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Lecture Notes: Clinical Anaesthesia GCAPR 7/2/04 5:31 PM Page Ii

GCAPR 7/2/04 5:31 PM Page i

Lecture Notes: Clinical Anaesthesia GCAPR 7/2/04 5:31 PM Page ii

To Karen, Matthew and Mark. Thank you for the never-ending help, encouragement, humour and always having so much patience. GCAPR 7/2/04 5:31 PM Page iii

Lecture Notes Clinical Anaesthesia

Carl L. Gwinnutt MB BS MRCS LRCP FRCA Consultant Anaesthetist Hope Hospital, Salford

Honorary Clinical Lecturer in Anaesthesia University of Manchester

Second Edition GCAPR 7/2/04 5:31 PM Page iv

© 2004 C. Gwinnutt © 1997 Blackwell Science Ltd Published by Blackwell Publishing Ltd

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First published 1997 Reprinted 1998, 1999, 2000, 2001, 2002 Second edition 2004

Library of Congress Cataloging-in-Publication Data Gwinnutt, Carl L. Lecture notes on clinical anaesthesia / Carl L. Gwinnutt.—2nd ed. p. ; cm. Includes bibliographical references and index. ISBN 1-4051-1552-1 1. . 2. . [DNLM: 1. Anesthesia. 2. —administration & dosage. WO 200 G9945L 2004] I. Title. RD81.G843 2004 617.9¢6—dc22 2004007261

ISBN 1-4051-1552-1

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Contents

Contributors vi Preface vii List of Abbreviations viii

1 Anaesthetic assessment and preparation for 1 2 Anaesthesia 15 3 Postanaesthesia care 71 4Management of perioperative emergencies and cardiac arrest 90 5 Recognition and management of the critically ill patient 112 6 Anaesthetists and chronic 139

Index 151

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Contributors

Tim Johnson Anthony McCluskey Consultant in and Anaesthesia Consultant in Anaesthesia and Intensive Care Hope Hospital Medicine Salford Stepping Hill Hospital Stockport Richard Morgan Consultant Anaesthetist Jas Soar Hope Hospital Consultant in Anaesthesia and Intensive Care Salford Medicine Southmead Hospital Bristol

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Preface

In the first edition, I asked the question, ‘Should will encounter before deciding on a career in medical students be taught anaesthesia?’ I firmly anaesthesia. On the other hand, it is also impor- believed that they should, and in the intervening tant that you are aware of the continuing essential years nothing has happened to change my view. role that many of my colleagues play in treating Indeed, with the continuing expansion of the roles and helping patients live with chronic pain prob- and responsibilities of anaesthetists, it is now more lems and the principles upon which these are important than ever that as medical students you based. understand that we do far more than provide the With this edition, I have endeavoured to identi- conditions under which surgery can be performed fy the skills you will need and the challenges you safely. I hope that this second edition reflects these will meet in the early years after qualification. The changes. book remains a skeleton on which to build, not Anaesthetists are increasingly responsible for the only from within other texts, but also with clinical development and care of patients preoperatively experience. I remain hopeful that if, after reading and postoperatively and in the recognition and this book, you feel motivated to learn by desire management of those who are critically ill. With rather than need I will be a little bit closer to the help of my colleagues, I have tried to reflect this achieving my aims. expanding role in the updated text, particularly as these are areas that as newly qualified doctors, you Carl Gwinnutt

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List of Abbreviations

AAGBI Association of Anaesthetists of Great GI gastrointestinal Britain & Ireland GTN glyceryl trinitrate ADH antidiuretic hormone HAFOE high airflow enrichment AED automated external defibrillator HDU high dependency unit ALS advanced life support HIV human immunodeficiency virus ALT alanine aminotransferase HR APC activated protein C HRT hormone replacement therapy APPT activated partial thromboplastin time ICP intracranial pressure ARDS acute respiratory distress syndrome ICU intensive care unit ASA American Society of Anesthesiologists I:E inspiratory:expiratory AST aspartate aminotransferase ILM intubating LMA ATN acute tubular necrosis IM intramuscular BLS basic life support INR international normalized ratio BNF British National Formulary IPPV intermittent positive pressure ventilation CAVH continuous arteriovenous haemofiltration IR immediate release CBF cerebral blood flow ITU intensive therapy unit CCU coronary care unit IV intravenous

CLCR creatinine clearance IVRA intravenous regional anaesthesia CNS JVP jugular venous pressure COPD chronic obstructive pulmonary LMA COX cyclo-oxygenase enzymes (COX-1, 2) LVEDP left ventricular end-diastolic pressure CPAP continuous positive airway pressure M6G -6-glucuronide CPR cardiopulmonary resuscitation MAC minimum alveolar concentration CSF cerebrospinal fluid MAP mean arterial pressure CT computerized tomography MET Medical Emergency Team CVP central venous pressure MH malignant hyperpyrexia () CVS cardiovascular system MI CVVH venovenous haemofiltration MOFS multiple organ failure syndrome DIC disseminated intravascular coagulation MR modified release DNAR do not attempt resuscitation MRI magnetic resonance imaging ECF extracellular fluid MRSA methicillin-resistant Staphylococcus aureus EMLA eutectic mixture of local anaesthetics NSAID non-steroidal anti-inflammatory drug ENT ear, nose and throat NICE National Institute for Clinical Excellence

FEV1 forced expiratory volume in 1 second NIPPV non-invasive positive pressure ventilation FFP fresh frozen plasma OCP oral contraceptive pill FRC functional residual capacity PAFC pulmonary artery flotation catheter FVC forced vital capacity PCA patient-controlled analgesia GCS Glasgow Coma Scale PCV pressure-controlled ventilation GFR glomerular filtration rate PEA pulseless electrical activity GGT gamma glutamyl transferase PEEP positive end expiratory pressure

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List of Abbreviations

PEFR peak expiratory flow rate TCI target controlled infusion PHN postherpetic neuralgia TENS transcutaneous electrical nerve stimulation PMGV piped medical gas and vacuum system TIVA total intravenous anaesthesia PONV postoperative and vomiting TNF tumour necrosis factor PT prothrombin time TOE transoesophageal echocardiography RS respiratory system TOF train-of-four RSI TPN total parenteral nutrition SIMV synchronized intermittent mandatory VF ventricular fibrillation ventilation VIE vacuum-insulated evaporator SIRS systemic inflammatory response syndrome V/Q ventilation/perfusion

SpO2 oxygenation of the peripheral tissues VT ventricular SVR systemic vascular resistance

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greater detail are advised to consult the document The process of preoperative produced by the Association of Anaesthetists (see assessment Useful websites). By virtue of their training and experience, anaes- thetists are uniquely qualified to assess the risks in- Stage 1 — Screening herent in administering an anaesthetic. In an ideal world, all patients would be seen by their anaes- Not all patients need to be seen in a preoperative thetist sufficiently ahead of the planned surgery to assessment clinic by an anaesthetist. This stage minimize all risks without interfering with the aims to ‘filter’ patients appropriately. Screening to smooth running of the operating list. Until determine who needs to be seen is achieved by recently, for elective procedures, this took place using either a questionnaire or interview, the con- when the patient was admitted, usually the day be- tent of which has been determined with the agree- fore surgery. This visit also allowed the most suit- ment of the anaesthetic department. The process able anaesthetic technique to be determined, can be carried out in a number of ways: completion along with an explanation and reassurance for the of a questionnaire by the patient, nursing or other patient. However, in the presence of any coexisting staff who have received training, or occasionally by illness, there would be little time to improve the the patient’s GP. patient’s condition before surgery or to seek advice The patients screened who do not need to attend from other specialists. For these patients, surgery the preoperative assessment clinic to see an was often postponed and operating time wasted. anaesthetist: The recent attempts to improve efficiency by ad- • have no coexisting medical problems; mitting patients on the day of their planned surgi- • require no or only baseline investigations, the re- cal procedure further reduces the opportunity for sults of which are within normal limits (see Table an adequate anaesthetic assessment. This has led 1.2); to significant changes in the way patients undergo- • have no potential for, or history of, anaesthetic ing elective surgery are managed preoperatively difficulties; and, more recently, the introduction of clinics • require peripheral surgery for which complica- specifically for anaesthetic assessment. A variety of tions are minimal. models of ‘preoperative’ or ‘anaesthetic assess- On admission these patients will need to be for- ment’ clinics exist; the following is intended as an mally clerked and examined by a member of the outline of their functions. Those who require surgical team.

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The most obvious type of patient who fits into Nurses who have been specifically trained are par- this class are those scheduled for day case (ambula- ticipating increasingly in the preparation of these tory) surgery. These patients should be seen at the patients, by taking a history, performing an exami- time of admission by the anaesthetist, who will: nation and ordering appropriate investigations • confirm the findings of the screening; (see below). Alternatively it may be a member of • check the results of any baseline investigations; the surgical team. • explain the type of anaesthetic appropriate for The patients, who will need to be seen by the the procedure; anaesthetist, are those identified for whatever rea- • have the ultimate responsibility for deciding it is son as having actual or potential anaesthetic prob- safe to proceed. lems. This is often symptomatic concurrent disease despite optimal treatment, or previous or potential anaesthetic problems. Patients may also have been Stage 2 — The preoperative deferred initially for review by a medical specialist, assessment clinic for example cardiologist, to optimize medical The patients seen here are those who have been treatment. This allows the anaesthetist to: identified by the screening process as having • make a full assessment of the patient’s medical coexisting medical problems that: condition; • are well controlled with medical treatment; • review any previous anaesthetics administered; • are previously undiagnosed, for example dia- • evaluate the results of any investigations; betes, ; • request any additional investigations; • are less than optimally managed, for example • explain and document: hypertension, angina; • the anaesthetic options available and the po- • have abnormal baseline investigations; tential side-effects; • show a need for further investigations, for exam- • the risks associated with anaesthesia; ple pulmonary function tests, echocardiography; • discuss plans for postoperative care. • indicate previous anaesthetic difficulties, for The ultimate aim is to ensure that when the patient example difficult intubation; is admitted for surgery, the chances of being can- • suggest potential anaesthetic difficulties, for celled as a result of ‘unfit for anaesthesia’ are mini- example , previous or family history of mized. Clearly the time between the patient being prolonged apnoea after anaesthesia; seen in the assessment clinic and the date admitted • are to undergo complex surgery with or without for surgery cannot be excessive, and is generally planned admission to the intensive therapy unit between 4 and 6 weeks. (ITU) postoperatively. Once again, not all these patients will need to be The anaesthetic assessment seen by an anaesthetist in the clinic, although it is essential that anaesthetic advice from a senior Whoever is responsible for the anaesthetic assess- anaesthetist is readily available. Those who may not ment must take a full history, examine each pa- need to be seen by an anaesthetist include: tient and ensure that appropriate investigations • Patients with well-controlled concurrent are carried out. When performed by non-anaes- medical conditions, for example hypertension, thetic staff, a protocol is often used to ensure all the . They may need additional investigations relevant areas are covered. This section concen- that can be ordered according to an agreed proto- trates on features of particular relevance to the col and then re-assessed. anaesthetist. • Patients with previously undiagnosed or less than optimally managed medical problems. They can be referred to the appropriate specialist at this stage and then re-assessed.

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cators of perioperative complications, associated Present and past medical history with increased risk of perioperative cardiac mor- Of all the aspects of the patient’s medical history, bidity and mortality. Its severity is best described those relating to the cardiovascular and respiratory using a recognized scale, for example the New York systems are relatively more important. Heart Association classification (Table 1.1). Untreated or poorly controlled hypertension may lead to exaggerated cardiovascular responses Cardiovascular system during anaesthesia. Both hypertension and hy- Symptoms of the following problems must be potension can be precipitated, which increase the sought in all patients: risk of myocardial and cerebral ischaemia. The • ischaemic heart disease; severity of hypertension will determine the action • heart failure; required: • hypertension; • Mild (SBP 140–159mmHg, DBP 90–99mmHg) No • conduction defects, ; evidence that delaying surgery for treatment •peripheral vascular disease. affects outcome. Patients with a proven history of myocardial • Moderate (SBP 160–179mmHg, DBP 100–109 infarction (MI) are at a greater risk of perioperative mmHg) Consider review of treatment. If un- reinfarction, the incidence of which is related changed, requires close to avoid to the time interval between infarct and surgery. swings during anaesthesia and surgery. This time is variable. In a patient with an uncom- • Severe (SBP > 180mmHg, DBP > 109mmHg) At this plicated MI and a normal exercise test elective sur- level, elective surgery should be postponed due to gery may only need to be delayed by 6–8 weeks. the significant risk of myocardial ischaemia, The American Heart Association has produced arrhythmias and intracerebral haemorrhage. In an guidance for perioperative cardiovascular evalua- emergency, will require acute control with invasive tion (see Useful websites). monitoring. Heart failure is one of the most significant indi-

Table 1.1 New York Heart Association classification of cardiac function compared to Specific Activity Scale

NYHA functional classification Specific Activity Scale classification

Class I: Cardiac disease without limitation of physical Can perform activities requiring ≥7 mets activity Jog/walk at 5 mph, ski, play squash or basketball, No fatigue, palpitations, dyspnoea or angina shovel soil

Class II: Cardiac disease resulting in slight limitation of Can perform activities requiring ≥5 but <7 mets physical activity Walk at 4 mph on level ground, garden, rake, Asymptomatic at rest, ordinary physical activity weed, have sexual intercourse without stopping causes fatigue, palpitations, dyspnoea or angina

Class III: Cardiac disease causing marked limitation of Can perform activities requiring ≥2 but <5 mets physical activity Perform most household chores, play golf, push Asymptomatic at rest, less than ordinary activity the lawnmower, shower causes fatigue, palpitations, dyspnoea or angina

Class IV: Cardiac disease limiting any physical activity Patients cannot perform activities requiring ≥2 mets Symptoms of heart failure or angina at rest, Cannot dress without stopping because of increased with any physical activity symptoms; cannot perform any class III activities

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serve. In such circumstances other methods of as- Respiratory system sessment are required. The most readily available Enquire specifically about symptoms of: method of non-invasive assessment of cardiac • chronic obstructive lung disease; function in patients is some type of echocardiogra- • emphysema; phy (see below). • asthma; Other conditions which are important if identi- • infection; fied in the medical history: • restrictive lung disease. • Indigestion, heartburn and reflux Possibility of a Patients with pre-existing lung disease are more hiatus . If exacerbated on bending forward prone to postoperative chest infections, parti- or lying flat, this increases the risk of regurgitation cularly if they are also obese, or undergoing upper and aspiration. abdominal or thoracic surgery. If an acute upper • Rheumatoid disease Limited movement of joints infection is present, anaesthesia makes positioning for surgery difficult. Cervical and surgery should be postponed unless it is for a spine and tempero-mandibular joint involvement life-threatening condition. may complicate . There is often a chronic anaemia. • Diabetes An increased incidence of ischaemic Assessment of exercise tolerance heart disease, renal dysfunction, and autonomic An indication of cardiac and respiratory reserves and peripheral neuropathy. Increased risk of intra- can be obtained by asking the patient about their and postoperative complications, particularly hy- ability to perform everyday physical activities be- potension and infections. fore having to stop because of symptoms of chest • Neuromuscular disorders Coexisting heart disease pain, , etc. For example: may be worsened by anaesthesia and restrictive •How far can you walk on the flat? pulmonary disease (forced vital capacity (FVC) < 1 • How far can you walk uphill? L) predisposes to chest infection and the possibility • How many stairs can you climb before stopping? of the need for ventilatory support postoperatively. • Could you run for a bus? Care when using muscle relaxants. • Are you able to do the shopping? • Chronic renal failure Anaemia and electrolyte ab- • Are you able to do housework? normalities. Altered drug excretion restricts the • Are you able to care for yourself? choice of anaesthetic drugs. Surgery and dialysis The problem with such questions is that they are treatments need to be coordinated. very subjective and patients often tend to overesti- • Jaundice Altered drug metabolism, coagulopathy. mate their abilities! Care with administration. • Epilepsy Well-controlled epilepsy is not a major How can this be made more objective? problem. Avoid anaesthetic drugs that are poten- The New York Heart Association (NYHA) tially epileptogenic (e.g. enflurane; see Table 2.4). Classification of function is one system, but even this uses some subjective terms such as ‘ordinary’ Previous anaesthetics and operations and ‘slight’. The Specific Activity Scale grades com- mon physical activities in terms of their metabolic These may have occurred in hospitals or, less com- equivalents of activity or ‘mets’, and classifies pa- monly, dental . Enquire about any difficul- tients on how many mets they can achieve. The ties, for example: nausea, vomiting, dreams, two classifications are shown for comparison in awareness, postoperative jaundice. Check the Table 1.1. Unfortunately, not all patients can be as- records of previous anaesthetics to rule out or sessed in this way; for example those with severe clarify problems such as difficulties with intuba- musculoskeletal dysfunction may not be able to tion, allergy to drugs given, or adverse reactions exercise to the limit of their cardiorespiratory re- (e.g. malignant hyperpyrexia, see below). Some

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patients may have been issued with a ‘Medic Alert’ riage is reduced by carboxyhaemoglobin, and nico- type bracelet or similar device giving details or a tine stimulates the sympathetic nervous system, contact number. Although is now less causing tachycardia, hypertension and coronary popular for maintenance of anaesthesia, the ap- artery narrowing. Apart from the risks of chronic proximate date of previous anaesthetics should be lung disease and carcinoma, smokers have a signifi- identified if possible to avoid the risk of repeat expo- cantly increased risk of postoperative chest infec- sure (see page 33). Details of previous surgery may tions. Stopping smoking for 8 weeks improves reveal potential anaesthetic problems, for example the airways; for 2 weeks reduces their irritability; cardiac, pulmonary or cervical spine surgery. and for as little as 24h before anaesthesia decreases carboxyhaemoglobin levels. Help and advice should be available at the preoperative assessment Family history clinic. All patients should be asked whether there are any • Alcohol This is measured as units consumed per known inherited conditions in the family (e.g. week; >50 units/week causes induction of liver en- sickle-cell disease, porphyria). Have any family zymes and tolerance to anaesthetic drugs. The risk members experienced problems with anaesthesia; of alcohol withdrawal syndrome postoperatively a history of prolonged apnoea suggests pseudo- must be considered. cholinesterase deficiency (see page 34), and an un- • Drugs Ask specifically about the use of drugs for explained death malignant hyperpyrexia (see page recreational purposes, including type, frequency 98). Elective surgery should be postponed if any and route of administration. This group of patients conditions are identified, and the patient investi- is at risk of infection with hepatitis B and human gated appropriately. In the emergency situation, immunodeficiency virus (HIV). There can be diffi- anaesthesia must be adjusted accordingly, for culty with venous access following IV drug abuse example by avoidance of triggering drugs in a due to widespread thrombosis of veins. With- patient with a family history of malignant drawal syndromes can occur postoperatively. hyperpyrexia. • Pregnancy The date of the last menstrual period should be noted in all women of childbearing age. The anaesthetist may be the only person in theatre Drug history and allergies able to give this information if X-rays are required. Identify all medications, both prescribed and self- Anaesthesia increases the risk of inducing a spon- administered, including herbal preparations. Pa- taneous in early pregnancy. There is an tients will often forget about the oral contraceptive increased risk of regurgitation and aspiration in pill (OCP) and hormone replacement therapy late pregnancy. Elective surgery is best postponed (HRT) unless specifically asked. The incidence of until after delivery. use of medications rises with age and many of these drugs have important interactions with The examination anaesthetics. A current British National Formulary (BNF), or the BNF website, should be consulted As with the history, this concentrates on the car- for lists of the more common and important ones. diovascular and respiratory systems; the remaining Allergies to drugs, topical preparations (e.g. io- systems are examined if problems relevant to dine), adhesive dressings and foodstuffs should be anaesthesia have been identified in the history. At noted. the end of the examination, the patient’s airway is assessed to try and identify any potential prob- lems. If a regional anaesthetic is planned, the ap- Social history propriate (e.g. lumbar spine for central • Smoking Ascertain the number of cigarettes or the neural block) is examined. amount of tobacco smoked per day. Oxygen car-

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Cardiovascular system Observation of the patient’s anatomy

Look specifically for signs of: Look for: • arrhythmias; • limitation of mouth opening; • heart failure; •a receding mandible; • hypertension; • position, number and health of teeth; • valvular heart disease; • size of the tongue; •peripheral vascular disease. • soft tissue swelling at the front of the neck; Don’t forget to inspect the peripheral veins to iden- • deviation of the or trachea; tify any potential problems with IV access. • limitations in flexion and extension of the cervi- cal spine. Finding any of these suggests that intubation may Respiratory system be more difficult. However, it must be remembered Look specifically for signs of: that all of these are subjective. • respiratory failure; • impaired ventilation; Simple bedside tests • collapse, consolidation, pleural effusion; • additional or absent breath sounds. • Mallampati criteria The patient, sitting upright, is asked to open their mouth and maximally pro- trude their tongue. The view of the pharyngeal Nervous system structures is noted and graded I–IV (Fig. 1.1). Chronic disease of the peripheral and central Grades III and IV suggest difficult intubation. nervous systems should be identified and any evi- • With the head fully ex- dence of motor or sensory impairment recorded. It tended on the neck, the distance between the bony must be remembered that some disorders will point of the chin and the prominence of the thy- affect the cardiovascular and respiratory systems, roid cartilage is measured (Fig. 1.2). A distance of for example dystrophia myotonica and multiple less than 7cm suggests difficult intubation. sclerosis. • Wilson score Increasing weight, a reduction in head and neck movement, reduced mouth open- ing, and the presence of a receding mandible or Musculoskeletal system buck-teeth all predispose to increased difficulty Patients with connective tissue disorders should with intubation. have any restriction of movement and deformities • Calder test The patient is asked to protrude the noted. Patients suffering from chronic rheumatoid mandible as far as possible. The lower incisors will disease frequently have a reduced muscle mass, lie either anterior to, aligned with or posterior to peripheral neuropathies and pulmonary involve- the upper incisors. The latter two suggest reduced ment. Particular attention should be paid to the view at . patient’s cervical spine and temperomandibular None of these tests, alone or in combination, pre- joints (see below). dicts all difficult intubations. A Mallampati grade III or IV with a thyromental distance of <7cm pre- dicts 80% of difficult intubations. If problems are The airway anticipated, anaesthesia should be planned ac- All patients must have an assessment made of their cordingly. If intubation proves to be difficult, it airway, the aim being to try and predict those must be recorded in a prominent place in the pa- patients who may be difficult to intubate. tient’s notes and the patient informed.

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Grade I Grade II

Grade III Grade IV

Figure 1.1 The pharyngeal structures seen during the Mallampati assessment.

Investigations Additional investigations

There is little evidence to support the performance The following is a guide to those commonly re- of ‘routine’ investigations, and these should only quested. Again these will also be dependent on the be ordered if the result would affect the patient’s grade of surgery and the age of the patient. Further management. In patients with no evidence of concur- information can be found in Clinical Guideline 3, rent disease (ASA 1, see below), preoperative investi- published by NICE (see Useful websites). gations will depend on the extent of surgery • Urea and electrolytes: patients taking digoxin, and the age of the patient. A synopsis of the diuretics, steroids, and those with diabetes, renal current guidelines for these patients, issued by the disease, vomiting, diarrhoea. National Institute for Clinical Excellence (NICE), is • Liver function tests: known hepatic disease, a his- shown in Table 1.2. For each age group and tory of a high alcohol intake (>50 units/week), grade of surgery, the upper entry, shows ‘tests metastatic disease or evidence of malnutrition. recommended’ and the lower entry ‘tests to be • Blood sugar: diabetics, severe peripheral arterial considered’ (depending on patient characteristics). disease or taking long-term steroids. Dipstick urinalysis need only be performed in • Electrocardiogram (ECG): hypertensive, with symptomatic individuals. symptoms or signs of ischaemic heart disease, a cardiac or diabetics >40 years of age. • Chest X-ray: symptoms or signs of cardiac or respiratory disease, or suspected or known

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malignancy, where thoracic surgery is planned, or (COPD) or asthma. Measure peak expiratory flow

in those from areas of endemic tuberculosis who rate (PEFR), forced expiratory volume in 1s (FEV1) have not had a chest X-ray in the last year. and FVC. Patients who are dyspnoeic or cyanosed

• Pulmonary function tests: dyspnoea on mild exer- at rest, found to have an FEV1 <60% predicted, or tion, chronic obstructive pulmonary disease are to have thoracic surgery, should also have arte- rial blood gas analysed while air. • Coagulation screen: anticoagulation, a history of a diatheses or a history of liver disease or jaundice. • Sickle-cell screen (Sickledex): a family history of sickle-cell disease or where ethnicity increases the risk of sickle-cell disease. If positive, electrophore- sis for definitive diagnosis. • Cervical spine X-ray: rheumatoid arthritis, a history of major trauma or surgery to the neck or when difficult intubation is predicted.

Echocardiography

This is becoming increasingly recognized as a use- ful tool to assess left ventricular function in pa- tients with ischaemic or valvular heart disease, but whose exercise ability is limited, for example by se- vere osteoarthritis. The ejection fraction and cont- ractility can be calculated and any ventricular wall motion abnormalities identified. Similarly, ven- tricular function post-myocardial infarction can be assessed. In patients with valvular lesions, the de- gree of dysfunction can be assessed. In aortic stenosis an estimate of the pressure gradient across the valve is a good indication of the severity of the Figure 1.2 The thyromental distance. disease. As an echocardiogram is performed in

Table 1.2 Baseline investigations in patients with no evidence of concurrent disease (ASA 1)

Age of patient Minor surgery Intermediate surgery Major surgery Major ‘plus’ surgery

16–39 Nil Nil FBC FBC, RFT Consider Nil Nil RFT, BS Clotting, BS 40–59 Nil Nil FBC FBC, RFT Consider ECG ECG, FBC, BS ECG, BS, RFT ECG, BS, clotting 60–79 Nil FBC FBC, ECG, RFT FBC, RFT, ECG Consider ECG ECG, BS, RFT BS, CXR BS, clotting, CXR ≥80 ECG FBC, ECG FBC, ECG, RFT FBC, RFT, ECG Consider FBC, RFT RFT, BS BS, CXR, clotting BS, clotting, CXR

FBC: full blood count; RFT: renal function tests, to include sodium, potassium, urea and creatinine; ECG: electrocardiogram; BS: random blood glucose; CXR: chest X-ray. Clotting to include prothrombin time (PT), activated partial thromboplastin time (APTT), international normalized ratio (INR). Courtesy of National Institute for Clinical Excellence.

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patients at rest, it does not give any indication of • Cushing’s or Addison’s disease. what happens under stress. A stress echocardio- • Hypopituitarism. gram can be performed during which drugs are given to increase heart rate and myocardial work, Renal disease simulating the conditions the patient may en- • Chronic renal failure. counter, while monitoring changes in myocard- • Patients undergoing renal replacement therapy. ial performance. For example the inotrope dobutamine acts as a substitute for exercise whilst Haematological disorders monitoring the ECG for ischaemic changes (dobu- • Bleeding diatheses, for example haemophilia, tamine stress echocardiography). thrombocytopenia. • Therapeutic anticoagulation. •Haemoglobinopathies. Medical referral • Polycythaemia. Patients with coexisting medical (or surgical) con- • Haemolytic anaemias. ditions that require advice from other specialists • Leukaemias. should have been identified in the preoperative assessment clinic, not on the day of admission. Risk associated with anaesthesia Clearly a wide spectrum of conditions exist; the and surgery following are examples of some of the more com- monly encountered. At the end of the day the question that patients ask is ‘Doctor, what are the risks of having an anaesthetic?’ Cardiovascular disease These can be divided into two main groups. • Untreated or poorly controlled hypertension or heart failure. Minor • Symptomatic ischaemic heart disease, despite treatment (unstable angina). These are not life threatening and can occur even • Arrhythmias: uncontrolled atrial fibrillation, when anaesthesia has apparently been uneventful. paroxysmal supraventricular tachycardia, and Although classed as minor, the patient may not second and third degree heart block. share this view. They include: • Symptomatic or newly diagnosed valvular heart • failed IV access; disease, or congenital heart disease. • cut lip, damage to teeth, caps, crowns; • sore throat; Respiratory disease • headache; • Chronic obstructive pulmonary disease, particu- • postoperative nausea and vomiting; larly if dyspnoeic at rest. • retention of urine. • Bronchiectasis. • Asthmatics who are unstable, taking oral steroids Major or have a FEV1 <60% predicted. These may be life-threatening events. They Endocrine disorders include: • Insulin and non-insulin dependent diabetics • aspiration of gastric contents; who have ketonuria, glycated Hb (HbA1c) >10% or • hypoxic brain injury; a random blood sugar >12mmol/L. Local policy • myocardial infarction; will dictate referral of stable diabetics for peri- • cerebrovascular accident; operative management. • nerve injury; •Hypo- or hyperthyroidism symptomatic on cur- • chest infection. rent treatment. In the United Kingdom, the Confidential Enquiry

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Table 1.3 ASA physical status scale

Absolute Class Physical status mortality (%)

IA healthy patient with no organic or psychological disease process. The pathological process 0.1 for which the operation is being performed is localized and causes no systemic upset II A patient with a mild to moderate systemic disease process, caused by the condition to 0.2 be treated surgically or another pathological process, that does not limit the patient’s activities in any way; e.g. treated hypertensive, stable diabetic. Patients aged >80 years are automatically placed in class II III A patient with severe systemic disease from any cause that imposes a definite functional 1.8 limitation on activity; e.g. ischaemic heart disease, chronic obstructive lung disease IV A patient with a severe systemic disease that is a constant threat to life, e.g. unstable angina 7.8 VA moribund patient unlikely to survive 24 h with or without surgery 9.4

Note: ‘E’ may be added to signify an emergency operation.

into Perioperative Deaths (CEPOD 1987) revealed gery being undertaken, which leads to a degree of an overall of 0.7% in ap- inter-rater variability. However, patients placed in proximately 500000 operations. Anaesthesia was higher categories are at increased overall risk of considered to have been a contributing factor in perioperative mortality (Table 1.3). 410 deaths (0.08%), but was judged completely re- sponsible in only three cases — a primary mortality Multifactorial risk indicators rate of 1:185000 operations. When the deaths where anaesthesia contributed were analysed, the The leading cause of death after surgery is predominant factor was human error. myocardial infarction, and there is significant Clearly, anaesthesia itself is very safe, particu- morbidity from non-fatal infarction, particularly larly in those patients who are otherwise well. in those patients with pre-existing heart disease. Apart from human error, the most likely risk is Not surprisingly, attempts have been made to iden- from an adverse drug reaction or drug interaction. tify factors that will predict those at risk. One sys- However, anaesthesia rarely occurs in isolation and tem is the Goldman Cardiac Risk Index, used in when the risks of the surgical procedure and those patients with pre-existing cardiac disease undergo- due to pre-existing disease are combined, the risks ing non-cardiac surgery. Using their history, of morbidity and mortality are increased. Not sur- examination, ECG findings, general status and prisingly a number of methods have been de- type of surgery, points are awarded in each scribed to try and quantify these risks. category (Table 1.4). The points total is used to assign the patient to one of four classes; the risks of a perioperative car- Risk indicators diac event, including myocardial infarction, pul- The most widely used scale for estimating risk is monary oedema, significant arrhythmia and death the American Society of Anesthesiologists (ASA) are: classification of the patient’s physical status. The • class I (0–5 points) 1% patient is assigned to one of five categories de- • class II (6–12 points) 5% pending on any physical disturbance caused by • class III (13–25 points) 16% either pre-existing disease or the process for which • class IV (=26 points) 56% surgery is being performed. It is relatively subjec- This has been shown to be a more accurate predic- tive and does not take into account the type of sur- tor than the ASA classification.

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Table 1.4 Goldman Cardiac Risk Index

Points

History Age >70 years 5 Myocardial infarction within 6 months 10

Examination Third heart sound (gallop rhythm), raised JVP 11 Significant aortic stenosis 3

ECG Rhythm other than sinus, or presence of premature atrial complexes 7 >5 ventricular ectopics per minute 7

General condition

PaO2 <8 kPa or PaCO2 >7.5 kPa on air + - K <3.0 mmol/L; HCO3 <20 mmol/L Urea >8.5 mmol/L; creatinine >200 mmol/L Chronic liver disease Bedridden from non-cardiac cause For each criterion 3

Operation Intraperitoneal, intrathoracic, aortic 3 Emergency surgery 4

JVP: jugular venous pressure.

Table 1.5 Overall approximate risk (%) of major cardiac based on type of surgery and patient’s cardiac risk index

Patient risk index score

Class I Class II Class III Class IV Grade of surgery (0–5 points) (6–12 points) (13–25 points) (>26 points)

Minor surgery 0.3 1 3 19

Major non-cardiac surgery, >40 years 1.2 4 12 48

Major non-cardiac surgery, >40 years, 3 10 30 75 significant medical problem requiring consultation before surgery

Apart from any risk as a result of pre-existing car- Table 1.5. Major cardiac complication includes diac disease, the type of surgery the patient is un- myocardial infarction, cardiogenic pulmonary dergoing will also have its own inherent risks; oedema, ventricular tachycardia or cardiac death. carpal tunnel decompression will carry less risk Assessing a patient as ‘low risk’ is no more of a than a hip replacement, which in turn will be less guarantee that complications will not occur than risky than aortic aneurysm surgery. In other words, ‘high risk’ means they will occur; it is only a guide- the sicker the patient and the bigger the operation, line and indicator of probability. For the patient the greater the risk. This is clearly demonstrated in who suffers a complication the rate is 100%!

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Ultimately it is the risk/benefit ratio that must be to establish the patient’s medical history, drugs considered for each patient; for a given risk, it is taken regularly and allergies. In the trauma patient more sensible to proceed with surgery that offers enquire about the mechanism of injury. All emer- the greatest benefit. gency patients should be assumed to have a full Further reductions in the perioperative mortality stomach. Details may only be available from rela- of patients have been shown to result from im- tives and/or the ambulance crew. proving preoperative preparation by optimizing the patient’s physical status, adequately resuscitat- ing those who require emergency surgery, moni- Informing the patient and consent toring appropriately intraoperatively, and by providing suitable postoperative care in a high de- What is consent? pendency unit (HDU) or intensive care unit (ICU). It is an agreement by the patient to undergo a spe- cific procedure. Only the patient can make the de- Classification of operation cision to undergo the procedure, even though the Traditionally, surgery was classified as being either doctor will advise on what is required. Although elective or emergency. Recognizing that this was the need for consent is usually thought of in terms too imprecise, the National Confidential Enquiry of surgery, in fact it is required for any breach of a into Perioperative Deaths (NCEPOD) devised four patient’s personal integrity, including examina- categories: tion, performing investigations and administering • Elective: operation at a time to suit both patient an anaesthetic. A patient can refuse treatment or and surgeon; for example hip replacement, vari- choose a less than optimal option from a range of- cose veins. fered (providing an appropriate explanation has • Scheduled: an early operation but not imme- been given — see below), but he or she cannot insist diately life saving; operation usually within 3 on treatment that is not on offer. weeks; for example surgery for malignancy. • Urgent: operation as soon as possible after resus- What about an unconscious patient? citation and within 24h; for example intestinal ob- struction, major fractures. This usually arises in the emergency situation, for • Emergency: immediate life-saving operation, re- example a patient with a severe head injury. Asking suscitation simultaneous with surgical treatment; a relative or other individual to sign a consent form operation usually within 1h; for example major for surgery on the patient’s behalf is not appropri- trauma with uncontrolled haemorrhage, extra- ate, as no one can give consent on behalf of dural haematoma. another adult. Under these circumstances medical All elective and the majority of scheduled cases can staff are required to act ‘in the patient’s best inter- be assessed as described above. However, with ur- ests’. This will mean taking into account not only gent cases this will not always be possible; as much the benefits of the proposed treatment, but also information as possible should be obtained about any views previously expressed by the patient (e.g. any concurrent medical problems and their treat- refusal of blood transfusion by a Jehovah’s ment, and allergies and previous anaesthetics. The Witness). This will often require discussion with cardiovascular and respiratory systems should be the relatives, and this opportunity should be used examined and an assessment made of any poten- to inform them of the proposed treatment and the tial difficulty with intubation. Investigations rationale for it. All decisions and discussions must should only be ordered if they would directly affect be clearly documented in the patient’s notes. the conduct of anaesthesia. With true emergency Where treatment decisions are complex or not cases there will be even less or no time for assess- clear cut, it is advisable to obtain and document ment. Where possible an attempt should be made independent medical advice.

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quires their co-operation; for example a patient- What constitutes evidence of consent? controlled analgesia device (see page 84). Most patients will be asked to sign a consent form • Information on any substantial risks with before undergoing a procedure. However, there is serious adverse consequences associated with the no legal requirement for such before anaesthesia or anaesthetic technique planned. surgery (or anything else); the form simply shows Although the anaesthetist will be the best judge of evidence of consent at the time it was signed. Con- the type of anaesthetic for each individual, patients sent may be given verbally and this is often the should be given an explanation of the choices, case in anaesthesia. It is recommended that a writ- along with the associated benefits and risks in terms ten record of the content of the conversation be they can understand. Most patients will have an un- made in the patient’s case notes. derstanding of general anaesthesia — the of a drug, followed by loss of and lack of awareness throughout the surgical procedure. If What do I have to tell the patient? regional anaesthesia is proposed, it is essential that In obtaining consent it is essential the patient the patient understands and accepts that remaining is given an adequate amount of information conscious throughout is to be expected, unless in a form that they can understand. This will some form of is to be used. vary depending on the procedure, but may Most patients will want to know when they can include: last eat and drink before surgery, if they are to take • The environment of the anaesthetic room and normal medications and how they will manage who they will meet, particularly if medical stu- without a drink. Some will expect or request a dents or other healthcare professionals in training premed and in these circumstances the approxi- will be present. mate timing, route of administration and likely ef- • Establishing intravenous access and IV infusion. fects should be discussed. • The need for, and type of, any invasive Finally, before leaving ask if the patient has any monitoring. questions or wants anything clarified further. • What to expect during the establishment of a regional technique. Who should get consent? • Being conscious throughout surgery if a regional technique alone is used, and what they may From the above it is clear that the individual seek- hear. ing consent must be able to provide the necessary • Preoxygenation. information for the patient and be able to answer • Induction of anaesthesia. Although most com- the patient’s questions. This will require the indi- monly intravenous, occasionally it may be by vidual to be trained in, and familiar with, the pro- . cedure for which consent is sought, and is best • Where they will ‘wake up’. This is usually the re- done by a senior clinician or the person who is to covery unit, but after some surgery it may be the perform the procedure. With complex problems ICU or HDU. In these circumstances the patient consent may require a multidisciplinary approach. should be given the opportunity to visit the unit a The issues around consent in children and adults few days before and meet some of the staff. who lack capacity are more complex, and the • Numbness and loss of movement after regional reader should consult the Useful websites section anaesthesia. for more information. • The possibility of drains, catheters and drips. Their presence may be misinterpreted by the pa- Useful websites tient as indicating unexpected problems. • The possibility of a need for blood transfusion. http://www.aagbi.org/pdf/pre-operative_ass.pdf • Postoperative pain control, particularly if it re- [Preoperative assessment. The role of the anaes-

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thetist. The Association of Anaesthetists of Great http://www.ncepod.org.uk/dhome.htm Britain and Ireland. November 2001.] [Confidential Enquiry into Perioperative Deaths http://www.americanheart.org/ (CEPOD).] presenter.jhtml?identifier=3000370 http://www.doh.gov.uk/consent/index.htm [American College of / American [Department of Health (UK) guidance on con- Heart Association (ACC/AHA) Guideline Update sent.] on Perioperative Cardiovascular Evaluation for http://www.bma.org.uk/ap.nsf/Content/consenttk2 Noncardiac Surgery. 2002.] [BMA consent toolkit, second edition. February http://www.nice.org.uk/pdf/ 2003.] Preop_Fullguideline.pdf http://www.youranaesthetic.info/ [National Institute for Clinical Excellence http://www.aagbi.org/pub_patient.html#KNOW (NICE) guidance on preoperative tests. June [Patient information guides from the Associa- 2003.] tion of Anaesthetists of Great Britain and Ireland http://info.med.yale.edu/intmed/cardio/ and The Royal College of Anaesthetists.] imaging/contents.html http://www.BNF.org [Chest X-ray interpretation.] [British National Formulary.]

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the administration of lorazepam (as above) to pro- vide anterograde . Premedication originally referred to drugs administered to facilitate the induction and main- Anti-emetic (reduction of nausea tenance of anaesthesia (literally, preliminary and vomiting) medication). Nowadays, premedication refers to the administration of any drugs in the period be- Nausea and vomiting may follow the administra- fore induction of anaesthesia. Consequently, a tion of , either pre- or intraoperatively. wide variety of drugs are used with a variety of Certain types of surgery are associated with a aims, summarized in Table 2.1. higher incidence of postoperative nausea and vomiting (PONV), for example gynaecology. Un- fortunately, none of the currently used drugs can Anxiolysis be relied on to prevent or treat established PONV. The most commonly prescribed drugs are the ben- Drugs with anti-emetic properties are shown in zodiazepines. They produce a degree of sedation Table 2.2. and amnesia, are well absorbed from the gastroin- testinal tract and are usually given orally, 45– Antacid (modify pH and volume of 90mins preoperatively. Those most commonly gastric contents) used include temazepam 20–30mg, diazepam 10–20mg and lorazepam 2–4mg. In patients who Patients are starved preoperatively to reduce suffer from excessive somatic manifestations of the risk of regurgitation and aspiration of gastric anxiety, for example tachycardia, beta blockers acid at the induction of anaesthesia (see below). may be given. A preoperative visit and explanation This may not be possible or effective in some is often as effective as drugs at alleviating anxiety, patients: and sedation does not always mean lack of anxiety. • those who require emergency surgery; • those who have received opiates or are in pain will show a significant delay in gastric emptying; Amnesia • those with a hiatus hernia, who are at an in- Some patients specifically request that they not creased risk of regurgitation. have any recall of the events leading up to anaes- A variety of drug combinations are used to try and thesia and surgery. This may be accomplished by increase the pH and reduce the volume.

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• Oral sodium citrate (0.3M):30mL orally operatively by glycopyrrolate, 0.2–0.4mg intra- immediately preinduction, to chemically neu- muscularly (IM). Many anaesthetists would con- tralize residual acid. sider an IV dose given at induction more effective.

• Ranitidine (H2 antagonist): 150mg orally 12 hourly and 2 hourly preoperatively. Antisympathomimetic effects • :10mg orally preoperatively. Increases both gastric emptying and lower Increased sympathetic activity can be seen at intu- oesophageal sphincter tone. Often given in bation, causing tachycardia and hypertension. conjunction with ranitidine. This is undesirable in certain patients, for example • Omeprazole (proton pump inhibitor):40mg 3–4 those with ischaemic heart disease or raised in- hourly preoperatively. tracranial pressure. These responses can be If a naso- or orogastric tube is in place, this can be attenuated by the use of beta blockers given used to aspirate gastric contents. preoperatively (e.g. atenolol, 25–50mg orally) or intravenously at induction (e.g. esmolol). Peri- operative beta blockade may also decrease the inci- Anti-autonomic effects dence of adverse coronary events in high risk patients having major surgery. An alternative is to effects give a potent at induction of anaesthesia, for example , alfentanil or . (a) Reduce salivation (antisialogogue), for exam- ple during fibreoptic intubation, surgery or instru- mentation of the oral cavity or Analgesia anaesthesia. Although the oldest form of premedication, anal- (b) Reduce the vagolytic effects on the heart, for gesic drugs are now generally reserved for patients example before the use of suxamethonium who are in pain preoperatively. The most com- (particularly in children), during surgery on the monly used are morphine, pethidine and fentanyl. extra ocular muscles (squint correction), or during Morphine was widely used for its effects elevation of a fractured zygoma. Atropine and but is relatively poor as an and has hyoscine have now largely been replaced pre- largely been replaced by the . Opi- ates have a range of unwanted side-effects, includ-

Table 2.1 The 6 As of premedication ing nausea, vomiting, respiratory depression and delayed gastric emptying. • Anxiolysis • Amnesia • Anti-emetic Miscellaneous • Antacid A variety of other drugs are commonly given pro- • Anti-autonomic • Analgesia phylactically before anaesthesia and surgery; for example:

Table 2.2 Commonly used anti-emetic drugs, dose and route of administration

Type of drug Example Usual dose

Dopamine antagonists Metoclopramide 10 mg orally or IV 5-hydroxytryptamine antagonists 4–8 mg orally or IV 50 mg IM or IV Hyoscine 1 mg patch

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• steroids: to patients on long-term treatment Patients at increased risk of aspiration or who have received them within the past 3 months; • Delayed gastric emptying: • : to patients with prosthetic or • recent trauma; diseased heart valves, or undergoing joint • ; replacement; • pregnancy; • anticoagulants: as prophylaxis against deep • alcohol, opiates, anticholinergics; venous thrombosis; •autonomic neuropathy (diabetes mellitus). • transdermal glyceryl trinitrate (GTN): as patches in • Gastro-oesophageal reflux: patients with ischaemic heart disease to reduce the • symptoms of, or known hiatus hernia; risk of coronary ischaemia; • obesity; • eutectic mixture of local anaesthetics (EMLA): a • pregnancy, children; topically applied local anaesthetic cream to reduce • position for surgery (steep head-down). the pain of inserting an IV cannula. These patients will benefit from the methods described above to reduce gastric volume and increase the pH of the contents. In the trauma The majority of the patient’s own regular medications patient the time from last meal to injury may be a should be taken as normal, unless instructed otherwise better indicator of the gastric volume. by the anaesthetist.

Managing the airway

Preoperative starvation Maintenance of a patent airway is an essential pre- requisite for the safe and successful conduct of Traditionally, patients were starved of both food anaesthesia. However, it is a skill that should be ac- and fluids for prolonged periods preoperatively, quired by all doctors, as during resuscitation pa- but it is now increasingly recognized that, apart tients often have an obstructed airway either as the from certain groups with an increased risk of aspi- cause or result of their loss of consciousness. The ration, this is not necessary. descriptions of airway management techniques that follow are intended to supplement practice Guidelines for normal healthy patients either on a manikin or, preferably, on an anaes- undergoing elective surgery thetized patient under the direction of a skilled anaesthetist. • No solid food for 6h preoperatively. • Clear fluids can be taken up to 2h preopera- tively; these include water, black tea or coffee, Basic techniques pulpless fruit juice. Anaesthesia frequently results in loss of the airway, • Milk is not allowed as it flocculates in gastric acid and this is most easily restored by a combination of and the fat delays gastric emptying. the head tilt and a jaw thrust (see page 100). When • Chewing gum does not increase gastric volume holding a facemask in position with the index fin- and is best treated as for clear fluids. ger and thumb, the jaw thrust is achieved by lifting • Normal medications can be taken with a small the angle of the mandible with the remaining fin- volume of water. gers of one or both hands. The overall effect desired • The use of opiates or anticholinergics as is that the patient’s mandible is ‘lifted’ into the premedicants has little effect on gastric volume. mask rather than that the mask is being pushed into the face (Fig. 2.1).

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Oropharyngeal airway

• Curved plastic tubes, flattened in cross-section and flanged at the oral end. They lie over the tongue, preventing it from falling back into the . •Available in a variety of sizes suitable for all pa- tients, from neonates to large adults. The com- monest sizes are 2–4, for small to large adults, respectively. • An estimate of the size required is given by com- paring the airway length with the vertical distance between the patient’s incisor teeth and the angle of the jaw. • Initially inserted ‘upside down’ as far as the back of the hard palate (Fig. 2.2a), rotated 180° (Fig. 2.2b) and fully inserted until the flange lies in front of the teeth, or gums in an edentulous patient (Fig. 2.2c,d). Figure 2.1 Mask being held on a patient’s face. Nasopharyngeal airway

• Round, malleable plastic tubes, bevelled at the Facemasks pharyngeal end and flanged at the nasal end. •A commonly used type in adults is the BOC •Sized on their internal diameter in millimetres, anatomical facemask (Fig. 2.1), designed to fit the length increasing with diameter. The common contours of the face with the minimum of sizes in adults are 6–8mm, for small to large adults, pressure. respectively. • Leakage of anaesthetic gases is minimized by an •A guide to the correct size is made by comparing air-filled cuff around the edge. the diameter to the external nares. • Masks are made in a variety of sizes, and the • Prior to insertion, the patency of the nostril smallest one that provides a good seal should be (usually the right) should be checked and the air- used. way lubricated. • Some masks have a transparent body allowing • The airway is inserted along the floor of the nose, identification of vomit, making them popular for with the bevel facing medially to avoid catching resuscitation. the turbinates (Fig. 2.3). • All masks must be disinfected between each •A safety pin may be inserted through the flange patient use. Alternatively single use masks are to prevent inhalation of the airway. available. • If obstruction is encountered, force should not be used as severe bleeding may be provoked. Instead, the other nostril can be tried. Simple adjuncts

The oropharyngeal (Guedel) airway, and to a lesser Problems with airways extent the nasopharyngeal airway, are used in con- junction with the techniques described above to Snoring, indrawing of the supraclavicular, help maintain the airway after the induction of suprasternal and intercostal spaces, use of the ac- anaesthesia. cessory muscles or paradoxical respiratory move-

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Anaesthesia Chapter 2

(a) (b)

Figure 2.2 The sequence of inserting (c) (d) an oropharyngeal airway.

ment (see-saw ) suggest that the above The laryngeal mask airway (LMA) methods are failing to maintain a patent airway. Other problems with these techniques include: Originally designed for use in spontaneously • inability to maintain a good seal between the pa- breathing patients, it consists of a ‘mask’ that sits tient’s face and the mask, particularly in those over the laryngeal opening, attached to which is a without teeth; tube that protrudes from the mouth and connects • fatigue, when holding the mask for prolonged directly to the anaesthetic breathing system. On periods; the perimeter of the mask is an inflatable cuff that • the risk of aspiration, due to the loss of upper air- creates a seal and helps to stabilize it (Fig. 2.4a). The way reflexes; LMA is produced in a variety of sizes suitable for all • the anaesthetist not being free to deal with any patients, from neonates to adults, with sizes 3, 4 other problems that may arise. and 5 being the most commonly used in female The laryngeal mask airway or and male adults. Patients can be ventilated via the may be used to overcome these problems. LMA provided that high inflation pressures are avoided, otherwise leakage occurs past the cuff. This reduces ventilation and may cause gastric in- flation. The LMA is reusable, provided that it is

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sterilized between each patient. There are now four additional types of LMAs available: •A version with a reinforced tube to prevent kink- ing (Fig. 2.4b). • The Proseal LMA (Fig. 2.4c): this has an addi- tional posterior cuff to improve the seal around the larynx and reduce leak when the patient is venti- lated. It also has a secondary tube to allow drainage of gastric contents. • The intubating LMA (Fig. 2.4d): as the name suggests this device is used as a conduit to perform tracheal intubation without the need for laryn- goscopy (see Tracheal intubation, below). •A disposable version of the original for single (a) use, for example in infected cases. The use of the laryngeal mask overcomes some of the problems of the previous techniques: • It is not affected by the shape of the patient’s face or the absence of teeth. • The anaesthetist is not required to hold it in po- sition, avoiding fatigue and allowing any other problems to be dealt with. • It significantly reduces the risk of aspiration of re- gurgitated gastric contents, but does not eliminate it completely. Its use is relatively contraindicated where there is an increased risk of regurgitation, for example in emergency cases, pregnancy and patients with a (b) hiatus hernia. The LMA has proved to be a valuable aid in those patients who are difficult to intubate, as it can usually be inserted to facilitate oxygena- tion while additional help or equipment is ob- tained (see below).

