CHAPTER 14 – GENERAL EMERGENCIES AND MAJOR TRAUMA

First Nations and Inuit Health Branch (FNHIB) Clinical Practice Guidelines for Nurses in Primary Care. The content of this chapter was revised October 2011.

Table of Contents

RESPONDING TO GENERAL EMERGENCIES AND MAJOR TRAUMA...... 14–1 GENERAL EMERGENCY SITUATIONS...... 14–1 ...... 14–1 ...... 14–5 Coma (Not Yet Diagnosed)...... 14–7 Overdoses, Poisonings and Toxidromes...... 14–9 Hypothermia...... 14–14 MAJOR TRAUMA SITUATIONS...... 14–16 Head Trauma...... 14–16 Cervical Spine and Trauma...... 14–19 Flail Chest...... 14–21 Pelvic Fracture...... 14–22 SOURCES...... 14–25

Clinical Practice Guidelines for Nurses in Primary Care 2011

General Emergency and Major Trauma 14–1

RESPONDING TO GENERAL EMERGENCIES AND MAJOR TRAUMA

For any emergency, always remember your ABCs The next priorities are as follows: (airway, breathing, circulation) as the priority. Primary –– Adequate ventilation survey and are followed by secondary survey, definitive care and, finally, transport. –– Treatment of shock –– Identification of life-threatening injuries The primary survey and resuscitation are done simultaneously. During this period, a patent airway See “Primary Survey” and “Resuscitation” sections is established while control of the cervical spine under “Responding to General Emergencies and is maintained. Maintenance of airway patency is Major Trauma” in the pediatric Chapter 20, “General obviously the most critical factor, and cervical spine Emergencies and Major Trauma” for a general injury should be assumed in every seriously injured approach to use with all clients in an emergency. individual, until proven otherwise.

GENERAL EMERGENCY SITUATIONS

ANAPHYLAXIS CAUSES Anaphylaxis is an acute hypersensitivity reaction The most common causes of fatal anaphylactic with multi-organ-system involvement that has a reactions are: rapid onset and may cause death.1,2 The symptoms –– Drugs (for example, penicillin and cephalosporin develop over several minutes to several hours,3 may antibiotics, NSAIDs [nonsteroidal anti- involve multiple body systems (for example, skin inflammatory drugs] including ASA [90% of episodes], respiratory [70% of episodes], [acetylsalicylic acid], anesthetics)1 gastrointestinal [40% of episodes], circulatory [35% of –– Foods (most common in children,5 for example, episodes]3) and may progress to unconsciousness as a peanuts, shellfish, nuts, sesame seeds, fish late event in severe cases. Rarely is unconsciousness products, eggs)5 the sole manifestation of anaphylaxis. The severity –– Insect venom (for example, bees, wasps) and differentiation of an anaphylaxis reaction can be implied by the presence of cutaneous or multi- In contrast, fatal reactions to vaccines and latex rubber system findings, in addition to the involvement of are rare.6 cardiovascular and/or respiratory findings.4 HISTORY Anaphylaxis is a medical emergency and must be distinguished from fainting (vasovagal syncope), Most anaphylactic episodes involve an immediate which is more common and benign. Rapidity of onset hypersensitivity reaction following exposure to 1 is a key difference. When a person faints, the change an allergen. Symptoms often occur within 5–30 from a normal to an unconscious state occurs within minutes of exposure to trigger factor. Anaphylaxis seconds. Fainting is managed simply by placing the can be biphasic with recurrence of symptoms patient in a recumbent position and elevating the feet. occurring, usually within eight to ten hours, but Fainting is sometimes accompanied by brief clonic occasionally up to 72 hours after the resolution of 7 seizure activity, but this generally requires no specific the initial anaphylactic event. Anaphylaxis may be treatment or investigation. fatal within minutes, usually through cardiovascular orrespiratory compromise.1

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The signs and symptoms may include:8 SEVERE REACTION –– Severe respiratory distress (lower respiratory Skin obstruction characterized by high-pitched –– Flushing wheezing, upper airway obstruction characterized –– Feeling of warmth by stridor) –– Itching (may begin on palms and soles, may –– Difficulty speaking, hoarseness include the external auditory canal) –– Difficulty swallowing –– Urticaria (hives) –– Agitation –– Angioedema (facial edema) –– Shock –– Morbilliform rash –– Loss of consciousness –– Piloerection (hair standing on end) PHYSICAL FINDINGS Oral –– Tachycardia –– Itching or tingling or edema of lips, tongue, –– Tachypnea, laboured respiration palate or uvula –– Blood pressure low-normal (client hypotensive if –– Metallic taste in shock) –– Pulse oximetry may show hypoxia Gastrointestinal –– Client in moderate-to-severe distress –– Nausea, vomiting, abdominal pain, diarrhea, –– Use of accessory muscles of respiration difficulty swallowing –– Chest: air entry reduced, mild-to-severe wheezing –– Stridor, rapid or shallow breathing, cyanosis9 Respiratory –– Client flushed and diaphoretic –– Pruritus of the larynx and tightness in the throat –– Generalized urticaria (hives) –– Dysphagia, dysphonia or hoarseness –– Facial edema, angioedema –– Respiratory difficulties: shortness of breath, –– Diminished level of consciousness wheezing, cough dyspnea, tightness of the chest –– Confusion, anxiety, agitation (caused by hypoxia)9 –– Nasal symptoms including, itching, congestion, –– Skin feels cool and clammy sneezing, rhinorrhea DIFFERENTIAL DIAGNOSIS Ocular –– Asthma –– Periorbital itching, erythema, tearing or edema –– Acute anxiety (panic attack), breath-holding –– Red, itchy eyes5 episode in a child9 –– Conjunctival erythema –– Foreign-body aspiration Neurologic –– Angioedema –– Pulmonary embolism –– Anxiety –– Vasovagal syncope (fainting) (pulse and BP are –– Apprehension, sense of impending doom generally normal, and there is usually no evidence –– Confusion of airway symptoms)9 –– Seizures –– Hypoglycemia9 –– Headache –– Seizure disorder9 9 Cardiovascular –– –– Mastocytosis, carcinoid syndrome, scromboid –– Feeling faint, dizziness, syncope poisoning9 –– Palpitations, tachycardia

Hypotension –– Lower back pain due to uterine cramping in women –– Cardiovascular collapse can occur without respiratory symptoms

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CASE DEFINITION Pharmacologic Interventions As anaphylaxis may present with a number of Epinephrine is the drug of choice for the treatment symptoms and/or signs, a case definition provides of anaphylaxis, and the IM route is preferred.11 a standard approach to describing the degree of There are no absolute contraindications to the use clinical severity and the level of diagnostic certainty. of epinephrine for the treatment of anaphylaxis.7,11 The case definition and guidelines for clinical application, including reporting adverse events, were Speedy intervention is of paramount importance. published by the Brighton Collaboration Anaphylaxis Failure to use epinephrine promptly is more Working Group in “Anaphylaxis: Case definition dangerous than using it quickly but improperly. and guidelines for data collection, analysis and Failure to administer epinephrine promptly and use of presentation of immunization safety data”.10 antihistamines and salbutamol rather than epinephrine are important errors in the treatment of anaphylaxis.7 COMPLICATIONS Promptly administer: –– Hypoxia epinephrine 1 mg/mL solution (may be labelled –– Shock 1:1000), 0.2–0.5 mg = 0.2–0.5 mL intramuscular –– Airway obstruction due to edema of upper airway (IM)7,11 in the midanterolateral thigh to achieve peak –– Convulsions plasma and tissue concentrations rapidly12 –– Aspiration Repeat at 5–15 minute intervals, as necessary, –– Death depending on the severity of the reaction, to control symptoms and to sustain or increase blood pressure.11 DIAGNOSTIC TESTS Published national anaphylaxis guidelines agree that 1 Diagnosis made on clinical findings. epinephrine is fundamental to acute management, although they do not agree on the initial dose or route MANAGEMENT of injection.12 The subcutaneous route and injecting Goals of Treatment in the opposite limb, when immunization is the cause, can also be used.13 –– Improve oxygenation –– Alleviate symptoms Epinephrine Dose in Children –– Prevent complications Calculations based on body weight are preferred when –– Prevent recurrence weight is known. When body weight is not known, –– Treat as a medical emergency and manage airway, the dose of epinephrine (1:1000) can be approximated breathing and circulation9 from the subject’s age (see Table 1, “Epinephrine Dose on the Basis of Age”).14 Early recognition and treatment of anaphylaxis is vital. Table 1 – Epinephrine Dose on the Basis of Age Nonpharmacologic Interventions Age Dose –– Place the client in a recumbent position 2–6 months* 0.07 mL (0.07 mg) (if tolerated), elevating the feet 12 months* 0.1 mL (0.1 mg) –– Establish an oral airway if necessary 18 months* to 4 years 0.15 mL (0.15 mg) 5 years 0.2 mL (0.2 mg) Adjuvant Therapy 6–9 years 0.3 mL (0.3 mg) Should anaphylaxis progressively become severe: 10–13 years 0.4 mL (0.4 mg) –– Give oxygen by mask, 10–12 L/min or more; ≥ 14 years 0.5 mL (0.5 mg) keep oxygen saturations > 97% to 98% *Doses for children between the ages shown are –– Start intravenous (IV) therapy with normal saline approximated (the volume being intermediate between or Ringer’s lactate to keep vein open, unless the values shown or increased to the next larger dose, severe anaphylaxis and signs of shock are evident; depending on practicability). see section “Shock” later on in this chapter for Source: Canadian Immunization Guide, 7th ed. details of fluid resuscitation in shock (Health Canada, 2006).