Technique for insertion of the standard LMA

The patient’s reflexes must be suppressed to a level similar to that required for the insertion of an (c) oropharyngeal airway to prevent coughing or . Figure 2.3 Insertion of a nasopharyngeal airway. • The cuff is deflated (Fig. 2.5a) and the mask lightly lubricated. •A head tilt is performed, the patient’s mouth opened fully and the tip of the mask inserted along the hard palate with the open side facing but not touching the tongue (Fig. 2.5b).

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• The mask is further inserted, using the index fin- ger to provide support for the tube (Fig. 2.5c). Eventually, resistance will be felt at the point where the tip of the mask lies at the upper oesophageal sphincter (Fig. 2.5d). • The cuff is now fully inflated using an air-filled attached to the valve at the end of the pilot tube (Fig. 2.5e). • The laryngeal mask is secured either by a length (a) of bandage or adhesive strapping attached to the protruding tube. •A ‘bite block’ may be inserted to reduce the risk of damage to the LMA at recovery.

Tracheal intubation

This is the best method of providing and securing a clear airway in patients during anaesthesia and re- (b) suscitation, but success requires abolition of the la- ryngeal reflexes. During anaesthesia, this is usually achieved by the administration of a (see below). Deep inhalational anaesthe- sia or local anaesthesia of the larynx can also be used, but these are usually reserved for patients where difficulty with intubation is anticipated, for example in the presence of airway tumours or im- (c) mobility of the cervical spine.

Common indications for tracheal intubation

•Where muscle relaxants are used to facilitate sur- gery (e.g. abdominal and thoracic surgery), thereby necessitating the use of . • In patients with a full stomach, to protect against aspiration. • Where the position of the patient would make airway maintenance difficult, for example the lateral or prone position. • Where there is competition between surgeon and anaesthetist for the airway (e.g. operations on (d) the head and neck). • Where controlled ventilation is utilized to im- Figure 2.4 From the top down: (a) standard laryngeal mask prove surgical access (e.g. neurosurgery). airway (LMA); (b) reinforced LMA with close-up of rein- forcement; (c) Proseal LMA; (d) intubating LMA with tra- • In those patients in whom the airway cannot be cheal tube passing through the mask. satisfactorily maintained by any other technique. • During cardiopulmonary resuscitation.

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(a)

(b) (c)

Figure 2.5 (a-e) Sequence of events (d) (e) in the insertion of a laryngeal mask airway (LMA).

• Syringe: to inflate the cuff once the tube is in Equipment for tracheal intubation place. The equipment used will be determined by the cir- • Catheter mount: or ‘elbow’ to connect the tube to cumstances and by the preferences of the indivi- the anaesthetic system or ventilator tubing. dual anaesthetist. The following is a list of the basic • Suction: switched on and immediately to hand in needs for adult oral intubation. case the patient vomits or regurgitates. • Laryngoscope: with a curved (Macintosh) blade • Stethoscope: to check correct placement of the and functioning light. tube by listening for breath sounds during • Tracheal tubes (cuffed): in a variety of sizes. The ventilation. internal diameter is expressed in millimetres and • Extras:a semi-rigid introducer to help mould the the length in centimetres. They may be lightly tube to a particular shape; Magill’s forceps, de- lubricated. signed to reach into the pharynx to remove debris • For males: 8.0–9.0mm internal diameter, or direct the tip of a tube; bandage or tape to secure 22–24cm length. the tube. • For females: 7.5–8.5mm internal diameter, 20–22cm length.

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• Double lumen tubes are effectively two tubes Tracheal tubes welded together side-by-side, with one tube ex- Mostly manufactured from plastic (PVC), and for tending distally beyond the other. They are used single use to eliminate cross-infection (Fig. 2.6B). during thoracic surgery, and allow one lung to be They are available in 0.5mm diameter intervals, deflated whilst ventilation is maintained via the and long enough to be used orally or nasally. A bronchial portion in the opposite lung (Fig. 2.6E). standard 15mm connector is provided to allow • Uncuffed tubes are used in children up to connection to the breathing system. approximately 10 years of age as the narrowing in In adult anaesthesia, a with an in- the subglottic region provides a natural seal (Fig. flatable cuff is used to prevent leakage of anaes- 2.6A). thetic gases back past the tube when positive pressure ventilation is used. This also helps prevent aspiration of any foreign material into the lungs. The technique of oral intubation The cuff is inflated by injecting air via a pilot tube, at the distal end of which is a one-way valve to pre- Preoxygenation vent deflation and a small ‘balloon’ to indicate when the cuff is inflated. A wide variety of All patients who are to be intubated are asked to specialized tubes have been developed, examples breathe 100% oxygen via a close-fitting facemask of which are shown in Fig. 2.6. for 2–3mins (‘preoxygenation’). This provides a • Reinforced tubes are used to prevent kinking and reservoir of oxygen in the patient’s lungs, reducing subsequent obstruction as a result of the position- the risk of if difficulty is encountered with ing of the patient’s head (Fig. 2.6C). intubation. Once this has been accomplished, the • Preformed tubes are used during surgery on the appropriate drugs will be administered to render head and neck, and are designed to take the con- the patient unconscious and abolish laryngeal nections away from the surgical field (Fig. 2.6D). reflexes.

Figure 2.6 Tracheal tubes: (A) paedia- tric (uncuffed); (B) adult (cuffed); (C) reinforced (close-up showing rein- forcement); (D) preformed (RAE); and (E) double lumen (close-up showing tracheal and bronchial cuffs).

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Tip of Tongue laryngoscope pushed in vallecula to left False cords — aryepiglottic folds True cords Laryngeal opening (tracheal rings just to left)

Figure 2.7 A view of the larynx at laryngoscopy.

Positioning Intubation

The patient’s head is placed on a small pillow with The tracheal tube is introduced into the right side the neck flexed and the head extended at the of the mouth, advanced and seen to pass through the atlanto-occipital joint, the ‘sniffing the morning cords until the cuff lies just below the cords. The air’ position. The patient’s mouth is fully opened tube is then held firmly and the laryngoscope is using the index finger and thumb of the right hand carefully removed, and the cuff is inflated suffi- in a scissor action. ciently to prevent any leak during ventilation. Finally the position of the tube is confirmed and secured in place. Laryngoscopy For nasotracheal intubation a well-lubricated The laryngoscope is held in the left hand and the tube is introduced, usually via the right nostril blade introduced into the mouth along the right- along the floor of the nose with the bevel pointing hand side of the tongue, displacing it to the left. medially to avoid damage to the turbinates. It is ad- The blade is advanced until the tip lies in the gap vanced into the oropharynx, where it is usually between the base of the tongue and the epiglottis, visualized using a laryngoscope in the manner de- the vallecula. Force is then applied in the direction in scribed above. It can then either be advanced di- which the handle of the laryngoscope is pointing. The rectly into the larynx by pushing on the proximal effort comes from the upper arm not the wrist, to end, or the tip picked up with Magill’s forceps lift the tongue and epiglottis to expose the larynx, (which are designed not to impair the view of the seen as a triangular opening with the apex anteri- larynx) and directed into the larynx. The proce- orly and the whitish coloured true cords laterally dure then continues as for oral intubation. (Fig. 2.7). The intubating LMA (ILM)

This is a modification of the LMA in which the mask part is almost unchanged, but a shorter,

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wider metal tube with a 90° bend in it replaces the Hypoxia flexible tube (Fig. 2.4d). A handle is attached to the tube. It is inserted by holding the handle rather Due to: than using one’s index finger as a guide, and sits • Unrecognized oesophageal intubation If there is opposite the laryngeal opening. A specially de- any doubt about the position of the tube it should signed reinforced, cuffed, tracheal tube can then be be removed and the patient ventilated via a inserted, and, due to the shape and position of the facemask. ILM, will almost always pass into the trachea. Once • Failed intubation and inability to ventilate the pa- it has been confirmed that the tube lies in the tient This is usually a result of abnormal anatomy trachea, the ILM can either be left in place or re- or airway pathology. Many cases are predictable at moved. This device has proved to be very popular the preoperative assessment (see page 6). in cases where direct laryngoscopy does not give a • Failed ventilation after intubation Possible causes good view of the larynx and tracheal intubation include the tube becoming kinked, disconnected, fails. or inserted too far and passing into one main bronchus; severe and tension pneumothorax. Confirming the position of the • Aspiration Regurgitated gastric contents can tracheal tube cause blockage of the airways directly, or secondary This can be achieved using a number of to laryngeal spasm and bronchospasm. Cricoid techniques: pressure can be used to reduce the risk of regurgita- • Measuring the in expired gas (capnog- tion prior to intubation (see below). raphy): less than 0.2% indicates oesophageal intubation. Trauma • Oesophageal detector: a 50mL syringe is attached to the tracheal tube and the plunger rapidly with- • Direct During laryngoscopy and insertion of the drawn. If the tracheal tube is in the oesophagus, re- tube, damage to lips, teeth, tongue, pharynx, lar- sistance is felt and air cannot be aspirated; if it is in ynx, trachea, and nose and nasopharynx during the trachea, air is easily aspirated. nasal intubation; causing soft tissue swelling or • Direct visualization: of the tracheal tube passing bleeding. between the vocal cords. • Indirect To the recurrent laryngeal nerves, and • Fogging: on clear plastic tube connectors during the cervical spine and cord, particularly where expiration. there is pre-existing degenerative disease or • Less reliable signs are: trauma. • diminished breath sounds on auscultation; • decreased chest movement on ventilation; Reflex activity • gurgling sounds over the epigastrium and ‘burping’ sounds as gas escapes; • Hypertension and arrhythmias Occurs in response •a decrease in detected by to laryngoscopy and intubation. May jeopardize . This occurs late, particularly if patients with coronary artery disease. In patients at the patient has been preoxygenated. risk, specific action is taken to attenuate the re- sponse; for example pretreatment with beta block- ers or potent (fentanyl, remifentanil). Complications of tracheal intubation • Vomiting This may be stimulated when laryn- The following complications are the more com- goscopy is attempted in patients who are inade- mon ones, not an attempt to cover all occurrences. quately anaesthetized. It is more frequent when there is material in the stomach; for example in emergencies when the patient is not starved, in

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patients with intestinal obstruction, or when gas- Cricoid pressure (Sellick’s manoeuvre) tric emptying is delayed, as after opiate analgesics or following trauma. Regurgitation and aspiration of gastric contents are • Laryngeal spasm Reflex adduction of the vocal life-threatening complications of anaesthesia and cords as a result of stimulation of the epiglottis or every effort must be made to minimize the risk. larynx. Preoperatively, patients are starved to reduce gas- tric volume and drugs may be given to increase pH. At induction of anaesthesia, cricoid pressure pro- Difficult intubation vides a physical barrier to regurgitation. As the Occasionally, intubation of the trachea is made is the only complete ring of carti- difficult because of an inability to visualize the lage in the larynx, pressure on it, anteroposteriorly, larynx. This may have been predicted at the forces the whole ring posteriorly, compressing the preoperative assessment or may be unexpected. A oesophagus against the body of the sixth cervical variety of techniques have been described to help vertebra, thereby preventing regurgitation. An as- solve this problem and include the following: sistant, using the thumb and index finger, applies •Manipulation of the thyroid cartilage by back- pressure whilst the other hand is behind the pa- wards and upwards pressure by an assistant to try tient’s neck to stabilize it (Fig. 2.8). Pressure is and bring the larynx or its posterior aspect into applied as the patient loses consciousness and view. maintained until the tube has been inserted, the • At laryngoscopy, a gum elastic bougie, 60cm cuff inflated and correct position confirmed. It long, is inserted blindly into the trachea, over should be maintained even if the patient starts to which the tracheal tube is ‘railroaded’ into place. actively vomit, as the risk of aspiration is greater •A fibreoptic bronchoscope is introduced into the than the theoretical risk of oesophageal rupture. If trachea via the mouth or nose, and is used as a vomiting does occur, the patient should be turned guide over which a tube can be passed into the tra- onto his or her side to minimize aspiration. chea. This technique has the advantage that it can be used in either anaesthetized or awake patients. Can’t intubate, can’t ventilate • An LMA or ILM can be inserted and used as a conduit to pass a tracheal tube directly or via a In most patients who are difficult to intubate, a fibreoptic scope. patent airway and ventilation can be maintained

Figure 2.8 Sellick’s manoeuvre. Note the position of the thyroid cartilage marked on the patient’s neck.

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using one or more of the techniques described Intravenous induction of anaesthesia above. Rarely, a patient may be both difficult to intubate and ventilate. This is a life-threatening This is most frequently achieved in adults by the IV emergency and may require the anaesthetist to re- injection of a drug. Consciousness is lost rapidly as sort to one of the emergency techniques described the concentration of the drug in the brain rises below. very quickly. The drug is then redistributed to other tissues and the plasma concentration falls; this is followed by a fall in brain concentration and Emergency airway techniques the patient recovers consciousness. Despite a short These must only be used when all other techniques duration of action, complete elimination, usually have failed to maintain oxygenation. by hepatic metabolism, may take considerably • Needle cricothyroidotomy The cricothyroid mem- longer and lead to accumulation. Consequently, brane is identified and punctured using a large bore most drugs are not given repeatedly to maintain cannula (12–14 gauge) attached to a syringe. Aspi- anaesthesia. Currently, the only exception to this ration of air confirms that the tip of the cannula is (see below). Whichever drug is used, lies within the trachea. The cannula is then angled the dose required to induce anaesthesia will be to about 45° caudally and advanced off the needle dramatically reduced in those patients who into the trachea (Fig. 2.9). A high-flow oxygen sup- are elderly, frail, have compromise of their ply is then attached to the cannula and insufflated cardiovascular system or are hypovolaemic. A for 1s, followed by a 4s rest. Expiration occurs via synopsis of the drugs commonly used is given in the upper airway as normal. This technique oxy- Table 2.3. genates the patient but only results in minimal car- bon dioxide elimination, and is therefore limited Inhalational induction of anaesthesia to about 30mins use while a definitive airway is created. Breathing an inhalational anaesthetic in oxygen or • Surgical cricothyroidotomy This involves making in a mixture of oxygen and can be an incision through the cricothyroid membrane to used to induce anaesthesia. As the concentration of allow the introduction of a 5.0–6.0mm diameter the anaesthetic in the brain increases slowly, tracheostomy tube or tracheal tube (Fig. 2.10). It is occurs but more slowly than more difficult to perform, and results in signifi- with an IV drug. Adequacy (‘depth’) of anaesthesia cantly more bleeding than the above. However, is assessed (and overdose avoided) using clinical once a tube has been inserted the patient can be signs or ‘stages of anaesthesia’; the original ventilated, ensuring oxygenation, elimination of description was based on using ether, but the main carbon dioxide and suction of the airway to re- features can still be seen using modern drugs. The move any blood or debris. signs are modified by the concurrent administra- tion of opiate or anticholinergic drugs. Currently, sevoflurane is the most popular anaesthetic used for Drugs used during general this technique. Inhalation induction of anaesthesia anaesthesia is used when IV induction is not practical, for exam- Anaesthetists have to be familiar with a wide range ple in: of drugs that, unlike in most other branches of •a patient with a lack of suitable veins; medicine, are almost always given parenterally: • an uncooperative child; either intravenously or via inhalation. In addition • patients with a needle phobia; to their effects on the central nervous system • patients with airway compromise, in which an (CNS), most drugs have undesirable actions on IV drug may cause apnoea, and ventilation and many other body systems, of which the anaes- oxygenation become impossible, with catastro- thetist must be fully aware. phic results.

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Cricothyroid membrane

Thyroid cartilage Cricoid cartilage Trachea

(a)

Figure 2.9 (a) Needle cricothyroido- tomy. (b) Photograph of oxygen deliv- ery system (Manujet) attached to an intravenous cannula. The pressure of oxygen delivered is controlled by the black knob and displayed on the dial. Inset; preformed cannula and stylet for use as an alternative to an IV can- nula for cricothyroid puncture, with integral wings to aid securing of the (b) device.

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Tracheostomy tube with 15 mm connector

Trachea

Figure 2.10 Surgical cricothyroido- tomy with insertion of small-diameter Thyroid cartilage Cricoid cartilage tracheostomy tube.

The stages of anaesthesia As well as the above, the anaesthetic will have ef- fects on all of the other body systems, which will need appropriate monitoring. First stage

This lasts until consciousness is lost. The pupils Maintenance of anaesthesia will be normal in size and reactive, muscle tone is normal and breathing uses intercostal mus- This can be achieved either by using one of a vari- cles and the diaphragm. ety of inhalational anaesthetics in oxygen with or without nitrous oxide, or by an intravenous infu- sion of a drug, most commonly propofol. Second stage

In this period there may be breath-holding, Inhalational anaesthesia struggling and coughing. It is often referred to as the stage of excitation. The pupils will be di- Inhalational anaesthetics are a group of halogena- lated and there is loss of the eyelash reflex. ted hydrocarbons with relatively low boiling points. A ‘vaporizer’ is used to produce an accurate concentration in the inspired gas mixture. Nitrous Third stage oxide is the only other drug in this category. The This is the stage of surgical anaesthesia. There is inspired concentration of all of these compounds reduction in respiratory activity, with progres- is expressed as the percentage by volume. A synop- sive intercostal . Muscle tone is also re- sis of the drugs used is given in Table 2.4. duced and laryngeal reflexes are lost. The pupils There are two concepts that will help in under- start by being slightly constricted and gradually standing the use of inhalational anaesthetics: dilate. This stage ends with diaphragmatic minimum alveolar concentration and solubility. paralysis. Minimum alveolar concentration To compare potencies and side-effects of the in- Fourth stage halational anaesthetics, rather than simply com- This constitutes an anaesthetic catastrophe, paring a fixed inspired concentration, the concept with apnoea, loss of all reflex activity and fixed of minimum alveolar concentration (MAC) is used. dilated pupils. This is the concentration required to prevent

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Chapter 2 Anaesthesia suppresses steroid suppresses synthesis prehospital (see TIVA) hiccoughs non-cumulative, but ssure; TIVA: total intravenous anaesthesia. TIVA: ssure; preserved, adverse preserved, bronchodilation e.g. circumstances, , worse if hypovolaemic or of depression diseasecardiac and ICP, ventilationpatients, bettertolerated if of depression anticonvulsantcardiovascular adverse compromise reactions maintained, ventilation, laryngeal better reflexes hallucinations garlic or onions! profound analgesia Cumulative, delayed hypotension, ventilation, doses cause worse if hypovolaemic or disease cardiac worse in elderly analgesia. Can be after repeat recovery used as sole doses anaesthetic drug in worse ifhypovolaemic or diseasecardiac of ventilation 60 s, depression and ICP involuntary movement, injections repeated or infusion used to hiccoughs maintain anaesthesia cardiovasculardepression ventilation and ICP, involuntary anticonvulsant movement, less painful. No histamine release, Speed of Duration Induction induction of action on Effects Intravenous drugs used for the induction of anaesthesia and their effects Thiopentone 2–6Ketamine 20–30 1–2 9–10 Dose dependent 50–70 Apnoea, 10–12 0.1–0.3 CBF Decreases Minimal in fit but severe Rare 40–70 Minimal Patients may ‘taste’ 10–15 CBF Dose dependent of Depression Mildly Vivid Subanaesthetic Causes amnesia DrugPropofol dose (mg/kg) 1.5–2.5 (s) 30–45 (mins) 4–7 CVS Hypotension, Apnoea up to on RS Effects CBF Decreases on CNS Effects Other side-effects Pain on injection, Comments Non-cumulative, 0.2–0.3 30–40 3–6 Relatively less of Depression CBF Decreases Pain on injection, Emulsion available, able 2.3 T blood flow; ICP: intracranial pre system; CNS: central nervous CBF; cerebral system; RS: respiratory CVS: cardiovascular

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Anaesthesia Chapter 2 for induction ICP May cause hepatitis on EEG activity Pungency limits use ≠ CBF and ICP Pungency limits use ≠ ≠ CBF, CBF, CBF, CBF, ≠ ≠≠ concentration concentration ral blood flow; ICP: intracranial pressure; ral blood flow; ICP: intracranial pressure; HR, ventilation Depresses Slight HR ventilation Depresses on Minimal effect Pungent, boils at 23°C ≠ ≠ BP ventilation Depresses BP, vasodilatation,BP, ventilation Depresses BP, BP, BP, BP, BP, vasodilatationBP, ventilation Depresses on Minimal effect Popular for inhalation Ø Ø Ø Ø Ø maintenance induction, 0.5–1% formaintenance depression, myocardial arrhythmias common exposure repeat induction, 1–1.5% formaintenance vasodilatation for induction maintenance of depth CBF at clinical induction, 2–3% formaintenance of depth CBF at clinical induction Inhalational anaesthetic drugs and their effects Enflurane Medium; 1.5–2% for Medium Halothane High; 3–4% for High Isoflurane Medium; 5% for Medium Desflurane Low; 6–9% for Low; rapid changes CompoundSevoflurane Potency Low; 6–7% for Low; rapid changes Solubility on CVS Effect on RS Effect on CNS Effect Comments able 2.4 T HR: heart rate; CBF: cereb system; CNS: central nervous BP: ; system; RS: respiratory CVS: cardiovascular ECG: electroencephalograph.

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Table 2.5 MAC values for inhalational anaesthetics

Sevoflurane Desflurane Isoflurane Halothane Enflurane (%) (%) (%) (%) (%)

In 100% oxygen 2.2 6.0 1.3 0.75 1.6 In 70% nitrous oxide 1.2 2.8 0.6 0.3 0.6

movement in 50% of subjects following a surgical ples in reverse. Only a small amount of an insolu- stimulus. At 1 MAC, or multiples thereof, the ble drug will have to be excreted to allow brain par- anaesthetic effect will be the same and a compari- tial pressure to fall. With a more soluble drug, a son of the side-effects can be made. Compounds larger amount will need to be excreted, which will with a low potency (e.g. desflurane) will have a take proportionately longer. high MAC, those with a high potency (e.g. Other factors that determine the speed at which halothane) will have a low MAC. the alveolar concentration rises include: The effects of inhalational anaesthetics are addi- • A high inspired concentration: limited clinically by tive, therefore two values for MAC are often quoted — the degree of irritation caused. the value in oxygen and the value when given with a • Alveolar ventilation: this is most pronounced for stated percentage of nitrous oxide (which has its own drugs with a high solubility. As large amounts are MAC), which will clearly be less (Table 2.5). removed from the alveoli, increasing ventilation The value of MAC is reduced in the elderly, in ensures more rapid replacement. those with hypotension, , and hy- • : if high, results in a greater pul- pothyroidism, and with concurrent use of opioids; monary blood flow, increasing uptake thereby it is increased in infants, patients with a pyrexia, lowering the alveolar partial pressure. If low, the and in those who are chronic drug abusers. converse occurs and the alveolar concentration rises more rapidly. Solubility Inhalational anaesthetics exert their effect on the Nitrous oxide central nervous system. It is the partial pressure in

the brain that is responsible for the anaesthetic ef- Nitrous oxide (N2O) is a colourless, sweet-smelling, fect and this follows closely the partial pressure in non-irritant gas with moderate analgesic proper- the alveoli. The rate at which the alveolar partial ties but low anaesthetic potency (MAC 105%). As pressure can be changed determines the rate of the maximum safe concentration that can be ad- change in brain partial pressure, and hence speed ministered without the risk of hypoxia is approxi- of induction, change in depth of, and recovery mately 70%, unconsciousness or anaesthesia from anaesthesia. sufficient to allow surgery is rarely achieved. Con- One of the main determinants of alveolar partial sequently, it is usually given in conjunction with pressure is how soluble the inhalational anaesthe- one of the other vapours. Nitrous oxide is pre- tic is in blood. Relatively insoluble anaesthetics (e.g. mixed with oxygen as a 50:50 mixture called sevoflurane, desflurane) are removed slowly from ‘Entonox’ which is used as an analgesic in obstet- the alveoli by the pulmonary blood. The alveolar rics and by the emergency services. (and brain) partial pressures rise quickly and anaes- thesia is induced rapidly. In contrast, a soluble Systemic effects anaesthetic (e.g. halothane) is removed rapidly •Cardiovascular depression, exacerbated in pa- from the alveoli into the pulmonary blood, limit- tients with pre-existing cardiac disease. ing the rate of rise of alveolar and brain partial pres- • Slight increase in the respiratory rate and a de- sure. Consequently, induction will be slower. crease in the tidal volume. Decreases the ventila- Recovery from anaesthesia follows similar princi- tory response to carbon dioxide and hypoxia.

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• Cerebral vasodilatation, increasing intracranial recovery, etomidate suppresses steroid synthesis pressure (ICP). and recovery after is prolonged due to •Diffuses into air-filled cavities more rapidly than their accumulation. nitrogen can escape, causing either a rise in pres- sure (e.g. in the middle ear) or an increase in TIVA using propofol volume (e.g. within the gut or an air embolus). • May cause bone-marrow suppression by inhibit- With this technique, an appropriate brain concen- ing the production of factors necessary for the syn- tration of propofol must be achieved and main- thesis of DNA. The length of exposure necessary tained to prevent awareness and any response to may be as short as a few hours, and recovery surgery. The simplest way is to give the usual IV in- usually occurs within 1 week. duction dose, followed by repeated injections at in- • At the end of anaesthesia, rapid excretion of tervals depending on the patient’s response. This nitrous oxide into the alveoli dilutes any oxygen method can be used for short procedures, but for present (diffusion hypoxia). If the patient is maintenance over a longer period, it is more com- breathing air, hypoxia can occur. This can be over- mon to use a microprocessor-controlled infusion come by increasing the inspired oxygen concentra- pump (e.g. ‘Diprifusor’). This is more accurate and tion during recovery. reliable as it uses the patient’s weight and age to calculate the rate of infusion required to achieve a constant plasma (and brain) concentration. Hav- Halothane hepatitis ing entered the appropriate data, on starting the The precise link between the use of halothane and pump an initial rapid infusion is given to render the subsequent development of hepatitis remains the patient unconscious, followed by an infusion unclear. The incidence is extremely low, being in at a slower rate to maintain anaesthesia. This is the region of 1:10000–20000 halothane adminis- often referred to as ‘target controlled infusion’ trations. The clinical picture is one of jaundice, (TCI). The infusion rate can also be adjusted with a massive rise in plasma aminotransferases manually to change the plasma concentration to several days after the exposure to halothane, asso- take account of individual patient variation and ciated with severe hepatic necrosis. The mortality the degree of surgical stimulation, in the same way rate is approximately 50%. Severe liver damage is that the concentration of a volatile anaesthetic unlikely to occur after a single exposure in adults, from the vaporizer can be changed. but repeat administration at an interval of less than Propofol alone can be used to maintain anaes- 3 months should be avoided, particularly in obese, thesia, but the infusion rates are very high, with middle-aged females. With the current range of al- significant cardiovascular side-effects. It is usually ternatives this should no longer be necessary. The combined with either IV opioids, given as repeated risk to children appears to be much less. injections (e.g. fentanyl), or an infusion (e.g. remifen- tanil). An alternative is to use a regional anaesthetic technique for analgesia. If muscle relaxation is re- Total intravenous anaesthesia quired, neuromuscular blocking drugs are given and When IV drugs alone are given to induce and the patient is usually ventilated with oxygen- maintain anaesthesia, the term ‘total intravenous enriched air. Nitrous oxide can be used, but this is not anaesthesia’ (TIVA) is used. For a drug to be of use strictly TIVA and some of the advantages are lost. in maintaining anaesthesia, it must be rapidly eliminated or metabolized to inactive substances Advantages of total intravenous to prevent accumulation and delayed recovery, anaesthesia and have no unpleasant side-effects. Currently, an infusion of propofol is the most widely used tech- • The potential toxic effects of the inhalational nique; ketamine is associated with an unpleasant anaesthetics are avoided.

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• The problems associated with nitrous oxide can •A massive rise in serum potassium may provoke be avoided. dysrhythmias in certain patients with: •A better quality of recovery is claimed. • burns, maximal 3 weeks to 3 months after the • It may be beneficial in certain types of surgery, burn; for example neurosurgery. • denervation injury, for example • Pollution is reduced. trauma, maximal after 1 week; • muscle dystrophies, for example Duchenne’s; • crush injury. Disadvantages of total intravenous Administration of suxamethonium is associated anaesthesia with a number of important side-effects: • Secure, reliable intravenous access is required. • malignant hyperpyrexia in susceptible patients • Risk of awareness if intravenous infusion fails. (see page 98); • Cost of electronic infusion pumps. • increased which may cause • May cause profound hypotension. loss of vitreous in penetrating eye injuries; • muscular pain around the limb girdles, most common 24h after administration in young Neuromuscular blocking drugs adults; These work by interfering with the normal action •histamine release: usually localized but may of at the motor end plate, blocking cause an anaphylactoid reaction; the receptors on the postsynaptic muscle mem- • prolonged apnoea in patients with pseudo- brane (and possibly other sites). Muscle relaxants cholinesterase deficiency. are divided into two groups, the names of which are thought to reflect their mode of action. Pseudocholinesterase deficiency A variety of genes have been identified which are involved in pseudocholinesterase production. The Depolarizing neuromuscular most significant genotypes are: blocking drugs • normal homozygotes: sufficient enzyme to hy- drolyse suxamethonium in 4–6mins (950 per 1000 Suxamethonium population); This is the only drug of this type in regular clinical use. • atypical heterozygotes: slightly reduced enzyme It comes ready-prepared (50mg/mL, 2mL ampoules). levels; suxamethonium lasts 10–20mins (50 per The dose in adults is 1.5mg/kg IV. After injection, 1000); there is a short period of muscle fasciculation due to • atypical homozygotes: marked deficiency of en- depolarization of the muscle membrane, followed by zyme; members of this group are apnoeic for up to muscular paralysis in 40–60s. Recovery occurs as a re- 2h after suxamethonium (1 per 1000). sult of hydrolysis by plasma (pseudo-) cholinesterase, Treatment of the third group consists of ventila- with restoration of normal neuromuscular transmis- tory support with maintenance of anaesthesia or sion after 4–6mins. This rapid onset makes it the drug sedation until recovery occurs. The patient should of choice to facilitate tracheal intubation in patients subsequently be warned and given a card that car- likely to regurgitate and aspirate. ries details and, because of its inherited nature, the remainder of the family should be investigated. Systemic effects • No direct effect on the cardiovascular, respira- Non-depolarizing neuromuscular tory or central nervous systems. sec- blocking drugs ondary to vagal stimulation is common after very large or repeated doses, necessitating pretreatment These drugs compete with acetylcholine and block with atropine. its access to the postsynaptic receptor sites on the

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muscle but do not cause depolarization. (They may • Its maximal effect is seen after approximately also block prejunctional receptors responsible for 5mins and lasts for 20–30mins. facilitating the release of acetylcholine.) They are • It is given concurrently with either atropine sometimes referred to as competitive neuromuscu- 1.2mg or glycopyrrolate 0.5mg. lar blockers. The time to maximum effect, that is when relaxation is adequate to allow tracheal intu- Assessment of neuromuscular blockade bation, is relatively slow compared with suxamethonium, generally 1.5–3mins. A synopsis This can be achieved either clinically or by using a of the drugs used is given in Table 2.6. peripheral nerve stimulator. They are used in two ways: • following suxamethonium to maintain muscle Clinical assessment relaxation during surgery; •to facilitate tracheal intubation in non-urgent This requires a conscious, co-operative patient situations. to perform a sustained activity and is therefore Although recovery of normal neuromuscular limited in its application. Tests commonly used function eventually occurs spontaneously after include: the use of these drugs, it is often accelerated by the • lifting the head off the pillow for 5s; administration of an anticholinesterase (see below). •a hand grip for 5s; •the ability to produce a vital capacity breath, 10mL/kg. Anticholinesterases > Inability to perform these activities and/or the The action of all the neuromuscular blocking presence of ‘see-sawing’ or paradoxical respiration drugs wears off spontaneously with time, but this is suggests a degree of residual neuromuscular block. not always clinically appropriate. In patients who A further dose of neostigmine and an anticholiner- require reversal of neuromuscular blocking drugs, gic may be required. an anticholinesterase is given. This inhibits the ac- tion of the enzyme acetylcholinesterase, resulting Peripheral nerve stimulation in an increase in the concentration of acetyl- choline at the (nicotinic This is used in anaesthetized patients, the details effect). The speed of recovery will depend upon the of which are outside the remit of this book. intensity of block when reversal is attempted — the The following is intended as no more than a brief more intense the block the slower the reversal. outline. Anticholinesterases cannot be used to reverse very A peripheral nerve supplying a discrete muscle intense block, for example if given soon after the group is stimulated transcutaneously with a cur- administration of a relaxant (no response to a rent of 50mA. The resulting contractions are ‘train-of-four’ sequence — see below). observed or measured. One arrangement is to stim- Anticholinesterases also function at parasympa- ulate the ulnar nerve at the wrist whilst monitor- thetic nerve endings (muscarinic effect), causing ing the contractions (twitch) of the adductor bradycardia, spasm of the bowel, bladder and pollicis. Although most often done by looking at or bronchi, increased bronchial secretions, etc. There- feeling the response, measuring either the force of fore they are always administered with a suitable contraction or the compound action potential is dose of atropine or glycopyrrolate to block the un- more objective. wanted muscarinic effects. Sequences of stimulation used include: The most commonly used anticholinesterase is • four stimuli each of 0.2s duration, at 2Hz for 2s, neostigmine: referred to as a ‘train-of-four’ (TOF); •A fixed dose of 2.5mg intravenously is used in • One stimulus at 50Hz of 5s duration, that is, a adults. tetanic stimulus;

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Chapter 2 Anaesthesia eversal often r unnecessary RSI isomer, more potent more isomer, HR Long-acting ≠ BP, BP, BP Cisatracurium a single ≠ large dose injectedrapidly plasma cholinesterase. Rapid recovery, Ø infusion release use dissolved before infusion 60 s suxamethonium for infusion release, degradation in plasma. Dose for Maintenance Time to Duration Non-depolarizing neuromuscular blocking drugs Non-depolarizing neuromuscular ecuronium 0.1 mg/kg 0.02–0.03 mg/kg; 6–10 mg/h 90–120 s 15–20 mins Minimal, no histamine White powder, Pancuronium 0.1 mg/kg 0.015 mg/kg 120–150 s 35–45 mins V Mivacurium 0.15–0.2 mg/kg 0.1 mg/kg 100–120 s 10–15 mins if Histamine released Metabolized by Rocuronium 0.6–0.7 mg/kg 0.15–0.2 mg/kg; 30–50 mg/h 90–100 s; after 1 mg/kg, 20–30 mins Minimal Alternative to DrugAtracurium 0.5–0.6 mg/kg intubation 0.15–0.2 mg/kg; 30–50 mg/h dose 90–120 s 20–25 mins intubation Cutaneous histamine Spontaneous of action Systemic effects Comments able 2.6 T BP: blood pressure; HR: heart rate; RSI: rapid sequence induction. BP: blood pressure;

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• two groups of three tetanic bursts at 50Hz, thetic compounds. The term ‘opiate’ is reserved for 750ms apart. naturally occurring substances, for example mor- During non-depolarizing neuromuscular block- phine. There are several opioid receptors, each ade, there is a progressive decremental response to identified by a letter of the Greek alphabet, at all the sequences, termed ‘fade’. In the TOF, the which this group of drugs can have either or ratio of the amplitude of the fourth twitch (T4) to antagonist actions. Two of the most important re- the first twitch (T1) is used as an index of the de- ceptors are m (mu) and k (kappa), and stimulation gree of neuromuscular blockade. During depolariz- (agonist actions) of these by a pure agonist pro- ing blockade, the response to all sequences of duces the classical effects of opioids: analgesia (m, stimulation is reduced but consistent, that is, there k), euphoria (m), sedation (k), depression of ventila- is no fade. tion (m, k) and physical dependence (m). The sys- temic effects of opioids due to both central and peripheral actions are summarized in Table 2.7. When is it useful to assess the degree of A synopsis of the pure used in anaesthe- neuromuscular block? sia is given in Table 2.8. Because of the potential for • During long surgical procedures to control the physical dependence, there are strict rules govern- timing of increments or adjust the rate of an infu- ing the issue and use of most opioid drugs under sion of relaxants to prevent coughing or sudden the Misuse of Drugs Act 1971 (see below). movement. This is particularly important during Opioid analgesics can also be partial agonists or surgery in which a microscope is used, for example partial agonists/antagonists. There are also drugs neurosurgery. that are pure antagonist, have no analgesic action • At the end of surgery, to plan reversal of residual and reverse all the central actions of a pure agonist. neuromuscular block to ensure adequate respira- It is in this role that they are used clinically. tory muscle function. •To differentiate between apnoea due to pro- The partial agonists and mixed longed action of suxamethonium, suggesting agonists/antagonists pseudocholinesterase deficiency, and residual non- depolarizing block, when both have been given. These drugs were introduced in the hope that, with • In recovery, to help distinguish between residual only partial agonist activity at m receptors or mixed neuromuscular block and opioids overdose as a agonist/antagonist actions at m and k receptors, cause of inadequate ventilation postoperatively. analgesia would be achieved without the problem The former will show reduced or absent response of depression of ventilation. Such an ideal has not to stimulation, the latter a normal response. yet been achieved.

Analgesic drugs Nalbuphine (Nubaine)

Analgesic drugs are used as part of the anaesthetic This is a synthetic analgesic with antagonist ac- technique to eliminate pain, reduce the auto- tions at m receptors and partial agonist actions at k nomic response and allow lower concentrations of receptors. It is similar in potency and duration of inhalational or intravenous drugs to be given to action to morphine, and exhibits a ceiling effect of maintain anaesthesia. analgesia. Unfortunately, being a partial antago- nist, giving morphine subsequently is relatively ineffective. Opioid analgesics

This term is used to describe all drugs that have an Tramadol (Zydol) analgesic effect mediated through opioid receptors and includes both naturally occurring and syn- A relatively complex analgesic, a weak opioid

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Table 2.7 Central and peripheral actions of opioids

Central nervous system Respiratory system Gastrointestinal tract Analgesia Antitussive effect Reduced peristalsis causing: Sedation Bronchospasm in susceptible patients • constipation Euphoria • delayed gastric emptying Cardiovascular system Nausea and vomiting Constriction of sphincters Peripheral venodilatation Pupillary constriction Bradycardia due to vagal stimulation Endocrine system Depression of ventilation: Release of ADH and • rate more than depth Skin •reduced response to carbon dioxide Itching Depression of vasomotor centre Addiction (not with normal clinical use)

Urinary tract Increased sphincter tone and urinary retention

ADH: antidiuretic hormone.

Table 2.8 The pure opioid agonists used in anaesthesia

Duration of Drug Route given Dose Speed of onset action (mins) Comments

Morphine Also given subcutaneously, rectally, epidurally, intrathecally IM 0.2–0.3 mg/kg 20–30 mins 60–120 Effective against IV 0.1–0.15 mg/kg 5–10 mins 45–60 visceral pain and pain of myocardial ischaemia. Less effective in trauma Fentanyl IV 1–3 mg/kg 2–3 mins 20–30 Short procedures, spontaneous ventilation 5–10 mg/kg 1–2 mins 30–60 Long procedures, controlled ventilation Alfentanil IV 10 mg/kg 30–60 s 5–10 Short procedures. May cause profound respiratory depression IV infusion 0.5–2 mg/kg/min 30–60 s Infusion Long procedures, dependent controlled ventilation Remifentanil IV infusion 0.1–0.3 mg/kg/min 15–30 s Infusion Major procedures. dependent Very rapid recovery. Profound respiratory depression. Widely used in TIVA Pethidine IM 1–2 mg/kg 15–20 mins 30–60 Marked nausea and vomiting. Less effect on smooth muscle

TIVA: total intravenous anaesthesia.

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agonist at m receptors, inhibits noradrenaline are classified into five schedules, each with a differ- uptake and release of 5-hydroxytryptamine (5-HT). ent level of control. When given intravenously, it is approximately one Schedule 1 Hallucinogenic drugs, including tenth as potent as morphine and roughly equiva- cannabis and LSD, which currently have no lent to pethidine, that is, the dose being 1–2mg/kg. recognized therapeutic use. It is claimed to cause less respiratory depression Schedule 2 This includes opioids, major stimulants than equivalent doses of morphine, but if this does (amphetamines and cocaine) and quinal- occur it is readily reversed by naloxone. A further barbitone. advantage is that it is not a controlled drug, and is Schedule 3 Drugs thought not as likely to be therefore more easily available. misused as those in schedule 2, and includes barbiturates, minor stimulants, buprenorphine (Temgesic) and temazepam. The pure antagonist Schedule 4 This is split into two parts: The only one in common clinical use is naloxone. • benzodiazepines, which are recognized as having the potential for abuse; •androgenic steroids, clenbuterol and growth Naloxone (Narcan) hormones. This has antagonist actions at all the opioid recep- Schedule 5 Preparations which contain very low tors, reversing all the centrally mediated effects of concentrations of codeine or morphine, pure opioid agonists. for example cough mixtures. • The initial IV dose in adults is 0.1–0.4mg, effec- tive in less than 60s and lasting 30–45mins. Supply and custody of schedule 2 • It has a limited effect against opioids, with par- drugs tial or mixed actions, and complete reversal may require very high (10mg) doses. In the theatre complex, these drugs are supplied by • Following a severe overdose, either accidental or the pharmacy, usually at the written request of a deliberate, several doses or an infusion of naloxone senior member of the nursing staff, specifying the may be required, as its duration of action is less drug and total quantity required, and signed. than most opioids. These drugs must be stored in a locked safe, cabinet • Naloxone will also reverse the analgesia pro- or room, constructed and maintained to prevent duced by acupuncture, suggesting that this is prob- unauthorized access. A record must be kept of their ably mediated in part by the release of endogenous use in the ‘Controlled Drugs Register’ and must opioids. comply with the following points: • Separate parts of the register can be used for differ- ent drugs or strengths of drugs within a single class. The regulation of opioid drugs •The class of drug must be recorded at the head of Some drugs have the potential for abuse and con- each page. sequent physical dependence, and their use in • Entries must be in chronological sequence. medicine is carefully regulated. The Misuse of • Entries must be made on the day of the transac- Drugs Act 1971 controls ‘dangerous or otherwise tion or the next day. harmful drugs’, which are designated ‘Controlled • Entries must be in ink or otherwise indelible. Drugs’ and include the opioids. The Act imposes a • No cancellation, alteration or obliteration may total prohibition on the manufacture, possession be made. and supply of these substances, in an attempt to • Corrections must be accompanied by a footnote prevent their misuse. The Misuse of Drugs Regula- that must be dated. tions 2001 permits the use of Controlled Drugs in • The register must not be used for any other medicine. The drugs covered by these regulations purpose.

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•A separate register may be used for each depart- Ketorolac ment (i.e. theatre). • Registers must be kept for 2 years after the last •A non-specific COX inhibitor, with predomi- dated entry. nantly analgesic activity, given orally, IM or IV. The specific details required with respect to supply • The initial parenteral dose is 10mg, subsequently of Controlled Drugs (i.e. for the patient) are: the 30mg (maximum 90mg/day), for up to 2 days. date of the transaction, name of person supplied •Effective after orthopaedic surgery, has opioid- (i.e. the patient’s name), licence of person to be in sparing effects after abdominal surgery. possession (doctor’s signature), amount supplied • No effect on ventilation or cardiovascular and form in which supplied. function. • Not subject to the Misuse of Drugs Regulations. As well as the usual contraindications to the use of Non-steroidal anti-inflammatory NSAIDs, ketorolac should be avoided when exces- drugs (NSAIDs) sive blood loss is anticipated, or when patients are These drugs inhibit the cyclo-oxygenase enzymes receiving other NSAIDs or anticoagulants, includ- (COX-1 and 2) and prevent the breakdown of ing low-dose . arachidonic acid to prostaglandins. Prostaglandins mediate inflammation peripherally and also the Parecoxib sensation of in the CNS. There is a ceil- ing effect to this action and a maximum recom- This is a selective inhibitor of COX-2 and is mended dose for each drug. Prostaglandins also claimed to have fewer adverse side-effects, particu- have important constitutive roles: larly on the GI tract and platelets. Only available • protect the integrity of the gastric mucosa; for parenteral use; the initial dose is 40mg, with • maintain renal blood flow, particularly during subsequent doses of 20–40mg, 6–12 hourly, maxi- shock; mum 80mg/day. • platelet aggregation to reduce bleeding; • bone healing. Older NSAIDs are non-specific COX inhibitors and associated with a significant incidence of renal fail- Not widely used during anaesthesia, but an intra- ure and haemorrhage — the elderly, frail or patients venous preparation is now available (see page 83). taking steroids are particularly vulnerable. Gastrointestinal (GI) ulceration is unusual with short-term use but the drugs may promote fluid The safe delivery of anaesthesia retention and delay fracture healing. More recent- ly, COX-2 specific NSAIDs have become available. The delivery of gases to the These target only the inducible form of the enzyme operating theatre at the site of inflammation. This reduces the chance of gastric ulceration or bleeding problems, Most hospitals use a piped medical gas and vacuum but they must still be used with great caution in system (PMGV) to distribute oxygen, nitrous oxide, potential or actual renal failure. Some asthmatic medical air and vacuum. The pipelines’ outlets act patients (especially those with recurrent nasal as self-closing sockets, each specifically configured, polyps) are prone to bronchospasm precipitated by coloured and labelled for one gas. Oxygen, nitrous NSAIDs. Most patients with asthma do not react to oxide and air are delivered to the anaesthetic room NSAIDs so it is not a general contraindication. at a pressure of 400 kilopascals (kPa) (4bar, 60 pounds per square inch (psi)). The gases (and vacu- um) reach the via flexible rein- forced hoses, colour coded throughout their length

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Figure 2.11 Wall-mounted outlets and gas-specific probes for (left to right) oxygen, nitrous oxide, air.

Table 2.9 Medical colours 12000kPa (120bar, 1980psi) and this falls in direct

Colour proportion to the cylinder contents.

Gas Body Shoulder Nitrous oxide Oxygen Black White Nitrous Oxide Blue Blue Piped nitrous oxide is supplied from large cylin- Entonox Blue Blue/white ders, several of which are joined together to form a Air Grey White/black bank, attached to a common manifold. There are Carbon dioxide Grey Grey usually two banks, one running with all cylinders turned on (duty bank), and a reserve. In addition, there is a small emergency supply. Smaller cylin- (oxygen white, nitrous oxide blue, vacuum yellow). ders are attached directly to the anaesthetic ma- These attach to the wall outlet via a gas-specific chine. At room temperature, nitrous oxide is a probe (Fig. 2.11) and to the anaesthetic machine via liquid within the cylinder, and while any liquid a gas-specific nut and union. Cylinders, the tradi- remains the pressure within the cylinder remains tional method of supplying gases to the anaesthetic constant (440kPa, 640psi). When all the liquid has machine, are now mainly used as reserves in case of evaporated, the cylinder contains only gas and as it pipeline failure. Cylinders are also colour coded to empties, the pressure falls to zero. indicate their contents (Table 2.9). Medical air Oxygen This is supplied either by a compressor or in cylin- Piped oxygen is supplied from a liquid oxygen re- ders. A compressor delivers air to a central reser- serve, where it is stored under pressure (10–12bar, voir, where it is dried and filtered to achieve the 1200kPa) at approximately -180°C in a vacuum- desired quality before distribution. Air is supplied insulated evaporator (VIE), effectively a thermos to the operating theatre for anaesthetic use at 400 flask. Gaseous oxygen is removed from above the kPa, and at 700kPa to power medical tools. liquid, or at times of increased demand, by vaporizing liquid oxygen using heat from the Vacuum environment. The gas is warmed to ambient air temperature en route from the VIE to the pipeline The final part of the PMGV system is medical system. A reserve bank of cylinders of compressed vacuum. Two pumps are connected to a system oxygen is kept adjacent in case of failure of that must be capable of generating a vacuum of at the main system. A smaller cylinder is attached least 400mmHg below atmospheric pressure. This directly to the anaesthetic machine as an emer- is delivered to the anaesthetic rooms, operating gency reserve. The pressure in a full cylinder is theatre and other appropriate sites. At several

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•A specific, calibrated flowmeter is used for each gas. •A needle valve controls the flow of gas through the flowmeter. •A rotating bobbin floats in the gas stream, its upper edge indicating the rate of gas flow. • Several flowmeters are mounted adjacent with oxygen to the left; the control for oxygen has a different knurled finish and is usually more prominent. • Flowmeters do not regulate pressure.