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Excessive doses of epinephrine can compound a Recommended Epinephrine Kit Contents patient’s distress by causing palpitations, tachycardia, The Canadian immunization guidelines suggest the flushing and headache. Although unpleasant, such side following content; regional policies may vary. effects pose little danger. Cardiac dysrhythmias may occur in older adults but are rare in otherwise healthy –– Copy of the anaphylaxis procedures and doses children and young adults. recommended of epinephrine and diphenhydramine for weight and age Some drugs can interfere with the efficacy of –– Two 1 cc syringes with attached needles (one epinephrine. Beta-blockers (for example, atenolol 25 gauge, 5/8" needle; one 25 gauge, 1" needle) and metoprolol) block the effects of epinephrine (and salbutamol). Patients taking beta-blockers –– 2 ampuls of epinephrine 1:1000 (check expiry date may have more severe anaphylactic reactions or monthly and replace once expired) reactions that are refractory to epinephrine. Glucagon –– 1 vial of diphenhydramine (pills or oral solutions (1–2 mg IV administered over 5 minutes in adults optional, check expiry date monthly and replace may be administered to counteract the effects of the once expired) beta‑blocker in such patients).14 –– One 25 gauge, 5/8" needle (extra) –– One 25 gauge, 1" needle (extra) Angiotensin converting enzyme inhibitors and 15 angiotensin II receptor blockers may also interfere –– 2 alcohol swabs (optional) with the effects of epinephrine and result in more Because anaphylaxis is rare, epinephrine vials and severe or prolonged symptoms.7 other emergency supplies should be checked regularly and should be replaced before they are outdated. In addition to epinephrine, the following medications may be administered depending on the circumstances: and Follow-up

7 Antihistamines Severe Anaphylaxis diphenhydramine hydrochloride (Benadryl) Monitor airway, breathing and circulation (ABC), vital for itching and hives 25–50 mg IV/IM in adults (1 mg/kg IV/IM to a maximum of 50 mg in children)7 signs and cardiorespiratory status every 15 minutes until client’s condition stabilizes. Diphenhydramine is an adjunct to rather than a substitute for epinephrine and Since 20% of anaphylaxis episodes follow a biphasic course of recurrence, the reaction after a 2–9 hour ranitidine 50 mg IV/IM in adults (1 mg/kg to a asymptomatic period, hospitalization or a long period maximum of 50 mg in children). Dilute in 5% of observation is recommended. For all but the mildest dextrose to a volume of 20 mL and inject over cases of anaphylaxis, patients should be hospitalized 5 minutes overnight or monitored for at least 12 hours.15 Corticosteroids7,14 Corticosteroids are commonly administered during Prevention anaphylactic reactions although there is little evidence If anaphylaxis is a potential recurrent risk, consider that they are of benefit. They are unlikely to be the use of an epinephrine self-injector (for example, helpful in the treatment of acute anaphylaxis, but Epipen or Twinject). Assess and educate potential may help to prevent biphasic or protracted reactions;7 users regarding the proper use and storage of the thus, preparation and administration of a dose of device.13 Consider having a personalized anaphylaxis corticosteroid should not take priority over prompt emergency action plan and an up-to-date medical administration (or re-administration) of epinephrine. identification.16 methylprednisolone 1–2 mg/kg/day IV/IM divided q6h Appropriate Consultation or Consult a physician as soon as client’s condition oral prednisone 0.5 mg/kg/day stabilizes; discuss use of IV steroids. Bronchodilator Referral salbutamol (Ventolin), via nebulizer 2.5–5 mg, repeat as necessary14 Medevac as soon as possible. In all but the mildest cases, clients with anaphylaxis should be hospitalized overnight or monitored for at least 12 hours.