Safety features

• The oxygen and nitrous oxide controls are linked such that less than 25% oxygen cannot be delivered. • If carbon dioxide is fitted, flow is limited to 500mL/min. • An emergency oxygen ‘flush’ device can be used to deliver pure oxygen into the breathing system. • An audible alarm to warn of oxygen failure. This discontinues the nitrous oxide supply and if the patient is breathing spontaneously air can be entrained. Figure 2.12 Oxygen, air and nitrous oxide flowmeters on •A non-return valve to minimize the effects of an anaesthetic machine. back-pressure on the function of flowmeters and vaporizers. stages between the outlets and the pumps there are •Pressure relief valves are fitted primarily to pro- drains and bacterial filters to prevent contamina- tect the equipment, not the patient! tion by aspirated fluids. The addition of anaesthetic vapours The anaesthetic machine Vapour-specific devices are used to produce an Its main functions are to allow: accurate concentration of each inhalational • the accurate delivery of varying flows of gases to anaesthetic: an anaesthetic system; •Vaporizers produce a saturated vapour from a • an accurate concentration of an anaesthetic reservoir of liquid anaesthetic. vapour to be added to the gas stream. • The final concentration of anaesthetic is con- In addition to these functions, many modern trolled by varying the proportion of gas passing anaesthetic machines contain integral monitoring into the vapour chamber. equipment and ventilators. • The vaporizers are temperature compensated (hence -tec suffix, e.g. Sevotec) to account for the loss of latent heat that causes cooling and reduces Measurement of flow vaporization of the anaesthetic. This is achieved on most anaesthetic machines by The resultant mixture of gases and vapour is the use of flowmeters (‘rotameters’; Fig. 2.12): finally delivered to a common outlet on the

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anaesthetic machine. From this point, specialized the patient’s peak inspiratory demands (30– breathing systems are used to transfer the gases 40L/min) to be met with a lower constant flow and vapours to the patient. from the anaesthetic machine. Its excursion gives an indication of ventilation and allows manual ventilation of the patient. It also acts as a further Checking the anaesthetic machine safety device, being easily distended at low pres- It is the responsibility of each anaesthetist to check sure if obstruction occurs. that the apparatus used will function in the man- • An adjustable expiratory valve To vent expired ner expected at the beginning of each operating gas, helping to eliminate carbon dioxide. During session. The main danger is that the anaesthetic spontaneous ventilation, resistance to opening is machine appears to perform normally, but in fact is minimal so as not to impede expiration. Closing delivering a hypoxic mixture to the patient. In the valve allows manual ventilation by squeezing order to minimize the risk of this, the Association the reservoir bag. of Anaesthetists of Great Britain and Ireland An example of a commonly used system is shown (AAGBI) has published a Checklist for Anaesthetic in Fig. 2.13. Machines. Its main aim is to ensure that oxygen flows through the oxygen delivery system and is The circle system unaffected by the use of any additional gas or vapour. Most modern anaesthetic machines now The traditional breathing systems relied on the po- have built-in oxygen analysers that monitor the in- sitioning of the components and the gas flow from spired oxygen concentration to minimize this risk. the anaesthetic machine to eliminate carbon diox- ide in expired gas, thereby preventing rebreathing and hypercapnia. Even the most efficient system is Anaesthetic breathing systems still wasteful; a gas flow of 4–6L/min is required The mixture of anaesthetic gas and vapour travels and the expired gas contains oxygen and anaes- from the anaesthetic machine to the patient via an thetic vapour in addition to carbon dioxide. anaesthetic circuit, or more correctly an anaesthetic The circle system (Fig. 2.14) overcomes these breathing system. Delivery to the patient is via a inefficiencies: facemask, laryngeal mask or tracheal tube (see pages • The expired gases, instead of being vented to the 18–25). There are a number of different breathing atmosphere, are passed through a container of systems (referred to as ‘Mapleson A’, B, C, D or E) soda lime (the absorber), a mixture of calcium, plus a circle system. The details of these systems are sodium and potassium hydroxide, to chemically beyond the scope of this book, but they all have a remove carbon dioxide. number of common features, described below. As • Supplementary oxygen and anaesthetic vapour several patients in succession may breathe through are added to maintain the desired concentrations, the same system, a low-resistance, disposable bacte- and the mixture rebreathed by the patient. Gas rial filter is placed at the patient end of the system, flows from the anaesthetic machine to achieve this and changed between each patient to reduce the can be as low as 0.5L/min. The circle system is risk of cross-infection. Alternatively, disposable sys- therefore the only true ‘anaesthetic circuit’. tems are used, and changed for each patient. • The gases are warmed and humidified as they pass through the absorber (by-products of the reac- tion removing carbon dioxide). Components of a breathing system There are several points to note when using a circle All systems consist of the following: system. • A connection for fresh gas input Usually the com- • As the inspired gas is a mixture of expired and mon gas outlet on the anaesthetic machine. fresh gas, the concentration of oxygen within the • A reservoir bag Usually of 2L capacity to allow circle is not known accurately. The inspired oxygen

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Connection to scavenging system Adjustable expiratory valve

Fresh gas input

Reservoir bag

Figure 2.13 The component parts of a breathing system and photograph of the system connected to the common gas outlet on the anaesthetic ma- chine. Note the port on the expiratory valve (white) to allow connection to the anaesthetic gas scavenging system.

concentration must be monitored to ensure Mechanical ventilation that the patient is not rendered hypoxic (see page 53). A wide variety of anaesthetic ventilators are avail- • The inspired anaesthetic concentration must be able, each of which functions in a slightly different monitored, particularly when a patient is being way. An outline of the principles of mechanical ventilated through a circle, to prevent awareness. ventilation is given and the interested reader •When unable to absorb any more carbon diox- should consult Further reading at the end of the ide, a change in the colour of the granules occurs as chapter. a result of the incorporation of an indicator. One of During spontaneous ventilation, gas moves into the commonly used preparations changes from the lungs by a negative intrathoracic pressure. This pink to white. process is reversed during mechanical ventilation. A positive pressure is applied to the anaesthetic gases to overcome airway resistance and elastic

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Fresh gas I input

Soda E lime Expiratory valve

Reservoir bag

Figure 2.14 Diagram and photograph of a circle system. The internal arrangement of the pipe-work in the system al- lows most of the components in the diagram to be situated on the top of the absorber. (I, inspiratory; E, expiratory one- way valves).

recoil of the chest, and flow occurs into the lungs. curs by passive recoil of the lungs and chest wall. In This technique is usually referred to as intermittent order to generate a positive pressure, the ventilator positive pressure ventilation (IPPV). In both sponta- requires a source of energy: gravity, gas pressure or neous and mechanical ventilation, expiration oc- electricity.

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ing the brain and heart, reducing blood flow. Un- Gravity derventilation will lead to hypercapnia, causing a The Manley is a typical example of a ventilator respiratory acidosis. The effects on the oxyhaemo- using this operating principle. Gas from the anaes- globin dissociation curve are the opposite of above, thetic machine collects within a bellows that is along with stimulation of the sympathetic nervous compressed by a weight. At a predetermined time a system causing vasodilatation, hypertension, valve opens and the contents of the bellows are tachycardia and arrhythmias. delivered to the patient (Fig. 2.15). • Excessive tidal volume may cause overdistension of the alveoli. In patients with pre-existing lung disease this may cause a pneumothorax, and, long Gas pressure term, a condition called ventilator-induced lung Gas from the anaesthetic machine collects in a bel- injury. lows or bag situated in a rigid container (Fig. 2.16). • The positive intrathoracic pressure reduces The ventilator controls the delivery of a gas venous return to the heart and cardiac output. (usually oxygen) at high pressure into the contain- • Both systemic and pulmonary blood flow are re- er to compress the bellows or bag, delivering the duced, the latter further increasing V/Q mismatch. contents to the patient. This system is often called a ‘bag-in-bottle’ ventilator. Minimizing theatre pollution

Unless special measures are taken, the atmosphere Electricity in the operating theatre will become polluted with Electrical power opens and closes valves to control anaesthetic gases. The breathing systems described the flow (and volume) of gas from a high-pressure and mechanical ventilators vent varying volumes source. Alternatively, an electric motor can power a of excess and expired gas into the atmosphere, the piston within a cylinder to deliver a volume of gas patient expires anaesthetic gas during recovery to the patient (Fig. 2.17). Modern ventilators rely and there are leaks from anaesthetic apparatus. increasingly on complex electronics to control gas Although no conclusive evidence exists to link delivery and the inspiratory and expiratory timing prolonged exposure to low concentrations of of ventilation. inhalational anaesthetics with any risks, it would seem sensible to minimize the degree of pollution within the operating theatre environment. This The effects of positive pressure can be achieved in a number of ways: ventilation • reduce the flow of gases, for example by use of a • There is an increase in both the physiological circle system; dead space relative to the tidal volume and ventila- • avoid use of gases, for example by use of TIVA, tion/perfusion (V/Q) mismatch, the effect of which regional anaesthesia; is to impair oxygenation. An inspired oxygen con- • use of air conditioning in the theatre; centration of around 30% is used to compensate • scavenging systems. and prevent hypoxaemia. • The arterial partial pressure of carbon dioxide Scavenging systems (PaCO2) is dependent on alveolar ventilation. Over- ventilation results in hypocapnia, causing a respi- These collect the gas vented from breathing sys- ratory alkalosis. This ‘shifts’ the oxyhaemoglobin tems and ventilators and deliver it via a pipeline dissociation curve to the left, increasing the af- system to the external atmosphere. The most finity of haemoglobin for oxygen. Hypocapnia will widely used is an active system in which a low neg- induce vasoconstriction in many organs, includ- ative pressure is applied to the expiratory valve

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A

C

B

Figure 2.15 Diagram and photo- graph of a gravity-powered ventilator. A, anaesthetic gas input; B, anaes- thetic gas output to patient; C, expired gas from patient.

of the breathing system or ventilator to remove ers of ozone, thereby adding to the greenhouse gases to the outside environment. The patient is effect. protected against excessive negative pressure being applied to the lungs by valves with very low open- Measurement and monitoring ing pressures. The use of such systems does not eliminate the problem of pollution; it merely shifts Measurement and monitoring are closely linked it from one site to another. Inhalational anaesthet- but are not synonymous. A measuring instrument ics, particularly nitrous oxide, are potent destroy- becomes a monitor when it is capable of delivering

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A B

Figure 2.16 Photograph and diagram of bag-in-bottle ventilator. A, high-pressure driving gas input; B, anaes- thetic gas output to patient.

a warning when the variable being measured falls • type of operation and operative technique; outside preset limits. During anaesthesia, both the • anaesthetic technique used; patient and the equipment being used are moni- • present and previous health of the patient; tored, the complexity of which depends upon a va- • equipment available and the anaesthetist’s riety of factors including: ability to use it;

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Monitoring is not without its own potential hazards: faulty equipment may endanger the pa- tient, for example from electrocution secondary to faulty earthing; the anaesthetist may act on faulty data, instituting inappropriate treatment; or the patient may be harmed by the complications of the technique to establish invasive monitoring, for ex- ample pneumothorax following central line inser- tion. Ultimately, too many monitors may distract the anaesthetist from recognizing problems occur- ring in other areas.

Monitoring the patient

The AAGBI recommends certain monitoring devices as essential for the safe conduct of anaes- thesia. These consist of: • ECG; • non-invasive blood pressure; • pulse oximeter; • ; •vapour concentration analyser. Figure 2.17 Modern electronic ventilator. None of the components are visible. Close-up of the control panel In addition, the following monitors should be im- shows soft keys, allowing choice of mode of ventilation and mediately available: volumes and pressures during controlled ventilation (IPPV). • peripheral nerve stimulator; • temperature. Finally, additional equipment will be required in • preferences of the anaesthetist; certain cases, to monitor, for example: • any research being undertaken. • invasive blood pressure; Clearly, the anaesthetist has a responsibility to • urine output; check the function of all monitoring equipment • central venous pressure; before use and ensure that the alarm limits are set • pulmonary artery pressure; appropriately. • cardiac output. There is good evidence that monitoring reduces the risks of adverse incidents and accidents. The combination of pulse oximetry, capnography and Essential monitors blood pressure monitoring detects the majority of serious incidents before the patient suffers serious The ECG injury. Monitoring should commence before the induction of anaesthesia and continue until the This is easily applied and gives information on patient has recovered from the effects of anaes- heart rate and rhythm, and may warn of the pres- thesia, and the information generated should be ence of ischaemia and acute disturbances of certain recorded in the patient’s notes. Ultimately, moni- electrolytes (e.g. potassium and calcium). It can be tors supplement clinical observation; there is no monitored using three leads applied to the right substitute for the presence of a trained and experi- shoulder (red), the left shoulder (yellow) and the enced anaesthetist throughout the entire operative left lower chest (green), to give a tracing equivalent procedure. to standard lead II of the 12-lead ECG. Many ECG

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monitors now use five electrodes placed on the an- reaching the photodetector is converted to an elec- terior chest to allow all the standard leads and V5 trical signal. The absorption due to the tissues and to be displayed. The ECG alone gives no informa- venous blood is static. This is then subtracted from tion on the adequacy of the cardiac output and it the beat-to-beat variation due to arterial blood, to must be remembered that it is possible to have a display the peripheral arterial oxygen saturation

virtually normal ECG in the absence of any cardiac (SpO2), both as a waveform and digital reading (see output. Fig. 2.18). Pulse oximeters are accurate to ±2%. The waveform can also be interpreted to give a reading of heart rate. Alarms are provided for levels of satu- Non-invasive blood pressure ration and heart rate. The pulse oximeter therefore This is the most common method of obtaining the gives information about both the circulatory and patient’s blood pressure during anaesthesia and respiratory systems and has the advantages of: surgery. A pneumatic cuff with a width that is 40% • providing continuous monitoring of oxygena- of the arm circumference must be used and the inter- tion at tissue level; nal inflatable bladder should encircle at least half • being unaffected by skin pigmentation; the arm. If the cuff is too small, the blood pressure • portability (mains or battery powered); will be overestimated, and if it is too large it will be • being non-invasive. underestimated. Auscultation of the Korotkoff Despite this, there a number of important limita- sounds is difficult in the operating theatre and au- tions of this device: tomated devices (Fig. 2.18) are widely used. An • There is failure to realize the severity of hypoxia; electrical pump inflates the cuff, which then un- dergoes controlled deflation. A microprocessor- controlled pressure transducer detects variations in cuff pressure resulting from transmitted arterial pulsations. Initial pulsations represent systolic blood pressure and peak amplitude of the pulsa- tions equates to mean arterial pressure. Diastolic is calculated using an algorithm. Heart rate is also de- termined and displayed. The frequency at which blood pressure is estimated can be set along with values for blood pressure, outside which an alarm sounds. Such devices cannot measure pressure continually and become increasingly inaccurate at extremes of pressure and in patients with an arrhythmia.

Pulse oximeter

A probe, containing a light-emitting diode (LED) and a photodetector, is applied across the tip of a digit or earlobe. The LED alternately emits red light at two different wavelengths in the visible and infrared regions of the electromagnetic spectrum. Figure 2.18 Integrated monitoring system displaying ECG These are transmitted through the tissues and and heart rate (beats/min), non-invasive blood pressure absorbed to different degrees by oxyhaemoglobin (mmHg), capnograph and end tidal carbon dioxide (kPa), and deoxyhaemoglobin. The intensity of light pulse oximeter waveform and saturation (%).

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a saturation of 90% equates to a PaO2 of 8kPa Table 2.10 Uses of end-tidal CO2 measurement (60mmHg) because of the shape of the haemoglo- • An indicator of the degree of alveolar ventilation: bin dissociation curve. • to ensure normocapnia during mechanical • It is unreliable when there is severe vasoconstric- ventilation tion due to the reduced pulsatile component of the • control the level of hypocapnia in neurosurgery signal. • avoidance of hypocapnia where the cerebral • It is unreliable with certain haemoglobins: circulation is impaired, e.g. the elderly • when carboxyhaemoglobin is present, it over- • As a disconnection indicator (the reading suddenly falls to zero) estimates SaO2; •To indicate that the tracheal tube is in the trachea • when methaemoglobin is present, at an SaO2 > (CO in expired gas) 85%, it underestimates the saturation. 2 • As an indicator of the degree of rebreathing • It progressively under-reads the saturation as the (presence of CO in inspired gas) haemoglobin falls (but it is not affected by 2 • As an indicator of cardiac output. If cardiac output polycythaemia). falls and ventilation is maintained, then end-tidal CO2 • It is affected by extraneous light. falls as CO2 is not delivered to the lungs, e.g.: • It is unreliable when there is excessive move- • hypovolaemia ment of the patient. • cardiac arrest, where it can also be used to indicate effectiveness of external cardiac compression • massive pulmonary embolus • It may be the first clue of the development of The pulse oximeter is not an indicator of the adequacy of malignant hyperpyrexia (see page 98) alveolar ventilation. Hypoventilation can be compensated for by increasing the inspired oxygen concentration to maintain oxygen saturation.

of respiratory gases. Care must be taken in inter- Capnography preting end-tidal CO2 concentrations in these cir- The capnograph (see Fig. 2.18) works on the prin- cumstances. Modern capnographs have alarms for

ciple that carbon dioxide (CO2) absorbs infrared when the end-tidal carbon dioxide is outside preset light in proportion to its concentration. In a limits. Other uses of carbon dioxide monitoring

healthy person, the CO2 concentration in alveolar are given in Table 2.10.

gas (or partial pressure, PACO2) correlates well with partial pressure in arterial blood (PaCO ), with the 2 Vapour concentration analyser former being slightly lower, by 5mmHg or 0.7kPa. Analysis of expired gas at the end of expiration Whenever a volatile anaesthetic is administered

(i.e. end-tidal CO2 concentration) reflects PaCO2. the inspired concentration in gas mixture should Capnography is used primarily as an indicator of be monitored. This is usually achieved using

the adequacy of ventilation; PaCO2 is inversely pro- infrared absorption, similar to carbon dioxide. The portional to alveolar ventilation. In patients with a degree of absorption is dependent specifically on low cardiac output (e.g. hypovolaemia, pulmonary the volatile and its concentration. A single device embolus), the gap between arterial and end-tidal can be calibrated for all of the commonly used carbon dioxide increases (end-tidal falls), mainly inhalational anaesthetics. due to the development of increased areas of venti- In many modern anaesthesia systems the above lation/perfusion mismatch. The gap also increases monitors are integrated and displayed on a single in patients with chest disease due to poor mixing screen (Fig. 2.18).

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Immediately available monitors Urine output

Measurement of urine output is performed during Peripheral nerve stimulator prolonged surgery to ensure maintenance of ade- See page 35. quate circulating volume where there is likely to be major blood loss, where diuretics are used (e.g. neurosurgery) and in all critically ill patients. Urine Temperature output needs to be measured at least hourly, aim- During anaesthesia the patient’s temperature is ing for a flow of approximately 1mL/kg/h. Failure usually monitored continually. The most com- to produce urine indicates that renal blood flow is monly used device is a thermistor, the resistance of inadequate, as well as the flow to the other vital which is temperature dependent. This can be organs (heart and brain). Catheterization also placed in the oesophagus (cardiac temperature) or eliminates bladder distension or incontinence. nasopharynx (brain temperature). The can be used but, apart from being unpleasant, faeces Central venous pressure (CVP) may insulate the thermistor, leading to inaccura- cies. An infrared tympanic membrane thermome- This is measured by inserting a catheter via a cen- ter can be used intermittently, but the external tral vein, usually the internal jugular or subclavian, auditory canal must be clear. Most patients’ core so that its tip lies at the junction of the superior temperature falls during anaesthesia as a result of vena cava and right atrium. It is then connected via exposure to a cold environment, evaporation of a fluid-filled tube to a transducer that converts the fluids from body cavities, the administration of pressure signal to an electrical signal. This is then cold intravenous fluids and breathing dry, cold amplified and displayed as both a waveform and anaesthetic gases. This is compounded by the loss pressure. of body temperature regulation and inability to Loss of circulating volume will reduce venous shiver. These can be minimized by forced air warm- return to the heart, diastolic filling and preload, ing, warming all fluids (particularly blood), heat- and be reflected as a low or falling CVP. Although ing and humidifying inspired gases, and covering absolute values of the CVP can be measured, trends exposed areas. Apart from monitoring cooling, a are usually more informative. Often a ‘fluid chal- sudden unexpected rise in a patient’s temperature lenge’ is used in the face of a low CVP. The CVP is may be the first warning of the development of ma- measured, a rapid infusion of fluid is given (3– lignant hyperpyrexia (see page 98). 5mL/kg) and the change in CVP noted. In the hy- povolaemic patient the CVP increases briefly and then falls to around the previous value, whereas in Additional monitors the fluid-replete patient the CVP will rise to a greater extent and be sustained. Overtransfusion will be seen as a high, sustained CVP. Invasive or direct blood pressure CVP is usually monitored in operations during This is the most accurate method for measuring which there is the potential for major fluid shifts blood pressure and is generally reserved for use in (e.g. prolonged abdominal surgery) or blood loss complex, prolonged surgery or sick patients. A can- (e.g. major orthopaedic and trauma surgery). It is nula is inserted into a peripheral artery and con- affected by a variety of other factors apart from fluid nected to a transducer that converts the pressure balance (Table 2.11), in particular cardiac function. signal to an electrical signal. This is then amplified Hypotension in the presence of an elevated CVP and displayed as both a waveform and blood pres- (absolute or in response to a fluid challenge) may in- sure (see Fig. 5.3). dicate heart failure, but most clinicians would now accept that measurement of the pressures on the

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Table 2.11 Factors affecting the central venous pressure Oxygen supply • The zero reference point • Patient posture All anaesthetic machines are fitted with a device • Fluid status warning of oxygen supply failure (see page 42). • Heart failure Continuous monitoring of the oxygen concentra- • Raised intrathoracic pressure: tion in the inspired gas mixture is considered es- • mechanical ventilation sential. This is usually achieved using a fuel cell • coughing oxygen analyser that produces a current propor- • straining tional to the oxygen concentration, displayed as a • Pulmonary embolism numeric value of oxygen concentration. It must be • Pulmonary hypertension remembered that the inspired oxygen concentration •Tricuspid valve disease does not guarantee adequate arterial oxygen saturation • Pericardial effusion, tamponade as it may be insufficient to compensate for the • Superior vena cava obstruction effects of hypoventilation and ventilation/perfu- sion mismatch (see page 72). left side of the heart using a pulmonary artery flota- tion catheter is preferable to assist in the manage- Breathing systems ment of this condition (see page 126). Irrespective of whether the patient is breathing spontaneously or being ventilated, capnography Pulmonary artery catheter and cardiac will detect most of the common problems, for output example disconnection (loss of reading), inade-

See page 126. quate gas flow (increased end-tidal CO2), hyper/hy-

poventilation (decreased/increased end-tidal CO2, respectively). In addition, when a patient is venti- Blood loss lated, airway pressures must be monitored to avoid Simple estimates of blood loss during surgery are excessive pressures being generated within the easily performed. Swabs can be weighed, dry and lungs. Airway pressure monitoring can also be used wet, the increase in weight giving an indication of as a secondary indicator of inadequate ventilation the amount of blood they have absorbed. The vol- in ventilated patients; high pressures may be the ume of blood in the suction apparatus can be meas- result of obstruction (e.g. blocked tracheal tube, ured, with allowance for irrigation fluids. Such bronchospasm), and loss of pressure the result of a methods are only estimates, as blood may remain disconnection. The latter function may be specifi- in body cavities, be spilt on the floor and absorbed cally used as a ‘disconnection alarm’. by drapes and gowns. In paediatric practice, where small volumes of blood loss are relatively more Many other physiological parameters can be, and important, all absorbent materials are washed to are, monitored during anaesthesia when appropri- remove the blood and the resultant solvent as- ate. Some examples are: clotting profiles in patients sayed colorimetrically to estimate blood loss. receiving a transfusion of a large volume of stored blood; blood glucose in diabetic patients; and arte- rial blood gas and acid–base analysis during the by- Monitoring the equipment pass phase of cardiac surgery. Recently, interest has With the increasing reliance on complex equip- been shown in the development of monitors that ment to deliver anaesthesia, the AAGBI recom- give information relating to the depth of anaesthe- mends that there should be continuous sia, but these are still under investigation. monitoring of the continuity of the oxygen supply Finally, it is essential to recognize that the above and correct functioning of the breathing system. standards apply not only to those patients

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undergoing general anaesthesia, but also those re- ceiving sedation, local or regional anaesthesia and during transfer. Cephalic vein

The anaesthetic record

On every occasion an anaesthetic is administered, a comprehensive and legible record must be made. The details and method of recording will vary with each case, the type of chart used and the equip- Dorsal metacarpal veins ment available. Apart from the value to future Figure 2.19 Typical distribution of veins on the dorsum of anaesthetists who encounter the patient, particu- the hand. After Warwick R & Williams PL (eds) Gray’s larly when there has been a difficulty (e.g. with in- Anatomy, 35th edn. Edinburgh: Churchill Livingstone, tubation), the anaesthetic record is a medicolegal 1973. document, to which reference may be necessary after several years. An anaesthetic chart typically allows the following to be recorded: The superficial veins in the upper limbs are most • preoperative findings, ASA grade, premedication; commonly used. • details of previous anaesthetics and any difficulties; • apparatus used for the current anaesthetic; Anatomy of the veins in the upper limb • monitoring devices used; •anaesthetic and other drugs administered: The dorsum of the hand and forearm timing, dose and route; • vital signs at various intervals, usually on a The veins draining the fingers unite to form three graphical section; dorsal metacarpal veins. Laterally these are joined by • fluids administered and lost: type and volume; veins from the thumb and continue up the radial • use of local or regional anaesthetic techniques; border of the forearm as the cephalic vein (Fig. 2.19). • anaesthetic difficulties or complications; Medially the metacarpal veins unite with the veins • postoperative instructions. from the little finger and pass up the ulnar border Increasingly, electronic records are being devel- of the forearm as the basilic vein. There is often a oped. These have the advantage of allowing the large vein in the middle of the ventral (anterior) anaesthetist to concentrate on caring for the pa- aspect of the forearm — the median vein of the tient, particularly during an emergency, rather forearm (Fig. 2.20). than having to stop and make a record or try to fill in the record retrospectively. The antecubital fossa

The cephalic vein passes through the antecubital Intravenous cannulation and fluid fossa on the lateral side and the basilic vein enters administration the antecubital fossa very medially, just in front of Intravenous cannulation is used to allow: the medial epicondyle of the elbow. These veins are •drugs to be given to induce and maintain joined by the median cubital or antecubital vein (see anaesthesia; Fig. 2.20). Veins in this region tend to be used • fluids to be given to maintain or restore the either in an emergency situation or when attempts patient’s circulating volume; to cannulate more peripheral veins have failed. It •monitoring of intravascular pressures. must be remembered that the brachial artery, the

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Cephalic vein Median cubital vein Biceps tendon

Figure 2.20 Typical distribution of veins of the forearm and antecubital fossa (right arm). After Warwick R & Williams PL (eds) Gray’s Anatomy, 35th edn. Edinburgh: Churchill Median vein of forearm Basilic vein Brachial artery Livingstone, 1973.

Figure 2.21 (A–D) Different types of intravenous cannula.

median nerve and branches of the medial and chamber’, which fills with blood once the needle lateral cutaneous nerves of the arm are in close bevel lies within the vein (Fig. 2.21A). Some de- proximity and easily damaged by needles or vices have flanges or ‘wings’ to facilitate attach- extravasated drugs. ment to the skin (Fig. 2.21B). All cannulae have a standard Luer-lock fitting for attaching a giving set and some have a valved injection port through Equipment which drugs can be given (Fig. 2.21C). Devices of different lengths and diameters are • Seldinger type This is used predominantly to used; the term ‘cannula’ is used for those 7cm or achieve cannulation of the central veins (see less in length, and ‘catheter’ for those longer than below), but peripheral devices are available, de- 7cm. The external diameter of these devices is signed mainly for use in resuscitation, for example quoted either in terms of its ‘gauge’ (diameter the Arrow EID cannula (Fig. 2.21D). increases with decreasing gauge) or millimetres. The main types of cannulae used are: Technique for cannulation of a • Cannula over needle The most popular device, peripheral vein available in a variety of sizes, most commonly 14 gauge (2.1mm) to 22 gauge (0.8mm). A plastic The superficial veins are situated immediately (PTFE or similar material) cannula is mounted on a under the skin in the superficial fascia, along with smaller diameter metal needle, the bevel of which a variable amount of subcutaneous fat. They are protrudes from the cannula. The other end of the relatively mobile and capable of considerable vari- needle is attached to a transparent ‘flashback ation in their diameters. The size of cannula used

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(a) (b)

(c) (d)

Figure 2.22 (a-d) Peripheral intravenous cannulation. Courtesy of Greaves I, Hodgetts T, Porter K. Emergency Care — A Textbook for Paramedics. London: Harcourt Brace, 1997.

will depend upon its purpose: large-diameter can- avoided as drugs or fluids may leak from the frac- nulas are required for giving fluid rapidly, smaller ture site. ones are adequate for giving drugs and mainte- • Encourage the vein to dilate by applying a nance fluids. tourniquet proximally and gently tapping the skin over the vein. Warming a cold hand will also help. • Clean the skin over the vein using either an As with any procedure where there is a risk of contact alcohol- or iodine-based solution (ensure there is with body fluids, gloves should be worn by the operator. no risk of allergy if iodine is used). •A small amount of local anaesthetic (0.2mL lignocaine 1%) should be infiltrated into the skin • Choose a vein capable of accommodating the at the site chosen for venepuncture using a 25 size of cannula needed, preferably one that is both gauge (0.5mm) needle, particularly if a large (>18 visible and palpable. gauge, 1.2mm) cannula is used. This reduces pain, • The junction of two veins is often a good site and makes the patient less likely to move and less as the ‘target’ is relatively larger. resistant to further attempts. •Avoid veins over joints as the cannula may • Immobilize the vein to prevent it being dis- kink if the joint is flexed, with loss of function. placed by the cannula, by pulling the overlying •Veins distal to fractures should also be skin tight, using your spare hand (Fig. 2.22a).

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• Advance the cannula through the skin at an with inadequate pressure applied over the punc- angle of 10–15° and then into the vein. Often a ture site to prevent bleeding, and made worse by slight loss of resistance is felt as the vein is entered forgetting to remove the tourniquet! and this should be accompanied by the appearance • Extravasation of fluid or drugs Failing to recognize of blood in the flashback chamber of the cannula that the cannula is not within the vein before use. (Fig. 2.22b). This indicates that the tip of the The degree of damage to the overlying tissues needle is within the vein. will depend primarily upon the nature of the • Reduce the angle of the cannula slightly and ad- extravasated fluid. vance it a further 2–3mm into the vein, keeping • Damage to local structures Secondary to poor the skin taut. This ensures that the first part of technique and lack of knowledge of the local the plastic cannula lies within the vein. Take care anatomy. not to push the needle out of the far side of the • Air embolus The peripheral veins normally col- vein! lapse when empty. However, a cannula may pre- •Withdraw the needle 5–10mm into the cannula vent this and allow air to enter the circulation. so that the bevel no longer protrudes from the end. Most likely following cannulation of a central vein As this is done, blood may be seen to flow between (see below). the needle body and the cannula, confirming that • Shearing of the cannula Usually a result of trying the tip of the cannula is within the vein (Fig. to reintroduce the needle after it has been with- 2.22c). drawn. The safest action is to withdraw the whole • The cannula and needle should now be ad- cannula and re-attempt at another site. vanced together along the vein. The needle is re- • Thrombophlebitis Related to the length of time tained within the cannula to provide support and the vein is in use and irritation caused by the sub- prevent kinking at the point of skin puncture (Fig. stances flowing through it. High concentrations of 2.22d). drugs and fluids with extremes of pH or high • Once the cannula is fully inserted the tourniquet osmolality are the main causes, for example anti- should be released, and the needle removed and biotics, calcium chloride, sodium bicarbonate. disposed of safely. Once a vein shows signs of thrombophlebitis (i.e. • Confirm that the cannula lies within the vein by tender, red and deteriorating flow) the cannula attaching an IV infusion and ensuring it runs must be removed to prevent subsequent infection freely. Alternatively, inject a small volume of or thrombosis. saline. Immediate, localized swelling or pain indi- cates that the cannula is incorrectly positioned. Do Central venous cannulation not persist; remove it and try at another site. • Finally, secure the cannula in an appropriate This may be used for a variety of reasons during manner with adhesive tape, or a commercial anaesthesia: to monitor the cardiovascular system; dressing. because of inadequate peripheral venous access; and to give certain drugs (e.g. inotropes). There are many different types of equipment and ap- Complications proaches to the central veins, and the following is Most are relatively minor but this must not be used intended as an outline. The use of an ultrasound as an excuse for carelessness and poor technique. scanner may improve the detection and needle • Failure Usually a result of pushing the needle localization of central veins. completely through the vein. It is always best to attempt cannulation distally in a limb and work proximally. If multiple attempts are required, fluid or drugs will not leak from previous puncture sites. • Haematoma Usually secondary to the above

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Table 2.12 Complications of central venous obstruction due to haematoma formation in the cannulation neck or bilateral pneumothoraces.

•Arterial puncture and bleeding causing haematoma or haemothorax Whenever a CVP catheter is inserted, a chest X-ray must • Air embolus be taken to ensure that the catheter is correctly posi- •Venous thrombosis tioned and a pneumothorax has not been caused. • Pneumothorax • Thoracic duct injury (left side) and chylothorax • Hydrothorax if the catheter is intrapleural and fluid given Equipment for central venous • Bacteraemia catheterization • Septicaemia Three types of catheter are commonly used for per- • Soft tissue infection at puncture site cutaneous cannulation of the central veins: • Injury to nerves: • brachial plexus • Catheter over needle Similar to a peripheral IV •recurrent laryngeal cannula, the main difference is that it is longer to • phrenic ensure that the tip lies in the correct position with- in a central vein. • Seldinger technique The vein is initially punc- tured percutaneously using a small-diameter needle. A flexible guidewire is then passed down Access to the central veins the needle into the vein and the needle carefully withdrawn, leaving the wire behind. The catheter The antecubital fossa is now passed over the wire into the vein, some- This route has a relatively low success rate, but times preceded by a dilator. The advantage of this fewer complications, the most important of which method is that the initial use of a small needle in- is thrombophlebitis after prolonged use (>48h). creases the chance of successful venepuncture and The basilic vein is preferable, as a catheter passed reduces the risk of damage to the vein. via this vein is most likely to reach beyond the • Catheter through needle A large-diameter needle clavipectoral fascia. is introduced into the vein, the catheter is threaded down the lumen and the needle is with- The internal jugular vein drawn, leaving the catheter in place. This approach is associated with the highest inci- dence of success (95%), and a low rate of complica- Fluid flow through a cannula tions (Table 2.12). The right internal jugular offers certain advantages: there is a ‘straight line’ to the This determined by four factors: heart, the apical pleura does not rise as high on this • Internal diameter Theoretically, flow is propor- side, and the main thoracic duct is on the left. tional to the fourth power of the radius. Doubling the diameter should result in flow increasing Subclavian vein 16-fold (24). This is rarely achieved in practice, but This can be approached by both the supra- and in- an increase of four- to fivefold will be seen. fraclavicular routes. Both are technically more dif- • Length Flow is inversely proportional to the ficult than the internal jugular route and there is a length of the cannula — doubling the length will significant incidence of causing a pneumothorax halve the flow. (2%). The main advantage of this route is com- • Viscosity Flow is inversely proportional to the fort for the patient during long-term use. viscosity of the fluid — increasing viscosity reduces Bilateral attempts at central venous cannulation flow. Colloids and blood flow more slowly than a must not be made because of the risk of airway crystalloid, particularly when they are cold.

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• Pressure Increasing the pressure across the can- concentrations to plasma are rapidly distributed nula will increase the flow. This is usually achieved throughout the extracellular fluid space (i.e. by either raising the height of the drip above the intravascular and interstitial volumes). Ultimately, patient or using external pressure. only 25–30% of the volume administered remains intravascular. If such fluids are used to restore the circulating volume, three to four times the deficit Always use a large-diameter, short cannula during will need to be given. If crystalloids containing a resuscitation as the rate of flow is determined primarily lower concentration of sodium than plasma (e.g. by the diameter. 4% glucose plus 0.18% saline) are given, then once the glucose is metabolized the remaining fluid is distributed throughout the entire body water (i.e. Intravenous fluids extracellular and intracellular volumes), and as During anaesthesia fluids are given intravenously little as 10% will remain intravascular. Crystalloids to replace losses due to surgery and provide the are used primarily either as an emergency resusci- patient’s normal daily requirements. Three types tation fluid or to provide a patient’s daily require- are used: crystalloids, colloids, and blood and its ments of water and sodium. components. Colloids Crystalloids These are suspensions of high molecular weight These are solutions of crystalline solids in water. A particles. The most commonly used are derived wide variety is available and a summary of the from gelatin (Haemaccel, Gelofusine), protein (al- composition of the most commonly used is shown bumin) or starch (Hespan, HAES-steril). A sum- in Table 2.13. Those containing sodium in similar mary of their composition is shown in Table 2.14.

Table 2.13 Composition of crystalloids

+ + ++ - - Na K Ca Cl HCO3 Osmolality Crystalloid (mmol/L) (mmol/L) (mmol/L) (mmol/L) (mmol/L) pH (mosmol/L)

Hartmann’s 131 5 4 112 29* 6.5 281 0.9% sodium chloride 154 0 0 154 0 5.5 300 4% glucose plus 0.18% 31 0 0 31 0 4.5 284 sodium chloride 5% glucose 000004.1278

*Present as lactate which is metabolized to bicarbonate by the liver.

Table 2.14 Composition of colloids

Average molecular + + ++ - - weight Na K Ca Cl HCO3 Osmolality Colloid (kDa) (mmol/L) (mmol/L) (mmol/L) (mmol/L) (mmol/L) pH (mosmol/L)

Haemaccel 35 145 5 6.2 145 0 7.3 350 Gelofusine 35 154 0.4 0.4 125 0 7.4 465 Albumin 69 130–160 2 0 120 0 6.7–7.3 270–300 Starch 140–400 154 0 0 154 0 5.5 310

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Colloids primarily expand the intravascular supplied as a pooled donation from six packs of FFP volume and can initially be given in a volume sim- in one unit and must be used as soon as possible ilar to the deficit to maintain the circulating vol- after thawing. ume. However, they have a finite life in the plasma and will eventually be either metabolized or ex- Risks of intravenous blood and creted and therefore need replacing. blood products

All blood donations are routinely tested for hepati- Blood and blood components tis B surface antigen, hepatitis C, syphilis and anti- There are several forms of blood and its compo- bodies to the HIV. However, a period exists nents available. In the intraoperative period the between exposure and the development of anti- most commonly used are red cell products, platelet bodies. The resultant infected red cells would not concentrates and clotting factors. be detected by current screening techniques. The • Whole blood Despite its name, this is basically risk is very small, and has been estimated for hepa- red cells, plasma proteins and clotting factors titis B at 1:105 and for HIV at 1:106 units trans- (levels of V and VIII are low). There are no platelets. fused. In order to try and eliminate these risks, Each unit contains approximately 510mL with a techniques now exist for using the patient’s own haematocrit of 35–45%. Not widely available. blood in the perioperative period. • Red cell concentrate This is the by-product of the • Predepositing blood Over a period of 4 weeks removal of plasma from whole blood. Each unit prior to surgery, the patient builds up a bank contains 250mL with a haematocrit of 60–75%, of two to four units of blood for retransfusion and is hence very viscous with a poor flow rate. perioperatively. • Red cells in optimal additive solution (SAG-M) A • Preoperative haemodilution Following induction red cell concentrate to which a mixture of saline, of anaesthesia 0.5–1.5L of blood is removed and re- adenine and glucose and mannitol has been placed with colloid. This can then be transfused at added. This improves both red cell survival and the end of surgery. flow characteristics. Each unit contains 300mL • Cell savers These devices collect blood lost dur- with a haematocrit of 50–70%. White cells are ing surgery via a suction system; the red cells are routinely removed in the UK to prevent the risk of separated, washed and resuspended, ready for re- prion transmission. transfusion to the patient. • Platelet concentrates Supplied either as ‘units’ containing 50–60mL (55 109 platelets) or as bags ¥ Intraoperative fluid administration equivalent to four units. Four units or one bag will raise the platelet count by 30–40000mm3. Given The type and volume of fluid administered during via a standard giving set without the use of a surgery varies for each and every patient, but must microaggregate filter, as this will result in the loss take into account: of significant numbers of platelets. • any deficit the patient has accrued; • Fresh frozen plasma (FFP) This consists of the • maintenance requirements during the plasma separated from a single donation and procedure; frozen within 6h. Each pack contains 200–250mL, • losses due to surgery; with normal levels of clotting factors (except factor • any vasodilatation secondary to the use of a VIII, 70% normal). It should be infused as soon as regional anaesthetic technique (see page 67). it has thawed. • Cryoprecipitate This is produced as a precipitate The accrued deficit formed on the controlled thawing of FFP, which is collected and suspended in plasma. It contains This may be due to preoperative fasting, or losses as large amounts of factor VIII and fibrinogen. It is a result of vomiting, haemorrhage or pyrexia. Any

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deficit due to fasting is predominantly water from Fluid losses from the first two causes are difficult to the total body water volume. The volume required measure and are extremely variable. If evaporative is calculated at the normal daily maintenance rate losses are considered excessive, then 4% glucose of 1.5mL/kg/h (from the point at which fasting plus 0.18% saline can be used. Third space losses began). Although this deficit can be replaced with should be replaced with a solution similar in com- a fluid such as 4% glucose plus 0.18% saline, position to extracellular fluid, and Hartmann’s is Hartmann’s solution is widely used intraoperative- commonly used. The rate of administration and ly. The other main cause of a preoperative deficit is volume required is proportional to surgical trauma losses either from or into the gastrointestinal tract. and may be as much as 10mL/kg/h. Blood pres- This fluid usually contains electrolytes and effec- sure, pulse, peripheral perfusion and urine output tively depletes the extracellular volume. It is best will give an indication as to the adequacy of re- replaced with a crystalloid of similar composition, placement, but in complex cases where there are particularly in respect of the sodium concentra- other causes of fluid loss, particularly bleeding, the tion; for example 0.9% sodium chloride or trend of the CVP is very useful (see page 52). Hartmann’s solution. Blood loss is slightly more obvious and easier to Acute blood loss preoperatively can be replaced measure. Most previously well patients will toler- with either an appropriate volume of crystalloid ate the anaemia that results from the loss of 20% of (remembering that only 30% remains intravascu- their blood volume, providing that the circulating lar) or colloid. If more than 20% of the estimated volume is adequately maintained by the use of blood volume has been lost (approximately crystalloids or colloids. Beyond this, red cell prepa- 1000mL), blood should be used, particularly if rations are used in order to maintain the oxygen- bleeding is ongoing. carrying capacity of the blood. A haemoglobin level between 8 and 10g/dL is a safe level even for those patients with serious cardiorespiratory Intraoperative requirements disease. In most cases, the equivalent of the pa- Maintenance fluids alone are usually only given tient’s estimated blood volume can be replaced when surgery is prolonged (>1–2h), or if there is with red cell concentrates, crystalloid and colloid the possibility of a delay in the patient resuming in the appropriate volumes. Occasionally, blood oral fluid intake. Most patients will compensate for loss is such that the haemostatic mechanisms are a preoperative deficit by increasing their oral in- affected. This may be seen as continuous oozing take postoperatively. When maintenance fluid is from the surgical wound or around IV cannulation used it should be given at 1.5mL/kg/h, and sites. If this is suspected, the patient’s coagulation increased if the patient is pyrexial by 10% for each status must be confirmed (platelet count, PT, APTT, degree centigrade above normal. fibrinogen levels). Platelets may not be required Losses during surgery are due to: until losses exceed 1.5 times the estimated blood • Evaporation This can occur during body cavity volume. Treatment is usually reserved for those surgery or when large areas of tissue are exposed, cases in which the INR reaches 1.7–2.0, fibrinogen depleting the total body water. levels fall below 0.5g/L or the platelet count falls • Trauma The formation of tissue oedema, the below 50 ¥ 109/L. volume of which is dependent upon the extent of tissue damage; it is similar in composition Local and regional anaesthesia to extracellular fluid. This fluid is often referred to as ‘third space loss’ and creates a deficit in When referring to local and regional techniques the circulating volume that can no longer be and the drugs used, the terms ‘analgesia’ and accessed. ‘anaesthesia’ are used loosely and interchangeably. • Blood loss This will depend upon the type and For clarity and consistency the following terms will site of surgery. be used:

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Table 2.15 Local anaesthetic drugs

Drug Dose Speed of onset Duration of action Comments

Lignocaine 3 mg/kg (plain), Rapid 60–180 mins, depending Used: topically, infiltration, max. 200 mg on the technique used nerve blocks, IVRA, 6 mg/kg (with epidurally, intrathecally epinephrine), max. 500 mg

Bupivacaine 2 mg/kg, max. : up Up to 24 h Mainly used for nerve blocks, 150 mg to 40 mins epidurally and intrathecally. (± epinephrine) Epidurally: 3–4 h, dose dependent Relatively cardiotoxic in any 4 h 15–20 mins period Intrathecal: 30 s 2–3 h, dose dependent

Levo bupivacaine An isomer of bupivacaine; most properties very similar, but less cardiotoxic. This allows slightly higher doses to be given

Ropivacaine 3 mg/kg, Similar to For the same concentration At lower concentrations, max. 200 mg bupivacaine and technique, shorter relatively less intense motor than bupivacaine block than bupivacaine

IVRA: intravenous regional anaesthesia.

• Analgesia The state when only relief of pain is Ametop provided. This may allow some minor surgical pro- cedures to be performed, for example infiltration This is a topical preparation of 4% amethocaine. It analgesia for suturing. is used like EMLA to produce surface analgesia, but • Anaesthesia The state when analgesia is accom- in a slightly shorter time. panied by muscle relaxation, usually to allow A synopsis of the drugs used for local and re- major surgery to be undertaken. Regional anaes- gional anaesthesia is given in Table 2.15. thesia may be used alone or in combination with general anaesthesia. Epinephrine () All drugs will be referred to as local anaesthetics ir- respective of the technique for which they are This is added to local anaesthetics to reduce the being used. rate of absorption, reduce toxicity and extend their duration of action. This is most effective during in- filtration anaesthesia and nerve blocks, and less ef- Local anaesthetic drugs fective in epidurals or spinals. Some authorities recommend that solutions containing epineph- rine should never be used intrathecally. Only very EMLA small concentrations of epinephrine are required This is a eutectic mixture of local anaesthetics to obtain intense vasoconstriction (a-adrenergic lignocaine and prilocaine in equal proportions effect). The concentration is expressed as the (25mg of each per gram). It is applied as a cream to weight of epinephrine (g) per volume of solution the skin and produces surface analgesia in approx- (mL). Commonly used concentrations range from imately 60mins. It is used to reduce the pain asso- 1:80000 to 1: 200000. ciated with venepuncture in children. Local anaesthetics containing vasoconstrictors must never be used around extremities (e.g. fin-

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gers, toes, penis), as the vasoconstriction can cause ness, slurred speech, twitching, restlessness, mild fatal tissue ischaemia. hypotension and bradycardia. • Severe or late: grand mal convulsions followed by 1:80000== 1g in 80000mL 1mg in 80mL coma, respiratory depression and, eventually, = 0.0125mg/mL or 12.5m g/mL apnoea, cardiovascular collapse with profound 1:200000== 1g in 200 0000mL 1mg in 2 0mL hypotension and bradycardia, and ultimately, car- = 0.005mg/mL or 5m g/mL diac arrest. The maximum safe dose in an adult is 250mg, that is, 20mL of 1:80000 or 50mL of 1:200000. This Management of toxicity should be reduced by 50% in patients with is- chaemic heart disease. If a patient complains of any of the above symp- toms or exhibits signs, stop giving the local anaes- thetic immediately! The next steps consist of: Calculation of doses • Airway Maintain using basic techniques. For any drug it is essential that the correct dose is Tracheal intubation will be needed if the protective given and the maximum safe dose never exceeded. reflexes are absent to protect against aspiration. This can be confusing with local anaesthetic drugs • Breathing Give oxygen (100%) with support of as the volume containing the required dose will ventilation if inadequate. vary depending upon the concentration (expressed • Circulation Raise the patient’s legs to encourage in per cent), and a range of concentrations exists venous return and start an IV infusion of crystal- for each drug. The relationship between concentra- loid or colloid. Treat a bradycardia with IV at- tion, volume and dose is given by the formula: ropine. If no major pulse is palpable, start external cardiac compression. If inotropes and vasopressors Concentration() %¥ Volume() mL¥= 10 dose() mg are required, invasive monitoring will be needed and this should be performed on the intensive care Local anaesthetic toxicity unit. This is usually the result of one of the following: • Convulsions These must be treated early. • Rapid absorption of a normally safe dose Use of an Diazepam 5–10mg intravenously can be used excessively concentrated solution or injection into initially but this may cause significant respiratory a vascular area results in rapid absorption. It can depression. If the convulsions do not respond or also occur during intravenous regional anaesthesia they recur, then seek assistance. (IVRA — see below) if the tourniquet is released too Because of the risk of an inadvertent overdose of a soon or accidentally. local anaesthetic drug, they should only be given • Inadvertent IV injection Failure to aspirate prior to where full facilities for monitoring and resuscita- injection via virtually any route. tion are immediately available. In this way the pa- • Administration of an overdose Failure or error in tient will recover without any permanent sequelae. either calculating the maximum safe dose or taking into account any pre-existing cardiac or hepatic The role of local and regional disease. anaesthesia Signs and symptoms of toxicity are due to effects on the central nervous system and the cardiovas- Regional anaesthesia is not just an answer to the cular system. These are dependent on the plasma problem of anaesthesia in patients regarded as not concentration and initially may represent either a well enough for general anaesthesia. The decision mild toxicity or, more significantly, the early stages to use any of these techniques should be based on of a more severe reaction. the advantages offered to both the patient and sur- • Mild or early: circumoral paraesthesia, numbness geon. The following are some of the considerations of the tongue, visual disturbances, lightheaded- taken into account.

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• Analgesia or anaesthesia is provided predomi- • Intravenous cannulae and a range of fluids. nantly in the area required, thereby avoiding the • Drugs, including epinephrine, atropine, vaso- systemic effects of drugs. pressors and . • In patients with chronic respiratory disease, • Suction. spontaneous ventilation can be preserved and res- •A surface for the patient that is capable of being piratory depressant drugs avoided. tipped head-down. • There is generally less disturbance of the control of coexisting systemic disease requiring medical Local and regional anaesthetic therapy, for example diabetes mellitus. techniques • The airway reflexes are preserved and in a patient with a full stomach, particularly due to delayed Local anaesthetics can be used: gastric emptying (e.g. pregnancy), the risk of aspi- • topically to a mucous membrane, for example ration is reduced. the eye or urethra; • Central neural blockade may improve access and • for subcutaneous infiltration; facilitate surgery, for example by causing contrac- • intravenously after the application of a tion of the bowel or by providing profound muscle tourniquet (IVRA); relaxation. • directly around nerves, for example the brachial •Blood loss can be reduced with controlled plexus; hypotension. • in the extradural space (‘epidural anaesthesia’); • There is a considerable reduction in the equip- • in the subarachnoid space (‘’). ment required and the cost of anaesthesia. This The latter two techniques are more correctly called may be important in underdeveloped areas. ‘central neural blockade’; however, the term • When used in conjunction with general anaes- ‘spinal anaesthesia’ is commonly used when local thesia, only sufficient anaesthetic (inhalational or anaesthetic is injected into the subarachnoid space IV) is required to maintain unconsciousness, with and it is in this context that it will be used. The fol- analgesia and muscle relaxation provided by the lowing is a brief introduction to some of the more regional technique. popular regional anaesthetic techniques; those • Some techniques can be continued postopera- who require more detail should consult the texts in tively to provide pain relief, for example an Further reading. epidural. • Complications after major surgery, particularly Infiltration analgesia (Fig. 2.23) orthopaedic surgery, are significantly reduced. Lignocaine 0.5% is used for short procedures, for example suturing a wound, and 0.5% bupivacaine A patient should never be forced to accept a local or for pain relief from a surgical incision. A solution regional technique. Initial objections and fears are best alleviated, and usually overcome, by explanation of the containing epinephrine can be used if a large dose advantages and reassurance. or a prolonged effect is required, providing that tis- sues around end arteries are avoided. Infiltration analgesia is not instantaneous and lack of patience Whenever a local or regional anaesthetic tech- is the commonest reason for failure. The technique nique is used, facilities for resuscitation must used is as follows: always be immediately available in order that aller- • Calculate the maximum volume of drug that can gic reactions and toxicity can be dealt with be used. effectively. At a minimum this will include the • Clean the skin surrounding the wound with an following: appropriate solution and allow to dry. • Equipment to maintain and secure the airway, • Insert the needle subcutaneously, avoiding any give oxygen and provide ventilation. obvious blood vessels.

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equivalent of a massive intravenous injection. Contraindications are relatively few but include patients with impaired peripheral circulation or sickle-cell disease.