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SHOCK HISTORY Shock is an acute widespread process of impaired –– Nausea tissue perfusion that results in cellular, metabolic and –– Lightheadedness, faintness hemodynamic alterations. Ineffective tissue perfusion –– Thirst occurs when an imbalance develops between cellular –– Loss of consciousness oxygen supply and cellular oxygen demand, which Other symptoms depend upon underlying cause. can occur for a number of reasons and eventually 17 result in cellular dysfunction and death. PHYSICAL FINDINGS Shock is categorized in many ways, for example, ABCs are the priority. according to the state of physiologic progression that has occurred: Physical findings depend on whether the client is in early or late shock. –– Compensated shock: vital organ perfusion is maintained by endogenous compensatory Early mechanisms Loss of approximately 15% to 25% of blood volume –– Decompensated shock: compensatory mechanisms is enough to cause significant signs and symptoms: have failed; associated with and impairment of tissue perfusion –– Tachycardia –– Irreversible shock: multiple end-stage organ failure –– Blood pressure normal and death occur, despite occasional return of –– Postural blood pressure drop present (orthostatic spontaneous cardiorespiratory function hypotension) Arterial blood pressure is often preserved by –– Narrowed pulse pressure compensatory vasoconstrictive mechanisms until –– Faint or weaker pulse very late in shock. An over-reliance on arterial blood –– Thirst pressure readings can delay recognition and timely –– Diaphoresis treatment of shock. –– Delayed capillary refill possible –– Anxiousness, restlessness TYPES OF SHOCK –– Tachypnea, increased respiratory depth17 –– Hypovolemic shock: inadequate perfusion of –– Decreased urine output17 vital organs results from a loss of circulating –– Pale cool skin17 or intravascular volume17 (hemorrhage, trauma, 17 gastrointestinal [GI] fluid loss) –– Jugular vein appears flat –– : due to the inability of the Late Hypovolemic Shock heart to pump blood to tissues (decreased cardiac output), as in congestive heart failure, myocardial Caused by loss of 30% to 45% of blood volume and ischemia can be life-threatening. –– : result from maldistribution of –– Hypotension circulating blood volume causing vasodilation. –– Tachycardia more pronounced It can be classified further as septic, neurogenic or –– Pulse weak and thready anaphylactic. Septic results from microorganisms –– Oxygen saturation decreased entering the body. Anaphylactic shock is the 17 result of a severe antibody-antigen reaction –– Respiratory distress 17 (histamine). is the result of loss –– Oliguria of sympathetic tone ()17 –– Skin becomes ashen, cold and clammy with 17 –– Obstructive (mechanical) shock: obstruction of marked, delayed capillary refill cardiac filling such as that caused by pericardial –– Confusion and decreased level of consciousness17 tamponade or tension pneumothorax Tachycardia is one of the early indicators of volume –– Dissociative shock: oxygen is not released from depletion. It may not be as apparent in elderly clients hemoglobin to the cells (as in carbon monoxide as in younger ones. Tachycardia may be mild if the poisoning) client is taking certain medications (for example, beta-blockers, calcium channel blockers).