Brachial plexus block

The nerves of the brachial plexus can be anaes- thetized by injecting the local anaesthetic drug either above the level of the clavicle (supraclavicu- lar approach) or where they enter the arm through the axilla along with the axillary artery and vein (axillary approach). A nerve stimulator is fre- quently used to locate the nerves more precisely. All of the drugs in Table 2.15 can be used. These Figure 2.23 Infiltration with local anaesthetic. techniques can be used for a wide range of surgical procedures below the elbow and will frequently provide good analgesia in the immediate postoper- ative period. As the block may last several hours, it • Aspirate to ensure that the tip of the needle does is important to warn both the surgeon and patient not lie in a blood vessel. of this. • Inject the local anaesthetic in a constant flow as the needle is withdrawn. Too-rapid injection will Epidural anaesthesia cause pain. • Second and subsequent punctures should be Epidural (extradural) anaesthesia involves the made through an area of skin already deposition of a local anaesthetic drug into the po- anaesthetized. tential space outside the dura (Fig. 2.24a). This When suturing, the needle is inserted into an area space extends from the craniocervical junction at of intact skin at one end of the wound and C1 to the sacrococcygeal membrane, and anaes- advanced parallel to the wound, and local anaes- thesia can theoretically be safely instituted at any thetic is injected as described. In a clean wound, level in between. In practice, an epidural is sited local anaesthetic can be injected directly into the adjacent to the nerve roots that supply the surgical exposed wound edge. This technique can be also site; that is, the lumbar region is used for pelvic and used at the end of surgery to help reduce wound lower limb surgery and the thoracic region for ab- pain postoperatively. dominal surgery. A single injection of local anaes- thetic can be given, but more commonly a catheter is inserted into the epidural space and either re- IVRA, bier’s block peated injections or a constant infusion of a local Local anaesthetic is injected into the veins of an anaesthetic drug is used. exsanguinated limb and retained by using an arte- To aid identification of the epidural space, a rial tourniquet. Anaesthesia is produced in 10– technique termed ‘loss of resistance’ is used. The 15mins and the duration is limited by discomfort (Tuohy) needle is advanced until its tip is embed- caused by the tourniquet. Sensation returns soon ded within the ligamentum flavum (yellow liga- after release of the tourniquet. This is a useful tech- ment). This blocks the tip and causes marked nique for surgery of the distal upper limb. Correct resistance to attempted injection of either air or functioning of the tourniquet is essential other- saline from a syringe attached to the needle. As the wise there is the risk of the patient being given the needle is advanced further, the ligament is pierced,

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Dura Dura — not punctured Epidural space Ligamentum flavum

Spinous process

Tuohy needle

(a)

Dura — pierced by needle Ligamentum flavum

Spinous process

Figure 2.24 (a) Placement of needle tip for epidural anaesthesia. (b) Place- ment of needle tip for spinal (intrathe- cal) anaesthesia. From Gwinnutt CL CSF (b) Clinical Anaesthesia. Oxford: Black- well Science, 1996.

resistance disappears dramatically and air or saline Varying concentrations of local anaesthetics are is injected easily. used depending on what effect is required. For ex- A plastic catheter is then inserted into the ample, bupivacaine 0.5–0.75% will be needed for epidural space via the needle. The catheter is surgical anaesthesia with muscle relaxation, but marked at 5cm intervals to 20cm and at 1cm only 0.1–0.2% for postoperative analgesia. Local intervals between 5 and 15cm. If the depth of the anaesthetic will spread from the level of injection epidural space is noted, this allows the length of both up and down the epidural space. The extent catheter in the space to be determined. of anaesthesia is determined by:

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• The spinal level of insertion of the epidural. For a given volume, spread is greater in the thoracic re- gion than in the lumbar region. • The volume of local anaesthetic injected. • Gravity: tipping the patient head-down encour- ages spread cranially, while head-up tends to limit spread. The spread of anaesthesia is described with refer- ence to the limits of the dermatomes affected; for example: the inguinal ligament, T12; the umbili- cus, T10; and the nipples, T4. An opioid is often given with the local anaesthetic to improve the Figure 2.25 Photomicrograph showing shape of bevel quality and duration of analgesia, for example fen- needle (top) and ‘pencil point’ needle (below). From Jones MJ, Selby IR, Gwinnutt CL & Hughes DG. Technical note: the tanyl 50mg. For details of infusions of local anaes- influence of using an atraumatic needle on the incidence of thetics and opioids for postoperative analgesia, see post-myelography headache. British Journal of page 87. 1994; 67: 396–98.

Spinal anaesthesia • Positioning of the patient either during or after Spinal (intrathecal) anaesthesia results from the in- the injection. Maintenance of the sitting position jection of a local anaesthetic drug directly into the after injection results in a block of the low lumbar cerebrospinal fluid (CSF), within the subarachnoid and sacral nerves. In the supine position, the block space (Fig. 2.24b). The spinal needle can only be in- will extend to the thoracic nerves around T5–6, the serted below the second lumbar and above the first point of maximum backwards curve (kyphosis) of sacral vertebrae; the upper limit is determined by the thoracic spine. Further extension can be ob- the termination of the spinal cord, and the lower tained with a head-down tilt. limit by the fact that the sacral vertebrae are fused • Increasing the dose (volume and/or concentra- and access becomes virtually impossible. A single tion) of local anaesthetic drug. injection of local anaesthetic is usually used, there- • The higher the placement of the spinal anaes- by limiting the duration of the technique. thetic in the lumbar region, the higher the level of A fine, 22–29 gauge needle with a ‘pencil point’ block obtained. or tapered point (for example Whitacre or Sprotte Small doses of an opioid, for example morphine needle) is used (Fig. 2.25). The small diameter and 0.1–0.25mg, may be injected with the local anaes- shape are an attempt to reduce the incidence of thetic. This extends the duration of analgesia for postdural puncture headache (see below). To aid up to 24h postoperatively. passage of this needle through the skin and inter- spinous ligament, a short, wide-bore needle is in- Monitoring during local and regional troduced initially and the spinal needle passed anaesthesia through its lumen. Factors influencing the spread of the local anaes- During epidural and spinal anaesthesia, the guide- thetic drug within the CSF, and hence the extent of lines on monitoring (see page 49) should be fol- anaesthesia, include: lowed. A conscious patient is not an excuse for • Use of hyperbaric solutions (i.e. its specific inadequate monitoring! Particular attention must gravity is greater than that of CSF), for example be paid to the cardiovascular system as a result of ‘heavy’ bupivacaine (0.5%). This is achieved by the the profound effects these techniques can have. addition of 8% dextrose. Posture is then used to Maintenance of verbal contact with the patient is control spread. useful as it gives an indication of cerebral perfu-

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Table 2.16 Incidence of common complications with Nausea and vomiting spinal anaesthesia These are most often the first indications of hy- • Hypotension 33% potension and cerebral hypoxia, but can also result • Nausea 18% from vagal stimulation during upper abdominal • Bradycardia 13% surgery. Any hypotension or hypoxia is corrected •Vomiting 7% as described above. If due to surgery, try to reduce • Dysrhythmias 2% the degree of manipulation. If this is not possible then it may be necessary to convert to general anaesthesia. Atropine 0.3–0.6mg is frequently sion. Early signs of inadequate cardiac output are effective, particularly if there is a bradycardia. Anti- complaints of nausea and faintness, and subse- emetics can be tried (e.g. metoclopramide 10mg quent vomiting. The first indication of extensive intravenously), but this must not be at the expense spread of anaesthesia may be a complaint of diffi- of the above. culty with breathing or numbness in the fingers. Clearly, these valuable signs and symptoms will be lost if the patient is heavily sedated. Postdural puncture headache

Caused by a persistent leak of CSF from the Complications of central neural blockade needle hole in the lumbar dura. The incidence is greatest with large holes, that is, when a hole is These are usually mild and rarely cause any lasting made accidentally with a Tuohy needle, and least morbidity (Table 2.16). Those commonly seen after spinal anaesthesia using fine needles (e.g. 26 intraoperatively are due predominantly to the gauge) with a pencil or tapered point (<1%). effects of the local anaesthetic. Their management Patients usually complain of a headache that is is covered below. Complications seen in patients frontal or occipital, postural, worse when standing receiving epidural analgesia postoperatively are and exacerbated by straining. The majority will covered on page 87. resolve spontaneously. Persistent headaches can be relieved (>90%) by injecting 20–30mL of the Hypotension and bradycardia patient’s own venous blood into the epidural space (epidural blood patch) under strict aseptic Anaesthesia of the lumbar and thoracic nerves conditions. causes progressive sympathetic block, a reduction in the peripheral resistance and venous return to the heart and fall in cardiac output. If the block ex- Regional anaesthesia, awake or after tends cranially beyond T5, the cardioaccelerator induction of anaesthesia? nerves are also blocked, and the unopposed vagal Major nerve blocks and epidural anaesthesia are tone results in a bradycardia. Small falls in blood often combined with general anaesthesia to reduce pressure are tolerated and may be helpful in reduc- the amount and number of systemic drugs given ing blood loss. If the blood pressure falls >25% of and to provide postoperative analgesia. Claimed resting value, or the patient becomes symptomatic advantages of performing the block with the pa- (see below), treatment consists of: tient awake: • oxygen via a facemask; • the block can be checked before surgery com- • IV fluids (crystalloids or colloids) to increase mences to ensure it works satisfactorily; venous return; • the risk of nerve injury is reduced as the patient • vasopressors to counteract the vasodilatation, will complain if the needle touches a nerve; either , an a- and b-agonist (3mg IV) • the patient can co-operate with positioning. or metaraminol, an a-agonist (0.25mg IV); Claimed advantages of performing the block after • atropine 0.5mg IV for a bradycardia. induction of anaesthesia:

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• it is more pleasant for the patient, with no dis- Further reading comfort during insertion of the needle; • there is no risk of the patient suddenly moving; Aitkenhead A, Rowbotham DJ, Smith G (eds). • it allows easier positioning of patients in pain, Textbook of anaesthesia, 4th edn. Edinburgh: for example due to fractures; Churchill Livingstone, 2001. • if the needle hits the nerve then the damage has Al-Shaikh B, Stacey S. Essentials of anaesthetic already been done. equipment, 2nd edn. Edinburgh: Churchill Fortunately, in experienced hands with either Livingstone, 2001. technique, the risk of nerve injury resulting in per- British Medical Association and the Royal manent sequelae is very rare. However, all patients Pharmaceutical Society of Great Britain. British who have a regional technique should be assessed National Formulary (BNF). London: British to ensure that there is full recovery of normal Medical Association and the Royal function. Pharmaceutical Society of Great Britain. (Current issue available at BNF website: Contraindications to epidural and http://www.bnf.org/) spinal anaesthesia Gan TJ, Meyer T, Apfel CC et al., and Department of Anesthesiology, Duke University Medical Hypovolaemia Either as a result of blood loss or de- Center. Consensus guidelines for managing hydration. Such patients are likely to experience postoperative nausea and vomiting. Anesthesia severe falls in cardiac output as compensatory and Analgesia 2003; 97: 62–71. vasoconstriction is lost. Gwinnutt C, Driscoll P (eds). Trauma resuscitation: A low, fixed cardiac output As seen with severe aortic the team approach, 2nd edn. Oxford: Bios or mitral stenosis. The reduced venous return Scientific, 2003. further reduces cardiac output, jeopardizing per- Gosling P. Salt of the earth or a drop in the ocean? fusion of vital organs. A pathophysiological approach to fluid Local skin Risk of introducing infection. resuscitation. Emergency Medicine Journal 2003; Coagulopathy Either as a result of a bleeding 20: 306–15. diathesis (e.g. haemophilia) or therapeutic anti- Wildsmith JAW, Armitage EN (eds). Principles and coagulation. This risks causing an epidural practice of regional anaesthesia, 2nd edn. haematoma. There may also be a very small risk Edinburgh: Churchill Livingstone, 1993. in patients taking aspirin and associated drugs Yentis SM, Hirsch NP, Smith GB. Anaesthesia and which reduce platelet activity. Where intensive care A to Z: an encyclopaedia of principles are used perioperatively to reduce the risk of and practice. Edinburgh: Butterworth deep venous thrombosis, these may be started Heinemann, 2003. after the insertion of the epidural or spinal. Raised intracranial pressure Risk of precipitating Useful websites coning. Known allergy to amide local anaesthetic http://www.nice.org.uk/pdf/ drugs. Ultrasound_49_GUIDANCE.pdf A patient who is totally uncooperative. [Guidance from the National Institute of Concurrent disease of the CNS Some would caution Clinical Excellence (NICE) on the use of against the use of these techniques for fear of ultrasound locating devices for placing central being blamed for any subsequent deterioration. venous catheters.] Previous spinal surgery or has abnormal spinal http://www.aagbi.org/ anatomy Although not an absolute contraindi- [The Association of Anaesthetists of Great cation, epidural or spinal anaesthesia may be Britain & Ireland.] technically difficult.

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http://www.rcoa.ac.uk/ http://www.jr2.ox.ac.uk/bandolier/booth/ [The Royal College of Anaesthetists.] painpag/ These two sites are a must if you want to have [The Oxford Pain site. Good for the latest the latest national UK guidance on anaesthetic evidence-based reviews in pain.] practice. http://www.mhra.gov.uk/ www.theairwaysite.com [Medicines and Healthcare products Regulatory [This site is aimed at emergency physicians and Agency. This agency ensures that medicines, orientated to American practice. It does, healthcare products and medical equipment however, contain some useful information.] meet appropriate standards of safety, quality, www.lmaco.com/ performance and effectiveness, and are used [The laryngeal mask airway company website, safely. Site contains latest drug and device which has instruction manuals for all the hazards.] variations in current use.] http://www.aagbi.org/pdf/blood_tran.pdf http://gasnet.med.yale.edu/ [Association of anaesthetists guidelines on [The best anaesthesia site on the Web, with free blood transfusion, 2001.] sign-on, and a virtual textbook of anaesthesia http://www.shotuk.org/ that includes a good section on airway [Serious Hazards of Transfusion (SHOT). management.] Contains latest UK data.] http://www.capnography.com/index.html http://www.nysora.com/ [This is an excellent site if you want to know [The best regional anaesthesia site.] more about capnography. Very detailed, so be warned.]

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• Circulation equipment A defibrillator, drugs for The recovery area cardiopulmonary resuscitation, a range of IV solu- The vast majority of patients recover from anaes- tions, pressure infusers and devices for IV access. thesia and surgery uneventfully, but a small and • Drugs For resuscitation and anaesthesia. unpredictable number suffer complications. It is • Monitoring equipment Transducers and a moni- now accepted that all patients recovering from tor capable of displaying two or three pressure anaesthesia should be nursed in an area with ap- waveforms, end-tidal carbon dioxide monitor and propriate facilities to deal with any of the problems thermometer. that may arise, and by trained staff. Most patients will recover on a trolley capable of being tipped Discharge of the patient head-down. Patients who have undergone pro- longed surgery, or where a prolonged stay is The anaesthetist’s responsibility to the patient expected, may be recovered on their beds to does not end with termination of the anaesthetic. minimize the number of transfers. Each patient Although care is handed over to the recovery staff should be cared for in a dedicated area equipped (nurse or equivalent), the ultimate responsibility with: remains with the anaesthetist until discharge from • oxygen supply plus appropriate circuits for the recovery area. If there are inadequate numbers administration; of recovery staff to care for a newly admitted pa- • suction; tient, the anaesthetist should adopt this role. • ECG monitoring device; • pulse oximeter; A patient who cannot maintain his/her own airway •non-invasive blood pressure monitor. should never be left alone. In addition the following must be available imme- diately: • Airway equipment Oral and nasal airways, a The length of time any patient spends in recovery range of endotracheal tubes, laryngoscopes, a will depend upon a variety of factors, including bronchoscope and the instruments to perform length and type of surgery, anaesthetic technique a cricothyroidotomy and tracheostomy. and the occurrence of any complications. Most • Breathing and ventilation equipment Self-inflating units have a policy determining the minimum bag-valve-masks, a mechanical ventilator and a length of stay, which is usually around 30mins, chest drain set. and agreed discharge criteria (Table 3.1).

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Table 3.1 Minimum criteria for discharge from recovery of the airways that plays no part in gas exchange. area No oxygen reaches the alveoli irrespective of the

• Fully conscious and able to maintain own airway inspired oxygen concentration and profound hy- (although patient may still be ‘sleepy’) poxaemia will follow. Hypoventilation is always • Adequate breathing accompanied by hypercapnia, as there is an in- • Stable cardiovascular system, with minimal bleeding verse relationship between arterial carbon dioxide

from the surgical site (PacO2) and alveolar ventilation. Common causes • Adequate pain relief of hypoventilation include: •Warm • Obstruction of the airway Most often due to the tongue. Consider vomit, blood or swelling (e.g. post-thyroid surgery). Partial obstruction causes noisy breathing; in complete obstruction there is Complications and their little noise despite vigorous efforts. There may be a management characteristic ‘see-saw’ or paradoxical pattern of ventilation. A tracheal tug may be seen. It is pre- vented by recovering patients in the lateral posi- Hypoxaemia tion, particularly those recovering from surgery This is the most important respiratory complica- where there is a risk of bleeding into the airway tion after anaesthesia and surgery. It may start at (e.g. ear, nose and throat (ENT) surgery), or regur- recovery and in some patients persist for 3 days or gitation (bowel obstruction or a history of reflux). more after surgery. The presence of cyanosis is very If it is not possible to turn the patient (e.g. after a

insensitive and when detectable the arterial PO2 hip replacement), perform a chin lift or jaw thrust will be <8kPa (55mmHg), a saturation of 85%. The (see page 100). An oropharyngeal or nasopharyn- advent of pulse oximetry has had a major impact geal airway may be required to help maintain the on the prevention of hypoxaemia and should be airway (see page 18). used routinely in all patients. If hypoxaemia is se- vere, persistent or when there is any doubt, arterial blood gas analysis should be performed. Hypox- No patient should be handed to the care of the recovery aemia can be caused by a number of factors, either nurse with noisy respiration of unknown cause. alone or in combination: • alveolar hypoventilation; • ventilation and perfusion mismatch within the • Central respiratory depression The residual effects lungs; of anaesthetic drugs decrease the ventilatory re- • diffusion hypoxia; sponse to hypoxia and hypercarbia and also reduce • pulmonary diffusion defects; the level of consciousness. Support ventilation •a reduced inspired oxygen concentration. until effects have worn off or reversed. Opioid analgesics (in excess) cause respiratory depression and reduce the level of consciousness. If severe, the Alveolar hypoventilation administration of the specific antagonist naloxone This is the commonest cause of hypoxaemia and may be required (see page 39). results in insufficient influx of oxygen into the • Hypothermia Reduces ventilation but, in the alveoli to replace that taken up by the blood. As a absence of any contributing factors, it is usually

result, alveolar PO2 (PAO2) and arterial PO2 (PaO2) adequate for the body’s needs. fall. In most patients, increasing their inspired oxy- • Cerebral haemorrhage or ischaemia May cause gen concentration will restore alveolar and arterial direct damage to the respiratory centre or, more

PO2. Eventually a point is reached where there is commonly, a deeply unconscious patient unable only ventilation of ‘dead space’, that is, the volume to maintain a patent airway.

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• Impaired mechanics of ventilation Pain, particu- venous, with an oxygen content of 15mL/100mL larly after upper abdominal or thoracic surgery, of blood. prevents coughing, leading to sputum retention • The final oxygen content of blood leaving the and atelectasis. Provide adequate analgesia (con- lungs will be dependent on the relative propor- sider central neural block). Residual neuromuscu- tions of shunted blood and non-shunted blood. lar blockade is suggested by unsustained, jerky movements with rapid, shallow breathing in a hy- pertensive, tachycardic patient. For test to confirm For an equivalent blood flow, areas of V/Q < 1 decrease the diagnosis see page 35. The patient should be oxygen content more than increasing the oxygen con- given oxygen, reassured, sat upright to improve centration in areas of V/Q > 1 increases content. the efficiency of ventilation, and a (further) dose of neostigmine and an anticholinergic given. • Pneumothorax or haemothorax Prevents ventila- The aetiology of V/Q mismatch is multifactorial tion of the underlying lung. Will require insertion but the following are recognized as being of of chest drain. importance: • Diaphragmatic splinting Abdominal distension •Mechanical ventilation reduces cardiac output. and obesity push the diaphragm into the This reduces perfusion of non-dependent areas of and increase the work of breathing. Such patients the lungs, whilst ventilation is maintained. This is are greatly helped by being sat up. worst in the lateral position, when the upper lung is better ventilated and the lower lung better perfused. Ventilation and perfusion mismatch •A reduced functional residual capacity (FRC). In within the lungs supine, anaesthetized patients, particularly those Normally, ventilation of the alveoli (V) and perfu- over 50 years of age, the FRC falls below their clos- sion with blood (Q) are well matched (V/Q = 1) to ing capacity — the lung volume below which some ensure that the haemoglobin in blood leaving the airways close and distal alveoli are no longer venti- lungs is saturated with oxygen. During anaesthesia lated. Eventually, areas of atelectasis develop, and the recovery period, this process is disturbed mainly in dependent areas of the lung that are (ventilation/perfusion (V/Q) mismatch). Areas perfused but not ventilated. develop where: • Pain restricts breathing and coughing, lead- • Perfusion exceeds ventilation (V/Q < 1): this results ing to poor ventilation of the lung bases, sputum in haemoglobin with a reduced oxygen content. retention, basal atelectasis and, ultimately, infec- • Ventilation exceeds perfusion (V/Q > 1): this can tion. This is more prevalent in the following be considered wasted ventilation. Only a small circumstances: additional volume of oxygen is taken up as the • smokers; haemoglobin is already almost fully saturated • obesity; (98%). • pre-existing lung disease; In the most extreme situation, there is perfusion • elderly; of areas of the lung but no ventilation (V/Q = 0). • after upper gastrointestinal or thoracic Blood leaving these areas remains ‘venous’ and is surgery; often referred to as ‘shunted blood’. This is then •3 days after surgery. mixed with oxygenated blood leaving ventilated The effects of small areas of V/Q mismatch can be areas of the lungs. The net result is: corrected by increasing the inspired oxygen con- • Blood perfusing alveoli ventilated with air has an centration. However, because of the dispropor- oxygen content of approximately 20mL/100mL of tionate effect of areas V/Q < 1, once more than 30% blood. of the pulmonary blood flow is passing through • Blood perfusing unventilated alveoli remains such areas, even breathing 100% oxygen will not

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Table 3.2 Effect of alveolar oxygen concentration on oxygen content of blood

Alveolar oxygen Haemoglobin Oxygen content concentration (%) saturation (%) (mL/100 mL blood)

Alveoli containing air 21 97 20 Alveoli containing oxygen 100 100 21 Non-ventilated alveoli Very low 75 15

eliminate hypoxaemia. The oxygen content of the Management of hypoxaemia pulmonary blood flow through areas ventilated with 100% oxygen will only increase by 1mL/100 All patients should be given oxygen in the imme- mL of blood (21mL/100mL of blood, Table 3.2), diate postoperative period to: insufficient to offset the lack from the areas of low • counter the effects of diffusion hypoxia when V/Q. nitrous oxide has been used; • compensate for any hypoventilation; Diffusion hypoxia • compensate for V/Q mismatch; • meet the increased oxygen demand when Nitrous oxide absorbed during anaesthesia has to shivering. be excreted during recovery. As it is very insoluble Patients who continue to hypoventilate, have per- in blood, it rapidly diffuses down a concentration sistent V/Q mismatch, are obese, anaemic or have gradient into the alveoli, where it reduces the par- ischaemic heart disease, will require additional tial pressure of oxygen in the alveoli, making the oxygen for an extended period of time. This is best patient hypoxaemic. This can be treated by giving determined either by arterial blood gas analysis or oxygen via a facemask to increase the inspired oxy- by using a pulse oximeter. gen concentration (see below).

Devices used for delivery of oxygen Pulmonary diffusion defects

Any chronic condition causing thickening of the Variable-performance devices: masks or alveolar membrane, for example fibrosing alveoli- nasal cannulae tis, impairs transfer of oxygen into the blood. In the recovery period it may occur secondary to the These are adequate for the majority of patients re- development of pulmonary oedema following covering from anaesthesia and surgery. The precise fluid overload or impaired left ventricular func- concentration of oxygen inspired by the patient is tion. It should be treated by first administering unknown as it is dependent upon the patient’s oxygen to increase the partial pressure of oxygen in respiratory pattern and the flow of oxygen used the alveoli and then by management of any under- (usually 2–12L/min). The inspired gas consists of a lying cause. mixture of: • oxygen flowing into the mask; • oxygen that has accumulated under the mask A reduced inspired oxygen concentration during the expiratory pause; As the inspired oxygen concentration is a prime • alveolar gas from the previous breath which has determinant of the amount of oxygen in the alve- collected under the mask; oli, reducing this will lead to hypoxaemia. There • air entrained during peak inspiratory flow from are no circumstances where it is appropriate to ad- the holes in the side of the mask and from leaks minister less than 21% oxygen. between the mask and face.

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Fig. 3.2 Hudson mask with reservoir and high airflow oxy- gen enrichment (HAFOE; Venturi) mask.

Fig. 3.1 Hudson mask (top left), MC mask (top right) and nasal catheters (bottom). Fixed-performance devices

Examples of this type of device are Hudson and MC These are used when it is important to deliver a masks (Fig. 3.1). As a guide, they increase the in- precise concentration of oxygen, unaffected by the spired oxygen concentration to 25–60% with oxy- patient’s ventilatory pattern. These masks work on gen flows of 2–12L/min. the principle of high airflow oxygen enrichment Patients unable to tolerate a facemask who can (HAFOE). Oxygen is fed into a Venturi that en- nose breathe may find either a single foam-tipped trains a much greater but constant flow of air. catheter or double catheters, placed just inside the The total flow into the mask may be as high as vestibule of the nose, more comfortable (see Fig. 45L/min. The high gas flow has two effects: it 3.1). Lower flows of oxygen are used, 2–4L/min meets the patient’s peak inspiratory flow, reducing increasing the inspired oxygen concentration to entrainment of air, and flushes expiratory gas, re- 25–40%. ducing rebreathing. Masks deliver either a fixed If higher inspired oxygen concentrations are concentration or have interchangeable Venturis to needed in a spontaneously breathing patient, a vary the oxygen concentration (Fig. 3.2). Hudson mask with a reservoir can be used (see Fig. The above systems all deliver dry gas to the 3.2). A one-way valve diverts the oxygen flow into patient that may cause crusting or thickening the reservoir during expiration. During inspira- of secretions and difficulty with clearance. For pro- tion, the contents of the reservoir, along with longed use, a HAFOE system should be used with a the high flow of oxygen (12–15L/min), result in humidifier. minimal entrainment of air, raising the inspired concentration to 85%. An inspired oxygen con- Hypotension centration of 100% can only be achieved by using either an anaesthetic system with a close-fitting This can be due to a variety of factors, alone or facemask or a self-inflating bag with reservoir and in combination, that reduce the cardiac output, non-rebreathing valve and an oxygen flow of the systemic vascular resistance or both (see also 12–15L/min. page 96): • hypovolaemia; • reduced myocardial contractility;

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• vasodilatation; Management (see also page 97) • cardiac arrhythmias. • Ensure adequate oxygenation and ventilation. • Intravenous fluid, either crystalloid or colloid, should be given, using a pressure infusor to speed Hypovolaemia administration. This is the commonest cause of hypotension after • Consider cross-matching blood if not already anaesthesia and surgery. Although intraoperative done. blood loss is usually obvious, continued bleeding, • Stop any external haemorrhage with direct especially in the absence of surgical drains, may pressure. not be. Fluid loss may also occur as a result of tissue • Get surgical assistance if internal haemorrhage damage leading to oedema, or from evaporation suspected. during prolonged surgery on body cavities, for Monitoring of the patient’s central venous pressure example the or thorax (see below). The (CVP) may be indicated if cardiac function is in diagnosis can be confirmed by finding: question. In the presence of significant hypo- •Reduced peripheral perfusion; cold clammy skin volaemia do not waste time inserting a CVP line or delayed capillary refill (>2s) in the absence of for venous access alone. The trend of the patient’s fear, pain and hypothermia. acid–base status is a useful indicator of therapeutic •Tachycardia; a pulse rate >100 beats/min of poor success. volume. • Hypotension. Initially, systolic blood pressure Reduced myocardial contractility may be reduced minimally but the diastolic eleva- ted as a result of compensatory vasoconstriction The commonest cause is ischaemic heart disease, (narrow pulse pressure). The blood pressure must causing any degree of left ventricular failure. The always be interpreted in conjunction with the diagnosis should be considered on finding: other assessments. • poor peripheral circulation; •Inadequate urine output (<0.5mL/kg/h), best • tachycardia; measured hourly via a catheter and urometer. • tachypnoea; Consider also the following as causes of reduced • distended neck veins; urine output: • basal crepitations on auscultation of the lungs; •a blocked catheter (blood clot or lubricant); • wheeze with a productive cough; • hypotension; •a triple rhythm on auscultation of the heart. • hypoxia; It is not uncommon to mistake this condition for • renal damage intraoperatively (e.g. during hypovolaemia based on the first three findings. A aortic aneurysm surgery). chest X-ray is usually diagnostic.

Management The commonest cause of oliguria is hypovolaemia; anuria is usually due to a blocked catheter. • Sit the patient upright. • Give 100% oxygen. • Monitor the ECG, blood pressure and peripheral The extent to which these changes occur will de- oxygen saturation. pend primarily upon the degree of hypovolaemia. If the diagnosis is unclear, a fluid challenge (maxi- A tachycardia may not be seen in the patient taking mum 5mL/kg) can be given and the response ob- beta blockers and up to 15% of the blood volume served; an improvement in the circulatory status may be lost without detectable signs in a fit, young suggests hypovolaemia. Where there is no doubt patient. An arterial blood sample should be about the diagnosis, fluids can be restricted ini- analysed; a metabolic acidosis is usually found tially and a diuretic (e.g. frusemide 20–40mg) after a period of poor tissue perfusion. given intravenously. Trends in the CVP can be

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monitored as a guide to therapy. Patients with ven- Cardiac arrhythmias tricular failure are best cared for in a critical care area. If there is acute myocardial infarction, con- Occur more frequently in the presence of: tractility may only improve with the use of in- • hypoxaemia; otropes in conjunction with vasodilators, and this • hypovolaemia; is best undertaken on the intensive care unit (ICU) • hypercarbia; (see page 121). Unfortunately thrombolysis is con- •hypothermia; traindicated after surgery. • sepsis; • pre-existing ischaemic heart disease; • electrolyte abnormalities; Vasodilatation • hypo/hyperkalaemia, hypocalcaemia, hypomag- This is common during spinal or epidural anaes- nesaemia; thesia (see page 67). Another example is following • acid–base disturbances; prostate surgery under spinal anaesthesia. As the • inotropes, antiarrhythmics, bronchodilators; legs are taken down from the lithotomy position, • antidepressants in overdose. vasodilatation in the lower limbs is unmasked, and result in insufficient time for ventric- as the patient is moved to the recovery area he ular filling, thereby reducing cardiac output, while becomes profoundly hypotensive. reduce the heart rate below the point The development of septic shock may present where no further increase in ventricular filling can initially as peripheral vasodilatation, hypotension occur to maintain cardiac output. and tachycardia in the absence of blood loss. The patient may be pyrexial and if the cardiac output Coronary artery flow is dependent on diastolic pressure is measured, it is usually elevated. Gradually, vaso- and time. Hypotension and tachycardia are therefore constriction ensues along with a fall in cardiac particularly dangerous. output. The diagnosis should be suspected in any patient who has had surgery associated with a sep- tic focus, for example free infection in the peri- Management toneal cavity or where there is infection in the Correction of the underlying problem will result in genitourinary tract. This usually presents several spontaneous resolution of most arrhythmias. Spe- hours after the patient has left the recovery area, cific intervention is required if there is a significant often during the night following daytime surgery. reduction in cardiac output and hypotension. The The causative micro-organism is often a Gram- Resuscitation Council (UK) publishes guidelines negative bacterium. that are regularly updated. • Sinus tachycardia (>100 beats/min) The common- Management est arrhythmia after anaesthesia and surgery, usu- Hypotension secondary to regional anaesthesia ally as a result of pain or hypovolaemia. If there is is corrected by the administration of fluids associated pyrexia, it may be an early indication of (crystalloid, colloid), the use of vasopressors (e.g. sepsis. Treatment consists of oxygen, analgesia and ephedrine), or a combination of both. Oxygen adequate fluid replacement. If the tachycardia per- should always be given. The combination of hypo- sists, then providing there is no contraindication a volaemia and vasodilatation will cause profound small dose of a may be given intra- hypotension. Patients developing septic shock re- venously whilst monitoring the ECG. Rarely, the quire early diagnosis, invasive monitoring and cir- development of an unexplained tachycardia after culatory support in a critical care area. anaesthesia may be the first sign of malignant therapy should be guided by a microbiologist. hyperpyrexia (see page 98). • Supraventricular tachycardia The most common is atrial fibrillation usually secondary to ischaemic

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heart disease or the presence of sepsis. Treatment Postoperative nausea and vomiting will depend on the rate and reduction in cardiac (PONV) output: • heart rate 100–150/min with critical perfusion This occurs in up to 80% of patients following will require cardioversion followed by IV amio- anaesthesia and surgery. A variety of factors have darone 300mg over 1h; been identified which increase the incidence: • heart rate <100/min with good perfusion, con- • Age and sex: more common in young women sider amiodarone 300mg IV over 1h. and children. • Sinus bradycardia (<60 beats/min) Usually the • Site of surgery: abdominal, middle ear or the result of: posterior cranial fossa. • an inadequate dose of an anticholinergic •Giving opioid analgesics pre-, intra- and post- (e.g. glycopyrrolate) given with neostigmine to operatively. reverse neuromuscular block; •Anaesthetic drugs: etomidate, nitrous oxide. • excessive suction to clear pharyngeal or tra- • Gastric dilatation, caused by manual ventilation cheal secretions; with a bag and mask without a clear airway. • traction on the viscera during surgery; • Hypotension associated with epidural or spinal • excessive high spread of spinal or epidural anaesthesia. anaesthesia; • Patients prone to travel sickness. • the development of acute inferior myocardial Patients identified as being at risk of PONV should infarction; be given an anti-emetic before emergence from • excessive beta-blockade preoperatively or in- anaesthesia. Failure of treatment may be addressed traoperatively. in the recovery area by giving a second or third Treatment should consist of removing any pro- drug from different classes of compound. voking stimuli and administering oxygen. If symp- tomatic, atropine 0.5mg intravenously may be Drugs used to treat nausea required. and vomiting

Before resorting to the administration of drugs to Hypertension treat nausea and vomiting, it is essential to make This is most common in patients with pre-existing sure that the patient is not hypoxaemic or hypertension. It may be exacerbated or caused hypotensive. by: • Antihistamines Cyclizine. Adults 50mg intra- • Pain muscularly, up to 6 hourly. Also has anticholiner- • Hypoxaemia gic actions; may cause a tachycardia when given IV. • Hypercarbia • 5-HT3 (hydroxytryptamine) antagonists Ondanse- • Confusion or tron (Zofran). Adults 4–8mg intravenously or • Hypothermia. orally, 8 hourly. Has both central and peripheral A coexisting tachycardia is particularly dangerous actions; in the gut it blocks 5-HT3 receptors in the in the presence of ischaemic heart disease as this mucosal vagal afferents. It does not cause dystonic may cause an acute myocardial infarction. If the movements. blood pressure remains elevated after correcting • Dopamine antagonists Metoclopramide (Max- the above, a vasodilator or beta blocker may be olon). Adults 10mg intravenously, intra- necessary. Senior help should be sought. muscularly or orally, 6 hourly. Although a specific anti-emetic, minimal effect against PONV. Not re- lated to the major tranquillizers and has no seda- tive or effects. Has an effect at the

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chemoreceptor trigger zone and increases gastric sue trauma), most patients start drinking within motility. An alternative is domperidone (Motili- 1–2h of surgery and IV fluid is not required. If a um) 10mg orally. patient has failed to drink within 4–6h (usually • Phenothiazine derivatives Prochlorperazine (Stem- as a result of nausea and vomiting), consideration etil). Adults 12.5mg intramuscularly 6 hourly should be given to commencing IV fluids. Provid- or 15–30mg orally, daily in divided doses. May ing that the volume of vomit is not excessive, only cause hypotension due to alpha-blockade. Some maintenance fluids are required. These are calcu- have antihistamine activity and may cause dystonic lated at 1.5mL/kg/h, but must take into account muscle movements. the accrued deficit. • Anticholinergic drugs Atropine and hyoscine; the For example, a 70kg patient starved from 0800 latter is available as a transdermal patch. Severe to 1400, who is still unable to take fluids by mouth side-effects, particularly dry mouth and blurred at 1800 will require: vision. • Steroids 8mg IV may be useful 1.5mL/kg/h to make up the deficit from in resistant cases. 0800 until 1800 = 1.5¥¥ 70 (kg) 10() hª 1000mL; Postoperative intravenous 1.5mL/kg/h from 1800 until 0800 the fluid therapy next morning: = 1.5¥¥ 70 (kg) 14 () hª 1400mL. Oral intake should be encouraged as not all pa- The total IV fluid requirement= 2400ml tients require routine IV fluids after anaesthesia in the next 14h. and surgery. For those that do, the volume and type of fluid will be determined by a variety of An appropriate rate for the IV fluid would be: factors, including: • 1000mL over the first 4h; • the site of surgery; • 1000mL over the following 6h; • the extent of tissue damage; • 500mL over the last 4h. • blood loss during and after surgery; This should contain the daily requirement of • any delay in starting to drink; Na++ 1–1.5mmol/kg and could be given either • continuing losses from the gastrointestinal tract. as: A wide range of fluids are available (see page 59), 2 ¥ 1000mL 5% glucose and 500mL 0.9% and for each patient the type and volume will (normal) saline; or be dependent upon the calculated maintenance 2 ¥ 1000mL 4% glucose/0.18% saline, and requirements of water and electrolytes plus the 500mL 4% glucose/0.18% saline. replacement of any abnormal losses. This is The patient should be reviewed at 0800 with complemented by clinical evaluation of the pa- regard to further management. tient to ensure that they are adequately hydrated, as assessed by degree of thirst, moisture of mucous Major surgery membranes, blood pressure, pulse, peripheral cir- culation and an adequate urine output. In complex Following major surgery, postoperative fluid bal- cases, monitoring the trend of the CVP may also ance is more complex. Assuming that appropriate prove useful. volumes of water, electrolytes and blood have been given during the operation, then postoperatively the fluid and electrolyte requirements will depend Minor surgery upon: Following minor surgical procedures (i.e. taking • the volume needed for ongoing maintenance, less than 30mins, with minimal blood loss and tis- which will be increased if the patient is pyrexial;

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• replacement of continuing losses from the measure and usually become evident as a result of gastrointestinal tract, for example via a nasogastric the above regimen failing to keep the patient ade- tube; quately hydrated. This is usually seen as thirst, a • any continued bleeding; dry mouth, cool peripheries with empty superficial • rewarming of cold peripheries causing veins, hypotension, tachycardia and a decrease vasodilatation. in the urine output to less than 0.5mL/kg/h. An The patient who has undergone major surgery will additional 1L of Hartmann’s solution per 24h may require close monitoring to ensure that sufficient need to be added to the above regimen to account volumes of the correct fluid are administered. A for such losses and adjusted according to the pa- standard postoperative regimen for the first 24h tient’s response. These losses may continue for up postoperatively might therefore consist of: to 48h after surgery and sufficient extra volumes of • 1.5mL/kg/h water, increased by 10% for each °C fluid should be administered to maintain hydra- if the patient is pyrexial; tion and an adequate circulating volume. Where • sodium, 1mmol/kg; large volumes of fluid are required and/or there is • replacement of measured gastrointestinal losses underlying heart disease, then the CVP should be with an equal volume of Hartmann’s solution; measured and the trend noted (see page 52) and • replacement of blood loss of <500mL with serum electrolytes monitored twice daily. either: • Hartmann’s solution (three times the volume The stress response of blood lost will be needed as it is distributed throughout the extracellular fluid (ECF)); or Following major surgery and trauma, various • colloid, the same volume as the blood loss; neuroendocrine responses result in an increased • blood loss >1000mL will require transfusion secretion of a variety of hormones. Antidiuretic with stored blood. hormone (ADH) secretion is maximal during sur- It is essential that the patient is reviewed at the end gery and may remain elevated for several days. The of the day as described above to ensure that the effect of this is to increase water absorption by the volumes and type of fluid prescribed are adequate kidneys and reduce urine output. Aldosterone se- for the patient’s needs. cretion is raised secondary to increased cortisol lev- On the second and subsequent days, the same els and activation of the renin–angiotensin system. basic principles are used. In addition: This results in sodium retention and increased uri- • The fluid balance of the previous 24h must be nary excretion of potassium. Despite this retention checked. of water and sodium, it is important that fluid • Ensure that all sources of fluid loss are recorded. input is not restricted in these patients, as the con- • The patient’s serum electrolytes must be checked tinued losses identified above more than offset the to ensure adequate replacement. volume retained. • The urine output for the previous 6 and 24h After 2–3 days, hormone levels return to normal should be noted; if decreasing, consider other and this is followed by an increase in the volume of causes of fluid loss, for example increasing pyrexia, urine passed, which may be augmented by loss of development of an ileus. fluid as tissue oedema resolves. • Potassium will be required (in addition to sodi- um) at the rate of 1mmol/kg per 24h. Postoperative analgesia If surgery is associated with significant tissue trau- ma (e.g. total hip replacement, major gastrointesti- After injury, acute pain limits activity until healing nal surgery), then there will be continued losses has taken place. Modern surgical treatment re- into the tissues, which have the same effect as any stores function more rapidly, a process facilitated other form of fluid loss and are often referred to as by the elimination of postoperative pain. A good ‘third space losses’. Such volumes are difficult to example is the internal fixation of fractures, fol-

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lowed by potent analgesia allowing early mobiliza- what to expect postoperatively, what types of anal- tion. Ineffective treatment of postoperative pain gesia are available and also by allowing patients to not only delays this process, but also has other im- explore their concerns. portant consequences: • Patients who have a pre-existing chronic pain •Physical immobility: problem are vulnerable to suffering with addition- • reduced cough, sputum retention and al acute pain. Their nervous systems can be consid- pneumonia; ered to be sensitized to pain and will react more • muscle wasting, skin breakdown and cardio- strongly to noxious stimuli. Bad previous pain ex- vascular deconditioning; periences in hospital or anticipation of severe pain • thromboembolic disease — deep venous for another reason suggest that extra effort will be thrombosis and pulmonary embolus; required to control the pain. • delayed bone and soft tissue healing. • Older patients tend to require lower doses of •Psychological reaction: analgesics as a result of changes in drug distribu- • reluctance to undergo further, necessary surgi- tion, metabolism, excretion and coexisting dis- cal procedures. ease. Prescribing should take these factors into • Economic costs: account rather than using them as an excuse for in- • prolonged hospital stay, increased medical adequate analgesia. There is no difference between complications; the suffered by the different sexes having the • increased time away from normal same operation. occupations. • Upper abdominal and thoracic surgery cause the • Development of chronic pain syndromes. most severe pain of the longest duration, control of Sometimes pain is a useful aid to diagnosis and which is important because of the detrimental ef- must be recognized and acted upon, for example: fects on ventilation. Pain following surgery on the • pain due to ischaemia from tissue swelling, body wall or periphery of limbs is less severe and haematoma formation restricting the circulation for a shorter duration. causing a compartment syndrome or by dressings becoming too tight; Management of postoperative pain • pain of infection from cellulitis, peritonitis or pneumonia; This can be divided into a number of steps: • referred visceral pain in myocardial infarction • assessment of pain; (arm or neck) or pancreatitis (to the back). •analgesic drugs used; • techniques of administration; Any patient who complains of pain that unexpectedly in- • difficult pain problems. creases in severity, changes in nature or site, or is of new onset should be examined to identify the cause rather Assessment of acute pain than simply be prescribed analgesia. Regular measurement of pain means that it is more difficult to ignore and the efficacy of interventions Factors affecting the experience of pain can be assessed. There are a variety of methods of Pain and the patient’s response to it are very assessing pain; Table 3.3 shows a simple, practical variable and should be understood against the system that is easily administered and understood background of the individual’s previous personal by patients. The numeric score is to facilitate experiences and expectations rather than com- recording and allows trends to be identified. Pain pared with the norm. must be assessed with appropriate activity for the • Anxiety heightens the experience of pain. The stage of recovery; for example, 5 days after a hip preoperative visit by the anaesthetist plays a joint replacement a patient would not be expected significant role in allaying anxiety by explaining to have pain while lying in bed, but adequate

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Table 3.3 A simple practical scoring system for acute pain

Pain Staff score view Patient’s view Action

0 None Insignificant or no pain Consider reducing dose or changing to weaker analgesic, e.g. morphine to NSAID plus paracetamol 1 Mild In pain, but expected and tolerable; no reason Continue current therapy, review regularly to seek (additional) treatment 2 Moderate Unpleasant situation; treatment desirable but Continue current therapy, consider additional not necessarily at the expense of severe regular simple analgesia, e.g. paracetamol treatment side-effects and/or NSAID 3 Severe Intolerable situation—will consider even Increase dose of opioid, or start opioid; unpleasant treatments to reduce pain consider alternative technique, e.g. epidural

analgesia should allow mobilization with only • : how the body distributes, mild to insignificant pain. metabolizes and eliminates the drug; • the nature of the stimulus; • the psychological reaction to the situation. Analgesic drugs used postoperatively The biggest step forward in the treatment of acute (Fig. 3.3) pain with opioids has been the recognition that The most commonly used drugs are opioids and individual requirements are very variable and the NSAIDs. dose needs to be titrated for each patient: • There is no minimum or maximum dose. Opioids • Even with best practice some pain will remain. The of opioid drugs and their side- •Minimum levels of monitoring and intervention effects are covered on page 37. In the UK, mor- are necessary for safe, effective use. phine is most commonly used to control severe • Additional methods of analgesia should be con- postoperative pain on surgical units, and dia- sidered if opioid requirements are high. morphine (heroin) on medical wards, for example coronary care units, mainly for historical reasons. Overdose There are few pharmacological differences be- Profound respiratory depression and coma due to tween these two drugs. Morphine can be given by opioids must be treated using the ABC principles several routes (Table 3.4). One of the principal described elsewhere (page 99). Having created a metabolites, morphine-6-glucuronide (M6G), has patent airway and supported ventilation using a potent opioid effects and may accumulate and bag-valve-mask with supplementary oxygen, the cause toxicity in patients with renal failure, effects of the opioid can be pharmacologically particularly the elderly. Fentanyl and reversed (antagonized) using naloxone. 0.4mg is have less active metabolites than morphine and so diluted to 5mL with 0.9% saline and given in may be more suitable for these patients. incremental doses of 1mL IV (adult dosing). Anal- For most painful clinical conditions there will be gesia will also be reversed, and careful thought a blood level of opioid that provides useful analge- must be given to continuing analgesia. HDU care is sia, that is, a reduction in pain level. The dose usually advisable in this situation. required to achieve this may vary enormously between patients as a result of differences in: Long-term complications of opioids • : the effect of the drug on the Adequate treatment of acute pain with opioids is body (via the receptors); not associated with dependency.

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Brain

Spinal cord B Oral Dura L i.m. OPIOIDS B O i.v. Oral L O sub cut. i.m. NSAIDs O D transdermal i.v. O transcutaneous p.r. D Intrathecal Anticonvulsants

Epidural Peripheral nerve

Local CSF anaesthetics

Fig. 3.3 Sites of action of analgesic drugs.

Less potent opioid agonists Non-steroidal anti-inflammatory • Codeine (3-methyl morphine) Well absorbed drugs (NSAIDs) orally, dose 30–60mg 6 hourly (can be given intra- The pharmacology of these drugs has been covered muscularly but never intravenously). Available in a on page 40. range of tablets, often combined with paracetamol, • Paracetamol An analgesic and antipyretic with for example co-codamol (8mg codeine, 500mg little anti-inflammatory action, but usually classi- paracetamol). Exerts its effect by a small amount fied with NSAIDs. Inhibits prostaglandin synthe- (10%) being metabolized to morphine in the liver. sis, mainly in the CNS. It is used to treat mild to Some patients lack the necessary enzyme and moderate pain. Well absorbed orally, causing little therefore get no effect from codeine. irritation of the gastrointestinal tract. Widely used • Tramadol Similar potency to codeine and used orally in a dose of 1g 4–6 hourly, maximum for mild to moderate pain (see page 37). 4g/day. Often incorporated into compound prepa- Neither is a controlled drug and so are more easily rations with aspirin or codeine. An intravenous accessible. preparation is available containing 10mg/mL, in 100mL vials (1g). This can be infused over 15mins and is effective in 5–10mins. The dose is the same as for the oral preparation. It is the safest of all

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Table 3.4 Administration of morphine

Oral Immediate release (IR) tablets or liquid • Absorption and effect within minutes • Usual adult dose 20 mg hourly prn • Less in elderly, more if opioid tolerant •Providing the gut is working, useful even after major surgery • Usually used for acute pain where the opioid requirement is unknown or changing rapidly Modified release (MR) tablets, capsules or granules • Dose released over either 12 or 24 h •Avoids frequent dosing with immediate release preparations • Useful when opioid requirement is prolonged and also for gradually weaning down the dose at the end of treatment The two formulations are usually used together to provide a steady background level of analgesia (MR) with additional breakthrough doses (IR) as required It is important that everybody understands the difference between MR and IR forms of morphine

Intravenous Morphine 10 or 20 mg diluted to 1 mg/mL with 0.9% sodium chloride can be given: • In increments initially of 1–3 mg at 3 min intervals; effective dose may range from 1 to 50 mg or more (the latter in opioid-tolerant patients) •Via patient controlled analgesia device (see below) • As a continuous infusion. Useful where patient cooperation is limited, e.g. in elderly patients or intensive care units. Problems occur in predicting the correct infusion rate, given the variability of dose requirement between patients Very close supervision is required to avoid underinfusion (pain) or overinfusion (toxicity) This method can be used to replace high doses of oral opioids during the perioperative period The intravenous dose of morphine is about one-third of the oral dose

Intramuscular • A predetermined dose (e.g. morphine 10 mg) at fixed minimum intervals, e.g. hourly • Delayed and variable rate of effect •Precise titration is difficult with repeated cycles of pain and relief • Does not require complex equipment or a co-operative patient •Widely available • Intermittent injections through an indwelling cannula may be more acceptable to staff and patients

analgesics but patients may need reassurance that • Activation is by the patient depressing a switch regular dosing of 1g every 6h is not associated with that is designed to prevent accidental triggering hepatic toxicity. A summary of the use of these (hence ‘patient-controlled’). drugs is given in Table 3.5. • There may be a background, low-dose, continu- ous infusion. Analgesic techniques used To prevent the administration of an overdose: postoperatively • The dose and any background infusion is preset (usually by a doctor). • After successful administration of a dose, a sub- Patient-controlled analgesia (PCA) sequent dose cannot be administered for a preset •A microprocessor-controlled syringe pump capa- period, the ‘lockout period’. ble of being programmed is used to deliver a pre- • The total quantity of drug given over a predeter- determined dose of a drug intravenously. mined period can be limited.