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DIFFERENTIAL DIAGNOSIS –– Control any external bleeding; use direct pressure –– to control bleeding from external wounds –– Myocardial infarction –– Put in head-down position –– Pulmonary embolism Adjuvant Therapy –– Anaphylaxis –– Give oxygen at 10–12 L/min or more by –– Status asthmaticus non‑rebreather mask; keep oxygen saturation 18 –– Head, spinal injury > 97% to 98% 18 –– Drug-induced symptoms –– Start 2 large-bore IV lines (14- or 16-gauge or greater) with normal saline or Ringer’s lactate COMPLICATIONS –– Give 1–2 L IV fluid rapidly as a bolus over –– Cardiovascular: ventricular failure, microvascular 15 minutes thrombosis, angina, myocardial ischemia or –– Reassess for signs of continuing shock infarction17 –– If shock persists, continue to administer fluid –– Neurologic: sympathetic nervous system in 1 L boluses and reassess after each bolus dysfunction, cardiac and respiratory depression, –– Adjust IV rate according to clinical response thermoregulatory failure, coma17 –– Ongoing IV therapy is based on response to –– Pulmonary: acute respiratory failure, acute lung initial fluid resuscitation, continuing losses and injury17 underlying cause –– Renal: acute tubular necrosis, renal failure17 –– Aim for heart rate < 100 bpm, systolic blood –– Hematologic: disseminated intravascular pressure > 90 mm Hg coagulation17 –– Gastrointestinal: gastrointestinal tract failure, The amount of fluid required for resuscitation hepatic failure, pancreatic failure17 is difficult to predict on initial assessment. 17 –– Multi-system organ failure Caution in Cases of Internal Hemorrhage –– Death The use of large amounts of IV fluids in a client with uncontrolled internal hemorrhage from blunt or DIAGNOSTIC TESTS penetrating trauma may increase the internal bleeding –– Pulse oximetry (oxygen saturation) and ultimately lead to death. Administration of IV –– ABG, serum lactate, CBC, electrolytes, BUN, fluids while increasing blood pressure will also dilute Cr, glucose, PTT, INR, AST, ALT18 clotting factors and cause more hemorrhage. Use fluids judiciously to maintain peripheral perfusion. MANAGEMENT Early blood transfusion and surgical intervention to ABCs are the priority. achieve homeostasis is very important in this situation. After Initial Resuscitation Goals of Treatment –– Insert indwelling urinary catheter –– Restore circulating blood volume –– Insert a nasogastric tube prn –– Improve oxygenation of vital tissues –– Prevent ongoing volume losses Monitoring and Follow-Up –– Identify underlying cause17 –– Monitor ABC, vital signs (including pulse –– Identify and correct cause of lactic acidosis17 oximetry) and level of consciousness every –– Maintain surveillance for complications and 15 minutes until condition is stable provide comfort17 –– Frequent reassessment for continuing blood loss is important Nonpharmacologic Interventions –– Monitor hourly intake and urine output –– Assess and stabilize ABC –– Identify and manage underlying cause of –– Ensure that airway is patent and ventilation is adequate –– Assess stability of pre-existing medical problems –– Insert oral airway and ventilate with Ambu bag (for example, diabetes mellitus) (using oxygen) as needed

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Referral Long-Term Coma Care 19 Medevac as soon as possible. –– Provide eye care –– Protect skin integrity19 19 COMA (NOT YET DIAGNOSED) –– Initiate range of motion exercises Altered level of consciousness indicating diffuse or Adjuvant Therapy bilateral cortical impairment of cerebral function, –– Give oxygen (10–12 L/min) by mask; keep oxygen failure of brainstem-activating mechanisms (or both). saturation > 97% to 98% Coma is the deepest state of unconsciousness where –– Start IV therapy with normal saline to keep vein both arousal and awareness are lacking. Coma is a open, unless there is evidence of shock (see section symptom, not a disease, and occurs as a result of some “Shock” in this chapter) underlying process.19 Pharmacologic Interventions CAUSES Rapidly administer: –– Bilateral cortical disease thiamine, 100 mg IV (to prevent Wernicke-Korsakoff –– Compromise of reticular-activating system encephalopathy) Causes of coma can also be divided into structural and or surgical and metabolic or medical: dextrose 50%, 25–50 mL preloaded IV (to treat –– Structural or surgical causes: ischemic stroke, hypoglycemia) intracerebral hemorrhage, trauma and brain Do not withhold dextrose if thiamine is not available. tumours19 A single dose of dextrose will not induce Wernicke- –– Metabolic or medical causes: drug overdose, Korsakoff encephalopathy. infection, endocrine disorder, poisoning19 For patients with signs and symptoms of opioid See “Differential Diagnosis” in this section. intoxication give:20,21 INITIAL APPROACH TO CLIENT WITH naloxone (Narcan), 0.4–2 mg IV, SC or IM to treat COMA OF UNKNOWN ORIGIN potential narcotic overdose (start with 2 mg; if no response in 3–5 minutes, give an additional 4 mg) Perform primary survey (see “Primary Survey” under the section “Responding to General Emergencies and Anticonvulsant therapy may also be necessary Major Trauma” in the pediatric Chapter 20, “General to prevent further ischemic injury to the brain.19 Emergencies and Major Trauma”). Restrain the client if you suspect that naloxone may The can help identify the level precipitate narcotic withdrawal. of consciousness (see “Glasgow Coma Scale” under If unsure whether naloxone is necessary discuss with the section “Head Trauma” in this chapter). a physician before administering. MANAGEMENT Once the immediate life-threatening concerns have been addressed, the secondary survey can be carried Nonpharmacologic Interventions out (see “Secondary Survey” under the section “Responding to General Emergencies and Major Acute Coma Trauma” in the pediatric Chapter 20, “General –– Assess and stabilize ABC Emergencies and Major Trauma”). –– Assess changes in neurologic status19 –– Monitor vital signs, including pulse oximetry –– Stabilize cervical neck until traumatic injury is ruled out19 –– Obtain abbreviated, targeted history –– Maintain surveillance for complications19 –– In particular, determine if person has had any recent illness, antecedent fever, rash, vomiting or –– Insert oral airway trauma or has any chronic illnesses; explore recent –– Place in recovery position, unless there are exposure to infection, medication or intoxicants contraindications –– Check finger-stick glucose Past medical history and family history should be obtained when time permits.