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Table 3.5 Non-steroidal anti-inflammatory drugs (NSAIDs)

Route given Non-specific (COX-1 + 2) COX-2 specific CNS effect only

Oral Ibuprofen Rofecoxib Paracetamol 200–400 mg 8-hourly 50 mg once daily 1 g 6-hourly Intravenous Ketorolac Paracoxib Paracetamol 10–30 mg 6-hourly, 40 mg 12-hourly 1 g equivalent max 90 mg/24 h

Effects Anti-inflammatory Yes Yes No Analgesic (central) Yes Yes Yes Side-effects Reduced renal blood flow Yes Probably No Gastric ulceration Yes Unlikely No Anti-platelet Yes Unlikely No Delay bone healing Possible Unlikely No

•Typical settings for an adult using morphine de- Table 3.6 Management of overdose with patient- livered by a PCA device might be: controlled analgesia (PCA)

• bolus dose: 1mg; • Stop the PCA • lockout interval: 5mins. • Give oxygen via a mask • Call for assistance Effective PCA requires: • Consider giving naloxone (as described on page 82) • That the patient be briefed by the anaesthetist • If the patient is apnoeic, commence ventilation using and/or nursing staff preoperatively and, if possible, a self-inflating bag-valve-mask device be shown the device to be used. •A loading dose of analgesic, usually intraven- ously before starting. Failure to do this will result in the patient being unable to get sufficient analgesia •Intravenous administration with greater cer- from the PCA device and the system will fail. tainty of adequate plasma levels. •A dedicated IV cannula or non-return valve on an IV infusion to prevent accumulation of the drug Disadvantages and failure of analgesia. • Equipment is expensive to purchase and Observation and recording of the patient’s maintain. pain score, sedation score and respiratory rate • Requires patient comprehension of the system. to ensure success. Any patient whose respiratory • Patient must be physically able to trigger the rate is less than 8 breaths/min and sedation score device. is 2 or 3 should be treated as described in Table • The elderly are often reluctant to use a PCA 3.6. device. • The potential for overdose if the device is Advantages of PCA incorrectly programmed. • Greater flexibility; analgesia matched to the pa- As pain subsides the PCA can be discontinued, and tient’s perception of the pain. oral analgesics can be used. The first dose should be •Reduced workload for the nursing staff. given 1h prior to discontinuing PCA, to ensure • Elimination of painful IM injections. continuity of analgesia.

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Supra-orbital: scalp surgery

Intercostal: Brachial plexus: rib fractures upper limb surgery

Wound Radial, ulnar and infiltration median at wrist: at the end hand surgery of surgery

Lumbar plexus: Femoral: anterior hip surgery thigh, knee, femoral fracture Sciatic: knee, foot surgery

Sural, saphenous, deep and superficial peroneal, post. tibial: foot surgery

Fig. 3.4 Some commonly used nerve blocks.

alone or in combination with opioids, act on the Regional analgesic techniques (Fig. 3.4) transiting nerve roots and the dorsal horn of the • Peripheral nerve blocks Used mainly for pain relief spinal cord, respectively, to provide dramatic relief after upper or lower limb surgery. A single injection of postoperative pain. It is essential that patients of local anaesthetic, usually bupivacaine, results who are offered an epidural receive an explanation in 6–12h of pain relief. An infusion of local by the anaesthetist at the preoperative visit of what anaesthetic via a catheter inserted close to the to expect postoperatively, in particular altered sen- nerve may enable the block to be continued for sation, weakness of the lower limbs and the po- several days. An alternative effective form of anal- tential need for a urinary catheter. The epidural is gesia must be prescribed for when the local anaes- often sited preoperatively and used as part of the thetic is discontinued to prevent the patient being anaesthetic technique. For upper abdominal sur- in severe pain. gery an epidural in the mid-thoracic region (T6/7) • Epidural analgesia (see also page 65) Infusions of a is used, while a hip operation would need a lumbar local anaesthetic into the epidural space, either epidural (L1/2).

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Different combinations of local anaesthetic and example haemorrhage, are particularly vulnerable opioid infusion have been used successfully. to severe hypotension. Check the extent of the Ideally, the concentration of local anaesthetic block; if extensive, reduce the rate of infusion. should block sensory nerves, leaving motor nerves • Respiratory depression Caused by opioid reaching relatively spared. The choice and dose of opioid the respiratory centre in the medulla. Highly lipid should be such that the drug passes through the soluble opioids (diamorphine, fentanyl) are rapid- dura into the CSF in sufficient quantities to block ly taken up by the spinal cord, limiting their spread the opioid receptors in the spinal cord but not and systemic absorption, and respiratory depres- spread cranially to cause respiratory depression. sion tends to occur early; less soluble opioids For example: (morphine) are taken up slowly, and respiratory de- • bupivacaine 0.167% plus diamorphine pression tends to occur later. A high infusion rate 0.1mg/mL; of either drug may also lead to respiratory depres- • bupivacaine 0.125% plus fentanyl 4mg/mL. sion. Prevented by regular assessment and record- Epidural infusions can be used to maintain an- ing of vital signs. Treat by supporting ventilation if algesia for several days. Opioid side-effects are less necessary; stop the epidural infusion; give nalox- common and less severe than when given systemi- one according to the severity; seek expert help. cally as the dose is much less. • Sedation Due to opioid reaching the brain either directly via the CSF or after absorption into the sys- Points to note temic circulation via the epidural veins. May be • The infusion rate and the site of the catheter secondary to hypotension and cerebral hypox- determine the spread of the solution. In the thor- aemia. Prevent by regular assessment and record- acic epidural space a starting infusion rate might be ing of vital signs. Treat by stopping the infusion; if 4mL/h; in the lumbar space commence at unresponsive or the level of sedation progresses, 8mL/h. give naloxone in 0.1mg increments intravenously; • The efficacy of the infusion must be monitored seek expert help. in a similar manner as for PCA. • Pruritus Can be severe and frequently localized • If analgesia is inadequate, a ‘top-up’ of 3–4mL of to the nose; may respond to antihistamines, at- solution may be necessary. ropine or naloxone. • Observations of the patient’s vital signs should • Retention of urine May be due to the effect of the then be made on a regular basis according to local opioid on bladder sphincter control or the local protocol. anaesthetic removing the sensation of a full blad- • In patients over the age of 60 years, the concen- der. More common in males, particularly if there tration of opioid is often halved. are already symptoms of prostatism. Prevented by routine monitoring of urine output in all Management of complications during postoperative patients. May require short-term postoperative epidural analgesia catheterization. This will depend upon whether local anaesthetics • Numbness and weakness of the legs Usually due to alone or in combination with opioids have been excessive rates of infusion or a too-high concentra- used. The complications arising as a result of the tion of local anaesthetic. May lead to pressure ul- use of local anaesthetics intraoperatively are cov- cers on the patient’s heels or sacrum due to lack of ered on page 63. movement, or falls whilst mobilizing. Prevented • Hypotension Sympathetic block causes vasodi- by regular observation of effects of epidural and latation and increased venous pooling. Treat correct adjustment of infusion rate. acutely with IV fluid and vasopressors (e.g. • Vertebral canal haematoma Can occur as a result ephedrine according to local policy). Prevented by of trauma by the needle or catheter insertion. ensuring the patient has an adequate fluid regimen Greater risk in patients on warfarin, heparin, prescribed. Patients with additional fluid losses, for NSAIDs and other antiplatelet drugs, those with a

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coagulopathy or when severely haemodiluted. • oral morphine immediate release (IR) tablets and Rare, but consider if profound motor and sensory paracetamol prescribed to be given as a spinal block far greater than anticipated. wears off. • Infection Introduced via the catheter. May cause the formation of an epidural abscess and compro- Difficult pain problems mise of the spinal cord. Patients complain typical- ly of increasing back pain but this may be delayed Patients in whom there is evidence of regular opi- for several weeks so that the connection to the sur- oid use preoperatively, for example drug addicts, gery and epidural may be missed. cancer and chronic pain patients and those pa- If there is any doubt about spinal cord function tients with a previous bad pain experience, will the epidural infusion should be stopped and a pose a particular problem postoperatively. They are magnetic resonance imaging (MRI) scan con- best managed using a team approach that will sidered. Damage to nerves or the spinal cord include: during insertion of the needle and systemic toxi- • Liaison with the Acute Pain Team to inform it of city of the local anaesthetic are both unusual the patient’s admission. complications. • Discussion with the anaesthetist, and surgical and nursing staff to plan perioperative care, to: Intrathecal (spinal) analgesia •ensure any current opioid medication is con- (see page 66) tinued on admission to prevent withdrawal; Spinal anaesthesia is of insufficient duration to • understand that much larger doses of opioids provide postoperative pain relief. However, if a than normal may be required; small dose of opioid, for example morphine • explain that toxicity from high doses of opioid 0.1–0.25mg, is injected along with the local anaes- is very unlikely; thetic, this may provide up to 24h of analgesia. • reassure that addiction is not a concern. Complications are the same as those due to opioids • Discussion with the patient to explain: given epidurally, and managed in the same way. • types and effectiveness of analgesic regimes available postoperatively; • that analgesia may not be 100% effective; Other techniques • that long-term continuation may be Entonox is a mixture of nitrous oxide (50%) and necessary; oxygen (50%). It is a weak analgesic with sedative • potential side-effects, especially if regional properties. Useful for short-term analgesia for analgesia planned. painful procedures, for example change of dress- •Plan regular reviews during postoperative ings. It should be avoided in patients with a pneu- period. mothorax because the nitrous oxide may diffuse • Coordination of care. into the gas-filled space, increasing the volume. Further reading Combining analgesic techniques Bay I, Nunn JF, Prys Roberts C. Factors affecting

Examples of good practice are: arterial PO2 during recovery from general • bupivacaine and fentanyl in an epidural anaesthesia. British Journal of Anaesthesia 1968; infusion; 40: 398–407. • intravenous PCA morphine and intravenous Gan TJ, Meyer T, Apfel CC et al., and Department paracoxib in the early postoperative period when of Anesthesiology, Duke University Medical nil by mouth; Center. Consensus guidelines for managing

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postoperative nausea and vomiting. Anesthesia http://oac.med.jhmi.edu/res_phys/ and Analgesia 2003; 97: 62–71. [The Johns Hopkins School of Medicine Shelly MP, Eltringham RJ. Rational fluid therapy interactive respiratory website.] during surgery. British Journal of Hospital http://www.resus.org.uk/pages/periarst.htm Medicine 1988; 39: 506–17. [Current Resuscitation Council UK guidelines Thomson AJ, Webb DJ, Maxwell SRJ, Grant IS. on peri-arrest arrhythmias.] in acute medical care. British http://www.jr2.ox.ac.uk/bandolier/booth/ Medical Journal 2002; 324: 1406–7. painpag/ West JB. Respiratory physiology: the essentials, 6th [The Oxford Pain site. Brilliant for the latest edn. Baltimore: Williams and Wilkins, 1999. evidence-based information on all aspects of acute pain.] http://www.jr2.ox.ac.uk/bandolier/ Useful websites Extraforbando/APain.pdf http://www.aagbi.org/pdf/Postanaes2002.pdf [Acute Pain. Bandolier extra. Evidence-based [Immediate postanaesthetic recovery. The healthcare. February 2003.] Association of Anaesthetists of Great Britain & Ireland. September 2002.]

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Anaesthesia is extremely safe and uneventful, but Cardiovascular collapse is the most common and occasionally problems occur in the perioperative severe feature. Asthmatics often develop bron- period that may be incidental or secondary to the chospasm that is resistant to treatment, and any anaesthetic and potentially life-threatening to the circumstance reducing the patient’s patient. Whatever their nature, most difficulties response (e.g. beta blockers, spinal anaesthesia) can be dealt with initially using the ABC principles will increase the severity. of resuscitation: maintain and secure the airway, These events are caused by one of two things: ensure adequate breathing or ventilation and sup- • An anaphylactic reaction This involves the libera- port the circulation. Assistance will be required fre- tion of histamine, 5-hydroxytryptamine (5-HT) quently and should always be sought early. and associated vasoactive substances from mast cells and basophils, following exposure to a foreign substance (the drug) to which the individual has Acute severe drug reactions become sensitized. It is usually an IgE-mediated Most drug reactions in anaesthesia are mild and reaction. transient, consisting mainly of localized urticaria • An anaphylactoid reaction This is clinically indis- as a result of cutaneous histamine release. The inci- tinguishable from the above, but the release of his- dence of severe reactions to anaesthetic drugs is ap- tamine, etc. from mast cells is triggered by non-IgE proximately 1:10000 drug administrations, and is mechanisms. more common in females. Of those reported to the Medicines Control Agency, 10% involved a fatality Causes of allergic reactions compared to 3.7% for drugs overall. This probably reflects the frequency with which anaesthetic • Anaesthetic drugs: drugs are given intravenously. Clinical features in- • muscle relaxants (>50%): rocuronium, suxa- clude (in order of frequency): methonium, atracurium, vecuronium; • severe hypotension; • induction agents (5%): thiopentone, propofol. • severe bronchospasm; • Antibiotics (8%): • widespread flushing; • penicillin (2% of patients may cross-react to • hypoxaemia; modern cephalosporins). • urticaria; • Intravenous fluids: •angioedema, which may involve the airway; • colloids (3%); haemaccel, gelofusin. •pruritus, nausea and vomiting. • Latex (17%)

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latex sensitivity) and prolonged. An infusion of ep- Immediate management inephrine (adrenaline) may be required. The possi- •Discontinue all drugs likely to have triggered the bility of a tension pneumothorax (secondary to reaction. barotrauma) causing hypotension must not be • Call for help. forgotten. • Maintain the airway, administer 100% oxygen, elevate the patient’s legs. Investigations • Give epinephrine (adrenaline), 50–100mg slowly intravenously (0.5–1mL of 1:10000) under The most informative is measurement of plasma ECG control. If no ECG available, give 0.5mg in- tryptase. A blood sample (10mL, plain tube) tramuscularly (0.5mL of 1:1000). Give further should be taken immediately after treatment, ap- doses according to the response. proximately 1h after the event and at 6h. Elevated • Ensure adequate ventilation: tryptase confirms anaphylactic or anaphylactoid • Intubation will be required if spontaneous reaction, but does not distinguish between them. ventilation is inadequate or in the presence of Expert advice about follow-up and identification of severe bronchospasm. It may be made exceed- the cause must be arranged. ingly difficult by the presence of severe laryngeal Finally, record all details in the patient’s notes, oedema. In these circumstances a needle and do not forget to inform the patient and the pa- cricothyroidotomy or surgical airway will be tient’s general practitioner of the events, both ver- required. bally and in writing. In the UK, report adverse drug • Support the circulation: events to the Medicines and Healthcare products • Start a rapid intravenous infusion of fluids Regulatory Agency by completing a ‘yellow card’. 10–20mL/kg. Crystalloids initially may be safer Generalized atopy does not help predict the risk than colloids. In the absence of a major pulse, of immunologically mediated reaction to anaes- start cardiopulmonary resuscitation using the thetic drugs. A previous history of ‘allergy to an protocol for PEA. anaesthetic’ is cause for concern and there is a • Monitoring: high risk of cross-reactivity between drugs of the • ECG, oxygenation of the peripheral tissues same group. These patients must be investigated

(SpO2), blood pressure, end-tidal CO2. Establish appropriately. an and check the blood gases. Moni- tor central venous pressure (CVP) and urine out- Aspiration of gastric contents put to assess adequacy of circulating volume. The greatest risk is during induction of anaesthe- sia, but some patients are also at risk during extu- Subsequent management bation and recovery. Postoperative patients on the • : 2.5–5.0mg nebulized or 0.25mg IV. ward who have received liberal amounts of opiates • Aminophylline: 6mg/kg as an infusion over for pain relief or have impaired pharyngeal reflexes 20mins (omit if the patient is taking regular may also aspirate. The incidence of complications theophylline). appears to be related to both the volume (>25mL) • Antihistamines: chlorpheniramine 8–16mg and pH (<2.5) of the material aspirated.

slowly IV (anti-H1), ranitidine 50mg IV (anti-H2). Factors predisposing to aspiration include: • Steroids: hydrocortisone 500mg or methylpred- •delayed gastric emptying; nisolone 2g IV. • obstetric patients; As soon as possible these patients should be trans- • drugs, especially opiates; ferred to an intensive care unit (ICU) for further • trauma patients, particularly head injury; treatment and monitoring. Reactions vary in sever- • intestinal obstruction or peritoneal irritation; ity, can be biphasic, delayed in onset (particularly • blood in the stomach;

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• sympathetic stimulation, pain and anxiety; • After allowing the patient to recover, continue •a full stomach: using either a regional technique or a rapid- • an inadequate period of starvation; sequence induction and intubation. • distension with mask ventilation; • After intubation, aspirate the tracheobronchial •a history of gastro-oesophageal reflux or a hiatus tree and consider . hernia; •Treat bronchospasm as above. • obesity; •Postoperatively, arrange for a chest X-ray and •head-down position; physiotherapy. • presence of a bulbar palsy; • Recover in the ICU or HDU with oxygen therapy. •oesophageal pouch or stricture. •Postoperative ventilation may be required. Signs suggesting aspiration include: (iii) Neuromuscular blocking drugs given: • coughing during induction or recovery from • Intubate with a cuffed tracheal tube to secure the anaesthesia; airway. • the presence of gastric contents in the pharynx • Aspirate the tracheobronchial tree before start- at laryngoscopy or around the edge of the ing positive pressure ventilation. facemask; •Consider bronchopulmonary lavage with • progressive hypoxia; saline. • bronchospasm; •Treat bronchospasm as above. • respiratory obstruction, if severe; • Pass a nasogastric tube and empty the stomach. • occasionally, aspiration may go completely un- • If the patient is stable (i.e. not hypoxic or noticed during anaesthesia, with the development hypotensive), surgery can be continued with post- of hypoxia, hypotension and respiratory failure operative care as described above. postoperatively. If aspiration is suspected in a patient postopera- tively, treat as for (i) above. There is no place for routine administration of Management large-dose steroids. Antibiotics should be given • Maintain the airway and place the patient head- according to local protocols. down and on his or her side, preferably the left; in- In those cases where bronchospasm is resistant tubation is relatively easier on this side. to treatment or there is persistent hypoxia or hy- • Aspirate any material from the pharynx, prefer- potension, unless surgery is life-saving the patient ably under direct vision (use a laryngoscope). should be transferred to the ICU for ventilation (i) Neuromuscular blocking drugs not given; surgery where, in addition, invasive cardiorespiratory not urgent: monitoring will also be needed. • Give 100% oxygen via a facemask. •Allow the patient to recover, give oxygen to Prevention of aspiration maintain a satisfactory SpO2. •Treat bronchospasm with salbutamol or amino- A variety of methods are used, alone or in phylline as described on page 91. combination: •Take a chest X-ray and organize regular physio- 1 Reduction of residual gastric volume therapy. • An adequate period of starvation. • Consider monitoring on the ICU or HDU, de- •Avoid drugs that delay gastric emptying. pending on degree of aspiration. • Insertion of a nasogastric tube. (ii) Neuromuscular blocking drugs not given; surgery • Use of gastrokinetic drugs, for example essential: metoclopramide. • Get help, empty the stomach with a nasogastric 2 Increase pH of gastric contents tube and instill 30mL sodium citrate. • Sodium citrate to neutralize gastric acid.

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•H2 antagonists, for example ranitidine. via a nasogastric tube, use awake fibreoptic intuba- • Proton pump inhibitors, for example omepra- tion under local anaesthesia. zole, rebeprazole. Intubation not essential for surgery: 3 Use of cricoid pressure • Use a LMA, Proseal LMA or Combitube. See page 26. • Consider using a regional anaesthetic technique.

Failed intubation Anaesthesia for elective surgery

The following plans concentrate on unexpected Assume that the patient is starved, minimizing failed intubation. The immediate management in the risk of aspiration, and a non-depolarizing these circumstances will depend upon: neuromuscular blocker given to facilitate tracheal • ability to maintain adequate oxygenation; intubation. •type of neuromuscular blocker used, either depo- • Get help. larizing or non-depolarizing; • Administer 100% oxygen via facemask. •urgency of surgery (and the likelihood of a full •Ventilate gently to minimize the risk of gastric stomach); distension, try one- or two-person technique, use • need for intubation. oral and/or nasal airway.

Anaesthesia for emergency surgery Oxygenation and ventilation successful

Assuming the patient has a full stomach, a rapid- Maintain anaesthesia with inhalational agent in sequence induction (RSI) technique of preoxy- oxygen. genation, cricoid pressure and suxamethonium is Intubation essential for surgery: used to facilitate intubation: • Attempt fibreoptic intubation. • get help; • Attempt intubation using an Intubating LMA. • maintain cricoid pressure; • Maintain anaesthesia and ventilation using an • administer 100% oxygen via facemask; LMA or facemask until neuromuscular block can • ventilate gently to minimize the risk of gastric be reversed; awaken patient and plan for elective distension, try one- or two-person technique, use fibreoptic intubation. oral and/or nasal airway; Intubation not essential for surgery: •consider reducing cricoid pressure if ventilation • Use an LMA, Proseal LMA or Combitube. Con- difficult. sider using a regional anaesthetic technique.

Oxygenation and ventilation successful Failed intubation, failed ventilation

Surgery essential: Whatever the surgical urgency, if intubation fails • Continue anaesthesia with inhalational agent in and the patient cannot be oxygenated via a face- oxygen. mask, LMA or any other means: • Maintain airway with LMA, Proseal LMA or • GET HELP. Combitube. • Perform needle cricothyroidotomy or surgical Surgery not essential: cricothyroidotomy (see page 28). • Maintain oxygenation and allow patient to • In any situation other than surgery for life- recover. threatening condition, maintain oxygenation and • Plan alternative technique. unconsciousness until neuromuscular block has Intubation essential for surgery: worn off or is reversible. •Allow the patient to recover, empty the stomach • In life-threatening circumstances, maintain oxy-

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genation, secure the airway using an alternative After induction of anaesthesia technique (tracheostomy, fibreoptic intubation). Any patient whose airway has been traumatized, • Asymptomatic. either as a result of repeated attempts at intubation • Obstruction apparent on attempting manually or following surgical intervention, is at risk of de- to ventilate the patient, due to a supraglottic lesion veloping oedema and airway obstruction at extu- acting as a ‘ball valve’. bation. These patients should be admitted to an appropriate critical care area postoperatively and During anaesthesia may require prior to extubation. Full details of the difficulties encountered and • Mechanical obstruction of the breathing system. any solutions must be documented in the patient’s • Intrinsic airway obstruction (e.g. broncho- notes. The patient must be given verbal and writ- spasm). ten details (consider ‘MedicAlert’ type device) and • Extrinsic obstruction (e.g. tension pneumo- details sent to his or her GP. thorax).

Acute airway obstruction Management

This may present in a variety of ways: Whatever the circumstances, the aim is to secure a patent airway to allow adequate oxygenation. • Increase the inspired oxygen concentration to Conscious patient 100%. • Usually distressed and unwilling to lie down. • Get help urgently. • Marked respiratory effort, using accessory • If not already available, request the emergency muscles (e.g. sternomastoids). airway equipment. •Indrawing of intercostal and supraclavicular re- gions and a tracheal tug. In the conscious patient • Stridor. If inspiratory, consider obstruction above the larynx. • If safe to do so, transfer rapidly to the anaesthetic •Tachycardia and hypertension secondary to hy- room in theatre. poxia and hypercarbia. • If ventilation is reasonable, induce anaesthesia • The history, if available, may indicate the cause; using an inhalational anaesthetic in oxygen. for example inhaled foreign body, oedema (allergic Increasing the inspired concentration too reaction, inhalational injury), infection (epiglotti- rapidly may cause coughing and worsen the tis), tumour or trauma. obstruction. • Gentle manual supplementation of ventilation may be possible. Unconscious patient •When anaesthesia is adequate perform direct • Usually secondary to unrelieved obstruction laryngoscopy. causing hypoxaemia and hypercarbia. • Intubate if possible. • Minimal respiratory effort. • If this fails, and the airway is adequate, carry out • Paradoxical movement of the chest and formal tracheostomy. abdomen (see-saw ventilation). • If this fails, and the airway is inadequate, carry • Minimal or no breath sounds (silent chest). out needle cricothyroidotomy. • Hypotension, a variety of arrhythmias, Under some circumstances it may be safer initially cyanosed. to carry out needle cricothyroidotomy under local anaesthesia to allow oxygenation before inducing anaesthesia and direct laryngoscopy.

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In the unconscious patient Immediate management

• Attempt ventilation with 100% oxygen. • High-flow oxygen. • Perform direct laryngoscopy quickly, once only. • High-dose beta-2 agonists via oxygen driven If possible: nebulizer. •Remove any foreign bodies under direct vision • Salbutamol 5mg, terbutaline 10mg. using Magill’s forceps. • Ipratropium bromide, 0.5mg via oxygen driven • Pass a small-diameter (5.0mm) tracheal tube nebulizer. past the obstruction into the larynx. • Prednisolone 40–50mg orally, or hydrocortisone • If this fails, proceed rapidly to either needle or 100mg IV, or both. surgical cricothyroidotomy. • Once oxygenation is restored, the patient may Monitor recover consciousness rapidly. Sedation and neuro- muscular blocking drugs may be required while the • PEF, 15–30min intervals.

airway is formally assessed. • Pulse oximetry: maintain SpO2 > 92%. • Arterial blood gases. •A chest X-ray is only indicated if: In the anaesthetized patient • there is suspected pneumothorax or pneumo- • Attempt to ventilate with 100% oxygen. mediastinum; • Perform direct laryngoscopy. • there is suspected consolidation; • If possible pass a small-diameter (5.0mm) • there is failure to respond to therapy; tracheal tube past the obstruction into the larynx. • mechanical ventilation is required. • If unsuccessful, proceed to cricothyroidotomy. Subsequent management Acute severe asthma If the patient is improving: This is characterized by any one of: • continue oxygen therapy; • Severe breathlessness: • give IV hydrocortisone 100mg 6 hourly or 40– • an inability to complete a sentence in one 50mg orally daily; breath; • give nebulized salbutamol and ipratropium 4–6 •a silent chest; hourly. • cyanosis. If the patient is not improving: •Tachypnoea: respiratory rate >25 breaths/min. • continue oxygen therapy; •Tachycardia: heart rate >110 beats/min. • give nebulized salbutamol 5mg more frequently, • Peak expiratory flow (PEF) 33–50% of best or every 15–30mins or 10mg continuously hourly; predicted. • continue ipratropium 0.5mg 4–6 hourly; Acute severe asthma is considered life threatening • give magnesium sulphate 1.2–2.0g IV as slow in a patient with any one of the following: infusion over 20mins; • feeble respiratory effort; • consider IV beta-2 agonist or aminophylline; • PEF <33% of best or predicted; • consider need for tracheal intubation and

• SpO2 <92%; mechanical ventilation.

• PaO2 <8kPa; Discuss with Critical Care team if there is:

• normal PaCO2 (4.6–6.0kPa); • need for tracheal intubation and ventilatory • cyanosis; support; • bradycardia, arrhythmias, hypotension; • continuing failure to respond to treatment; • exhaustion, confusion, coma. •a deteriorating PEF; • persistent or worsening hypoxia;

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• hypercapnia; • chest trauma with associated rib fractures; • development of acidosis (fall in pH or increase in •insertion of central venous line, particularly hydrogen ion concentration); when the subclavian route is used; • exhaustion; • use of local anaesthetic nerve blocks, for • drowsiness or confusion; example intercostal nerves, supraclavicular • coma; ; • respiratory arrest. • rupture of an emphysematous bulla. The concurrent use of positive pressure ventilation will increase the rate at which the pressure rises Tension pneumothorax as gas is forced through the defect into the A pneumothorax exists when any gas accumulates pleural cavity, resulting in rapid cardiovascular in the pleural cavity. This leads to collapse of the collapse. underlying lung as a result of perfusion (Q) but no A simple pneumothorax can tension when ventilation (V) (V/Q < 1) and hypoxaemia. If the nitrous oxide is given. The nitrous oxide diffuses gas accumulates under pressure, then a tension into the air-filled space in a greater volume and at a pneumothorax exists. In addition to hypoxaemia, rate faster than nitrogen can escape, causing ex- the increasing pressure causes the mediastinum to pansion and a rise in the pressure. shift, impeding venous return, severely reducing the cardiac output. If unrelieved, it is rapidly fol- Management lowed by cardiovascular collapse and death. • If using nitrous oxide, this should be discontinued. Characteristics of a tension • Increase the inspired oxygen concentration to pneumothorax 100%. The conscious patient will be tachypnoeic and in • Insert a 14 or 16 gauge cannula in the second severe respiratory distress. intercostal space, midclavicular line (immediately In addition, and in the anaesthetized patient, above the third rib to avoid the neurovascular signs on the affected side will include: bundle). • reduced movement; • If successful, this is often accompanied by an • hyperresonance on percussion; obvious release of gas under pressure, decreased • decreased air entry; respiratory distress (or inflation pressures) and • distension of the hemithorax. an improvement in the cardiac output. There may also be: The insertion of a cannula has the effect of con- • surgical emphysema; verting the tension pneumothorax to a simple • tachycardia, hypotension; pneumothorax. This can then be treated by the •deviation of the trachea away from the affected insertion of a chest drain in the fifth intercostal side; space, midaxillary line on the affected side. Finally, • distended neck veins (if the patient is not a chest X-ray is taken. hypovolaemic); N.B. Very rarely there may be bilateral tension •a gradual rise in the inflation pressure, if the pneumothoraces. patient is being ventilated, or failure to deliver a preset tidal volume. Severe hypotension

Hypotension is a result of a reduction in either the Causes cardiac output or the peripheral resistance, alone Puncture of the pleura lining the surface of the or in combination (blood pressure = cardiac output lung (visceral pleura). This can be due to: ¥ peripheral resistance). Severe hypotension may

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be defined as a systolic pressure 40% less than the usually the result of a combination of the above preoperative value. factors; for example, vasodilatation caused by the anaesthetic drugs in a hypovolaemic patient. Reduced cardiac output Management Decreased venous return to the heart: • Hypovolaemia: blood loss, extracellular fluid Initially, time should not be spent trying to iden- loss (diarrhoea, vomiting). tify the cause. Treatment is symptomatic using the • Position, for example head up, prone with ab- ABC system. dominal compression. • Airway Clear and secure. If hypotension renders • Mechanical obstruction impeding venous re- the patient unconscious, intubation will be needed turn: pulmonary embolus, tension pneumothorax, to protect the airway. cardiac tamponade (rare). • Breathing and ventilation Increase the inspired Decreased myocardial contractility: oxygen concentration to 100%. Support ventila- • Intravenous and inhalational anaesthetic tion if inadequate or absent, using a facemask ini- agents. tially and then via a tracheal tube. • Ischaemic heart disease, hypoxia, hypothermia, • Circulation If not already done, insert a short, acidosis. wide-bore cannula in the most obvious peripheral Extremes of heart rate: vein, often in the antecubital fossa. Raise the legs • Profound bradycardia, <40 beats/min. to encourage venous return. Fluid, either crystal- •Tachycardia, >160 beats/min. loid or colloid, should be given, using a pressure in- fusor to speed administration. Stop any external haemorrhage with direct pressure. Seek urgent sur- Reduced peripheral resistance gical assistance if any internal haemorrhage. If a Anaesthetic drugs: bradycardia is present (heart rate <60/min), then •A direct action on vascular smooth muscle in the consider atropine 0.5–1mg IV. arteriolar wall, for example isoflurane. At this point, treatment should be directed towards • The release of histamine, for example specific causes that may be suggested by the find- atracurium. ings on examination or by the patient’s past • Reducing sympathetic tone, for example central medical history. neural block. Additional measures Sepsis: • Vasopressors: for example ephedrine to counter- •Toxins released can cause failure of the precapil- act vasodilatation. lary sphincters, leading to widespread vasodilata- • Inotropes: for example dopamine or dobutamine tion of the vascular bed. to increase myocardial contractility. Spinal cord injury: • Antiarrhythmics. •Injury to the cervical or upper thoracic cord • A change in position or relief of a tension pneumo- causes loss of sympathetic tone to blood vessels thorax: to allow venous return. and vasodilatation. • Needle pericardiocentesis: in the very rare circum- • If above T5, loss of cardiac sympathetic supply stances of cardiac tamponade. will result in a bradycardia. • Monitoring of CVP or pulmonary artery pressure: to Miscellaneous: guide therapy in complex cases. • Hypercarbia and a pyrexia will both cause vasodilatation. Severe hypotension requiring intervention is

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Malignant hyperpyrexia Immediate management (hyperthermia) (MH) • GET HELP. This is a rare inherited disorder of • Stop all anaesthetic agents. metabolism. The release of abnormally high con- • Hyperventilate with 100% oxygen. centrations of calcium from the sarcoplasmic • Change the anaesthesia machine and circuits. reticulum causes increased muscle activity and •Terminate surgery as soon as practical. metabolism. Excess heat production causes a rise in • Monitor core temperature. core temperature of at least 2°C/h. •Give 1mg/kg IV (up to 10mg/kg may Triggered by exposure to certain anaesthetic be needed, average dose 2.5–4mg/kg). agents: • Start active cooling: • all the inhalational anaesthetic agents, of which • cold 0.9% saline IV; halothane is the most potent; • expose the patient completely; • suxamethonium. • surface cooling — ice where vessels run close to Associated with certain operations: skin, for example over axillary and femoral arter- • squint surgery; ies, or by using wet sponging and fanning to en- • hernia repair; courage cooling by evaporation; • corrective orthopaedic surgery; • consider gastric or peritoneal lavage with cold • cleft palate repair. saline. Incidence of between 1:10000 and 1:40000 •Treat acidosis with 8.4% sodium bicarbonate in anaesthetized patients. 50mmol (50mL) IV titrated to acid–base results. •Treat hyperkalaemia. Transfer the patient to the ICU as soon as possible Presentation to: •A progressive rise in body temperature (which • monitor temperature; may be labile for up to may go unnoticed unless the patient’s temperature 48 hours; is being monitored). • continue dantrolene to alleviate muscle rigidity; •An unexplained tachycardia. • monitor urine output for myoglobin, and treat-

• An increased end-tidal CO2. ing to prevent renal failure; •Tachypnoea in spontaneously breathing • treat DIC if it develops. patients. • Muscle rigidity, despite the use of relaxants. Dantrolene •Failure to relax after suxamethonium, especially persistent masseter spasm. The specific treatment for MH. It inhibits calcium • Cardiac arrhythmias. release, inhibiting excitation–contraction and pre- •A falling oxygen saturation and cyanosis. venting further muscle activity. Dantrolene is Analysis of an arterial blood sample will orange in colour and supplied in vials containing demonstrate: 20mg (plus 3g mannitol); it requires 60mL water •a profound metabolic acidosis (low pH and for reconstitution and is very slow to dissolve. bicarbonate); •a low PaO despite a high inspired oxygen 2 Investigation of the family concentration;

•a high PaCO2; Following an episode, the patient and his or her • hyperkalaemia; family should be referred to an MH unit for inves- •a coagulopathy (disseminated intravascular tigation of their susceptibility to MH. coagulation (DIC)).

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tient’s forehead and shaking his or her shoulders Anaesthesia for malignant gently with the other hand, whilst at the same time hyperpyrexia-susceptible patients asking loudly ‘Are you all right?’ • Employ a regional technique using plain The head is held stable during the assessment to bupivacaine. guard against the possibility of aggravating an in- • General anaesthesia: jury to the cervical spine. • use a designated vapour-free machine and new Always assume the victim may be deaf; therefore circuits and hoses; ensure that he or she can see your lips move when • propofol, thiopentone, opioids, atracurium, assessing responsiveness. vecuronium, pancuronium are thought to be safe; Airway control • employ a total IV technique, using an infusion In most unconscious victims the airway will be- of propofol and remifentanil, with oxygen- come obstructed at the level of the hypopharynx, enriched air for ventilation; as the reduced tone in muscles of the tongue, jaw • consider pretreatment with dantrolene (orally and neck allows the tongue to fall against the pos- or IV) in those who have survived a previous terior pharyngeal wall (Fig. 4.1). Correction, using episode; the following techniques, may allow recovery •ensure that appropriate monitoring and without the need for further intervention. cooling are available; • Head tilt plus chin lift (Fig. 4.2) The rescuer’s hand • continue to monitor temperature and ECG nearest the head is placed on the forehead, gently postoperatively. extending the head backwards. The chin is then lifted using the index and middle fingers of the res- cuer’s other hand. If the mouth closes, the lower lip Cardiac arrest should be retracted downwards by the thumb. • Jaw thrust (Fig. 4.3) This is used if the above tech- Adult basic life support (BLS) nique fails to create an airway, or there is a suspi- cion that the cervical spine may have been injured. BLS is performed to limit hypoxic damage of the The patient’s jaw is ‘thrust’ upwards (forwards) by vital organs and maximize the chances of the rescuer applying pressure behind the angles of advanced life support restoring a spontaneous the mandible. circulation. A sequence of actions is performed in which the airway, breathing and circulation are supported without the use of any equipment other than a simple protective shield interposed between the mouths of the rescuer and patient (e.g. Laerdal pocket mask). This is increasingly re- ferred to as ‘Layperson BLS’. The reader should consult the current Resuscitation Council (UK) guidelines, for details of the latest algorithm put- ting together the techniques below (see Further reading).

Techniques used in BLS

Patient evaluation Figure 4.1 Saggital section of the airway, showing how the This is achieved by placing one hand on the pa- tongue contributes to obstruction.

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Figure 4.2 Head tilt, chin lift. Figure 4.4 Look, listen and feel for evidence of breathing. The hand on the chest may also detect chest movement during breathing.

• Finger sweep The mouth must be opened and in- spected, and any obvious material contributing to the obstruction removed by placing a finger in the mouth and gently sweeping from side to back, ‘hooking’ out loose material. At the same time, broken, loose or partial dentures should be re- moved, but well-fitting ones may be left in place (see later).

Breathing Checking for evidence of breathing. Maintain an airway using one of the above techniques, then (Fig. 4.4): • Look: down the line of the chest to see if it is rising and falling. • Listen: at the mouth and nose for breath sound, gurgling or snoring sounds. • Feel: for expired air at the victim’s mouth and nose with the side of one’s cheek. If there is no evidence of spontaneous ventilation, expired-air ventilation will be required.

Expired-air ventilation (rescue breathing or mouth-to-mouth ventilation) • There must be a clear path, with no leaks, be-

Figure 4.3 Jaw thrust. Note the application of pressure be- tween the rescuer’s lungs and the victim’s lungs. hind the angles of the mandible. The tips of the thumbs can • Keep the victim’s airway patent by performing a be used to open the mouth. head tilt, while using the index finger and thumb

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Well-fitting dentures are often usefully left in situ as they help maintain the contour of the mouth and make it easier to create a good seal. • The rescuer then breathes out into the victim’s mouth for 1.5–2s. •At the same time look down the victim’s chest: each breath should be sufficient to make the chest rise clearly (Fig. 4.5b). • Maintaining the head tilt/chin lift, the rescuer now moves away from the mouth to allow passive exhalation for 2–4s, watching to ensure the chest (a) falls (Fig. 4.5c). Each complete cycle of expired-air ventilation should take 5–6s, thereby allowing 10–12 breaths/min.

Mouth-to-nose ventilation This technique is used where mouth-to-mouth ventilation is unsuccessful, for example if an ob- struction in the mouth cannot be relieved, or when the rescuer is a child. (b) • The airway is maintained with a head tilt, but the mouth is closed with the fingers of the lower hand. • The seal is made by the rescuer’s lips around the base of the victim’s nose. • Inspiration is as above, checking to ensure that the chest rises. • The victim’s mouth is opened to assist with expi- ration, the rescuer watching to ensure that the chest falls.

Common causes of inadequate ventilation • Obstruction: failing to maintain head tilt, chin lift. (c) • Leaks: inadequate seal around the mouth or failure to occlude the patient’s nose. Figure 4.5 (a–c) Expired air (mouth-to-mouth) ventilation. • Exhaling too hard: trying to overcome an obstructed airway, resulting in gastric distension. • Foreign body: unrecognized in the patient’s airway. of the same hand to pinch the nose to prevent leaks. Circulation • The fingers of the lower hand are then used to Check for evidence of a circulation: perform a chin lift, and if necessary open the vic- •Look, listen and feel for normal breathing, tim’s mouth (Fig. 4.5a). coughing or movement by the victim. • The rescuer takes a deep breath in and makes a • If you are trained, check for the presence of a seal with their lips around the victim’s mouth. pulse:

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second hand placed on the back of the hand on the sternum. The fingers may then be interlocked. • The sternum is depressed vertically 4–5cm and then released rapidly. • This is repeated at a rate of approximately 100/min, compression and relaxation each taking the same length of time. To optimize compression and reduce rescuer (a) fatigue chest compressions are best performed with the rescuer leaning well forward over the patient, arms straight and hands, elbows and shoulders ex- tended in a straight line. This allows use of the res- cuer’s upper body weight to achieve compression, rather than the arm muscles, which will rapidly tire and reduce efficiency (Fig. 4.6b).

Common errors

Wrong hand position: • too high: the heart is not compressed; (b) • too low: the stomach is compressed and risk of Figure 4.6 (a,b) External cardiac compression. aspiration increased; •too laterally: injures underlying organs, for example liver, spleen, bowel. Overenthusiastic effort: • Central arteries are more reliable than periph- • causes cardiac damage; eral ones as a pulse will be palpable even with a • fractures ribs which may damage underlying very low cardiac output. organs, particularly lungs and liver. • The carotid artery is usually the most accessi- Inadequate effort: ble and acceptable. • the rescuer is not high enough above the patient •Take no more than 10s to make the check. to use his/her body weight; • If there is no evidence of a spontaneous circula- • fatigue during prolonged resuscitation or be- tion, then chest compressions will be required. cause of poor technique. Failure to release between compressions: Chest compressions • prevents venous return and filling of the heart. This technique only results in a maximum cardiac When a collapsed person is not breathing and has output 30% of normal, and in order to achieve this no spontaneous circulation, they will require both the position of the hands is critical: rescue breathing and chest compressions; this is • The rescuer positions him/herself on one side of often referred to as cardiopulmonary resuscitation the victim. (CPR). A ratio of 15 chest compressions to 2 breaths • The victim’s chest is exposed and the xiphister- should be used, irrespective of the number of per- num identified. sons present. If two or more laypersons are present, • The index and middle fingers of the rescuer’s they should take turns to provide single-person lower hand are placed on the xiphisternum and CPR, to prevent fatigue and maintain quality. If the heel of the other hand is placed adjacent to two or more healthcare professionals are present, them on the sternum (Fig. 4.6a). then one person should perform chest compres- • The fingers are then removed and the heel of the sions while another provides rescue breathing. The

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same ratio of 15:2 must still be used. It is impor- Healthcare Professional BLS tant to remember that whenever two or more peo- ple are present, irrespective of their background, Clearly, in a healthcare environment, there is al- one person must initially summon help, even if most always help available and access to resuscita- this results in one rescuer having to start CPR tion equipment, usually oxygen, a bag-valve-mask alone. apparatus and a monitor/defibrillator or auto- When there is only a single rescuer, the situation mated external defibrillator (AED). First-responder is more difficult. Having discovered a collapsed healthcare professionals with appropriate training person, if the victim is an adult, assume the pri- should use these devices to supplement BLS, in par- mary problem is cardiac. BLS is a ‘holding proce- ticular to reduce the time to defibrillation in those dure’ and advanced skills will be required for the patients in a shockable rhythm. This is increa- best chance of survival. The first action should be singly referred to as ‘Healthcare Professional BLS’ to telephone for help, even if it means leaving the and an outline plan is given below. However, if victim; on returning, BLS can then be commenced. there is any delay in obtaining resuscitation equip- However, if there is evidence that the primary ment, or trained personnel are not available, BLS problem is trauma, drowning, or drug or alcohol must be started immediately. induced, or that the victim is a child or infant, then On discovering a collapsed patient in a clinical it is appropriate to perform resuscitation for about area: 1min before going for help. • Shout for help. • Assess the patient’s responsiveness, ‘Are you right?’ The recovery position • Confirm cardiac arrest: When the victim is breathing and has a sponta- • Look, listen, feel for breathing for up to 10s. neous circulation, if safe to do so he or she should • Check for presence of a carotid pulse for up to be placed in the recovery position to minimize the 10s. risks of airway obstruction and aspiration of gastric • If two persons are present, both should leave the contents. patient: • Place the victim supine, with legs extended, and • No. 1 calls the cardiac arrest team. ensure airway is open (Fig. 4.7a). • No. 2 collects resuscitation equipment and • Kneeling against the victim’s chest, the victim’s monitor/defibrillator or AED. closest arm is abducted to lie at 90° so that the palm • If more than two persons present, in addition to lies facing upwards. above: • The victim’s far arm is then brought to lie across • No. 3 starts BLS while equipment is collected, his or her chest, so that the back of the hand lies 15 compressions to 2 ventilations. against the cheek (Fig. 4.7b). •Ventilate with airway equipment plus oxygen as • The far leg is then flexed at the hip and knee, soon as available (e.g. bag-valve-mask). keeping the foot on the ground. • Attach monitor/defibrillator or AED as soon as • The far shoulder is grasped. possible. • The victim is then rolled. The shoulder is pulled • Defibrillate if appropriate; do not delay for venti- towards the rescuer whilst at the same time the lations or chest compressions. flexed leg is rotated over the lower leg using a com- • Perform two-person CPR if appropriate. bination of pulling on the thigh and gentle down- • Hand over to the cardiac arrest team leader when ward pressure (Fig. 4.7c). the team arrives. The upper leg is adjusted so that the hip and knee are flexed and the hand under the cheek is Advanced life support (ALS) adjusted to help maintain the head tilt (Fig. 4.7d). The aim of ALS is to identify and reverse the underlying cause of the cardiac arrest using a

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(b)

(a)

(d)

(c)

Figure 4.7 (a–d) The recovery position.

defibrillator, airway devices, oxygen, intravenous shockable rhythms, much of the remainder of the cannulation and drugs, correcting reversible management is common to all rhythms. ALS man- causes. The most important first step is to identify agement is summarized in the Universal Treatment the cardiac arrest rhythm, which can belong to one Algorithm (Fig. 4.8). Only the key features of ALS of two groups: not covered elsewhere are included here. The inter- • Shockable: ventricular fibrillation (VF), pulseless ested reader should refer to the Resuscitation ventricular tachycardia (VT). Council (UK) for further details and is encouraged • Non-shockable: and pulseless electrical to undertake the Resuscitation Council (UK) ALS activity (PEA). course. Apart from attempting to defibrillate patients in

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Cardiac arrest

Precordial thump if appropriate

BLS algorithm if appropriate

Attach defibrillator-monitor

Assess rhythm

+/– check pulse

VF/VT Non-VF/ During CPR VT Correct reversible causes

If not already: Defibrillate x3 • Check electrodes, paddle as necessary position and contact • Attempt/verify:

airway and O2 intravenous access • Give epinephrine every 3 min CPR 3 min CPR 1 min Consider: (1 min if immediately amiodarone, atropine/pacing after defibrillation) buffers

Potential reversible causes: • Hypoxia • Hypovolaemia • Hypo/hyperkalaemia and metabolic disorders • Hypothermia • Tension pneumothorax • Tamponade • Toxic/therapeutic disorders • Thrombo-embolic and mechanical obstruction

Figure 4.8 The Universal Algorithm. Courtesy of the Resuscitation Council (UK).

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Ventricular fibrillation

The onset of VF may be preceded by a period of VT. The most effective treatment of both conditions is identical — electrical defibrillation (a direct current, DC, shock). The time to delivery of the first shock is critical in determining the outcome, and there- fore once the diagnosis has been made, defibrilla- tion is the first manoeuvre to be carried out in ALS. The only exception to this is when it is preceded by a precordial thump. This manoeuvre should only be used if the cardiac arrest was witnessed and/or monitored. A sharp blow is delivered to the pa- tient’s sternum with a closed fist. This delivers a small amount of mechanical energy to the myocardium and, if done early enough after the onset of VF, may cause the rhythm to revert to one capable of restoring the circulation.