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Observations in the secondary survey should attempt With cerebral lesions, the eyes will deviate toward to uncover signs of occult infection, trauma or toxic or the side of the lesion, whereas with brainstem lesions, metabolic derangements. Signs suggestive of specific the eyes deviate away from the lesion. toxidromes should be sought (see section “Overdoses, About 5% of the normal population has anisocoria Poisonings and Toxidromes” in this chapter). (asymmetric pupils). PHYSICAL FINDINGS A brief funduscopic exam may reveal papilledema or retinal hemorrhage. Level of Consciousness Assess level of consciousness using the Glasgow Motor Examination Coma Scale (see “Glasgow Coma Scale” under –– Evaluation of motor function focuses on two areas: the section “Head Trauma” in this chapter). 1) evaluation of muscle size and tone and; 2) estimation of muscle strength19 Respiratory Status –– Muscle tone is assessed for signs of flaccidity, Respiratory status focuses on the evaluation of two hypotonia, hypertonia, spasticity or rigidity19 things: 1) respiratory pattern and 2) airway status.19 –– Try to elicit motor response to verbal or physical stimuli Respiratory Pattern –– Assess muscle tone, strength and reflexes for –– Control of breathing is centered in the brain, lower normality and symmetry pons and medulla and is modulated by the cortical –– Ability of client to localize, as well as absence or centres in the forebrain presence of abnormal posture, helps in assessment –– Respiratory abnormalities signify either metabolic of severity of involvement derangement or neurologic insult –– Several patterns exist (for example, Cheyne-Stokes Classifications of abnormal posturing include: respiration, apneustic breathing, post-ventilation –– Spontaneous: occurs without regard to external apnea, cluster, ataxic, central neurogenic stimuli and possibly not by request19 19 hyperventilation) –– Localization: occurs when extremity opposite to Airway Status the extremity receiving stimuli crosses the midline to remove the noxious stimuli19 Airway maintenance, secretion control, cough, gag and swallow reflexes responsible for airway protection19 –– Withdrawal: occurs when the extremity receiving the stimuli flexes normally in order to avoid the 19 Ocular Findings noxious stimuli –– Decorticate posturing (flexion of the upper Pupillary Function extremities with extension of the lower extremities) –– Focuses on three areas: 1) estimation of pupil size suggests involvement of the cerebral cortex and and shape; 2) evaluation of pupillary reaction to subcortical white matter 19 light and; 3) assessment of eye movement –– Decerebrate posturing (rigid extension of the –– Remember that dilatation of pupils may be arms and legs) usually represents added brainstem secondary to topical or systemic drugs involvement at the level of the pons –– Dilatation of pupils in an alert person is not likely attributable to increased intracranial pressure and herniation –– Dilatation of pupils in an unconscious patient may herald imminent uncal herniation –– Small reactive pupils generally indicate metabolic problem or diencephalic lesion –– Unilateral, dilated, fixed pupils indicate lesion of third nerve or uncal lesion –– Bilateral pinpoint pupils indicate pontine lesion –– Pupils fixed in midposition indicate midbrain lesion –– Bilateral large, fixed pupils indicate tectal lesion

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DIFFERENTIAL DIAGNOSIS MANAGEMENT

Coma with no localizing central nervous system signs Nonpharmacologic Interventions may be caused by: –– Nothing by mouth –– Metabolic insult, including hypoglycemia, –– Insert nasogastric tube unless there is suspicion uremia, Addison’s disease, diabetic ketoacidosis, of associated basilar skull fracture or facial trauma hypothyroidism, liver disease –– Insert Foley catheter –– Children and young adults will often experience hypoglycemia and may present with coma after Pharmacologic Interventions ingesting alcohol, including alcohol-containing mouthwashes If you suspect meningitis, do not withhold antibiotics. Antibiotics should be started before the client goes –– Respiratory problems, including hypoxia, to the hospital. Discuss with physician. If unable to hypercapnia contact physician within a reasonable time frame, –– Intoxication, including that caused by initiate the following: barbiturates, alcohol, opiates, carbon monoxide, benzodiazepines For adults, antibiotics:22,23 –– Infections (severe, systemic), including sepsis, ceftriaxone (Rocephin) or cefotaxime 2 g IV stat pneumonia, typhoid fever plus –– Shock, including hypovolemic, cardiogenic, septic, anaphylactic vancomycin 1 g IV stat –– Epilepsy Vancomycin should be infused by infusion pump no –– Hypertensive encephalopathy more rapidly than 1 g/hour to avoid a characteristic –– Hyperthermia (heat stroke), hypothermia infusion reaction associated with rapid, uncontrolled administration. Coma with meningeal irritation but without localizing signs may be caused by: Monitoring and Follow-Up –– Meningitis Monitor ABC, vital signs, pulse oximetry, level of –– Subarachnoid hemorrhage from ruptured consciousness, respiratory status and sensory motor aneurysm, arteriovenous malformation deficits every 15 minutes until stable. Coma with focal brainstem or lateralizing signs may Appropriate Consultation be caused by: Consult a physician as soon as possible, once –– Pontine hemorrhage the client’s condition has stabilized. –– Stroke (cerebrovascular accident [CVA]) –– Brain abscess Referral –– Subdural or epidural hemorrhage Medevac as soon as possible. Coma in which client appears awake but is unresponsive may be caused by: OVERDOSES, POISONINGS –– Abulic state: frontal lobe function depressed, AND TOXIDROMES so client may take several minutes to answer a question DEFINITION –– Locked-in syndrome: destruction of pontine motor Ingestion of a substance in sufficient quantity to tracts; is able to look upward induce symptom complexes associated with toxic –– Psychogenic state: unresponsive effects. Poisoning is an exposure to an amount of substance that is likely to produce untoward effects DIAGNOSTIC TESTS in an individual.24 If poisoning is suspected contact –– Determine blood glucose level your poison control centre for management.

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SPECIFIC POISONINGS AND Salicylates (for example, Aspirin [ASA]) CLINICAL TOXIDROMES Main toxic effects: tinnitus, nausea, vomiting, Opiates hyperventilation (primary respiratory alkalosis) metabolic acidosis, hallucinations, stupor, cerebral –– Examples: heroin, morphine, codeine, edema, oliguria, renal failure, hemorrhage, diphenoxylate (Lomotil) cardiovascular failure,27 fever, hypokalemia, –– Toxidrome characterized by sedation, hypotension, hypoglycemia, seizures and coma. bradycardia, respiratory depression, usually Many patients are misdiagnosed on initial presentation pinpoint pupils (may not be present with mixed as having sepsis or gastroenteritis (because of fever, overdose), somnolence progressing to stupor or acidosis, vomiting and other symptoms). This coma, flaccidity of skeletal muscle, cold clammy misdiagnosis is particularly common in the elderly. skin, apnea, circulatory collapse, cardiac arrest and convulsions (may occur in children)25 For treatment, see section “Management of Specific For treatment, see section “Assessment and Overdoses and Toxidromes” in this chapter, including Management General Approach” in this chapter, the management specific to salicylates. including the management specific to opiates. Acetaminophen (Tylenol)28 Petroleum Distillates Main toxic effects are hepatic. –– Examples: gasoline, fuel oil, model airplane glue –– Symptoms may progress in a sequential 3-phase –– Main toxic effect: pulmonary (from inhalation) pattern and include from anorexia, nausea and general malaise to confusion, stupor, For treatment, see section “Management of Specific hepatic necrosis, jaundice, coagulation defects, Overdoses and Toxidromes” in this chapter, including hypoglycemia and encephalopathy28 the management specific to petroleum distillates. –– The first begins shortly after ingestion and lasts Tricyclic Antidepressants for 12–24 hours. Client may have nausea and vomiting, anorexia, diaphoresis, pallor and general –– Main toxic effects: cardiac arrhythmias, malaise anticholinergic effects (see Toxidrome for opiate –– If toxicity continues there is a latent phase of up poisoning), vomiting, hypotension, confusion and to 48 hours (during this second phase the patient seizures may feel better; however, hepatotoxicity is ongoing –– Cardiac complications: prolonged QRS and QT as evidenced by increasing hepatic enzymes (ALT intervals, other arrhythmias, sinus tachycardia, and AST), bilirubin, PTT, INR widening QRS complex, prolonged PR intervals, –– Symptoms of third phase depend on the severity right bundle branch and AV block, ventricular of hepatic damage and usually occur from 3–5 days tachyarrhythmias (including torsades de pointes after overdose and fibrillation)26 –– Neurologic complications: agitation, seizures For treatment, see section “Management of Specific –– Patients may occasionally become hypothermic26 Overdoses and Toxidromes” in this chapter, including the management specific to acetaminophen. –– Hypotension: Treat initially with IV fluids (see section “Shock” in this chapter) The client may appear fine and then rapidly deteriorate. He or she will need to be admitted to a monitored unit. Be prepared to manage the client’s airway. Even if the client is asymptomatic 6 hours after ingestion, he or she must be admitted to hospital for psychiatric examination. Minimize external stimulation to reduce the risk of seizures.26 For treatment, see section “Management of Specific Overdoses and Toxidromes” in this chapter, including the management specific to tricyclic antidepressants.