Defibrillation Defibrillation (and cardioversion) depolarizes a critical mass of the myocardium, allowing the nat- Figure 4.9 Paddle position for external cardiac ural pacemaker of the heart to take over and restore defibrillation. a normal coordinated contraction. Defibrillators have a power source, either mains or battery, which charges a capacitor to a predetermined level. Safety This energy is discharged through specially de- The discharge of a defibrillator delivers enough signed electrodes or ‘paddles’, usually 13–14cm in current to cause as well as to treat VF. A manual de- diameter, placed on the patient’s chest wall (see fibrillator must only be charged when the paddles below). Success depends on the current flow are on the patient’s chest and must not be moved through the myocardium and therefore to reduce between defibrillator and patient whilst charged. the resistance between paddles and the chest wall, The user must ensure that nobody is in contact ‘gel’ pads are used. This is often referred to as with the patient or trolley, directly or indirectly ‘manual defibrillation’. Increasingly, ‘hands free’ (via spilt electrolyte solution), when the defibrilla- systems consisting of two large, self-adhesive tor is discharged. Care must be taken to ensure that electrodes are being used, particularly with the paddles are not touching when on the chest, or AEDs. These allow both ECG monitoring and de- connected by misplaced gel pads, as this will cause fibrillation without operator contact with the arcing on discharge, insufficient current delivery patient. and the patient to be burned. Any nitrate patches The paddles or self-adhesive electrodes are should be removed from the patient’s chest placed anterolateral: one to the right of the ster- along with any high-flow oxygen to eliminate num, just below the clavicle; and the other over the risk of fire. Finally, a clear verbal warning, usu- the apex, below and to the left of the nipple. Al- ally a shout of ‘stand back’, and a visual check of though the paddles are marked positive and nega- the area are mandatory before discharging the tive, each can be placed in either position (Fig. 4.9). defibrillator. An alternative is to place them anteroposterior to If further shocks are required, the paddles should the heart. remain on the patient’s chest while the defibrillator

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is recharged. If the defibrillator has been charged IV access cannot be obtained, larger doses (2–3mg) in error while the paddles are on the patient, most can be administered via a tracheal tube diluted to devices will allow the charge to be ‘dumped’ safely 10mL with sterile water. by changing the energy level setting. Amiodarone Synchronized defibrillation Defibrillation can be attempted at any point on the The main indication for this drug in cardiac arrest VF waveform (an unsynchronized shock). How- is during shock-refractory VF or pulseless VT, when ever, when the rhythm is pulseless VT, the shock is it should be considered as early as before the deliv- best delivered co-ordinated with the ‘r’ wave, that ery of the fourth shock. The adult dose in cardiac is, synchronized. This may also be referred to as arrest is 300mg, diluted to 20mL and given prefer- cardioversion. If the shock is delivered on the ‘t’ ably via a central line, or alternatively a peripheral wave when the heart is refractory, then VF may be line. precipitated. Some defibrillators automatically de- fault to synchronized mode when switched on, Asystole and unless cancelled this may delay delivery of a shock if the patient is in VF. This represents electrical standstill of the heart with no contractile activity and is seen on the ECG as a gently undulating baseline. It is essential to Technique of safe defibrillation rule out the possibility of VF having been misdiag- •Turn on the power switch (ensure the synchro- nosed before the diagnosis of asystole is made, nization switch is set to ‘OFF’). consequently: • Put gel pads on patient’s chest. • check equipment function; • Place paddles firmly onto gel pads. • ensure that the ECG leads are connected; • Select correct energy level. • check the gain setting; • Check oxygen has been removed. • check the lead setting, lead I or II. •Warn team members that you are charging the If there is any doubt about the diagnosis, treatment defibrillator. should begin as for VF. The risks of not treating VF • Charge the defibrillator. are greater than that of three unnecessary shocks. A •Shout ‘stand back’ and make a visual check of precordial thump can be used under the same cri- the area. teria as for VF. Occasionally, if monitoring the pa- • Perform a final check of patient’s ECG rhythm. tient’s rhythm via the paddles, ‘spurious’ asystole • Deliver shock by pressing both buttons on the may be seen after the delivery of a shock (more paddles simultaneously. likely when successive sequences of shocks have • Check patient’s rhythm. been delivered via the same pads). It is essential that the rhythm is confirmed rapidly using ECG electrodes. In general, the outcome from asystole is Epinephrine (adrenaline) poor unless there are ‘p’ waves present that may re- This is a naturally occurring catecholamine, ad- spond to cardiac pacing. ministered during CPR for its profound a-agonist (vasoconstrictor) properties. This leads to an in- Atropine crease in the peripheral vascular resistance that tends to divert blood flow to the vital organs An anticholinergic acting at muscarinic receptors, (heart, brain). It is the first drug used in cardiac ar- causing block of the vagus nerve at both the sinoa- rest of any aetiology. The adult dose is 1mg intra- trial (SA) and atrioventricular (AV) nodes, causing venously, that is, 1mL of 1:1000 or 10mL of an increase in heart rate. In cardiac arrest due to 1:10000, administered during ALS every 3mins. If asystole or PEA where the heart rate is less than

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Table 4.1 Causes of pulseless electrical activity of children. Furthermore, if the optimum support is to be given, the techniques must be adjusted ac- • Hypoxia • Hypovolaemia cording to the size of the child. ‘Infant’ is used to • Hypo/hyperkalaemia and metabolic disorders mean those less than 1 year old and ‘small chil- • Hypothermia dren’ less than 8 years old. •Tension pneumothorax The evaluation of the victim is as for adults, ac- •Tamponade (cardiac) cepting that infants and very small children who •Toxic/therapeutic disorders cannot yet talk, and older children who are very • Thrombo-embolic and mechanical obstruction scared, are unlikely to reply meaningfully, but they may make some sound or open their eyes to the rescuer’s voice. 60 beats/min, the adult dose is 3mg IV. A dose of 6mg can be given via a tracheal tube. Airway control

If the child is not breathing it may be because the Pulseless electrical activity (PEA) airway has been blocked by the tongue falling back This is the term used to describe the situation when to obstruct the pharynx. Correction of this there are recognizable complexes on the ECG com- problem may result in recovery without further patible with a cardiac output but the patient is intervention. pulseless. It is usually a result of conditions that • Head tilt plus chin lift A hand is placed on the mechanically restrict cardiac filling or outflow, or forehead, and the head is gently tilted back as for biochemically disrupt cardiac contractility. Com- an adult. In an infant, the tilt should be just suffi- mon causes are listed in Table 4.1. The patient’s cient to place the head in a neutral position. The best chance of survival is rapid identification and fingers of the other hand should then be placed treatment of the underlying cause. under the chin, lifting it upwards. Care should be taken not to injure the soft tissue by gripping too hard. It may be necessary to use the thumb of the Open chest cardiac compression same hand to part the lips slightly. The output generated by direct compression of the • Jaw thrust This is achieved by placing two or heart is two to three times greater than closed chest three fingers under the angle of the mandible bilat- compression and coronary and cerebral perfusion erally, and lifting the jaw upwards. This technique pressures are significantly higher. The procedure is may be easier if the rescuer’s elbows are resting on performed via a left thoracotomy through the the same surface as the child is lying on. A small de- fourth or fifth intercostal space. It is of most use fol- gree of head tilt may also be applied. lowing penetrating trauma, but unlikely to benefit The finger sweep technique often recommended those in which cardiac arrest follows blunt trauma. for adults should not be used in children. The It can also be considered in those patients in whom child’s soft palate is easily damaged, causing bleed- closed chest compression is less effective, namely ing, and foreign bodies may become impacted in severe emphysema, a rigid chest wall, severe valvu- the child’s cone-shaped airway and be even more lar heart disease or recent sternotomy. There is no difficult to remove. evidence to support its use as a routine procedure. Breathing Paediatric basic life support Having created an airway using one of the above The general principles are the same as for adult techniques, the adequacy of ventilation should BLS, but specific techniques are required to take then be assessed rapidly in the same manner as for into account the altered anatomy and physiology adults, by looking, listening and feeling for up

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Table 4.2 General guidance for expired-air ventilation

• The chest should be seen to rise and fall • Inflation pressures may be relatively high as the airways are smaller • Slow breaths at the lowest pressure reduce gastric distension

to 10s; if absent, expired-air ventilation will be required.

The technique of expired-air ventilation The airway is kept open using the techniques described above. If the mouth of the child alone is used, then the nose should be pinched closed using the thumb and index fingers of the Figure 4.10 Infant cardiac compression. hand, that is, maintaining the head tilt. In infants and small children, mouth-to-mouth and nose ventilation should be used. Each breath should provide sufficient volume to make the child’s chest rise. Since children vary in size, only general guid- The technique of external cardiac ance can be given regarding the volume and pres- compression in children sure of inflation (Table 4.2). Children vary in size, and the technique used must If the chest does not rise then the airway is not reflect this. In children over 8 years of age, the clear: method used in adults can be applied with appro- • readjust the head tilt/chin lift position; priate modifications for their size. •try a jaw thrust; • if both fail to provide a clear airway, suspect that Infants a foreign body is causing obstruction. The infant heart is lower compared to external landmarks; the area of compression is found by imagining a line running between the nipples and Circulation compressing over the sternum one finger’s breadth Because of the difficulties in identifying the pres- below this line. Two fingers are used to compress ence of a pulse, lay persons should look for signs of the chest to a depth of approximately 1.5–2.5cm a circulation (normal breathing, coughing or (Fig. 4.10). movement) in response to ventilation. Healthcare An alternative in infants is the hand-encircling professionals should check for a pulse; in children technique. The infant is held with both the res- the carotid artery can be palpated, but in infants cuer’s hands encircling the chest. The thumbs are the neck is generally short and fat, and it may be placed over the correct part of the sternum (see difficult to identify; alternatives are the brachial above) and compression carried out. artery on the medial aspect of the upper arm or the femoral artery. Assessment must take no more than Small children 10s. If a pulse cannot be detected or there are no The area of compression is one finger’s breadth signs of a circulation, or if in an infant the heart above the xiphisternum. The heel of one hand is rate is less than 60 beats/min, chest compressions used to compress the sternum to a depth of ap- will be required. proximately 2.5–3.5cm (Fig. 4.11).

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at a rate of at least 100 times per minute. One ventila- Larger children tion should be delivered for every five compres- The area of compression is two fingers’ breadth sions. Clearly, time spent readjusting the airway or above the xiphisternum. The heels of both hands re-establishing the correct position for compres- are used to compress the sternum to a depth of ap- sions will seriously decrease the total number of proximately 3–4cm, depending on the size of the compressions given per minute. This can be a very child. real problem for the solo rescuer and there is no Infants and children have a requirement for easy solution. The CPR manoeuvres recommended higher rates of ventilation and compression than for infants and children are summarized in Table adults. The aim should be to compress the sternum 4.3.

Further reading

Adnet PJ, Gronert GA. : advances in diagnostics and management. Current Opinion in Anaesthesiology 1999; 12: 353–8. Marik PE. Aspiration pneumonitis and . New England Journal of Medicine 2001; 344: 665–7. Mendelson CL. The aspiration of stomach contents into the lungs during obstetric anesthesia. American Journal of Obstetrics and Figure 4.11 Cardiac compression in a small child. Gynecology 1946; 52: 191–205.

Table 4.3 Summary of CPR manoeuvres in children

Infant Small child Larger child

Airway Neutral Sniffing Sniffing Head tilt position

Breathing 555 Initial slow breaths

Circulation Pulse check Brachial or femoral Carotid Carotid

Landmark 1 finger’s breadth 1 finger’s breadth 2 fingers’ breadth below nipple line above xiphisternum above xiphisternum

Technique 2 fingers or encircling 1 hand 2 hands

Depth 1.5–2.5 cm 2.5–3.5 cm 3–4 cm

CPR Ratio 1 : 5 1 : 5 1 : 5 Cycles per minute 20 20 20

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Useful websites http://www.asahq.org/publicationsAndServices/ Difficult%20Airway.pdf http://www.aagbi.org/pdf/Anaphylaxis.pdf [American Society of Anesthesiologists. Practice [The Association of Anaesthetists of Great Guidelines for Management of the Difficult Britain & Ireland. Anaphylactic reactions Airway. Revised October 2002.] associated with anaesthesia. Revised 2003.] http://www.brit-thoracic.org.uk/sign/ http://www.resus.org.uk/pages/reaction.htm [The British Thoracic Society (BTS) & Scottish [Resuscitation Council UK. The Emergency Intercollegiate Guidelines Network (SIGN). Medical Treatment of Anaphylactic Reactions British Guidelines on the Management of for First Medical Responders and for Asthma. February 2003.] Community Nurses. Revised January 2002.] http://www.leeds.ac.uk/medicine/LeedsMH.html http://www.mhra.gov.uk/ [The Leeds malignant hyperthermia unit. Leeds [Medicines and Healthcare products Regulatory is the national testing centre in the UK.] Agency (UK) ensures that medicines, healthcare http://www.resus.org.uk/ products and medical equipment meet [The Resuscitation Council UK. This site appropriate standards of safety, quality, contains the current UK guidelines for performance and effectiveness, and are used cardiopulmonary resuscitation.] safely. Report adverse events to this agency in the UK.]

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The necessary prerequisites for the successful The organization of critical care implementation of this integrated approach to the Critically ill patients have a high morbidity and organization of provision of care for critically ill mortality. Although prompt recognition and early patients are summarized in Table 5.2 and described appropriate management of such patients helps in more detail below. both to minimize further deterioration and maxi- mize the chances of recovery, it is equally impor- ‘Critical care is a process, not a location’ tant to identify and monitor closely those patients who are at risk of becoming critically ill. The Department of Health (UK) has recently identified Training and education of ward- standards for the provision and organization of based medical and nursing staff hospital care required by critically ill patients and those at risk of developing critical illness. This pro- Recognition of patients at risk of becoming criti- poses a shift in emphasis away from defining the cally ill is a key point and often the limiting step in needs of such patients in terms of hospital geogra- initiating appropriate management. Even when phy (ICU, HDU, etc.) and towards a classification this is achieved, there is no substitute for experi- system that describes escalating levels of care for ence when it comes to the management of critical individual patients, independent of their location illness, and the importance of referring such pa- within the hospital (Table 5.1). Although this does tients to senior colleagues at an early stage cannot not obviate the requirement for ICUs and HDUs be emphasized enough. All too often, misinterpre- within most acute hospitals in the UK, it does tation of the clinical picture may lead either to a envisage less direct focus on these areas, towards lack of action or to treatment being commenced a more generalized, hospital-wide approach. which is inappropriate. A common example is the One of the key benefits that it is hoped will be elderly postoperative patient who is breathless, hy- achieved by this reorganization of care of critically potensive, oliguric and has crackles on ausculta- ill patients is a reduction in referral to ICU and tion of the chest. Acute heart failure is diagnosed HDU by earlier recognition of warning signs that and a large dose of an intravenous diuretic is given. often presage the development of critical illness The correct diagnosis is often pneumonia, sepsis and cardiac arrest, thereby prompting earlier and pre-renal failure, secondary to hypovolaemia initiation of resuscitation and treatment — the so- and hypotension. Although the intravenous called ‘intensive care without walls’ philosophy. diuretic may initially result in a slight increase

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Table 5.1 Levels of care for critically ill patients Table 5.2 Key features of an integrated approach to the provision and organization of care of critically ill patients Level 0 • Patients whose needs can be met through normal • Earlier recognition of the deteriorating condition of ward care susceptible patients • Earlier initiation of appropriate Level 1 treatment/resuscitation • Patients at risk of their condition deteriorating • Earlier referral of patients to the critical care team • Patients recently relocated from higher levels of care • Extension of the resources of the ICU/HDU beyond whose needs can be met with additional advice and their geographical limits support from the critical care team These aims may be facilitated by the introduction of: Level 2 (HDU) • Improved training and education of clinical ward staff • Patients requiring more detailed monitoring, •Doctors including support for a single organ system failure • Nurses • Certain postoperative patients (e.g. after major • Healthcare assistants surgery in high-risk patients) • Use of clinical early warning scoring systems • Patients stepping down from intensive care •Provision of an outreach team Level 3 (ICU) • Patients requiring advanced respiratory support (tracheal intubation and mechanical ventilation) • Advanced Life Support (ALS) Focuses on the • Patients with MOFS prevention and management of cardiorespiratory Adapted from Comprehensive critical care: a review of arrest. adult critical care services. Department of Health, 2000. • Advanced Trauma Life Support (ATLS) Focuses on Reproduced with permission of the Controller of HMSO. the management of major life-threatening acute trauma. • Advanced Paediatric Life Support (APLS) Focuses in urine output, ultimately it will exacerbate the on recognition and management of the sick child. dehydration and pre-renal failure, and may even Attendance on courses such as these is highly precipitate acute cardiovascular collapse. Clinical recommended. experience is essential to correctly identify the It is essential that all healthcare professionals problem and institute appropriate management, recognize their limitations and know when to call which in this case might include transfer of the for senior help, particularly when initial manage- patient to a high dependency area, oxygen, chest ment has not led to a timely improvement in the physiotherapy, a fluid challenge (perhaps guided condition of the patient. This assistance is often by invasive CVP and arterial pressure monitoring), one’s immediate clinical superior (e.g. specialist antibiotics and intravenous inotrope or vasopres- registrar or consultant) but may also include a sor therapy. medical emergency team (MET), an outreach team In an attempt to overcome the deficiencies in (see below) or a doctor/nurse from the ICU. How- training and education, a diverse range of courses ever, as stated previously, these judgements are is now available which aim to ‘short-circuit’ the often quite complex. Accordingly, formal clinical knowledge and experience gap, including: scoring systems have been introduced in many • Acute Life-threatening Event Recognition and Treat- hospitals to facilitate the process of assessing ill- ment (ALERT) Focuses on the recognition and ness severity and response to treatment. management of patients in the early stages of developing critical illness. Clinical scoring systems • Care of the Critically Ill Surgical Patient (CCrISP) Focuses on the management of critically ill surgical Several schemes have been described including: patients. • The Medical Emergency Team Calling Criteria.

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Table 5.3 The Modified Early Warning Scoring System

Score 3 2 1 0 1 2 3

HR <40 40–50 51–100 101–110 111–129 ≥130 BP >45% Ø 30% Ø 15% Ø Normal* 15% ≠ 30% ≠>45% ≠ RR £8 9–14 15–20 21–29 ≥30 Temp <35.0°C 35.0–38.4°C ≥38.5°C CNS** A V P U Urine NIL <0.5 mL/kg/h <1mL/kg/h >1.5 mL/kg/h

HR: heart rate; BP: blood pressure; RR: respiratory rate; CNS: central nervous system. * Normal for patient. ** Assessment of conscious level; A: alert; V: responsive to verbal stimulus; P: responsive to painful stimulus; U: unresponsive. Adapted from Stenhouse C, Coates S et al. Prospective evaluation of a modified Early Warning Score to aid earlier detection of patients developing critical illness on a surgical ward. British Journal of Anaesthesia 2000; 84: 663P.

• The Patient At Risk Team (PART) Protocol. • that staff require a minimum of training; • The Critical Care Liaison Service Protocol. •their applicability to trainee doctors, nurses • The Early Warning Scoring System (EWSS). (both qualified and student) and other health • The Modified Early Warning Scoring System professionals. (MEWSS). With these systems, patients at risk of developing All of these are based on recording observations re- critical illness are highlighted at an earlier stage lating to the physiological and clinical status of the than perhaps they otherwise would be, and appro- patient and the allocation of ‘points’ according to priate treatment commenced. The other advantage the presence and severity of any derangement is that referral arrangements by nurses and inexpe- from a reference range. The variables used include rienced doctors for more senior help and advice heart rate, arterial blood pressure, respiratory rate, can be formalized into the protocol. Thus the ward body temperature, conscious level and urine out- nurse may be required to contact the house officer put. The points derived from each variable are to- for assistance if the trigger threshold is reached. talled, and advice on further clinical management The house officer is then required to contact the is sought either on the basis of a trigger threshold senior house officer or registrar if immediate being reached or because of a continued adverse management does not result in an objective, trend in a patient’s score. Another subjective cate- timely improvement in the patient’s condition gory is sometimes added to include any patient based on an improving score. This leads ultimately about whom there are serious concerns, independ- to direct clinical input from either a senior doctor ent of the objective scoring assessment. The (consultant) or outreach team from critical care if importance of this latter point cannot be overem- the patient is still not improving. phasized, particularly when the concern is voiced The use of such scoring systems cannot and must by an experienced nurse who ‘doesn’t like the look’ not substitute entirely for appropriate training and of a particular patient. An example of one of these education of clinicians and there are several unre- scoring systems is shown in Table 5.3. solved issues relating to their use. As their intro- The main advantages of such scoring systems duction into clinical practice has been relatively are: recent, there is as yet insufficient data available as •their simplicity, with the need for only the basic to which physiological parameters are most impor- monitoring equipment, normally present on acute tant, and the weighting of the variables to achieve hospital wards; the overall score has not been validated. A doctor • their reproducibility between different with experience in treating critically ill patients observers; will not need to formally score his or her patients

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Table 5.4 Aims of outreach patients and ideally be either an intensivist doctor (consultant or experienced specialist registrar • Early identification of patients with actual or potential critical illness (SpR)) or a senior intensive-care nurse practitioner. • Appropriate early intervention, which may prevent Other members of the team should include trainee deterioration and avert the need for admission to doctors from acute medical and surgical special- HDU or ICU ties. The team should have easy access to other spe- • Liaison with the HDU and ICU cialized personnel such as physiotherapists, • Facilitate early admission to HDU and ICU when pharmacists and dieticians. The proper resourcing necessary of an effective outreach team is problematic in • Identification of patients for whom HDU or ICU care many hospitals, and ad hoc arrangements may is deemed inappropriate then operate whereby patients giving rise to con- • Appropriate early designation of patients as ‘not for cern are referred to the ICU, and a ‘team’ consisting attempted resuscitation’ in the event of of an ICU trainee and/or nurse is dispatched to cardiorespiratory arrest •To assist ward nurses in the management of patients assess the situation and act accordingly. Clearly with actual or potential critical illness this is a less satisfactory approach and leads to a • Education and training of trainee doctors and more fragmented level of care. medical students •Promote continuity of care following step-down of patients to the ward from HDU and ICU Definition and causes of critical illness

before deciding on the correct management. Multiple organ failure syndrome Nevertheless, it seems intuitive that scoring sys- tems will be useful in helping less-experienced per- Critical illness may be defined as the failure of one sonnel identify patients at risk and in assessing the or more organ systems, the most immediately life- effects of their clinical intervention. threatening being failure of the respiratory and cardiovascular systems. Failure of other systems (e.g. renal, gastrointestinal, hepatic, central Outreach teams nervous system, haematological, immunological, Outreach teams have been established in many metabolic, etc.) have their own intrinsic morbidity hospitals in accordance with the ‘intensive care and mortality, as well as increasing that associated without walls’ philosophy as one facet of the criti- with primary cardiorespiratory failure. Critical ill- cal care service. The aims of outreach are summa- ness due initially to a primary failure of one organ rized in Table 5.4. Although one of the primary system may rapidly escalate to fulminant multiple aims is to avoid admission to a critical care area, the organ failure syndrome (MOFS), particularly when following are also implicit: resuscitative management is delayed, inadequate • Outreach is not a substitute for the adequate pro- or inappropriate. Mortality correlates with the vision and resourcing of HDU and ICU beds. number of organ system failures and their • The effective use of outreach may, paradoxically, duration: increase demand for HDU and ICU beds by identi- • Patients with two or more organ system failures fying more patients who might benefit from them. have a mortality of approximately 50% on the first • Outreach is not a substitute for adequate staffing day, rising to 66% by the fourth day. of the general ward. • Patients with three or more organ system failures Membership of the outreach team should be have a mortality of approximately 80% on the first multidisciplinary, although its precise makeup will day, rising to 95% or more by the fourth day. vary from hospital to hospital. The team leader A common aetiological factor in the development should be experienced in managing critically ill of MOFS in critically ill patients is ischaemia of the

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gastrointestinal tract due to poor splanchnic level, leading inevitably to damage, dysfunction perfusion and oxygenation in unresuscitated, and ultimately cell death. shocked, hypoxic patients. The ischaemia produces damage to the mucosal integrity of the Initial assessment and gut, a breach of its normal barrier function management of critically and translocation of bacteria into the circulation ill patients (septicaemia). The causes of organ dysfunction may be classi- Cardiorespiratory arrest has a high overall morta- fied as either primary or secondary: lity, even when it occurs in hospital. Patients who • Primary organ dysfunction A result of direct tissue arrest secondary to severe myocardial ischaemia or injury; for example, pneumonia in acute respira- infarction have a relatively better outcome as the tory failure or myocardial infarction in acute car- presenting rhythm is more likely to be ventricular diovascular failure (cardiogenic shock and/or acute fibrillation or pulseless ventricular tachycardia. heart failure). Both are amenable to treatment by electrical defib- • Secondary organ dysfunction Results from indirect rillation, particularly when a patient is in a moni- tissue injury and is often the major contributor tored environment such as the coronary care unit to MOFS. For example, diverticular perforation (CCU), due to rapid recognition and treatment. of the colon may initially cause peritonitis and Unfortunately, the largest group of hospital pa- septicaemia. However, the resulting release of in- tients who have a cardiac arrest do so as the final flammatory and toxic mediators from bacteria step in a sequence of progressive deterioration of and host tissues may go on to trigger an escalating their presenting illness. The arrest rhythm is more cascade of inflammatory mediators throughout likely to be either asystole or pulseless electrical ac- the body, causing widespread tissue damage tivity (when the ECG displays complexes that and organ dysfunction (systemic inflammatory would normally be associated with a cardiac out- response syndrome, SIRS). Secondary organ dys- put). Only a very small minority of these patients function may also develop from hospital-acquired are successfully resuscitated and discharged home. (nosocomial) infections. Critically ill patients Prevention of cardiac arrest in this situation is are at greatly increased risk of these because their therefore the only approach likely to be successful. immune cellular defence mechanisms are im- Studies have shown that in this latter group of paired by the effects of SIRS and also because natu- patients cardiac arrest is often predictable, with ral host defence barriers are breached by invasive most patients exhibiting signs of clinical deteriora- monitoring lines, urinary catheters, tracheal tion over the preceding 12–24h. Features are typi- tubes, etc. cal of those listed above in clinical scoring systems, and include: • respiratory distress and tachypnoea (respiratory SIRS rate >30/min); Any cause of systemic sepsis or major trauma may • tachycardia (heart rate (HR) >120/min); activate inflammatory mediators giving rise to this •a fall in cardiac output manifest as hypotension, condition. Within the lungs there are non-cardio- confusion, drowsiness and metabolic acidosis. genic alveolar and interstitial oedema, ventila- If these warning signs are heeded and appropriate tion–perfusion imbalance and respiratory failure resuscitative measures commenced, cardiac arrest (acute respiratory distress syndrome, ARDS). Else- may be prevented and lives saved. Alternatively, if where SIRS causes profound circulatory vasodilata- it is decided (by a senior clinician) in advance of tion, hypotension, impaired control of regional the event that cardiac arrest is inevitable and that perfusion, capillary leak and systemic oedema. The resuscitation is unlikely to benefit the patient, a final outcome of this derangement is impaired DNAR (do not attempt resuscitation) order may be oxygen delivery and consumption at a cellular made. It should be noted that a DNAR order does

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not preclude appropriate resuscitative measures up very well, doctor’ tells you at the very least that the to the point of actual cardiac arrest. patient has control of his or her airway, is breath- ing, and has sufficient cerebral perfusion to process the question and formulate an appropriate answer. Action on receiving a call to a Failure to respond appropriately to the question sick patient should immediately suggest the possibility of an When requested to see a patient who is giving acute life-threatening physiological disturbance cause for concern, it is helpful to have asked a few and the possibility of cardiorespiratory arrest. pertinent questions of the referrer concerning the patient’s recent history, so that you are already Airway — assessment and management thinking about potential diagnoses and treatment as you make your way there. For example: Acute upper airway obstruction may be either • How old is the patient? complete or partial. If left untreated the patient • When was the patient admitted to hospital? may die within minutes. Assuming the patient is • What did the patient come into hospital with? attempting to breath: • Is the patient conscious, and if so what is he or • Look and listen for evidence of obstruction: she complaining of? • partial obstruction results in noisy breathing •How quickly has the patient deteriorated? (gurgling, snoring, crowing); • What are the patient’s pulse rate, blood pressure, • complete obstruction is silent; respiratory rate, temperature, skin colour? • movements of the chest are usually exaggera- • Does the patient have a DNAR order? ted and a see-saw pattern is often observed, with Do not attempt to acquire a comprehensive the chest being drawn in on inspiration as the medical and surgical history since birth in a abdomen rises; the opposite movements occur patient whose airway, breathing or circulation may during expiration; be threatened, or in whom cardiorespiratory arrest • accessory muscles may be used, for example is imminent! sternomastoids. The effective management of these patients has Common causes of airway obstruction are listed in two key elements: Table 5.5. •A systematic approach must be used that deals On the general medical or surgical ward, im- with the greatest potential threat first. paired consciousness is the most common cause of • Call early for senior help if the situation appears airway obstruction. It can usually be relieved using beyond your capabilities, or if the patient con- basic airway-opening manoeuvres such as the head tinues to deteriorate despite what you consider to tilt plus chin lift or jaw thrust (see page 99). Inser- be appropriate management. tion of simple airway adjuncts (Guedel oral airway

Initial approach Table 5.5 Causes of upper airway obstruction In assessing any critically ill patient, it is essential to follow the ABC system, that is Airway, • Impaired conscious level—reduced muscle tone Breathing, Circulation. The principles of ABC allows the tongue to fall back and occlude the airway management are discussed in the chapter on car- • Blood, vomit or other secretions diorespiratory arrest and the application of this •Trauma • Laryngeal oedema due to or thermal system in relation to the patient who has not yet injury progressed to cardiac arrest is given below. • Inhaled foreign body (e.g. food bolus) On approaching the patient for the first time, •Tumour much useful information may be gleaned by sim- • Infection (e.g. retropharyngeal abscess) ply asking: ‘Are you alright?’ The reply: ‘I don’t feel

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or nasopharyngeal airway) may also be required There are numerous causes of respiratory failure. (see page 18). Airway obstruction due to vomit, They may be classified as to whether respiratory blood, food or secretions in the mouth and phar- failure from lung disease is the primary problem or ynx may be apparent on inspection and dealt with secondary to other problems (Table 5.6). Both pri- by careful suction using a rigid, wide-bore sucker. mary and secondary causes may coexist in the Even if these simple steps relieve the airway ob- same patient. struction, it is vital to call for experienced help at The treatment for hypoxaemia is administration this stage, often from an anaesthetist, who may de- of oxygen in high concentration, ideally to achieve

cide that tracheal intubation and transfer to the a normal PaO2 (12–14kPa) or peripheral oxygen ICU is necessary. Airway obstruction secondary to saturation (=95%). At the very least, minimum re- pathology in and around the upper airway itself, spective targets of 8kPa and 90% should be aimed such as a laryngeal tumour or trauma to the head for. This is most easily achieved by using a face- and neck, mandates a call for immediate expert mask with an attached reservoir bag connected to assistance. oxygen at a flow rate of 15L/min (see Fig. 3.2). En- sure the reservoir is filled with oxygen before plac- ing it on the patient’s face. This apparatus will Breathing assessment and management provide an inspired oxygen concentration of ap- Breathing is initially assessed using the look, listen proximately 85%. Oxygen therapy per se does not and feel approach (see page 100). Assuming the air- treat the cause of hypoxaemia and respiratory way has been cleared and the patient is breathing: failure; the next step is to ascertain the cause and • Count the respiratory rate: treat appropriately. • Rapid breathing (>30 breaths/min) is an early sign of clinical deterioration that may progress The patient with chronic obstructive to cardiac arrest. pulmonary disease (COPD) • Abnormally slow breathing (rate <8/min) may indicate terminal exhaustion of the patient or The spectre of the patient with severe chronic res- brain stem depression due to ischaemia, hypoxia piratory disease, chronic hypoxia and a hypoxic or drugs (e.g. opioids). drive to breathing is a frequent cause of concern • Look for the presence of cyanosis (peripheral or and confusion for the inexperienced. The worry is central). that administration of a high concentration of • Examine the chest, palpating, percussing and oxygen will remove the respiratory drive of such auscultating for primary and secondary respiratory patients and produce hypoventilation with in- problems. creasing hypercapnia, progressing to unrespon- • Pulse oximetry and arterial blood gas analysis siveness and respiratory arrest. However, these provide useful additional information. patients represent a minority. There are two key Do not forget: points to remember: • Severe respiratory failure may be masked by ad- • Patients will die as a consequence of withhold- ministration of a high concentration of inspired ing oxygen in high concentration because of an

oxygen to the patient. A normal PaO2 (12–14kPa) unwarranted concern about hypoxic drive.

breathing 100% O2 is NOT normal! • Patients do not die of hypercapnia — they die of •When the oxygen saturation of arterial blood is hypoxia.

90% the PaO2 is only 8kPa. Unless the patient’s history strongly suggests severe •A hypoxaemic patient will usually hyperventi- chronic respiratory disease, give a high concentra-

late, resulting in a low PaCO2. tion of oxygen.

•A high PaCO2 in the presence of hypoxaemia is an Oxygen should be administered at a lower con- ominous sign: it usually indicates exhaustion of centration (e.g. 28–40%) to patients in whom a hy- the patient. poxic drive is strongly suspected and the response

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Table 5.6 Causes of respiratory failure on the ICU

Primary lung dysfunction Secondary causes

• Pneumonia • Exhaustion • Acute asthma • ARDS • Acute exacerbation of COPD • Acute heart failure • Emphysema • Pulmonary embolism • Pulmonary fibrosis • Airway obstruction • Pneumothorax/haemothorax • Neuromuscular problems • Pulmonary contusion • Myopathies • Neuropathies • Guillain–Barré syndrome • Myasthenia gravis • CNS depression •Drugs • Head injury • Meningitis/encephalitis • Cerebral haemorrhage • Cerebral tumour • Cerebral hypoxia • Diaphragmatic splinting • Morbidly obese patients • Abdominal pain • Abdominal distension

carefully observed, both clinically and by repeat- flow greater than the patient’s peak inspiratory ing arterial blood gas analysis at frequent intervals flow rate to minimize the work of breathing. The (e.g. every 30mins). The aim should still be to positive airway pressure improves oxygenation by achieve the minimum targets stated above, al- increasing functional residual capacity (FRC, the though it is acknowledged that in a small group of resting volume of the lungs at the end of a normal patients with severe chronic respiratory disease, expiration), re-expanding collapsed areas of the

even lower target levels for PaO2 may be acceptable. lungs (recruitment) and reducing the tendency of However, these patients require the early involve- airways to collapse during expiration. Nasal CPAP ment of an expert to make what are complex may also be administered. judgements of the risks/benefits of intervention. • NIPPV A mechanical ventilator is connected to a In patients who fail to improve with simple close-fitting facemask to avoid leaks and allow oxygen therapy, call for expert help early. They positive pressure assistance of the patient’s own may require: respiratory efforts. A nasal mask can also be used • continuous positive airway pressure (CPAP); and CPAP may be applied. The patient is not sedat- • non-invasive positive pressure ventilation ed as this would inhibit spontaneous respiratory (NIPPV); effort. Such patients may be managed on the med- • invasive ventilation. ical HDU or a specific respiratory care unit. • CPAP A breathing system is attached to a tightly • Invasive ventilation The patient is anaesthetized, fitting facemask to ensure that a positive pressure is intubated and then sedated to tolerate the tracheal maintained throughout the respiratory cycle dur- tube. Full mechanical ventilation is provided, in- ing the patient’s spontaneous respiratory efforts dependent of the patient’s own efforts. Admission (Fig. 5.1). The apparatus is designed to maintain a to the ICU is necessary.

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Figure 5.1 Demonstration of a CPAP system. (A) High flow of oxygen to pa- tient; (B) tight-fitting facemask; (C) ex- piratory valve to maintain a positive pressure throughout the respiratory cycle.

Although a full discussion of the respective Do not forget: merits of these two approaches to ventilation is •A thready, weak, rapid pulse with peripheral pal- beyond the scope of this book, there is increasing lor and cool skin is suggestive of circulatory shock evidence that the morbidity and mortality of pa- associated with a low cardiac output. tients with an acute exacerbation of COPD is re- •A bounding, easily felt rapid pulse with a warm duced when non-invasive ventilation is used prior periphery may be due to septic shock. Cardiac out- to consideration of tracheal intubation. Acute ven- put is often normal or even elevated despite a low tilatory failure due to other causes, particularly in blood pressure. the context of a critically ill patient with multiple Automated non-invasive blood pressure devices organ system failure, usually necessitates ICU are less reliable if the peripheral pulse is weak or ir- admission and invasive ventilation. regular. Obtain a systolic reading by manual use of a , noting the point at which the brachial pulse is just palpable. An arterial line Circulation — assessment and provides reliable, continuous blood pressure data. management However, appropriate skill is required to insert one, Circulation is once again assessed using the look, and operate the specialized monitoring equip- listen and feel approach. Assuming the patient ment, and nurses must be experienced in manag- has a pulse, observe for signs of an adequate ing such patients. Accordingly, it will usually be circulation: necessary to transfer such patients to a high de- • rate, volume and rhythm of the pulse (it may pendency area. only be possible to detect a large central pulse over Heart rate and blood pressure must be placed in the carotid, brachial or femoral arteries); the context of what is normal for that individual • respiratory rate, conscious level; patient. An elderly patient with poor myocardial • peripheral skin temperature, colour and capil- reserve may be in extremis with a heart rate of lary refill time (apply firm pressure to the patient’s 60/min and a blood pressure of 90/50mmHg, al- finger or toe for 5s and release: capillaries should though the same values may be well tolerated or refill within 2s); even normal for a fit young adult. A relative brady- •measure the blood pressure; cardia developing after a tachycardia must never • measure urine output. be assumed to indicate an improvement in the

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Table 5.7 Causes of systemic hypotension • Observe the patient for signs of improvement — decreased pulse and respiratory rate, improved level Hypovolaemia • Dehydration/inadequate fluid intake of consciousness, increased blood pressure, etc. • Haemorrhage • Repeat the fluid challenge, as indicated by the • Severe vomiting/diarrhoea patient’s response. • Burns The choice of what type of fluid to use at this stage • Abnormal fluid losses into the gut (crystalloid or colloid) is probably less important • High output fistula of the small bowel than the fact that fluid (any fluid) is being given. Cardiogenic causes However, dextrose-containing solutions are not • Acute myocardial ischaemia/infarction used for initial resuscitation as they rapidly dis- • Severe valvular heart disease tribute throughout the entire intracellular and ex- • Cardiomyopathy tracellular fluid compartments of the body, with • Acute myocarditis little remaining in the circulation. Where there is • Constrictive pericarditis evidence of significant blood loss or ongoing Sepsis haemorrhage, give blood or arrange urgent • Any cause of systemic sepsis cross-match. The aim of this initial treatment is to buy time by Neurogenic stabilizing the condition of the patient in order to • High spinal cord injury make a definitive diagnosis and arrange for more Anaphylaxis expert management. Patients who are unrespon- sive to fluid resuscitation alone may have ongoing fluid losses (e.g. bleeding or extravasation of circu- condition of the patient as it may herald an im- lating fluid through leaky capillaries in sepsis syn- pending cardiac arrest — the patient’s overall condi- drome) that require addressing, or complementary tion and progress must be considered. treatment with inotropes, vasopressors and inva- The causes of systemic hypotension are summa- sive haemodynamic monitoring (e.g. CVP and pul- rized in Table 5.7. monary artery flotation catheter (PAFC); see page It may be possible, from the history and clinical 125). These patients should be referred to the ap- examination, to arrive at a reasonably certain work- propriate expert. ing diagnosis and treat accordingly. For example: Patients with severe hypotension due to poor left •A patient on the CCU with acute myocardial in- ventricular performance after acute myocardial in- farction and severe hypotension probably has car- farction (cardiogenic shock) may not tolerate a diogenic shock. rapid, large fluid bolus because the filling pressure •A hypotensive patient found on a surgical ward of the left ventricle is already increased and its on the day after major abdominal surgery with ab- muscle fibres are overstretched. If the clinical diag- dominal distension and surgical drains full of nosis is fairly certain: blood is probably hypovolaemic. • If not already done, establish intravenous access. •A patient with pneumonia, a high pyrexia and • Give fluid in slower, smaller aliquots (250mL). elevated white cell count who is hypotensive with • Monitor the response very closely, preferably a rapid, bounding pulse is probably septic. with the aid of invasive haemodynamic monitor- As a general rule, nearly all patients with clinical ing (e.g. arterial line, CVP and PAFC). signs of an inadequate circulation such as tachy- These patients often need: cardia and hypotension respond well to a fluid • reduction of the high preload to the left ventricle challenge: using diuretics and intravenous nitrates (e.g. glyc- • If not already done, establish intravenous access. eryl trinitrate, GTN); • Give a rapid bolus of 500mL over approximately • reduction of afterload using intravenous arterial 15mins. vasodilators;

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• inotropic support to assist in supporting the fail- A standard 12 lead ECG should also be per- ing myocardium. formed in any patient with warning cardiorespira- Dobutamine, a synthetic catecholamine, is most tory signs, and will provide valuable information commonly used. Its actions are predominantly via of significant myocardial ischaemia or infarction. b-adrenoceptors, increasing myocardial con- A rapid irregular pulse is likely to be due to atrial tractility and causing arteriolar vasodilatation in fibrillation. This may need additional treatment

skeletal muscle reducing afterload via b2-adreno- with either anti-arrhythmic drugs (e.g. digoxin, ceptors. amiodarone) or synchronized electrical cardiover- Such patients should be considered as being at sion using a defibrillator (see page 106). Patients very high risk of cardiac arrest from which the causing serious concern should be continuously prognosis is likely to be poor. They must be monitored by ECG, pulse oximeter and invasive managed in a high dependency area (e.g. CCU) by arterial monitoring. experienced clinicians. Acute heart rhythm disturbances and their im- mediate management are summarized in Table 5.8. Cardiac arrhythmias

Common tachycardias and sinus bradycardia and their causes have been covered on pages 77–78.

Table 5.8 Acute heart rhythm disturbances and their immediate management

Sinus tachycardia Sinus bradycardia Usually an appropriate cardiovascular response to Identify and treat the underlying cause: maintain cardiac output and blood pressure—treat • Impending cardiac arrest the cause, not the tachycardia itself: • Hypoxia • Hypovolaemia • Drug toxicity • Myocardial ischaemia/infarction • Hypothermia • Sepsis • May be normal in young fit adults • Severe pain • Raised intracranial pressure • Anxiety • Heart block • Thyrotoxicosis • May pre-exist or be associated with acute myocardial ischaemia/infarction Supraventricular tachycardia • Second- and third-degree heart block may quickly • In critically ill patients usually atrial fibrillation, progress to ventricular standstill (cardiac arrest) particularly the elderly • Needs insertion of a temporary transvenous pacing • Often indicates inadequate intravascular volume wire •Treat using synchronized electrical cardioversion or drugs depending on the degree of urgency (see Ventricular tachycardia page 77) • Usually associated with acute myocardial ischaemia/infarction • Relatively uncommon presentation in critical illness due to other causes • Potentially compatible with a pulse but may also rapidly deteriorate into a cardiac arrest • Requires immediate treatment, usually by defibrillation unless ‘well tolerated’ by the patient, when drugs (e.g. amiodarone) may be tried initially

Ventricular fibrillation, asystole and pulseless electrical activity See pages 105–108

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Figure 5.2 Typical view of an ICU pa- tient to show the large amount of equipment required. Ventilator and monitors are on the patient’s right, sy- ringe pumps delivering drugs are on the left.

Complementing, or in lieu of the ICU, there may The intensive care unit be a high dependency unit (HDU) where the level of care is intermediate between that found on the ICU and the general ward (Level 2 care). Patients An overview on the HDU are not normally mechanically venti- The intensive care unit (ICU) is a designated area lated. Patients suffering from acute myocardial in- within a hospital where specialized treatment of farction are generally admitted to specialized critically ill patients takes place (Level 3 care, Fig. coronary care units (CCUs), while neurosurgical 5.2). In order to achieve this, there is a concentra- and head-injured patients may be admitted to a tion of resources, including: specialized area of the neurosurgical ward for short •a wide range of complex monitoring equipment; periods of mechanical ventilation. • mechanical ventilators; The demand for intensive care is increasing • facilities for organ support; steadily as a result of advances in clinical manage- • the use of potent drugs, which are often given by ment, and also because of the ever-increasing ex- continuous intravenous infusion; pectations from society that almost no patient, •a high nurse to patient ratio, typically 1:1; regardless of age or co-morbidity, should be denied •a medical resident who is continuously available admission to the ICU. Currently the UK has rela- exclusively for the ICU. tively fewer general or specialist intensive care The service is genuinely consultant-led; that is, beds, 2.6% of all acute hospital beds, compared consultants (predominantly anaesthetists in the with 4.1% in Denmark and approximately 8% in UK) are closely involved with all day-to-day the United States. This under-provision, coupled management of critically ill patients, and with with average ICU bed occupancy rates (80–90%) supervising, directing and training nurses and that tend to be much higher than the ideal doctors. The out-of-hours commitment of such (60–70%), means that there are relatively frequent consultants is onerous as they are normally present occasions when no local ICU bed can be found for on the ICU to directly supervise the initial manage- a critically ill patient. Hospitals now have for- ment of all newly referred critically ill patients, ad- malized arrangements for transferring patients to missions to the ICU and inter-hospital ICU other ICUs in such circumstances. It has been sug- transfers. gested that in order to maximize clinical and

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financial efficiency, much larger regional ICUs should be established although little progress has been made in this regard. The challenge for those involved in the care of critically ill patients is to aim precious resources at those patients likely to survive, by providing artifi- cial support of one or more failing physiological systems until natural recuperation and/or thera- peutically assisted recovery can take place. Patients may be admitted to the ICU electively following major surgery, or as medical or surgical emergen- cies. In an attempt to differentiate potential sur- vivors from non-survivors, a number of scoring Figure 5.3 ICU monitor displaying ECG, invasive blood systems have been developed which take into ac- pressure and waveform, CVP and waveform, SpO2. count various aspects of the patient’s acute physio- logical upset, age and any chronic health problems (e.g. APACHE II — Acute Physiology and Chronic Arterial blood pressure Health Evaluation). However, none of these scor- ing systems is sufficiently accurate to be used as the In health, systemic arterial blood pressure is sole basis for deciding whether or not to treat an in- closely regulated to maintain an adequate pressure dividual patient. Ultimately, there is no substitute to ensure tissue perfusion. In critically ill patients, for the clinical judgement of an experienced inten- mean arterial pressure (MAP) should normally be sivist (consultant). maintained above a minimum value of 70mmHg. However, it may be appropriate to aim for a higher value in elderly patients (as blood pressure tends to Monitoring on the intensive care unit increase with age) and in patients with known Physiological monitoring is an essential aid in the hypertension. It is very helpful to know what diagnosis and management of critically ill pa- is ‘normal’ for an individual patient and such tients, in evaluating their response to treatment information may be available in the patient’s case and alerting staff to the onset of a sudden deterio- notes. ration in the patient’s condition. There is a spec- MAP is dependent on cardiac output and sys- trum of monitoring. At its most basic level it temic vascular resistance (SVR) according to the comprises clinical observation and examination formula: MAP = CO ¥ SVR. Measurement of arterial (which, although ‘low technology’, remains of blood pressure is thus a relatively crude indicator vital importance), extending to complex, invasive of cardiac performance and circulatory flow, as it methods for the measurement of haemodynamic, may be normal or elevated in the presence of a low oxygen transport and other variables (Fig. 5.3). cardiac output and poor tissue perfusion. Interpre- tation of the blood pressure must be taken in the context of other clinical measurements such as the Electrocardiogram (ECG) state of the peripheral circulation, urine output All patients should have a continuously displayed and trends in acid–base balance. In critically ill pa- ECG for the detection of acute arrhythmias, and to tients it is often more useful to measure the cardiac a lesser extent (except on the CCU), acute is- output itself (see below). chaemia. In critically ill patients on the general Arterial blood pressure is usually monitored in- ICU, supraventricular tachycardias predom- vasively on the ICU as it is more accurate, and con- inate, especially sinus tachycardia and atrial tinuous, and the presence of an indwelling arterial fibrillation. cannula allows blood sampling without the need

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Table 5.9 Advantages and disadvantages of direct arterial Table 5.10 Uses of central vein catheterization blood pressure measurement • Measurement of central venous pressure Advantages • Infusion of: • Accuracy •irritant solutions, e.g. KCl • Continuous measurement gives immediate warning • vasoconstrictor agents, e.g. noradrenaline, of important changes in blood pressure dopamine • Shape of arterial waveform gives information relating • parenteral nutrition to myocardial contractility and other haemodynamic • Insertion of temporary cardiac pacing wire variables • Insertion of pulmonary artery flotation catheter • Facility for frequent arterial blood sampling •Venous access: • for haemodialysis, haemofiltration, Disadvantages plasmaphoresis, etc. • Complex to perform • in the absence of peripheral veins • Potentially inaccurate if apparatus is not set up • during cardiac arrest correctly • Haematoma at puncture site • Infection at puncture site/bacteraemia/septicaemia • Disconnection haemorrhage measured dose of lithium is injected intravenously • Embolization and cardiac output is calculated from the •Arterial thrombosis resultant lithium dilution curve. This value is used to calibrate the pulse contour analysis and is nor- for repeated puncturing of veins or arteries. The ad- mally performed only 2–3 times per day. The clear vantages and disadvantages of direct measurement advantage of this system is that continuous cardiac are shown in Table 5.9. A cannula is inserted percu- output monitoring of critically ill patients is pos- taneously into a suitable artery, usually the radial sible without requiring an invasive technique artery of the non-dominant hand (common alter- other than the arterial line itself, which is already natives being the femoral and dorsalis pedis routinely inserted into nearly all patients on the arteries, less commonly the brachial and axillary ICU. arteries). The arterial blood pressure is transmitted via a saline-filled catheter to a pressure transducer Central venous pressure (CVP) that converts the mechanical signal to a very small electrical signal, proportional to the pressure. This This is an index of the patient’s circulating volume signal is amplified and displayed on a monitor as (or more correctly right ventricular preload). It is both a waveform and pressure readings: systolic, useful for directing fluid therapy in cases of diastolic and mean. Exposing the transducer to at- dehydration, hypovolaemia due to haemorrhage mosphere and ensuring that the monitor reads and sepsis syndrome, and in the diagnosis and zero pressure ensures accuracy of the system. To management of heart failure. The routes com- prevent the system becoming blocked, it is flushed monly used to measure CVP are discussed on page constantly with heparinized saline at approxi- 58. A central venous cannula may also be used for mately 3mL/h from a pressurized source to prevent a variety of other purposes in the ICU, as shown in backflow. Central venous and pulmonary artery Table 5.10. pressures are measured using the same system. The main limitation in monitoring CVP is that Recently, devices have become available that therapy is directed towards optimizing the filling analyse the shape of the arterial waveform (pulse pressures on the right side of the heart. While the contour analysis) and derive stroke volume, and, filling pressures of the right and left sides are nor- by knowing heart rate, allow cardiac output to be mally closely related, this relationship may not determined. The arterial line is modified to incor- always be reliable in critically ill patients, porate an electrode sensitive to lithium. A particularly those with pre-existing cardiac or

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Figure 5.4 Pressure trace on insertion of PA catheter; (A) in right atrium, (B) in right ventricle, (C) in pulmonary artery, (D) in pulmonary artery with balloon inflated (‘wedged’).

respiratory disease. In this situation it is of greater Table 5.11 Complications of pulmonary artery therapeutic value to monitor and optimize condi- catheterization

tions for the left ventricle. • All of the complications associated with central venous catheterization Pulmonary artery pressures •Ventricular dysrhythmias • Pulmonary infarction Pressures in the pulmonary artery are monitored • Pulmonary artery rupture using a PAFC. This is a multi-lumen catheter with • Knot formation an inflatable balloon and a temperature thermistor • Balloon rupture at its distal end. • Subacute bacterial endocarditis • Pericardial tamponade A PAFC is inserted percutaneously via either the • Damage to tricuspid or pulmonary valve internal jugular or subclavian vein in the same manner as inserting a CVP line. Once the catheter is in a central vein, as indicated by the pressure waveform, the balloon is inflated. The flow of cently, PAFCs have become available that incorpo- blood through the heart carries the balloon for- rate two fibreoptic channels and measure mixed ward so that it can be advanced through the right venous oxygen saturation continuously. One atrium and ventricle until the tip lies in a main channel transmits near infrared light that is branch of the pulmonary artery (Fig. 5.4). In this reflected by the passing red cells; a second fibreop- position, an indirect assessment of the filling pres- tic channel conducts the reflected light to a pho- sure in the left ventricle can be made. The pressure todetector that determines the oxygen saturation obtained is commonly referred to as the wedge of the haemoglobin. pressure because the balloon is advanced until it ‘wedges’ in the pulmonary artery. The wedge pres- Pulse oximetry sure is usually closely related to the left ventricular end-diastolic pressure (LVEDP). This is a more ac- The pulse oximeter provides a simple, non-inva- curate indication of the preload to the left ventricle sive, continuous assessment of the oxygenation of

than the CVP. The wedge pressure is influenced by the peripheral tissues (SpO2). It therefore gives a many of the factors affecting CVP and trends are simultaneous indication of the degree of oxygena- more useful than absolute values. Complications tion of the blood by the respiratory system and the associated with PAFC insertion are listed in Table ability of the cardiovascular system to deliver it to 5.11. the tissues. By providing continuous monitoring it In addition to invasive pressure data, the can be used to give an early warning of deteriora- catheter can also be used to measure cardiac output tion in a patient’s condition. The principles of and allow mixed venous blood to be sampled. Re- operation are described on page 50.

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Transoesophageal echocardiography adequate renal perfusion pressure (pre-renal fail- ure) due, for example, to hypovolaemia. The kid- Transoesophageal echocardiography (TOE) can neys attempt to maintain blood pressure and provide sophisticated information relating to ven- circulating volume by producing a minimal tricular size and performance, valvular function volume and maximal concentration of urine. and cardiac output. The technique is relatively However, once urine production falls below non-invasive, the sensor being positioned via the approximately 500mL/day, the kidneys are unable oesophagus to lie behind the heart, similar to the to excrete all the waste products of metabolism, technique for inserting a gastroscope. Monitoring with the result that uraemia, metabolic acidosis is continuous, and acute changes in cardiac output and hyperkalaemia develop. can be detected. The use of TOE on the ICU is in- If the reduction in renal perfusion and oxygena- creasing and many intensivists now prefer TOE to tion is severe enough, not only does urine produc- insertion of a PAFC. The main limitation to more tion stop but the kidneys also become ischaemic. widespread adoption of TOE is the expense of the Severe widespread necrosis may then ensue, apparatus. mainly affecting the tubules (acute tubular necrosis, ATN), culminating in oliguria or anuria. Renal function Once ATN has developed, even restoration of a sat- isfactory blood pressure and circulating volume In critically ill patients, acute renal failure is a com- will not lead to immediate restoration of urine pro- mon problem. Although there are many causes of duction. However, if the patient is appropriately renal failure (Table 5.12), in the critically ill it resuscitated, there is a good chance that renal usually results from failure to maintain an function will eventually recover as the patient re- covers, although there is often a delay of 2–3 weeks before urine production restarts. When it does, Table 5.12 Aetiology of acute renal failure it is typically high output, low concentration in Pre-renal nature, when particular attention needs to be paid • Dehydration, e.g. vomiting, diarrhoea to fluid and electrolyte balance. • Haemorrhage Although pre-renal factors are commonly impli- • Cardiogenic shock cated in acute renal failure affecting critically ill • ‘Third space losses’, e.g. trauma, major surgery, patients, some patients may already have pre-exist- bowel obstruction, etc. ing intrinsic chronic renal failure due to other Renal causes. The two may also be present together • Acute tubular necrosis (usually secondary to severe (acute on chronic renal failure). The distinction be- pre-renal failure) tween pre-renal and intrinsic renal failure may be • Sepsis • Severe obstructive jaundice aided by biochemical investigations (Table 5.13). • Blood transfusion reaction All patients on the ICU should have their plasma • Myoglobinaemia urea, creatinine and electrolytes (Na, K, Ca, Mg, • Peritonitis phosphate, etc.) measured at least once daily, and ‘Medical’ causes urine output monitored hourly. Estimation of • Acute pyelonephritis glomerular filtration rate (GFR) from the creatinine • Acute glomerulonephritis clearance (CLCR) is a more precise index of renal • Acute pancreatitis function and is easily derived from a sample of • Nephrotic syndrome urine taken overnight: • Bowel obstruction •Vasculitis rate of urinary output¥ urine [] Cr GFRª= CR . • Burns CL plasma []Cr • Renal vein thrombosis

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Table 5.13 Differentiation of pre-renal from intrinsic renal failure

Index Pre-renal Intrinsic renal

Urine concentration High Dilute Specific gravity ≥1020 Specific gravity 1010 Osmolarity >550 mosmol/L Osmolarity <350 mosmol/L Urine (Na) <20 mmol/L >40 mmol/L Urine/plasma osmolar ratio ≥2:1 1.1:1 Urine/plasma urea ≥20 : 1 <10 : 1 Urine/plasma creatinine ≥40 : 1 <10 : 1

Table 5.14 Causes of hepatic dysfunction Neurological assessment Primary Neurological assessment of patients on the ICU is •Viral hepatitis, A, B, C, cytomegalovirus, Epstein–Barr often difficult because of the use of and virus, etc. neuromuscular blocking drugs. Ideally, muscle re- • Alcoholic liver disease laxants should be avoided unless absolutely neces- •Drug-induced hepatitis: halothane, sodium valproate, sary for the safe management of the patient. A isoniazid, paracetamol overdosage minimal level of sedation should be employed, • Autoimmune hepatitis/cirrhosis titrated for each individual and compatible with a • Acute fatty liver of pregnancy • Inborn error of metabolism, e.g. Wilson’s disease comfortable, settled patient who is nonetheless easily rousable. Formalized scoring systems such as Secondary The Glasgow Coma Scale (GCS) and Ramsay seda- • Sepsis syndrome tion scale (see Table 5.16) can be used, provided • Hypoxia that allowances are made for the effects of drugs • Hypotension • Cardiac failure and the presence of a tracheal tube. Patients who • Cholestasis have undergone major intracranial surgery or sus- • Cholangitis tained a severe head injury may have their in- tracranial pressure (ICP) monitored. A variety of devices are available that are placed, via a small (burr) hole in the skull, into the brain parenchyma, the most sensitive indicator of hepatic reserve and lateral ventricle, subarachnoid or extradural space. prognosis in fulminant liver failure. The aim is to keep the ICP below 20mmHg whilst maintaining cerebral perfusion pressure Miscellaneous (MAP–ICP) above approximately 70mmHg. Routine haematology (haemoglobin concentra- tion, white cell count, platelet count) should be as- Hepatic function sessed daily. Trace elements (e.g. Cu, Zn, Se) may Hepatic dysfunction may be primary, or more com- need monitoring in patients who are resident on monly in the context of critically ill patients, the ICU for more than a week, particularly during secondary to another disease process (Table 5.14). parenteral nutrition. Serum lactate levels are Liver function is monitored by serum bilirubin measured on some ICUs as a more specific indica- (conjugated/unconjugated), albumin, transami- tor of metabolic acidosis associated with tissue nases (AST, ALT, GGT), alkaline phosphatase, hypoxia. prothrombin time (PT) and activated partial thromboplastin time (APTT). The PT is probably

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level (the closing volume). In turn, this reduces the Mechanical ventilation on the extent of collapse of small airways, thus improving intensive care unit ventilation/perfusion matching. One of the commonest interventions on the ICU is Positive pressure ventilation may also relieve a mechanical ventilation of critically ill patients failing left ventricle and alleviate cardiogenic pul- who have developed respiratory failure, or when monary oedema by reducing venous return to the respiratory failure is thought to be imminent in an heart as the intrathoracic pressure rises during in-

exhausted patient. Hypoxaemia (PaO2 £ 8kPa) with spiration. The abnormally high left ventricular

or without accompanying hypercapnia (PaCO2 preload accompanying left ventricular failure is re- ≥ 6.6kPa) is usually present despite high-flow oxy- duced and the overstretched muscle fibres are able gen therapy. The aim of mechanical ventilation is to return to a more optimal size for efficient con- to optimize oxygenation of the patient and to traction. Mechanical ventilation may also reduce allow a period of respite by relieving the patient of left ventricular afterload as it produces a positive the work of breathing. The causes of respiratory pressure gradient between the thoracic and ab- failure are diverse (Table 5.6). A common presenta- dominal aorta during inspiration. Although the tion in patients admitted to the ICU is the acute gradient is relatively small, the reduction in work respiratory distress syndrome (ARDS). Following a required of the left ventricle may be significant. variety of insults, pulmonary capillaries become Critically ill patients requiring ventilation often hyperpermeable, with leakage of fluid and the de- have a reduction in lung compliance and an velopment of non-cardiogenic pulmonary oede- increase in resistance to respiratory gas flow. ma. This results in areas of ventilation/perfusion Consequently, ICU ventilators are principally mismatch, severe hypoxaemia, tachypnoea and, electronically controlled and programmed to en- eventually, physical exhaustion as the patient tries sure that the desired tidal volume is delivered (Fig. to compensate. 5.5). They allow the intensivist a great deal of con- During mechanical ventilation, the physiologi- trol over the pattern of inspiratory gas flow and ad- cal negative pressure phase of spontaneous inspira- justment of the time taken for inspiration and tion is replaced by a positive pressure phase in expiration, usually expressed as the inspiratory to which respiratory gas is driven into the lungs by expiratory (I:E) ratio. Furthermore, a variety of the ventilator. As a result, the distribution of gas modes are available which allow patients’ own flow through the lungs, and the shape of the chest inadequate respiratory efforts to be assisted, such wall and the pattern and extent of diaphragmatic as pressure support ventilation and synchronized movement is altered. This tends to lead to a small intermittent mandatory ventilation (SIMV). increase in ventilation/perfusion mismatching. However, the net result of mechanical ventilation Intubation and tracheostomy in patients with respiratory failure is usually bene-

ficial in improving arterial PaO2 and PaCO2 values. The majority of patients on the ICU are ventilated The reasons for this include: through a cuffed tracheal tube inserted via the

• reliable administration of up to 100% O2; mouth or, much less commonly, via the nasal • reduced oxygen consumption by a sedated, ven- route. The cuff should have a large volume to tilated patient; minimize the pressure exerted on the tracheal • ventilation with larger tidal volumes than can be mucosa. An orotracheal tube is very uncomfort- achieved by the dyspnoeic patient breathing spon- able; patients usually require sedation and analge- taneously; sia to tolerate its presence and it is associated with • application of positive end expiratory pressure difficult oral hygiene, infection and ulceration. (PEEP). These factors become a much more significant The latter two measures increase the functional problem during the period of recovery when residual capacity (FRC) of the lungs above a critical attempts are being made to wean the patient off

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Figure 5.5 ICU ventilator. Soft keys allow control of ventilator settings with display of volumes and pressures generated.

However, most tracheostomies are now performed using a percutaneous technique on the ICU by the intensivists using purpose-designed kits. In the most popular method, a tapered dilator is passed along a guidewire through a small incision, until the track is large enough to accommodate the tra- cheostomy tube (Fig. 5.6). Percutaneous tra- cheostomy is simple and quick to perform (usually less than half an hour), and is associated with a very low incidence of complications. Consequent- ly, it is increasingly performed relatively soon after the patient’s admission to the ICU, particularly when it is anticipated that weaning of the patient Figure 5.6 Percutaneous tracheostomy kit showing needle may be delayed or difficult. for initial puncture, Seldinger wire and tapered dilator. Sedation and analgesia

ventilatory support, as it now becomes necessary Critically ill patients admitted to the ICU require to reduce the level of sedation and analgesia to fa- varying degrees of sedation and analgesia. These cilitate this process. Furthermore, it is well known are not synonymous terms and require different that the prolonged presence of an orotracheal tube drugs and techniques. Many critically ill patients is associated with a higher incidence of long-term are confused and disorientated by their illness and complications, particularly tracheal stenosis. Ac- are likely to become agitated by their environ- cordingly, if the period of tracheal intubation ex- ment. For patients with insight, the realization of tends beyond approximately 7–10 days, it is usual the seriousness of their condition and the contem- to perform a tracheostomy. Until recently, this plation of their own mortality can be frightening, necessitated a formal surgical procedure in the and the psychological trauma engendered may operating theatre, usually by an ENT surgeon. hinder recovery. An appropriate level of sedation

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Table 5.15 Problems associated with deep sedation with Table 5.17 Indication for total parenteral nutrition and paralysis associated complications

• Immunosuppression Indications • Increased incidence of infection • Ileus following major bowel surgery •Prolonged recovery times • Acute pancreatitis • Loss of contact with reality, with an adverse effect on • Inflammatory bowel disease psychological well-being • Short bowel syndromes • Increased incidence of ICU neuropathy (weakness • Malabsorption syndromes and wasting of skeletal muscle) • Multiple organ failure • Postoesophagectomy • Severe catabolic states, e.g. extensive burns, sepsis, trauma Table 5.16 Ramsay sedation scale Complications Level Conscious level • Central line sepsis 1 Restless and agitated • Acute gastric erosion 2 Co-operative, calm, orientated • Hyperglycaemia 3 Asleep, responds to verbal command • Specific mineral or vitamin deficiencies 4 Asleep, responds briskly to glabellar tap • Less satisfactory nutrition of the luminal mucosa of 5 Asleep, responds sluggishly to glabellar tap the gut 6 No response

produces calm, co-operative patients who are thus concentration of local anaesthetic and opioid (see easier to nurse and treat. Similarly, patients admit- page 86). This technique is suitable for pain relief ted to the ICU following major surgery or trauma following surgery or trauma to the thorax, ab- will suffer if good analgesia is not provided. Many domen, pelvis and lower limbs. It is often easier to of the invasive procedures that are undertaken on wean patients off mechanical ventilation more patients are also painful and, as mentioned above, quickly in the presence of epidural analgesia as even the presence of the tracheal tube itself can be they are more able to take deep breaths and cough distressingly uncomfortable. As recently as 10–20 forcefully, uninhibited by pain or the respiratory years ago, it was common practice to deeply sedate depressant effects of systemic opioids. and paralyse all patients so that they were com- pletely unaware of their surroundings. It is now Nutrition realized that such deep sedation is not only unnec- essary, but may also be harmful (Table 5.15). Maintenance of adequate nutrition is an essential The ideal level of sedation is one in which the pa- element of the care of critically ill patients. Where tient is calm, awake and orientated during appro- possible, patients should be fed enterally and there priate periods of the day. The Ramsay sedation is no reason why feeding cannot be commenced scale (Table 5.16) is used on many ICUs, a score of on day one in many patients. If the gut is working, 2–4 being considered satisfactory depending on use it! Enteral feeding is simpler to administer, less the clinical situation, time of day, etc. expensive, more physiological and associated with The most commonly used sedative drugs are mi- fewer complications than total parenteral nutri- dazolam and propofol. Opioids such as morphine, tion (TPN). The presence of food within the gut fentanyl, alfentanil and remifentanil are used also stimulates blood flow and facilitates earlier re- when analgesia is required. Regional anaesthetic covery of normal gastrointestinal function. Indica- techniques are also used, particularly continuous tions for TPN and associated complications are epidural analgesia using a combination of a low listed in Table 5.17.

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Table 5.18 Risk factors for nosocomial infection on the Table 5.19 Prevention of nosocomial infection on the ICU ICU Good basic hygiene standards • Extremes of age • Scrupulous washing of hands immediately before •Pre-existing medical conditions and after contact with patient; wearing of gloves and • Poor nutritional status aprons • Immunosuppressive effect of illness, drugs • Regular disinfection of ventilator tubing or use of • ICU is a breeding site for antibiotic-resistant strains of disposable equipment bacteria • Use of bacterial/viral filters between patient and •Breach of body surface defences: ventilator •Tracheal intubation • Insertion of IV lines, catheters under full • Urinary catheter • Regular toileting of patient, particularly surgical • IV and arterial lines wounds and sites of insertion of IV lines, catheters

• Raised intragastric pH due to H2-antagonists • Routine changing of IV and arterial lines after a defined period (not proven to be effective)

Optimize nutritional status of patient Avoid overuse of ‘prophylactic’ broad-spectrum antibiotics Critically ill patients are at risk of developing acute erosion and ulceration of the gastric mucosa, particularly those who are unable to tolerate enteral feeding when the action of gastric acid is unopposed. The most appropriate method of ulcer Common conditions treated on the prophylaxis is provision of enteral nutrition at the intensive care unit earliest opportunity. Inhibition of gastric acid pro- duction itself (e.g. with ranitidine or omeprazole) Respiratory failure provides prophylaxis against acute gastric ulcera- tion when enteral feeding is not possible. However, The causes of respiratory failure and the principles abolishing the acid environment of the stomach of mechanical ventilation have already been dis- also risks causing bacterial overgrowth that may cussed. The most important therapy is oxygen — a lead to the development of so-called ventilator- life-saving ‘drug’. It must be administered in

associated pneumonia. sufficient concentration to raise the PaO2 to an acceptable level, usually = 10.5kPa (80mmHg). All severely hypoxic patients should be given as close Infection control to 100% oxygen as possible, by facemask initially. Hospital-acquired (nosocomial) infections are Unfortunately, as described earlier, many patients common on the ICU and are associated with are denied high-flow oxygen therapy, due to un- increased morbidity and mortality. They are warranted concern that their respiration is de- increasingly due to multiply antibiotic-resistant or- pendent on a hypoxic drive. Only a minority of ganisms such as methicillin-resistant Staph- patients with severe chronic obstructive airways ylococcus aureus (MRSA). Critically ill patients on disease (classically described as blue bloaters) are the ICU have a number of risk factors for develop- dependent on a hypoxic ventilatory drive and ing infection (Table 5.18). Common infections these patients should have their oxygen therapy involve the lower respiratory tract in ventilated carefully titrated. It is not that unusual to find patients, septicaemia associated with IV and arter- patients without any previous history of chronic ial lines, and surgical wound infections. Prevention obstructive airways disease receiving 28% oxygen of nosocomial infection should be a priority (Table because of such fears, and the authors have even 5.19). The single most important aspect of preven- seen young, fit patients admitted with acute severe tion is the practice of good hygiene standards. asthma being denied 100% oxygen. It is important

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to remember that it is the partial pressure of oxy- Appropriate antibiotics should be given in the

gen in arterial blood (PaO2) that is responsible for presence of a chest infection. It is essential to ob- respiratory drive, not the inspired oxygen concen- tain a specimen of sputum for microbiological tration. If there are serious concerns regarding a se- examination and antibiotic-sensitivity testing, verely hypoxic patient with chronic respiratory ideally from the lower respiratory tract. Bron- disease and a suspected hypoxic ventilatory drive, chodilators may be useful in patients with bron- immediate referral to an expert is advised. chospasm associated with asthma or chronic Although pulmonary oxygen toxicity may occur obstructive airways disease, chest infection, pul- when oxygen is administered in a concentration monary aspiration or ARDS. Bronchodilators are >40% for a prolonged period, it is both illogical and commonly administered as a nebulized mist di- dangerous to withhold higher concentrations in rectly to the respiratory tract (e.g. salbutamol, hypoxic patients with severe respiratory failure. In ipratropium). They may also be given by IV any case, oxygen toxicity is more closely correlated infusion (salbutamol, adrenaline, aminophylline),

with PaO2 than inspired oxygen concentration. although there is a greater risk of arrhythmias. The majority of patients admitted to the ICU re- Effective physiotherapy is an essential part of quire mechanical ventilation. Many of these have respiratory care for all patients on the ICU. Tech- ARDS and require the use of high inflation pres- niques used by physiotherapists in helping to sures to provide an adequate tidal volume. In expectorate secretions from the lungs include ARDS, the lungs become very stiff (decreased com- the positioning of patients to facilitate postural pliance) due to alveolar and interstitial oedema, drainage of secretions and percussion of the chest acute inflammatory infiltrates, atelectasis and pul- to help loosen secretions. Suctioning of the trachea monary fibrosis. Although it is obvious that these and upper airways is important as nearly all criti- patients would die without mechanical ventila- cally ill patients, whether sedated and paralysed or tion, in recent years it has become increasingly ap- not, are incapable of coughing effectively because parent that mechanical ventilation itself may of generalized muscle weakness. further injure the lung in critically ill patients. This Two other techniques practised on many ICUs in lung damage is caused by high inflation pressures severe respiratory failure and ARDS are: (barotrauma), over-distension of more compliant areas of the lung (volutrauma) and trauma due to Pulmonary arterial vasodilator therapy repeated ‘snapping’ open and closed of collapsed (inhaled nitric oxide (NO) gas or alveoli during inspiration and expiration (atelec- nebulized prostacyclin) trauma). There is now good evidence that limiting inflation pressures by accepting lower tidal The rationale for vasodilator therapy is that the volumes (e.g. 6mL/kg rather than 10–12mL/kg) inhaled drug is delivered only to well-ventilated may reduce ICU length of stay and mortality. Ap- alveoli where it is a potent pulmonary arterial va- plication of a high PEEP pressure (approximately sodilator. Pulmonary arterioles associated with

15cmH2O) also helps to minimize the extent of poorly ventilated alveoli remain unaffected. It may alveolar collapse and atelectrauma. This ‘protec- be anticipated that this will lead to an improve- tive ventilatory strategy’ is therefore becoming ment in the ventilation to perfusion ratio and in more widespread in the UK, using a combination practice the initial response of the patient is often of a specialized mode of ventilation called pres- a significant improvement in oxygenation. How- sure-controlled ventilation (PCV), a reversed I:E ever, the results of clinical trials have been disap- ratio and high PEEP. One of the consequences of pointing and there is as yet insufficient data

protective ventilation is an increased PaCO2 and available to demonstrate a beneficial effect on respiratory acidosis — permissive hypercapnia. actual mortality from ARDS. However, this is tolerated by most critically ill patients.

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citated. Intravenous amiodarone is the most effec- Prone ventilation of patients tive drug used to treat atrial fibrillation in critically The potential benefits of this technique are derived ill patients, and acts either by reducing the from the fact that prolonged adoption of the ventricular response rate or by pharmacological supine posture leads to collapse of dependent cardioversion back into sinus rhythm. (posterior) areas of the lung, increasing ventila- • Improving myocardial contractility An inotropic tion–perfusion mismatch. Reversing the posture agent (e.g. dobutamine) may be required to in- facilitates re-expansion of the dependent lung. crease cardiac output to a satisfactory level. Cardiac Prone ventilation has become common practice on output may be monitored using a PAFC, oe- many intensive care units after the publication sophageal Doppler ultrasound probe or arterial of several relatively small studies that showed pulse wave contour analysis. beneficial results. However, a recent much larger In severe sepsis syndrome, MAP is often inade- study failed to demonstrate any effect on mortality quate in spite of a normal or even elevated cardiac and the place of routine prone ventilation of pa- output. In this situation a vasopressor (a drug that tients with ARDS is now questionable. Turning vasoconstricts systemic arterioles) is necessary, for patients prone is potentially hazardous and may example noradrenaline. result in accidental extubation of the patient, the Vasodilators are only occasionally useful on pulling out of CVP and arterial lines, and pressure the ICU to ‘offload’ a failing left ventricle. The damage affecting the eyes and face. However, majority of patients who benefit from these drugs when undertaken by teams of doctors and nurses have usually suffered a myocardial infarction. experienced in the procedure, the risk of complica- They are not usually mechanically ventilated and tions is low. are admitted to the CCU rather than the ICU. The use of inotropes and vasopressors require in- vasive monitoring of the cardiovascular system to Cardiovascular failure direct therapy. The principles of treatment of cardiovascular failure are to optimize: What targets should be aimed for with • conditions for the left ventricle in order to respect to MAP and cardiac output in achieve an appropriate preload, stroke volume, critically ill patients with multiple cardiac output and hence oxygen delivery to the organ failure? tissues; • the state of the so that the Useful clinical variables include the state of the cardiac output is distributed to vital organs at suffi- peripheral circulation (cold and shut down or cient pressure for capillary beds to be well perfused. warm and well perfused), trends in acid–base bal- In clinical practice, these principles are followed ance and urine output (although urine output is of by: little use in the context of acute renal failure). Lac- • Correcting hypovolaemia with fluid challenges tic acid is produced by anaerobic metabolism and Increasing left ventricular preload so that it is trends in serum lactate concentration can provide functioning at the peak of the Frank–Starling useful information on whether or not oxygen de- curve. This first step is the single most impor- livery to the tissues and oxygen consumption by tant prerequisite for optimal cardiovascular the tissues is adequate. performance. It is usually appropriate to aim for a MAP of at • Treating arrhythmias adversely affecting cardiac per- least 70mmHg. However, elderly patients and pa- formance The most common on the ICU is atrial tients with pre-existing hypertension may require fibrillation and this sometimes resolves sponta- a significantly higher arterial pressure. On the neously when the patient is adequately fluid resus- other hand, younger patients may tolerate a lower

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pressure. Defining a satisfactory cardiac output in critical illness is more problematic. It is known that oxygen requirements are elevated during critical illness. Thus, values of cardiac output within the ‘normal range’ may be inadequate. Until relatively recently, it was quite commonplace to attempt to drive the cardiac output to the maximum attain- able using a combination of fluid loading and inotropic support. However, most intensivists now adopt a more conservative approach, following evidence that driving the cardiovascular system towards ‘supranormal goals’ did not improve mortality and could even increase it. Accordingly, when cardiac output is measured, values at the upper end of normal or moderately above it are ac- cepted as satisfactory, taken in the overall context of a stable or improving clinical situation.

Acute renal failure

Critically ill patients who have acute renal failure as a component of their multiple organ failure have significantly different requirements in terms of renal support from patients with isolated acute or chronic renal failure. An inherently unstable cardiovascular system, the need for continued in- fusion of large volumes of fluid to combat the ex- travasation of circulating volume through leaky capillaries and the use of potent inotropic and va- Figure 5.7 CVVH equipment. The vertical, central struc- sopressor drugs mean that these patients are often ture is the filter/dialysis membrane. There are four pumps: bottom right pumps blood in from a central vein into the fil- unable to tolerate the rapid fluid and ionic shifts ter; bottom left pumps fresh dialysate fluid into the filter; associated with intermittent haemodialysis tech- top left pumps out effluent from the filter (consisting of niques, which may precipitate cardiovascular col- dialysate fluid plus ultrafiltrate); and top right pump delivers lapse. Peritoneal dialysis is also of limited value in replacement fluid to the patient to maintain fluid balance. the ICU as it does not have the capacity to main- tain homeostasis in hypermetabolic patients or remove fluid rapidly enough when required. In pressure (continuous arteriovenous haemofiltra- addition, it is often not possible in patients after tion, CAVH). It is now more usual to employ ven- abdominal surgery and those with abdominal ovenous haemofiltration (CVVH) driven by a sepsis. Therefore, continuous haemofiltration mechanical roller pump (Fig. 5.7). In addition, (a process analogous to the filtration that occurs modern equipment permits the use of combina- naturally in the glomeruli of the kidneys) is tion therapy in which both haemofiltration and generally used as the preferred method of renal dialysis occur simultaneously (CVVHD). The max- support on the ICU. An extracorporeal circulation imum creatinine clearance obtained is much less is set up, containing a filter with an artificial semi- than that during haemodialysis. Consequently, permeable membrane. Previously, flow through CVVH must be run continuously in contrast to the the filter was driven by the patient’s own arterial short (several hours) intermittent (2–3 times per

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Table 5.20 The systemic inflammatory response syndrome result of all these derangements is lactic acidosis due to oxygen supply–demand imbalance, the de- Defined as the presence of two or more of the following: velopment of an oxygen debt and an increase in •Temperature >38°C or <36°C anaerobic metabolism. • Heart rate >90 beats/min Like any other inflammatory response, SIRS is a

•Tachypnoea >20 breaths/min or PaCO2 <32 mmHg physiological mechanism for defence of the body • White blood cell count >12 ¥ 109/L, or <4 ¥ 109/L, or after a major insult, facilitating eradication of in- >10% immature forms fection and tissue repair. The problem is that the host response becomes amplified and uncon- week) episodes of standard haemodialysis. How- trolled, contributing to further tissue damage and ever, as alluded to above, this disadvantage is also dysfunction. an advantage in that it promotes haemodynamic The principles of treating sepsis syndrome and stability. SIRS are the provision of support for failing organ systems (optimization of oxygenation of arterial blood, mechanical ventilation, fluid resuscitation, Sepsis syndrome and SIRS inotropic and vasopressor drugs, haemofiltration, These two terms are often used interchangeably. clotting factors, etc.), and targeting any infecting Although there is considerable overlap between organism with appropriate antibiotic therapy. This them, they describe subtly different clinical may require repeated blood cultures and analysis conditions. of specimens of sputum, urine, and wound and • Sepsis syndrome A condition in which the host is catheter sites to identify the organism responsible. overwhelmed by an infecting organism, classically If a collection of pus within the thorax, abdomen, a Gram-negative bacterium, producing endotoxin pelvis or elsewhere is a clinical possibility, it must and/or exotoxins. Endotoxin is a lipopolysaccha- be sought aggressively using ultrasound scanning, ride component of the cell membrane of computerized tomography (CT) scan or laparo- Gram-negative organisms, whereas exotoxins are tomy. Such patients do not recover if surgical bacterial products that may be released into the drainage is not undertaken. circulation. There have been attempts to target the abnormal • SIRS The clinical manifestations of the hyper- inflammatory cascade caused by the circulating in- metabolic state seen after any major insult to the flammatory mediators. Earlier studies examining body, and defined in Table 5.20. The insult may be the efficacy of monoclonal antibodies to one of the infection in which case SIRS and sepsis syndrome principle cytokines, tumour necrosis factor (TNF) describe the same pathophysiology. However, in- were disappointing and failed to demonstrate any fection is not the only trigger for SIRS and other clinical advantage. However, it is possible that ad- causes include major trauma, burns and acute vances in this area may be made as further research pancreatitis. elucidates more detailed information concerning The clinical features of sepsis syndrome and SIRS the pathophysiology of sepsis syndrome and SIRS. are similar, with hypermetabolism, circulatory More recently, evidence has emerged of the effi- shock due to systemic vasodilatation and extrava- cacy of activated protein C (APC), a natural circu- sation of fluid (via leaky capillaries). In the lungs, lating anticoagulant. APC levels are decreased in these manifestations present as ARDS. Elsewhere, severe sepsis due to both excessive consumption oxygen delivery to cells is compromised by shunt- and reduced activation, and the size of the decrease ing of blood away from capillary beds through ar- correlates with mortality. Consequently, micro- teriovenous channels that open in response to the thrombi develop throughout the circulation in inflammatory response. Oxygen consumption by sepsis syndrome and this is one of the main causes cells may also be reduced as a consequence of in- of end-organ dysfunction. The process is inhibited tracellular dysfunction of the mitochondria. The by APC. In a recent large double-blind, placebo-

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controlled study, administration of APC to patients of chronic obstructive pulmonary disease: with multiple organ failure associated with sepsis Cochrane systematic review and meta-analysis. syndrome resulted in a decrease in mortality from British Medical Journal 2003; 326: 185. 30.8 to 24.7%. APC is currently being evaluated in McQuillan P, Pilkington S, Allan A et al. the UK. Tight control of blood sugar during critical Confidential inquiry into quality of care before illness also improves survival. When intensive in- admission to intensive care. British Medical sulin therapy is used to maintain blood sugar be- Journal 1998; 316: 1853–8. tween 4.4 and 6.1mmol/L, ICU mortality is Meduri GU, Headley AS, Golden E et al. Effect of reduced (4.6 versus 8%) when compared with stan- prolonged methylprednisolone therapy in dard therapy. unresolving acute respiratory distress syndrome. Journal of the American Medical Association 1998; 280: 159–65. Further reading NHS Estates. Facilities for critical care. Health The Acute Respiratory Distress Syndrome Building Note 57. London: The Stationary Network. Ventilation with lower tidal volumes Office, 2003. as compared with traditional tidal volumes for Nolan J, Baskett P, Gabbott D et al. Advanced life acute lung injury and the acute respiratory support provider course manual, 4th edn. London: distress syndrome. New England Journal of Resuscitation Council (UK), 2000. Medicine 2000; 342: 1301–8. Oh TE. Intensive care manual, 5th edn. London: Bernard GR, Vincent JL, Laterre PF et al., and the Butterworths, 2003. Recombinant human protein C Worldwide Rivers E, Nguyen B, Havstad S et al. Early Evaluation in Severe Sepsis (PROWESS) study Goal-Directed Therapy Collaborative Group. group. Efficacy and safety of recombinant Early goal-directed therapy in the treatment of human activated protein C for severe sepsis. severe sepsis and septic shock. New England New England Journal of Medicine 2001; 344: Journal of Medicine 2001; 345: 1368–77. 699–709. Smith GB, Osgood VM, Crane S. ALERT: a Boldt J. Clinical Review: hemodynamic multiprofessional training course in the care of monitoring in the intensive care unit. Critical the acutely ill adult patient. Resuscitation 2002; Care 2002; 6: 52–9. 52: 281–6. Galley HF. Critical care focus 1: renal failure, 1st Van den Berghe G, Wouters P, Weekers F et al. edn. London: BMJ Books, 1999. Intensive insulin therapy in the critically ill Galley HF. Critical care focus 2: respiratory failure, patients. New England Journal of Medicine 2001; 1st edn. London: BMJ Books, 1999. 345: 1359–67. Galley HF. Critical care focus 5: antibiotic resistance and infection control, 1st edn. London: BMJ Useful websites Books, 2001. Gattinoni L, Tognoni G, Pesenti A et al. Effect of http://www.doh.gov.uk/compcritcare/index.htm prone positioning on the survival of patients [Department of health (UK). Comprehensive with acute respiratory failure. New England Critical Care. Review of adult critical care Journal of Medicine 2001; 345: 568–73. services. June 2000.] Hodgetts TJ, Kenward G, Vlackonikolis I et al. http://www.ics.ac.uk/ Incidence, location and reasons for avoidable [The Intensive Care Society (ICS). The in-hospital cardiac arrest in a district general publication section contains current UK hospital. Resuscitation 2002; 54: 115–23. national guidance on all aspects of critical care.] Lightowler JV, Wedzicha JA, Elliott MW. Non- http://www.sccm.org/professional_resources/ invasive positive pressure ventilation to treat guidelines/table_of_contents/index.asp respiratory failure resulting from exacerbations [This site contains current publications from

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the Society of Critical Care medicine (SCCM) http://www.pacep.org/ and reflects North American practice.] [Pulmonary artery catheter resource with http://www.ccmtutorials.com/ haemodynamic monitoring tutorials. Free to [Excellent, up-to-date interactive critical care use once registered.] tutorials.] http://www.sfar.org/s/article.php3?id_article=60 http://www.americanheart.org/ [This site has information on all the various presenter.jhtml?identifier=9181 scoring systems used in critically ill patients, [The American Heart Association scientific- including on-line calculators.] statements section has numerous up-to-date http://www.dicm.co.uk/papers.htm guidelines.] [This is a personal website aimed at those taking http://www.modern.nhs.uk/criticalcare/5021/ the Diploma in Exam. 7117/78001-DoH-CareOutreach.pdf It claims to list the top 100 critical care [NHS Modernisation Agency. Critical Care references and succeeds in most areas.] Outreach 2003. This report contains guidance http://www.ardsnet.org/ on current best practice in this area.] [The ARDS clinical network site. This contains http://www.brit-thoracic.org.uk/pdf/NIV.pdf updates on ARDS studies performed by the [Guidelines on non-invasive ventilation in network.] acute respiratory failure. British Thoracic Society Standards of Care Committee. Thorax 2002; 57: 192–211.]

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Chapter 6 Anaesthetists and chronic pain

Anaesthesia is concerned with reducing sensation • Distraction A kick on the shin during a game of during surgery; it does not in itself cure patients football is likely to provoke very different pain be- but enables important treatment to take place haviour when possession is maintained with a without the experience of pain. This is achieved by clear shot at goal compared to losing the tackle and the careful application of clinical physiology, phar- with it the chance of victory! macology and therapeutics. With this expertise in • Meaning of pain In the previous example, the pain and symptom control, some anaesthetists football injury and the sensations that go with it have specialized in the management of pain as a will have a positive meaning. A display of pain be- problem in its own right, leading to the establish- haviour may bring about a reward, particularly for ment of modern pain relief clinics where they work being brought down in the penalty area. Similar with a team of nurses, physiotherapists and sensations in a cancer patient with a bone metasta- psychologists. sis in the tibia may provoke anxiety, and fear of pain as yet another problem to be endured — cer- tainly a negative meaning. The definition of pain • Significance of pain The symptoms of headache, The International Association for the Study of Pain photophobia and vomiting in a medical student defines pain as: would normally result in presentation at the local ‘An unpleasant sensory and emotional experience casualty department with a self-made diagnosis of associated with actual or potential tissue damage meningitis. Exactly the same symptoms would be or described in terms of such damage’. ignored in the knowledge that he (or she) had Many interactions within the central nervous drunk 10 pints of lager the night before! Thus pain system, previous experiences and present emo- behaviour is conditioned by knowledge and tional state will all determine the reactions to tis- understanding. sue injury. • Memory and culture of pain Pain may leave a The following are examples of this: memory that will discourage repeating an action. • Effect of changed environment A hospital admis- Alternatively a response may be learned from ob- sion where painful treatment is expected may re- serving the behaviour and attitudes of others. This sult in an apparently minor stimulation, such as can have both beneficial and detrimental effects. venepuncture, which may otherwise be tolerated, Cultural differences are important when treating initiating an overwhelming state of distress. patients of different nationality and race. Age is

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important: children may not have the means to may not resolve with healing of the tissues; in understand pain, or otherwise they express both other words the protective mechanisms have not pain and distress by crying. The elderly may be too extinguished themselves. This may lead to confu- ashamed to admit to needing help with pain. sion for both doctors and patients, with repeated attempts at surgical intervention which only ex- acerbate the problem (e.g. postsurgical back pain Acute versus chronic pain does not usually respond to further operations). Chronic benign pain can also occur without injury if hyperaesthesia and allodynia occur for reasons Acute pain other than injury; a similar pain state will result as When injury has taken place, pain normally limits when injury is responsible. activity and promotes healing. The pain from a • Cancer pain (pain associated with a malignant blister on the heel when wearing new shoes is a tumour) This is usually included as a chronic pain warning in an attempt to prevent more severe but it is best thought of as a combination of damage to the skin. A healing wound is guarded, several acute pains from destructive effects of the preventing stress on newly formed connective tis- tumour. Once established, even with treatment, sues and the risk of wound breakdown. The region pain is usually a feature of remaining life. of the body surrounding the injury, even the whole We live in a society with high expectations of med- limb, may also undergo change, becoming sensi- ical intervention for injury and illness. Severe pain tive to even minor stimulation. The changes normally elicits sympathy and naturally we strive comprise: to relieve it whenever possible. Once severe pain is • hyperaesthesia: increased appreciation of any established, however, the resistance to further pain stimulus; is reduced — the physiological pain threshold is • hyperalgesia: more intense appreciation of a lowered and normally innocuous stimuli may not painful stimulus; be tolerated. Symptoms from mild degenerative • allodynia: sensation of pain in response to a nor- conditions may be amplified. Prolonged illness or mally non-painful stimulus. distress results in emotional changes, particularly They are mediated partly by locally released sub- depression of mood. The questioning of the sever- stances in the tissues (inflammation), but also by ity of pain exacerbates depression in patients with changes in the spinal cord processing of neuronal chronic pain. information. Hyperaesthesia, hyperalgesia and al- To summarize: lodynia usually resolve as injuries heal. These pro- • Acute pain: the normal body responds to nox- tective and incapacitating functions are an acute ious stimuli with the experience of pain. response to trauma, surgery or acute illness. • Chronic pain: the sensitized nervous system re- sponds more readily to both noxious and innocu- ous stimuli. Chronic pain The remainder of this chapter considers the under- This suggests persistence of the pain for a long standing, mechanisms and management of the time. There are several useful subdivisions: pain problems seen in pain relief clinics. • Pain from continuing tissue damage Rheumatoid arthritis pain is an example. Pain usually restricts Mechanisms of pain generation movement and is useful in preventing further damage to the joint. In contrast, neuropathic The following account separates pain mechanisms joints that have lost sensation, for example in dia- into distinct entities, but it must be remembered betes, degenerate rapidly. that in reality most pain results from activation of • Chronic benign pain (pain despite tissue healing) several mechanisms, such that the final experience The hyperaesthesia and allodynia of acute injury is complex.

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•5-hydroxytriptamine (5-HT); • hydrogen and potassium ions. • Prostaglandins These sensitize nerve endings to Experience and expression of pain react more intensely to further stimulation; for ex- ample a fingernail when hit with a hammer, al- though perhaps not showing signs of damage, is very sensitive to further touch and movement. • Other stimuli Impulses from pain and tempera- Higher pains ture receptors are carried in similar small nerve BRAIN fibres and the threshold for stimulation may be re- duced at low temperatures. For example, arthritis patients commonly complain of increased pain Central pain during cold weather. It is not necessary for there to -brain injury be tissue damage to elicit pain from the periphery; -thalamic pain pathways may be stimulated by unusual stimuli: eating ice-cream too quickly often provokes an in- Denervation SPINAL tense headache but is not usually perceived as a CORD threat to bodily integrity! • Peripheral nerve damage Damage to the nerves Peripheral supplying an area of the body may result in pain. nerve injury Peripheral nerves are not normally sensitive to mechanical stimuli, but attempts at regeneration Prostaglandins within a damaged nerve may result in a neuroma Tissue injury that can be exquisitely tender. The pain will Simple stimuli be referred to the area served by the nerve, al- TISSUES though obviously there is no damage to the painful Other stimuli (temperature) area. • Denervation Pain may occur even when sensory receptors are absent, for example after amputation. Figure 6.1 Mechanisms of pain generation. Sensation can be attributed to an area of the body that does not exist because the brain still has a rep- resentation of the absent part (e.g. the painful ‘phantom limb’). Pain may be generated in a number of ways • Central pain Damage of the thalamic pathways (Fig. 6.1): which carry nociceptive information can lead to • Simple stimulation Normal activity causing the experience of pain. As with many chronic stimulation of tissues can lead to pain; for example pains, the problem is within the central nervous the sensation of pressure when maintaining an system and it rarely responds to conventional uncomfortable posture is relieved on shifting analgesia. position. It is often subconscious and protects us • Higher pains We have probably all suffered grief, from damage when attention may be focused perhaps the death of a loved relative or failure in elsewhere. an important examination. We describe this as • Tissue injury This results in structural elements painful and although the pain cannot be localized being damaged and an inflammatory response to a particular body part, it is nevertheless very real. occurs. Many chemicals are released, including: This pain exists with no physical input to the body. • histamine; The pain of a broken heart is no less real than the • bradykinin; pain of a broken leg.

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• Both of these nerve types synapse onto central We all have the facility to experience excruciating pain from any part of the body and are prevented from this transmission neurones in the dorsal horn of the only by the normal functioning of our nervous system. spinal cord (the substantia gelatinosa). Both noxious stimulation and disorders of transmission •Transmission is modified by inhibitory interneu- or perception have identical results — the experience of rones which are switched on by large-fibre input pain. and off by small-fibre input. This explains the effect of stimulation-induced analgesia: large-fibre input activating the inhibi- tory neurones reduces the input from smaller The variability of pain fibres. We are all familiar with this effect: when we It can be seen that pain experience and expression suffer a minor injury, our instinct is to ‘rub it bet- can be triggered and conditioned by many factors ter’. This action stimulates large fibres with touch other than peripheral noxious stimulation. The and vibration and thereby reduces the transmis- body is subjected to millions of stimuli each day; sion of nociceptive information from the small most are of no significance or threat and need to be fibres activated in the injury. filtered from entering consciousness or producing The Gate Control Theory is only one example of a response. The fact that responses to stimulation how the nervous system can modify in response to can vary in intensity according to factors both electrical and chemical activity in nerves. The within and outside the body led Melzack and Wall brain also contributes by exerting ‘central control’ to propose the Gate Control Theory of Pain (Fig. via the descending pathways of the spinal cord, 6.2). It notes that: thereby helping to explain how mood and behav- • Sensory information from the periphery is car- iour affect processing within the spinal cord. The ried to the spinal cord in large-diameter (pressure, whole state is referred to as one of neuroplasticity touch and vibration) or small-diameter (pain and that occurs in a changing matrix of electrical and temperature) nerve fibres. activity, rather than a simple • An injury usually produces a brief, sharp ‘first fixed electrical circuit. pain’ via the large fibres that is well localized to the injury and produces withdrawal. A dull, aching Clinical assessment of chronic pain ‘second pain’ transmitted by the smaller fibres fol- lows after a fraction of a second and this is more The correct management of the patient with prolonged. chronic pain is based upon the basic principles of

CENTRAL CONTROL

Large fibres

- + + ACTION IN INPUT SG T SYSTEM (brain) - - + Small fibres Synapses + excitatory - inhibitory IN, inhibitory interneurones; SG, substantia gelatinosa; T, transmission cell Figure 6.2 The gate theory of pain.

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taking a full history and performing a physical used to help patients choose a suitable description examination prior to ordering investigations and (e.g. the McGill pain questionnaire). Trigeminal initiating treatment. Chronic pain is a specific neuralgia may be described as shooting, fibromyal- condition that must be recognized and treated, gia as exhausting, burning and nauseating. rather than a diagnosis of exclusion because • The pain history Past treatment and investiga- nothing else will account for the pain. Patients’ tions are often long and complex, and involve dif- symptoms may previously have been dismissed — ferent hospitals and specialists. A complete history listening and understanding are as important as will include: any prescription. • the time-course of the pain; •accentuating or relieving factors; • the pattern of activity and relation to pain; History • the effect on sleep; • Site This may be obvious and related to a • previous and current treatment, including: previous injury. Diffuse or non-dermatomal pat- • medications; terns of pain distribution are related to central • type and effects of physiotherapy; sensitization and do not imply that the symptoms • aids and appliances; are not genuine. Pain may be felt in structures • alternative therapies tried; with common innervation (e.g. heart with left • the effect on employment; arm, leg with low back). Pain diagrams are helpful •financial support: (Fig. 6.3). • invalidity benefits; • Character Some conditions are associated with • pensions; pain of a particular nature. Lists of words have been • Disability Living Allowance, etc.;

Left Right Left

Figure 6.3 Pain drawings showing the typical pain distribution resulting from an S1 nerve root compression (post view) compared with the pain S1 nerve root entrapment Fibromyalgia experience of a patient with fibro- (posterior view) (anterior view) myalgia (anterior view).

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• social and family losses because of pain; • skin: signs of sympathetic dysfunction: • concerns about the future; • temperature change; • uncertainties about diagnosis and treatment; • loss of hair growth; • past medical history, including episodes of •vascular changes and discoloration; vague or unexplained illnesses; • disorders of sensation. • family history, which may reveal clues as to In addition, loss of confidence in movements, coping mechanisms and attitude to chronic ill- guarding and abnormal posture are noted as possi- ness within the family. ble contributions to maintaining chronic pain. Some patients have no physical signs despite se- vere symptoms — again this does not imply that the Psychological assessment pain is not genuine. An assessment of mood is important and fre- quently reveals evidence of depression. This may Measurement of pain be related to the pain itself, but is also associated with frustration or anger at many previous at- It is impossible to measure an experience directly tempts at treatment or the failure of treatment, so we rely on written or verbal self-report, as well as lack of a clear diagnosis or disease, and loss of social facial expression, body language and behaviour to and financial status. These are all common with assess pain. Surrogate measures such as the number chronic pain. The assistance of a psychologist is in- of breakthrough analgesia tablets taken may be valuable to explore emotional issues associated useful as a measure of pain or of the effectiveness of with, or caused by, the pain. Wherever possible, treatment. Psychological measures of coping, dis- patients should be seen with a partner in order to tress and depression are all valuable tools in assess independently the degree of physical and exploring the pain; however, they should be emotional disturbance at home and with the interpreted carefully in conjunction with a clinical family. Depression is a normal human response to psychologist. an uncertain future full of pain. Investigations Physical examination Patients with chronic pain have usually had many It is unusual for patients to present with ‘put on’ investigations and may be frustrated that nothing symptoms of pain. Malingering is very rare. Often has been found. They may not understand that symptoms and the reaction to examination are ex- pain cannot be seen on their scans and X-rays. Care aggerated, but this is not surprising considering must be taken to explain that the absence of posi- that most patients with years of suffering are likely tive findings does not mean that the pain is in any to be distressed and anxious. Exaggeration may be way ‘imaginary’, ‘all in the mind’ or ‘psychologi- to convince rather than to deceive. Most patients cal’. One danger of sensitive tests, such as MRI, is experience worse pain after even limited clinical that abnormalities that are coincidental to the pain examination. may be revealed — careful feedback of information Pain may be associated with the following is always required. Figure 6.4 demonstrates that structures: disease does not always cause pain. • bones: deformity, tenderness; Some well-meaning explanations may increase • joints: swelling, tenderness, limitation of anxiety. Using terms such as ‘crumbling spine’ or movement; ‘degenerative changes’ in chronic low back pain • nerves: function, swelling or tenderness over the may invoke fear for the future and a life of increas- course of a peripheral nerve; ing disability, whereas in fact both back pain and • muscles: power and tone, localized or general- the preferable term ‘age-related change’ are com- ized tenderness; mon and are not well correlated.

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Figure 6.4 X-rays of lumbar spine. The patient on the left had been confined to bed for 2 years with back pain; the pa- tient on the right had never had a day’s back pain in her life.

cident pain, and the amount of this that is taken Treatment of chronic pain can be used as a guide for increasing the long- There are very few effective ‘cures’ for chronic pain acting preparation. problems. Intervention is only appropriate if there Respiratory depression (often a feared compli- is a realistic chance of success — an honest opinion cation) is not seen, even with very high doses, is appreciated. For some conditions associated with provided that doses are increased in a stepwise ongoing tissue damage, such as rheumatoid arthri- fashion — for example by 30% increments accord- tis, it is possible to suppress the inflammation and ing to effect. Sedation may be a problem for some the associated pain. This may not be completely patients but with careful titration it can be mini- successful, so the treatment of pain may have to mized. Increased doses of opioids can produce proceed alongside treatment of the condition. sedation and calming effects at the end of life that may be very useful. Alternative potent opioids are: • diamorphine (heroin): used for subcutaneous infu- Pharmacological treatments sions as it is more soluble than morphine and can be dissolved in a smaller volume for administra- tion using a compact pump. Opioids • fentanyl: absorbed from a patch applied to the Morphine is commonly used in the management skin and changed every 3 days. Useful because it of acute pain and has a major role in control of avoids the oral route and popular with patients chronic pain. In the latter, it is frequently taken because it avoids needles. May have reduced orally; the dose might start at 10mg every 4h, but side-effects compared with morphine. eventually range up to 2000mg per 24h in some • methadone: inexpensive and has a long plasma patients. Large daily doses are conveniently given half-life; may be given as a once daily dose orally. as a long-acting sustained-release preparation once • oxycodone and : alternative opioids or twice a day depending on the formulation. Ad- to morphine, usually given orally, with fewer side- ditional breakthrough doses of morphine solution effects in some patients. or immediate release tablets, usually 10% of the Less potent opioids such as dextropropoxyphene total daily dose, are made available for extra or in- (combined with paracetamol in coproxamol),

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tramadol, codeine or dihydrocodeine are com- postherpetic neuralgia (PHN) are all examples monly prescribed for chronic pain. They have the of pain syndromes that may respond to same effects and side-effects as morphine but the anticonvulsants. maximum analgesic effect is limited. There is no doubt that the proper (generous) use Steroids of opioids in cancer pain has revolutionized re- maining life for cancer patients. Debate continues, These are often injected into joints or tendon however, about the use of opioids in chronic be- sheaths for arthritis or inflammatory pain, but are nign pain (such as low back pain). Modest doses of not generally indicated for chronic benign pain be- opioids continued on a regular prescription with cause of the risk of osteoporosis and gastric ulcera- careful monitoring of dose and effect appear to be tion. Injections of steroid into the epidural space safe and very helpful for some patients, especially may be tried when nerve roots are thought to be if other physical and psychological treatments are compressed or inflamed: the benefit may be due to made available. a reduction in nerve root oedema. There may be a useful reduction in swelling and compression from Non-steroidal anti-inflammatory drugs solid tumours associated with improved appetite and well-being in cancer patients. NSAIDs are often used alone or in combination with opioids, particularly where there is inflamma- tory or bone pain. Their mechanism of action and Capsaicin side-effects are discussed on page 40. A wide range Applied topically as a cream, this extract of the of both non-specific and COX-2 inhibitors are chilli pepper can depress C-fibre nerve function. It available; the latter are preferable for long-term use has been found useful in cutaneous pain problems in vulnerable groups, for example the elderly and such as scar pain and postherpetic neuralgia. It pro- those on steroids. duces a burning sensation, so may be used with a topical local anaesthetic. Tricyclic antidepressants

The mechanism of action is thought to be due to Non-pharmacological interventions the potentiation of and noradrenaline in (Fig. 6.5) the CNS. Amitriptyline is the most commonly used drug, and has been used extensively to treat neuro- Nerve blocks pathic pain. The sedative effect may be useful for sleep disturbance where this is a problem. The an- These may be performed on any nerves thought to tidepressant effect may be an additional benefit. be part of the pain pathway and may help in the Newer antidepressants with fewer anticholinergic understanding of the contribution of peripheral side-effects are not as useful for chronic pain. input to the overall pain. Sometimes simple nerve blocks with local anaesthetic give prolonged relief, perhaps by reducing central sensitization. At- Anticonvulsants tempts to make blocks permanent with neurolytic Carbamazepine, phenytoin and, more recently, agents (alcohol or phenol) often result in worse gabapentin have been shown to be useful for pain pain, as central neurones lose peripheral inhibi- associated with nerve damage and are now also tory input and become spontaneously active or often tried for other pain syndromes where there respond to previously non-painful stimuli from may be sensitization of the central nervous system. other pathways (allodynia). Indwelling epidural or Trigeminal neuralgia, denervation of the upper intrathecal catheters delivering local anaesthetic limb following avulsion of the brachial plexus and or opioid can provide sustained analgesia, for

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Brain Thalamic stimulation

Cordotomy Spinal cord Sympathectomy Sympathetic nerve Spinal cord and ganglion stimulation Dorsal root (epidural ganglion electrodes)

Alcohol or phenol rhizolysis Thermocoagulation of Peripheral dorsal root ganglion nerve Guanethidine block

Transcutaneous electrical Tissue nerve stimulation (TENS)

Manipulation Vibration Counter irritation Figure 6.5 Non-pharmacological Acupuncture methods of providing analgesia.

example in severe and otherwise uncontrollable Stimulation cancer pain. Damaged peripheral nerves are very sensitive to Stimulation of the nervous system appears to be an noradrenaline, so reducing sympathetic activity effective method of decreasing some pains. Mas- may be helpful. Guanethidine intravenous region- sage may be temporarily helpful, but electrical al block or cervical or lumbar sympathetic chain stimulation using electrodes on the skin (transcu- blocks with local anaesthetic may help. The latter taneous electrical nerve stimulation (TENS)), or in can be performed with phenol and is a useful treat- the epidural space (spinal cord stimulation) may ment for the pain and ischaemia of peripheral vas- enable continued benefit. Acupuncture involves cular disease. identifying and needling specific points on the The spinothalamic tracts carry nociceptive body surface according to patterns determined by information from the contralateral side of the traditional Chinese medical practice. The stimula- body, and may be interrupted at the level of the tion is thought to reinforce intrinsic or natural cervical spine by a cordotomy (cutting the cord) analgesia. performed surgically at open operation or percuta- neously with a radio-frequency heated lesion- Manipulation generating needle. Fortunately this is rarely neces- sary because the other techniques are usually The aim is to restore movement and function. effective. Osteopathy and chiropractic techniques are com-

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monly sought by patients for chronic muscu- relaxation, with the object of helping the patient loskeletal pain, usually following unsuccessful to return to useful function with less impact from conventional treatment. The Alexander Technique the persistent pain. or yoga offer self help for motivated patients. Specific chronic pain problems Physiotherapy

Physical structure and function, which often be- Neuropathic pain (postoperative pain) come abnormal as a result of chronic pain, can be Although usually acute and self-limiting, postoper- assessed by physiotherapists. Confidence needs to ative pain may progress to chronic pain. Peripheral be rebuilt and patients encouraged to exercise de- nerve damage is one cause; for example post- spite pain in order to restore activities. thoracotomy intercostal nerve damage or ilio-in- guinal nerve damage from repair. A strong painful body is better than a weak painful body. Both are surprisingly frequent, persistent and trou- blesome, requiring a wide range of treatments. Psychology

It is unusual for patients to present with chronic Postherpetic neuralgia (PHN) pain without distress or depression. This is often as a result of the frustration of limited activity and PHN is a common consequence of infection with many failed attempts at treatment. Psychologists the herpes zoster virus, with damage to the sensory are essential in helping to overcome these prob- nerve cells in the dorsal root ganglion. The painful lems. Common obstacles to coping with chronic crusted lesions on the skin (on the dermatome cor- benign pain are: responding to the infected nerve) heal after several • fear of not being believed: patients often have weeks but the site often has persistent abnormal nothing to show for their pain; sensation, with light touch producing pain (allo- • fear of deterioration and dependency; dynia). Antiviral agents, applied topically or sys- • failure to accept that the pain is permanent; temically during the initial infection, may limit • anger directed at the cause of the pain, for exam- nerve damage and subsequent neuralgia, and early ple a road traffic accident causing whiplash injury sympathetic blocks may be of benefit, for example to the cervical spine; stellate ganglion or lumbar sympathetic blocks. •guilt at not being able to fulfil perceived role: let- ting others down because of the pain; Phantom limb pain • side-effects of unhelpful medical treatments, for example sedative effects of benzodiazepines. Normal sensory input from the periphery is neces- Careful assessment and treatment using cogni- sary for the proper regulation of nerves in the tive–behavioural methods need to be more widely CNS — loss after amputation may still result in ac- available. tivity of the central nerves that originally repre- sented the amputated part. Phantom sensation is very common and may include pain. It is one of Pain management programmes the most challenging conditions to treat and there Many patients with chronic benign pain can be are many potential treatments available. helped by a team of medical, physiotherapy and psychology therapists working together to address Neuroma many of the above physical and psychological is- sues. The aim is to develop understanding and pro- Regeneration of damaged peripheral nerves may vide useful coping strategies such as pacing and result in tender neuromata that are very painful

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spontaneously or with pressure. They are a particu- spinal degenerative changes are common, but lar problem if compressed by a prosthesis and may these changes do not correlate well with back pain then have to be surgically resected or repositioned. symptoms. Unfortunately, treatment is not avail- able for most degenerative changes — there is little evidence that replacing worn discs or fusing spinal Complex regional pain syndrome segments has long-term beneficial effects. Most (previously known as reflex important is early exclusion of specific causes of sympathetic dystrophy) back pain. These are: Sometimes the neuronal processes of acute pain • prolapsed intervertebral disc with spinal cord or (see page 140) do not extinguish themselves after nerve root compression; an injury and when tissues have apparently • tumour of bone, meninges or nerves; healed. This results in continued sensitivity and • infection of the spine. pain. The condition may progress, with signs of New episodes of back pain should be properly severe tissue inflammation and later atrophy. The investigated and the patient reassured if appropri- pathophysiology is not fully understood but it ate. Early mobilization and activity are important can be a severe and very disabling problem. Early to prevent dysfunction and guarding of move- mobilization appears to be important in prevent- ments of the back. Even 2 days of bed rest may be ing progression and analgesia is provided to harmful. Most patients are given advice to rest encourage this. Specific treatment may involve until the pain subsides, and investigation is under- sympathectomy. taken only after a long delay. This leads to unnec- essary suffering and dissatisfaction with the medical profession. Treatment involves acknowl- Trigeminal neuralgia edging the pain, education, gradual return to activ- Many cases are thought to be caused by vascular ity under strict supervision and the introduction of compression of the trigeminal nerve as it emerges coping skills for pain. from the pons in the posterior fossa — in fit pa- tients, surgical decompression may be considered. Fibromyalgia In others, anticonvulsant medication or injection of the trigeminal ganglion with phenol or glycerol A generalized disorder of pain sensation probably is usually effective. related to abnormal central neuronal activity. It in- volves widespread tenderness accompanied by sleep disturbance, fatigue and, not surprisingly, de- Arthritis pression. Most common in women in their middle In this debilitating condition, pain is a frequent years and associated with other pain problems symptom of joint inflammation and destruction. such as migraine and irritable bowel syndrome. Pa- Most patients are managed by general practitioners tients benefit most from explanation and reassur- or by rheumatologists. Patients with severe arthri- ance. Amitriptyline may help restore more normal tis have visible deformity and disability, which sleep. leads to their suffering and pain being understood by others and it is often well tolerated. NSAIDs and Cancer pain opioids are usually effective when used in addition to specific therapy for the disease. Cancers involving destruction of tissue are painful. Two-thirds of patients with cancer as a terminal ill- ness have significant pain. Modern chemotherapy, Back pain radiotherapy and surgery can reduce the growth of More than half the population will suffer back pain tumour, but pain may persist even despite techni- at some time in their lives. With advancing age, cally successful therapy. Pain may be feared more

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than death itself. Symptoms can become over- aimed at coping with pain, which in turn depends whelming — a mixture of pain, fear, depression, on: panic and denial — the so-called ‘total pain • understanding that chronic pain is harmless (but syndrome’. painful); Unfortunately morphine is not easily available •stopping looking for a cure; for clinical use in many developing countries. Even • accepting some limitations; in Western countries, use is inadequate due to fear • knowing that nothing is being hidden; of side-effects. Large doses of morphine may be re- •a willingness to change (that effort is required). quired (compared to those used to treat acute pain), but when correctly used it is safe and effec- tive for most cancer pain. Preventing chronic pain It is always possible to do something for cancer It may be possible to prevent chronic benign pain pain, and it may be reassuring for patients to know by more aggressive treatment of acute pain. Identi- that there are alternative treatments should their fication of risk factors, early education and discus- symptoms progress. sion may help to prevent the loss of function and frustration that often lead to chronic pain. The chronic pain syndrome

The precise cause and mechanism of many pain Useful websites syndromes remains unknown. Many chronic pain- clinic patients have the following characteristics: http://www.jr2.ox.ac.uk/bandolier/booth/ •a long history; painpag/ • many consultations; [The Oxford Pain website. An excellent site for • multiple negative investigations; the latest evidence-based reviews in pain.] •a high incidence of functional disturbance, for http://www.theacpa.org/resources/ example headache, irritable bowel syndrome; ACPAdrugsupplement2003.pdf • few standard physical findings; [The American Chronic Pain Association guide • distress; on drugs used in chronic pain. Although • depression. primarily aimed at patients, it is full of useful Medicolegal proceedings are common but only information and links to other sites.] rarely result in deliberate exaggeration of symp- http://www.nysora.com/ toms. The medical examination of these patients [This is the best website for information about requires experience and understanding of the con- regional anaesthesia techniques.] text in which the pain is being experienced. Even http://www.painsociety.org/ experienced clinicians have been known to accuse [The UK Pain Society website gives guidance on these patients of malingering. UK practice.] Patients may have coped well with the pain for a http://www.iasp-pain.org/index.html long period of time — it is usually a series of events [The International Association for Study of Pain as a consequence of the pain that precipitates re- (IASP), giving guidance on international ferral. Measures aimed at dealing with the pain practice.] may be useless if, for example, the patient has be- http://www.ninds.nih.gov/health_and_medical/ come depressed, is dependent on medication, has disorders/chronic_pain.htm lost his or her employment and self-respect, and [The National Institute of Neurological has been accused of malingering. Treatment is Disorders and Stroke chronic pain homepage.]

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Index

Page numbers in italics refer to figures and those in bold to tables; note that figures and tables are only indicated when they are separated from their text references.

ABC of resuscitation airway obstruction 94–5 anaesthetic assessment see adult basic life support 99–102 anaesthetized patient 95 preoperative assessment critically ill patients 117–22 basic life support 99–100, 108 anaesthetic breathing systems see paediatric basic life support causes 117 breathing systems, 108–10 conscious patient 94 anaesthetic perioperative emergencies 90 critical illness 117–18 anaesthetic drugs 27–40 abdominal surgery, upper 81 postoperative 72 allergic reactions 90, 91 activated protein C (APC) 136–7 unconscious patient 94, 95, inducing hypotension 97 acupuncture 147 117–18 anaesthetic gases see inhalational Acute Life-threatening Event airway pressure, monitoring 53 anaesthetics Recognition and Treatment albumin solution 59 anaesthetic machine 42–3 (ALERT) 113 alcohol consumption 5 checking 43 acute renal failure 127, 135–6 aldosterone 80 oxygen failure alarm 42, 53 acute respiratory distress Alexander technique 148 analgesia syndrome (ARDS) 129, 133 alfentanil 38 chronic pain 145–8 prone ventilation 134 allergic reactions, acute severe defined 62 pulmonary arterial vasodilator 90–1 ICU patients 130–1 therapy 133 allergies, history 5 non-pharmacological methods acute tubular necrosis (ATN) 127 allodynia 140 146–8 Addison’s disease 9 alpha-agonists 68 patient-controlled (PCA) 84–5 adrenaline see epinephrine alveolar hypoventilation 72–3 postoperative see postoperative advanced life support (ALS) alveolar ventilation analgesia 103–8, 113 inhalational anaesthesia 32 analgesic drugs advanced paediatric life support monitoring 51 for anaesthesia 37–40 (APLS) 113 American Heart Association 3 chronic pain 145–6 advanced trauma life support American Society of postoperative 82–3 (ATLS) 113 Anesthesiologists (ASA) premedication 16 air, medical 41 difficult airway guidelines 111 sites of action 83 air embolus 57 physical status scale 10 anaphylactic reaction 90, 91 airway adjuncts, simple 18, amethocaine, topical 62 anaphylactoid reaction 90, 91 117–18 aminophylline 91, 95 antacids 15–16 airway assessment amiodarone 78, 107, 134 antecubital fossa critical illness 117 amitriptyline 146 central venous cannulation via preoperative 6, 7, 8 amnesia 15 58 airway management 17–27 anaesthesia 15–70 veins 54–5 acute severe allergic reactions airway management 17–27 antibiotics 91 defined 62 allergic reactions 90 basic life support 99–100 induction 27 ICU patients 133 basic techniques 17–18 maintenance 29–33 preoperative 17 critical illness 117–18 measurement and monitoring anticholinergic agents 16, 79 emergency techniques 27 47–54 anticholinesterases 35 local anaesthetic toxicity 63 premedication 15–17 anticoagulant therapy 9, 17 paediatric basic life support 108 previous history 4–5 anticonvulsants 146 problems 18–19 risk 9–12 antidiuretic hormone (ADH) 80 recovery room equipment 71 safe delivery 40–7 anti-emetic drugs 78–9 see also laryngeal mask airway; stages 29 preoperative 15, 16 tracheal intubation useful websites 69–70 spinal anaesthesia 69

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Index

antihistamines 78, 91 paediatric 108–10 bupivacaine 62, 64 anxiety 81 patient evaluation 99 epidural anaesthesia 66, 87 anxiolysis 15 basilic vein 54, 55, 58 hyperbaric 67 aortic stenosis 8 benzodiazepines 15 ARDS see acute respiratory distress beta-agonists 68, 95 Calder test 6 syndrome beta blockers 15, 16, 77 cancer pain 140, 146, 149–50 arrhythmias Bier’s block 65 cannulae, peripheral intravenous critically ill patients 122, 124, bleeding diatheses 9 55 134 blood fluid flow 58–9 induced by tracheal intubation components 60 internal diameter 58, 59 25 predeposition 60 length 58 management 77–8 whole 60 over needle 55 postoperative 77–8 blood loss shearing 57 preoperative assessment 3, 6, 9 monitoring during anaesthesia capnography suxamethonium-induced 34 53 during anaesthesia 51, 53 arterial line, indwelling 52, 124–5 volume replacement 61, 80 to confirm tracheal tube arthritis 149 see also fluid losses position 25 aspiration of gastric contents blood pressure website 70 91–3 critically ill patients 120–1, capsaicin, topical 146 management 92 124–5 carbamazepine 146

prevention 26, 92–3 invasive or direct monitoring carbon dioxide (CO2) risk factors 17, 91–2 52, 120, 124–5 absorber 43, 44, 45

before tracheal intubation 25 monitoring during anaesthesia arterial partial pressure (PaCO2) assessment, preoperative see 50, 52 46, 51, 118 preoperative assessment see also hypertension; cylinders 41 Association of Anaesthetists of hypotension end-tidal 25, 51 Great Britain (AAGBI) 69, blood products 60 carboxyhaemoglobin 51 111 blood transfusion 60, 80 cardiac arrest 99–110, 116 checklist for anaesthetic bougie, gum elastic 26 advanced life support 103–8 machines 43 brachial artery 54–5 basic life support 99–103 monitoring recommendations brachial plexus block 65 Universal Algorithm 105 49, 53–4 bradycardia 122 useful websites 111 asthma complicating spinal anaesthesia warning signs 116–17 acute severe 95–6, 111 68 cardiac compressions allergic drug reactions 90 postoperative 77, 78 external 102 NSAIDs and 40 profound 97 paediatric patients 109–10 preoperative assessment 4, 9 breathing open chest 108 asystole 104, 107 assessment 100, 118 cardiac output

atelectasis, postoperative 73 basic life support 100–1 end-tidal CO2 measurement atenolol 16 critically ill patient 118–20 51 atracurium 36 local anaesthetic toxicity 63 ICU monitoring 125, 126, 134 atrial fibrillation 77–8, 122, 134 noisy 72, 117 inhalational anaesthesia 32 atropine paediatric basic life support low fixed, regional anaesthesia bradycardias 68, 78, 97 108–9 and 69 cardiac arrest 107 recovery room equipment 71 reduced 97, 120 nausea and vomiting 68, 79 rescue 100–1 targets in ICU patients 134–5 neuromuscular blockade breathing systems, anaesthetic cardiogenic shock 121–2 reversal 35 43–4 cardiopulmonary resuscitation preoperative 16 circle system 43–4, 45 (CPR) 99–110 components 43, 44 infants and children 108–10 back pain, chronic low 144, 145, disconnection indicators 51, useful websites 111 149 53 see also advanced life support; basic life support (BLS) 99–103 monitoring correct functioning basic life support airway control 99–100 53 cardiorespiratory arrest 116 breathing 100–1 breathlessness 95 cardiovascular disease circulation 101–2 bronchiectasis 9 medical referral 9 common errors 102–3 bronchodilators 133 preoperative assessment 3, 6 healthcare professional 103 bronchoscopy, fibreoptic 26 cardiovascular failure 134 layperson 99 bronchospasm 90, 92 cardioversion 78, 106, 107

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Care of the Critically Ill Surgical postoperative pain intensity coronary care unit (CCU) 116, Patient (CCrISP) 113 and 81 122, 123 carotid artery pulse 102, 109 prevention 150 corticosteroids see steroids

catheters psychological assessment 144 creatinine clearance (CLCR) 127 central venous 58 specific problems 148–50 cricoid pressure 26 over needle 58 treatment 145–8 cricothyroidotomy terminology 55 vs acute pain 140 needle 27, 28, 94 through needle 58 chronic pain syndrome 150 surgical 27, 29 cell savers 60 circle system 43–4, 45 critical care 112–38 central nervous system (CNS) circulation integrated approach 112, 113 disease 69 acute severe allergic reactions levels 113 central neural blockade 64 91 organization 112 complications 68 assessment 101–2, 120 outreach teams 115 see also epidural basic life support 101–2 training and education 112–13 anaesthesia/analgesia; critically ill patient 120–2 useful websites 137–8 spinal local anaesthetic toxicity 63 see also intensive care unit anaesthesia/analgesia paediatric basic life support critical illness central pain 141 109–10 clinical scoring systems central venous cannulation recovery room equipment 71 113–15 57–8 severe hypotension 97 definition and causes 115–16 complications 58 clinic, preoperative assessment 2 initial assessment and equipment 58 clotting tests 8, 61 management 116–22 routes 58 coagulopathy, regional cryoprecipitate 60 uses 125 anaesthesia 69 crystalloids 59 central venous pressure (CVP) co-codamol 83 cultural differences, pain response factors affecting 53 codeine 83, 146 139–40 ICU monitoring 125–6 colloids 59–60 Cushing’s disease 9 monitoring during anaesthesia complex regional pain syndrome cyanosis 72, 95, 118 52–3 149 cyclizine 16, 78 postoperative monitoring 76–7, complications, postoperative cyclo-oxygenase (COX) inhibitors 80 72–9 40 cephalic vein 54 conduction defects 3 cyclo-oxygenase type 2 (COX-2) cerebral haemorrhage 72 Confidential Enquiry into inhibitors 40, 85 cerebral ischaemia 72 Perioperative Deaths cylinders, medical gas 41 cervical spine X-ray 8 (CEPOD) 9–10, 12 chest compressions, external congenital heart disease 9 dantrolene 98, 99 adult 102 consent 12–13 day case surgery 2 infants, children 109–10 defined 12 dead space, ventilation 72 chest drain 96 information required 13 defibrillation 106–7 chest X-ray obtaining 13 safety 106 acute severe asthma 95 unconscious patient 12 synchronized 107 after central venous useful websites 14 technique 107 cannulation 58 written evidence 13 defibrillators, automated external preoperative 7–8 continuous arteriovenous (AEDs) 106 children haemofiltration (CAVH) denervation pain 141 basic life support 108, 109–10 135 depression 144, 148 see also paediatric patients continuous positive airways desflurane 31, 32 chiropractic techniques 147–8 pressure (CPAP) 119, 120 dexamethasone 79 chlorpheniramine 91 continuous venovenous dextropropoxyphene 145–6 chronic obstructive pulmonary haemofiltration (CVVH) diabetes 4, 9 disease (COPD) 135 dialysis, ICU patients 135 critical care 118–20, 132–3 controlled drugs 39–40 diamorphine preoperative assessment 4, 9 convulsions, local anaesthetic chronic pain 140 chronic pain 139–50 toxicity 63 epidural anaesthesia 87 benign 140 cooling measures 98 see also morphine clinical assessment 142–4 COPD see chronic obstructive diaphragmatic splinting 73 history 143–4 pulmonary disease diazepam 15, 63 investigations 144, 145 coproxamol 145–6 dihydrocodeine 146 physical examination 144 cordotomy 147 distraction 139

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Index

diuretics 76–7 eutectic mixture of local functional residual capacity (FRC) dobutamine 9, 122, 134 anaesthetics (EMLA) 17, 62 73, 129 domperidone 79 evaporation, intraoperative fluid do not attempt resuscitation loss 61 gabapentin 146 (DNAR) orders 116–17 examination, physical gases dopamine antagonists 78–9 chronic pain 144 anaesthetic see inhalational dorsal metacarpal veins 54 preoperative 5–6 anaesthetics drug abuse 5, 39 exercise tolerance 4 anaesthetic breathing systems drug history 5 expiratory valve 43 43–4 drugs expired-air ventilation 100–1 anaesthetic machine 42–3 acute severe reactions 90–1 paediatric patients 109 delivery to operating theatre anaesthetic see anaesthetic extravasation, fluid or drugs 57 40–2 drugs eye injuries, penetrating 34 gastric emptying, delayed 17 controlled 39–40 gastric ulcers, critically ill patients facemasks 18 132 ECG see electrocardiogram oxygen delivery 74–5 gastrointestinal tract echocardiography 8–9 problems 19 fluid losses 61 stress 9 technique of holding 17, 18 ischaemia 116 transoesophageal (TOE) 127 family see relatives gastro-oesophageal reflux 4, 17 education, critical care 112–13 family history 5 gate control theory of pain 142 elective surgery 12 fasting, preoperative 17 Gelofusine 59 failed intubation 93 fentanyl 38, 82 general anaesthesia, drugs used preoperative starvation 17 chronic pain 145 27–40 electrical stimulation, chronic epidural anaesthesia 67, 87 Glasgow Coma Scale (GCS) 128 pain 147 fibrinogen levels 61 glomerular filtration rate (GFR) electrocardiogram (ECG) fibromyalgia 149 127 during anaesthesia 49–50 finger sweep technique 100, 108 gloves 56 cardiac arrest 106, 107 flowmeters, anaesthetic machine glucose, blood (BS) critically ill patients 122, 42 control in critical illness 137 124 fluid intraoperative 53 preoperative 7, 8 flow through cannulae 58–9 preoperative testing 7, 8 emergencies, perioperative intraoperative requirements glucose solutions 59, 61 90–111 61 glyceryl trinitrate (GTN), emergency surgery 12 intravenous 59–60 transdermal 17 failed intubation 93 viscosity 58 glycopyrrolate 16, 35 EMLA (eutectic mixture of local fluid administration 54–61 Goldman Cardiac Risk Index 10, anaesthetics) 17, 62 critical illness 121–2 11 emphysema 4 intraoperative 60–1 guanethidine intravenous endocrine disorders 9 postoperative 76, 77, 79–80 regional block 147 endotoxin 136 maintenance requirements Guedel (oropharyngeal) airway enflurane 31, 32 79 18, 19 enteral feeding 131, 132 major surgery 79–80 gum elastic bougie 26 Entonox 32, 41, 88 fluid challenge 52, 76, 121, 134 epidural abscess 88 fluid losses Haemaccel 59 epidural anaesthesia/analgesia 64, accrued perioperative 60–1 haematological disorders 9 65–7 intraoperative causes 61 haematological tests 7, 8 chronic pain 146–7 postoperative 76, 80 haematoma complications 77, 87–8 third space 61, 80 after peripheral vein contraindications 69 see also blood loss cannulation 57 ICU patients 131 fogging 25 vertebral canal 87–8 postoperative 86–8 forced expiratory volume in 1s haemodilution, preoperative 60

epidural blood patch 68 (FEV1)8 haemofiltration, continuous epilepsy 4 forceps, Magill’s 22, 24 135–6 epinephrine (adrenaline) forearm, veins 54, 55 haemoglobin concentration 61 allergic reactions 91 foreign bodies, inhaled 95, 101, haemoglobinopathies 9 cardiopulmonary resuscitation 108 haemolytic anaemias 9 107 fresh frozen plasma (FFP) 60 haemorrhage 76, 97 local anaesthesia 62–3 frusemide 76–7 see also blood loss etomidate 30, 33 full blood count (FBC) 8 haemothorax 73

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halothane 31, 32 hypertension malignant hyperpyrexia 98 hepatitis 33 intubation induced 25 minimizing theatre pollution malignant hyperpyrexia 98 postoperative 78 46–7 previous exposure 5 preoperative assessment 2, 3, 6, minimum alveolar hand, veins of dorsum 54 9 concentration (MAC) Hartmann’s solution 59, 61 hyperthyroidism 9 29–32, 32 headache, postdural puncture 68 hypopituitarism 9 scavenging systems 46–7 head injury 123, 128 hypotension solubility 32 head position, oral tracheal causes in critically ill 121 see also specific agents intubation 24 complicating epidural analgesia inotropes 97, 122, 134 head tilt plus chin lift 99, 100 87 inspiratory to expiratory (I : E) paediatric patients 108 complicating spinal anaesthesia ratio 129 heart block 122 68 insulin therapy 137 heartburn 4 postoperative 75–8 Intensive Care Society (ICS) 137 heart failure severe 96–7 intensive care unit (ICU) 112, monitoring during anaesthesia hypothermia, postoperative 72 113, 123–37 52–3 hypothyroidism 9 common conditions treated preoperative assessment 3, 6, 9 hypoventilation, alveolar 72–3 132–7 see also left ventricular failure hypovolaemia 76, 97 infection control 132 heart rate critically ill patients 121, 134 intubation and tracheostomy critically ill patient 120–1 epidural or spinal anaesthesia 129–30 monitoring during anaesthesia 69 mechanical ventilation 129 50 management 76 monitoring 124–8 see also bradycardia; tachycardia hypoxia/hypoxaemia nutrition 131–2 hepatic function, ICU patients acute severe asthma 95 outreach teams 115 128 COPD 118–20 sedation and analgesia 130–1 hepatitis, halothane 33 critical illness 118 under-provision 123–4 hepatitis B 60 diffusion 33, 74 see also critical care heroin see diamorphine management 74 ‘intensive care without walls’ 112, hiatus hernia 17 mechanical ventilation 129 115 high airflow oxygen enrichment postoperative 72–4 intermittent positive pressure (HAFOE) 75 tension pneumothorax 96 ventilation (IPPV) 45 high dependency unit (HDU) tracheal intubation-related 25 internal jugular vein, cannulation 112, 113, 123 hypoxic ventilatory drive 118–19, 58 histamine release 34, 36, 90, 97 132–3 International Association for history taking Study of Pain (IASP) 139, chronic pain 143–4 ibuprofen 85 150 preoperative 3–5 ICU see intensive care unit intracranial pressure (ICP) HIV infection 60 indigestion 4 monitoring 128 hormone replacement therapy induction of anaesthesia raised, regional anaesthesia 69 (HRT) 5 inhalational 27 intrathecal anaesthesia see spinal hospital-acquired infections 116, intravenous 27, 30 anaesthesia/analgesia 132 infants, basic life support 108, intravenous anaesthesia, total Hudson mask 75 109, 110 (TIVA) 33–4 with reservoir 75 infection control, ICU 132 intravenous cannulation 54–61 hydrocortisone 91, 95 infections central see central venous hydromorphone 145 complicating epidural analgesia cannulation 5-hydroxytryptamine 3(5-HT3) 88 complications 57 antagonists 78 hospital-acquired 116, 132 equipment 55 hygiene standards, ICU 132 transfusion risks 60 failure 57 hyoscine 16, 79 infiltration analgesia 64–5 relevant anatomy 54–5 hyperaesthesia 140 information, patient 13 technique 55–7 hyperalgesia 140 inhalational anaesthetics intravenous fluids 59–60 hyperbaric solutions 67 anaesthetic machine 42–3 administration see fluid hypercapnia induction of anaesthesia 27 administration permissive 133 inspired concentration 32, 44, intravenous induction of postoperative 72 51 anaesthesia 27, 30 hyperpyrexia, malignant see maintenance of anaesthesia intravenous regional anaesthesia malignant hyperpyrexia 29–33 (IVRA) 65

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intubating laryngeal mask airway loss of resistance technique 65–6 Modified Early Warning Scoring (ILM) 20, 21, 24–5, 26 lung disease, pre-existing 4 System (MEWSS) 114 investigations, preoperative 7–9 monitoring additional 7–9 Magill’s forceps 22, 24 during general anaesthesia baseline (ASA 1) 7, 8 magnesium sulphate 95 47–54 ipratropium bromide 95, 133 maintenance of anaesthesia additional 49, 52–3 ischaemic heart disease 29–33 blood loss 53 postoperative complications major surgery breathing systems 53–4 76, 77–8 postoperative fluid therapy essential 49–51 preoperative assessment 3, 9 79–80 immediately available 49, isoflurane 31, 32 risk of major cardiac 52 complication 11 integrated systems 50, 51 jaundice 4 malignant hyperpyrexia oxygen supply 53 jaw thrust 17, 99, 100 (hyperthermia) (MH) 5, 34, potential hazards 49 paediatric patients 108 98–9, 111 intensive care unit 124–8 anaesthesia for susceptible during local and regional ketamine 30, 33 patients 99 anaesthesia 67 ketorolac 40, 85 management 98 perioperative emergencies 91 monitoring during anaesthesia recovery room 71 lactate, serum 128, 134 51, 52 morphine 38 laryngeal mask airway (LMA) Mallampati criteria 6, 7 cancer pain 150 19–21, 26, 70 manipulation 147–8 chronic pain 145 insertion technique 20–1, 22 Mapleson breathing systems 43 patient-controlled analgesia intubating (ILM) 20, 21, 24–5, masks see facemasks (PCA) 85 26 MC mask 75 postoperative analgesia 82 relative contraindications 20 mean arterial pressure (MAP) routes of administration 84 types available 20, 21 124–5, 134 mortality, perioperative 10 laryngeal spasm 26 targets in ICU patients 134–5 risk indicators 10–12 laryngoscope 22 median cubital vein 54–5 mouth-to-mouth ventilation laryngoscopy 24, 26 median nerve 55 100–1, 109 latex allergy 90, 91 median vein of forearm 54, 55 mouth-to-nose ventilation 101, left ventricular failure medical problems, coexisting 109 ICU management 129, 134 history taking 3–4 multiple organ failure syndrome postoperative 76–7 preoperative assessment 2 (MOFS) 115–16 see also heart failure preoperative referral 9 MAP and cardiac output targets left ventricular function, medical staff, critical care training 134–5 preoperative assessment 112–13 muscle relaxants see 8–9 Medicines and Healthcare neuromuscular blocking legs, numbness and weakness products Regulatory Agency drugs 87 70, 111 muscle rigidity 98 leukaemias 9 memory, pain 139 musculoskeletal disorders 6 levo bupivacaine 62 metaraminol 68 myocardial contractility lignocaine 62, 64 methadone 145 reduced 76–7, 97 liver function tests 7, 128 methaemoglobin 51 therapy to improve 134 LMA see laryngeal mask airway methicillin-resistant myocardial infarction (MI) local anaesthesia 61–7 Staphylococcus aureus acute 77, 121–2, 123 monitoring during 67 (MRSA) 132 perioperative risk 10–12 peripheral venous cannulation methylprednisolone 91 previous history 3 56 metoclopramide 16, 78–9 role 63–4 midazolam 30 nalbuphine 37 techniques 64–5 minimum alveolar concentration naloxone 39, 82 local anaesthetic drugs 62 (MAC) 29–32, 32 nasal cannulae 74–5 calculation of doses 63 minor surgery nasopharyngeal airway 18, 20 epidural anaesthesia 66, 87 postoperative fluid therapy National Institute for Clinical inadvertent overdose 63 79 Excellence (NICE) 7, 8, known allergy 69 risk of major cardiac 69 techniques using 64–7 complication 11 nausea toxicity 63 Misuse of Drugs Act 1971 39 complicating spinal anaesthesia lorazepam 15 mivacurium 36 68

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drugs used to treat see operating theatre peripheral arterial (SpO2) 50, anti-emetic drugs delivery of gases 40–2 126 postoperative 15, 78 minimizing pollution 46–7 oxygen therapy neostigmine 35 operations COPD 118–19 nerve blocks 146–7 classification 12 critical illness 118 peripheral 85, 146 previous history 4–5 perioperative emergencies 92, nerve stimulation, peripheral opioid analgesics 37–40 93, 95 35–7 antagonists 39 postoperative hypoxaemia 74 neurological assessment central and peripheral actions respiratory failure 132–3 ICU patients 128 38 oxyhaemoglobin dissociation preoperative 6 chronic pain 145–6 curve, hypocapnia and neuroma 148–9 complications 38, 72, 82 46 neuromuscular blockade epidural anaesthesia 66–7, 87 assessment 35–7 ICU patients 131 paediatric patients residual postoperative 73 less potent 83 basic life support 108–10 reversal 35 overdose 82 monitoring of blood loss 53 neuromuscular blocking drugs partial agonists and mixed tracheal intubation 23 34–7 agonists/antagonists 37–9 pain depolarizing 34 postoperative analgesia 82–3, acute 140 non-depolarizing 34–5, 36 84 assessment 81–2 neuromuscular disorders 4 premedication 16 cancer 140, 146, 149–50 neuropathic pain 148 pure agonists 38 chronic see chronic pain neurosurgical patients 123 regular preoperative users 88 continuing tissue damage 140 New York Heart Association regulation 39 definition 139 (NYHA) functional spinal anaesthesia 67, 88 experience 142 classification 3, 4 supply and custody 39–40 factors affecting 81, 139–40 nitric oxide (NO), inhaled 133 opioid receptors 37 gate control theory 142 nitrous oxide 29, 32–3 oral contraceptive pill (OCP) 5 management programmes 148 anaesthetic machine 42 oral fluid intake, postoperative 79 measurement 144 diffusion hypoxia 33, 74 oropharyngeal (Guedel) airway mechanisms of generation and oxygen see Entonox 18, 19 140–1 in pneumothorax 96 osteopathy 147–8 postoperative see postoperative supply to operating theatre outreach teams, critical care 115 pain 41 oxycodone 82, 145 useful websites 70, 89, 150 systemic effects 32–3 oxygen variability 142 non-invasive positive pressure alveolar concentration 74 pancuronium 36 ventilation (NIPPV) 119 anaesthetic machine 42 paracetamol 40, 83–4, 85

non-steroidal anti-inflammatory arterial partial pressure (PaO2) parecoxib 40, 85 drugs (NSAIDs) 40, 83–4, 118 parenteral nutrition, total (TPN) 85 delivery devices 74–5 131 chronic pain 146 inspired concentration 43–4, 46 patient-controlled analgesia (PCA) COX-2 specific 40, 85 anaesthetic machine controls 84–5 nosocomial infections 116, 42 peak expiratory flow (PEF) 95 132 continuous monitoring 53 pericardiocentesis, needle 97 nurses COPD 118–19 peripheral nerve blocks 85, 146 critical care training 112–13 critical illness 118 peripheral nerve damage 141 preoperative assessment 2 delivery devices 74–5 peripheral nerve stimulation 35–7 nutrition, ICU patients 131–2 postoperative hypoxaemia peripheral perfusion, assessment 72, 73–4 76, 120 obesity 17 reduced 74 peripheral resistance, reduced 97 oesophageal detector 25 respiratory failure 132–3 peripheral vascular disease 3, 6 oesophageal intubation, masks 74–5 pethidine 38 inadvertent 25 nasal cannulae 74–5 phantom limb pain 148 older patients supply to operating theatre 41 phenothiazine derivatives 79 epidural anaesthesia 87 toxicity 133 phenytoin 146 postoperative analgesia 81 oxygen saturation physiotherapy 133, 148 oliguria, postoperative 76 after tracheal intubation 25 piped medical gas and vacuum omeprazole 16 mixed venous, monitoring system (PMGV) 40–2 ondansetron 16, 78 126 platelet concentrates 60, 61

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platelet count 61 prostacyclin, nebulized 133 renal function pneumonia prostaglandins 40, 141 ICU patients 127 ICU patients 132, 133 prostate surgery 77 preoperative testing 8 ventilator-associated 132 protective ventilatory strategy renal replacement therapy 9 pneumothorax 73 133 renin–angiotensin system 80 tension 96 prothrombin time (PT) 128 rescue breathing 100–1 positioning, patient pruritus, opioid-induced 87 reservoir bag 43 cardiac output and 97 pseudocholinesterase 34 respiratory depression 72, 82, 87 epidural anaesthesia 66 deficiency 34 respiratory disease postanaesthesia 72 psychological assessment, chronic local or regional anaesthesia 64 recovery position 103, 104 pain 144 medical referral 9 spinal anaesthesia 67 psychological therapy, chronic preoperative assessment 4, 6 tracheal intubation 24 pain 148 respiratory distress 95, 96 positive end expiratory pressure pulmonary arterial vasodilator respiratory failure 6, 118, 132–4 (PEEP) 129, 133 therapy 133 causes 118, 119 positive pressure ventilation pulmonary artery flotation mechanical ventilation 129 44–5, 46, 129 catheter (PAFC) 126 prone ventilation 134 postanaesthesia care 71–89 pulmonary artery pressures 126 pulmonary arterial vasodilator postdural puncture headache 68 pulmonary diffusion defects 74 therapy 133 postherpetic neuralgia (PHN) 148 pulmonary function tests 8 respiratory rate 118 postoperative analgesia 80–8 pulmonary oedema 74 respiratory tract infections 4 combination techniques 88 pulse 101–2, 120 resuscitation difficult problems 88 pulse contour analysis 125 ABC principles see ABC of drugs used 82–3 pulseless electrical activity (PEA) resuscitation techniques 84–8 104, 107 cardiopulmonary see postoperative complications 72–9 pulse oximetry 50–1, 126 cardiopulmonary postoperative nausea and resuscitation vomiting (PONV) 15, 78 Ramsay sedation scale 128, 131 critically ill patients 117–22 postoperative pain 80–8, 148 ranitidine 16, 91 do not attempt (DNAR) orders adverse consequences 73, 81 rebreathing, indication 51 116–17 difficult problems 88 record, anaesthetic 54 opioid-induced respiratory management 81–8 recovery area 71 depression 82 potassium, postoperative discharge from 71, 72 severe hypotension 97 replacement 80 recovery position 103, 104 see also advanced life support; precordial thump 106, 107 red cell concentrate 60, 61 basic life support prednisolone 95 red cells in optimal additive Resuscitation Council (UK) 111 pregnancy 5, 17 solution 60 arrhythmia guidelines 77, 89 premedication 15–17 reflex activity, tracheal cardiopulmonary resuscitation preoperative assessment 1–9 intubation-induced 25–6 guidelines 99 airway 6, 7, 8 reflex sympathetic dystrophy 149 Universal Algorithm 105 clinic 2 reflux, gastro-oesophageal 4, 17 rheumatoid arthritis examination 5–6 regional anaesthesia 61–9 pain 140, 145 history 3–5 awake vs after induction 68–9 preoperative assessment 4, 6, 8 investigations 7–9 ICU patients 131 risk (anaesthesia and surgery) screening 1–2 monitoring during 67 9–12 urgent and emergency surgery postoperative analgesia 85–8 indicators 10–12 12 role 63–4 major 9–10 useful websites 13–14 techniques 64–7 minor 9 preoxygenation, tracheal relatives by type of surgery 11–12 intubation 23 malignant hyperpyrexia 98 rocuronium 36 pressure, fluid flow rate and 59 unconscious patient and rofecoxib 85 pressure-controlled ventilation consent 12 ropivacaine 62 (PCV) 133 remifentanil 38 rotameters 42 primary organ dysfunction 116 renal disease 9 Royal College of Anaesthetists 70 prochlorperazine 79 renal failure prone ventilation 134 acute 127, 135–6 SAG-M solution 60 propofol 30, 33 chronic 4, 9 salbutamol 91, 95, 133 Proseal laryngeal mask airway 20, morphine therapy 82 saline (sodium chloride) solutions 21 pre-renal vs intrinsic 127, 128 59, 61

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scavenging systems 46–7 suxamethonium 34 transoesophageal scheduled surgery 12 adverse effects 34, 98 echocardiography (TOE) scoring systems, critical care apnoea 34 127 113–15, 124 sympathetic activity, intubation- trauma screening, preoperative 1–2 associated 16 chest compression causing 102 secondary organ dysfunction 116 sympathetic blockade 147 intraoperative fluid loss 61 sedation systemic inflammatory response stress response 80 complicating epidural analgesia syndrome (SIRS) 116, during tracheal intubation 25 87 136–7 tricyclic antidepressants 146 harmful effects of deep 131 trigeminal neuralgia 143, 149 ICU patients 128, 130–1 tachycardia 122 tryptase, plasma 91 preoperative 15 extreme 97 Tuohy needle 65, 66, 68 Seldinger technique 55, 58 perioperative emergencies 94, Sellick’s manoeuvre 26 95 unconscious patient sepsis 97, 121 postoperative 76, 77–8 acute airway obstruction 94, sepsis syndrome 134, 136–7 tachypnoea 95, 98, 118 95, 117–18 septic shock 77, 120 target controlled infusion (TCI) basic life support 99–100 sevoflurane 27, 31, 32 33 consent issues 12 shock, circulatory 121–2 temazepam 15 upper limb, anatomy of veins sickle-cell screen (Sickledex) 8 temperature, monitoring during 54–5 sinus bradycardia 78, 122 anaesthesia 52 urea and electrolytes 7, 8 sinus tachycardia 77, 122 thiopentone 30 urgent surgery 12 smoking 5 third space fluid losses 61, 80 urine output social history 5 thoracic surgery 81 ICU monitoring 127 sodium chloride solutions 59, thrombophlebitis 57 monitoring during anaesthesia 61 thyromental distance 6, 8 52 sodium citrate 16, 92 tidal volume 46, 133 reduced postoperative 76, 80 Specific Activity Scale 3, 4 tissue injury 140, 141 urine retention 87 spinal anaesthesia/analgesia 64, topical anaesthesia 64 67 total intravenous anaesthesia vacuum, medical 41–2 chronic pain 146–7 (TIVA) 33–4 vacuum-insulated evaporator complications 67–8, 77 total parenteral nutrition (TPN) (VIE) 41 contraindications 69 131 valvular heart disease 6, 9 postoperative 88 tracheal intubation 21–7 vaporizers 29, 42–3 spinal cord injury 97 in airway obstruction 95 vapour concentration analyser 51 spinal cord stimulation 147 complications 25–6 vasodilatation 77, 97 spinal surgery, previous 69 cricoid pressure 26 vasodilator therapy 134 stages of anaesthesia 29 difficult 26 pulmonary arterial 133 starch solution 59 preoperative prediction 6, 7, vasopressors 68, 97 starvation, preoperative 17 8 vecuronium 36 steroids equipment 22 veins, upper limb 54–5 acute severe asthma 95 failed 25, 26–7, 93–4 venepuncture see intravenous allergic reactions 91 ICU patients 129–30 cannulation anti-emetic use 79 indications 21 venous return, decreased 97 chronic pain 146 nasal 24 ventilation preoperative 17 technique of oral 23–4 alveolar see alveolar ventilation stethoscope 22 tracheal tubes 23 expired-air 100–1, 109 stress response 80 confirming position 25 failed 25, 26–7, 93–4 stridor 94 cuffed 23 impaired 6, 73 subclavian vein, cannulation 58 sizes 22 mechanical 44–6 suctioning, airway 22, 133 types 23 COPD 119–20 sugar, blood see glucose, blood tracheostomy 129–30 ICU patients 129 supraventricular tachycardia training, critical care 112–13 respiratory failure 133 77–8, 122 train-of-four (TOF) stimulation ventilation/perfusion surgery 35 mismatch 73 classification 12 tramadol 37–9, 83, 145–6 weaning 129–30 previous history 4–5 transcutaneous electrical monitoring adequacy 51, 53 risk 9–12 nerve stimulation (TENS) mouth-to-nose 101 stress response 80 147 positive pressure 44–5, 46, 129

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ventilation (cont.) ventricular fibrillation (VF) 104, induced by tracheal intubation prone 134 105–7 25–6 protective strategy 133 see also defibrillation postoperative 15, 78 recovery room equipment 71 ventricular tachycardia (VT) 104, see-saw 72, 94, 117 122 weaning, ventilatory support ventilation/perfusion (V/Q) management 105–6, 107 129–30 mismatch 46, 73–4, 129 Venturi mask 75 Wilson score 6 ventilators viscosity, fluid 58 anaesthetic 44–6 vomiting X-rays bag-in-bottle 46, 48 complicating spinal anaesthesia chest 7, 8, 58, 96 gravity-powered 46, 47 68 cervical spine 8 ICU 129, 130 drugs used to treat see modern electronic 46, 49 anti-emetic drugs yoga 148

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Lecture Notes on Tropical Medicine Fifth Edition

Geoff Gill and Nick Beeching February 2004. 368 pages 86 illustrations ISBN 063206496X Paperback £16.95

*Emphasis on the clinical aspects of problem solving Lecture Notes on Tropical Medicine is a core text with an emphasis on the and management in the practical aspects of problem-solving in the tropics. It is a very practical tropics companion for the increasing number of medical students and junior doctors who have the opportunity to practice medicine in the tropics. *Emphasises a problem- based clinical approach using This new, revised edition includes a more global and syndromic approach to clinical presentations tropical medicine. In addition to covering the serious and relevant tropical , the book also covers conditions and diseases that are becoming *An increased global more widespread in the tropics such as epilepsy, diabetes and AIDS. approach to medicine in the tropics not just tropical and Carefully selected colour plates and an increased number of illustrations, exotic diseases effectively portray clinical conditions. This edition includes a separate section on HIV and reflects the impact that AIDS has had on the tropics. *New chapter on non- communicable diseases, such as epilepsy, diabetes and heart disease, which are becoming more widespread in the tropics

*New chapter on refugee ORDER FORM health that covers humanitarian disasters, To place an order for this book, simply complete and return this order form to: control of epidemics and Marston Book Services, PO Box 269, Marston, Oxon OX14 4YN, UK health assessment of asylum Tel: +44 (0)1235 465500 Fax: +44 (0)1235 465556 E-mail: [email protected] Web: www.blackwellmedicine.com seekers Please send me ______copies of Lecture Notes on Tropical Medicine *Over 25 expert contributors (ISBN 063206496X) at £16.95 each I enclose a cheque for £______made payable to Marston Book Services Ltd.

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Index Lecture Notes on Infectious Diseases

Sixth Edition

BK Mandal, EGL Wilkins, EM Dunbar and Richard Mayon-White December 2003. 280 pages 16 illustrations ISBN 1405108207 Paperback £16.95

This core text provides an excellent concise introduction to infectious diseases. The Integrates the basic science book integrates basic science with clinical practice, with disease-orientated with clinical practice descriptions and clinical presentations on a system-by-system basis. It is therefore ideal for both the student and the practitioner. Core introductory text for the For this new sixth edition the text has been brought fully up to date throughout.The student and the practitioner highly structured and improved text is designed to facilitate easy access to information, making the book an ideal resource for clinical attachments and revision. Major update throughout and There is a new chapter that covers infections in special groups, as well as coverage new chapter on infections in of sepsis and septic shock. The Introductory chapter also takes into account new special groups e.g. travellers control measures, emerging infections, and infections linked with bioterrorism. and drug users Information on global occurrence is added to the epidemiology sections where relevant and web site information has been included to provide up-to-date resources Includes information on the on fast moving topics such as AIDS, and travel-related infections such as SARS. new control measures and The result is a text that is a compact yet comprehensive guide to infectious diseases. emerging infections, It will appeal to medical students, junior doctors, general practitioners, and allied especially those with health professionals who want a concise introduction to the subject or an ideal bioterrorism potential revision companion.

Information is provided on global occurrence where relevant ORDER FORM Update information on SARS To place an order for this book, simply complete and return this order form to: Marston Book Services, PO Box 269, Marston, Oxon OX14 4YN, UK Tel: +44 (0)1235 465500 Fax: +44 (0)1235 465556 E-mail: [email protected] Web: www.blackwellmedicine.com

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Index Medical Genetics at a Glance First Edition

Dorian Pritchard and Bruce R Korf December 2002. 120 pages 48 illustrations ISBN 0632063726 Paperback £15.95

Medical Genetics at a Glance is a concise, well-illustrated and accessible genetics textbook. It follows the now familiar, easy-to-use, double page spread format of the * Concise introduction and at a Glance series. Each double page presents clear, memorable diagrams that revision text illustrate essential information with accompanying text that covers key topics and issues in more detail.

* Covers the core principles Structured into three distinct sections, Medical Genetics at a Glance, takes the of cell biology & genetics student through developmental biology, medical genetics and the clinical application of genetics. The first section focuses on basic biological concepts such as cell and * Three section structure chromosome structure, molecular biology and the cell cycle, as well as human covering developmental embyronic development and sexual maturation. The second section applies these biology, medical genetics principles to medicine through the essential 'laws' of inheritance, the chromosome and clinical application of anomolies, multifactorial inheritance, normal polymorphism and gene frequency, then genetics moving on to gene mapping, mutagenisis, cancer and immunogenetics. The final section addreses the clinical application of the above principles in pedigree drawing and molecular diagnostic procedures based on the human gene map, PCR and * Considers the essential Southern techniques, risk assessment, genetic counselling, gene therapy and much practical and philosophical more. aspects of medical genetics Medical Genetics At A Glance is an ideal resource that fits the budget and reading * Presents clinical material time of medical students and those seeking a quick yet thorough, introduction to this in context fast moving field. It can be used as primary or supplementary reading in a lecture- based course and is perfect for exam preparation. * Contains useful glossary of terms ORDER FORM

To place an order for this book, simply complete and return this order form to: Marston Book Services, PO Box 269, Marston, Oxon OX14 4YN, UK Tel: +44 (0)1235 465500 Fax: +44 (0)1235 465556 E-mail: [email protected] Web: www.blackwellmedicine.com

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