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Caustic Agents ASSESSMENT AND MANAGEMENT: GENERAL APPROACH –– Examples: alkaline (drain cleaner), bleach and battery acid (household bleach is usually not a First priority is ABC. problem, except for superficial burns), ethylene –– Insert IV and administer 500 mL of 0.9% saline glycol (major constituent in antifreeze)24 solution if patient hypotensive. Up to 1000 mL –– Main toxic effects: local tissue necrosis of the can be infused if hypotension persists24 esophagus with alkali and of the stomach with –– If advised to do so by poison control, induce acids, as well as respiratory distress; obvious facial vomiting by pharyngeal stimulation24 or oral burns and emesis; hoarseness and stridor reflecting epiglottic edema (especially with acids), –– Remember to decontaminate the gastrointestinal headache, hypotension, metabolic acidosis, shock, tract, any clothing, skin and environment (see renal failure, hypocalcemia and central nervous “Gastrointestinal Decontamination” in this section) system damage24 –– If client is unconscious, see section “Coma (Not Yet Diagnosed)”, in this chapter For treatment, see section “Management of Specific –– Determine to the best of your ability what was Overdoses and Toxidromes” in this chapter, including ingested the management specific to caustic agents. –– For any client with overdose, draw blood sample Carbon Monoxide for determination of serum acetaminophen level (see section “Management of Specific Overdoses Main toxic effects:29 and Toxidromes” in this chapter, including –– Central nervous system: headache (the most management specific to acetaminophen) common presenting symptom), dizziness, fatigue, –– Contact the nearest poison control centre for confusion. Syncope, coma, and seizures may occur further information about the toxin in question in severe cases Appropriate Consultation –– Gastrointestinal: nausea –– Other: arrhythmias and cardiac ischemia are Consult a physician as soon as you are able after the possible initial assessment and stabilization of ABC. Discuss –– Diagnosis: clinical background (for example, management with regional poison control centre. exposure to furnace or car exhaust [especially in children who have been riding in the back of Gastrointestinal Decontamination pick-up trucks with enclosed “caps”]); level of Activated Charcoal carboxyhemoglobin needed to confirm –– Treatment of choice in most overdoses involving Arterial oxygen saturation as measured by pulse ingestion. It is most effective if administered within oximetry is frequently normal in cases of carbon one hour of ingestion monoxide poisoning. –– May be indicated for overdose with For treatment, see section “Management of Specific acetaminophen, theophylline, tricyclic Overdoses and Toxidromes” in this chapter, including antidepressants, phenobarbital, phenytoin, digoxin the management specific to carbon monoxide. –– Does not work for metals such as iron or lithium –– Administer 10–25 g for children, 50–100 g for Cocaine adults (1 g/kg) suspended in 300 mL of water Main toxic effects: seizures, hypertension, –– If client will drink the mixture, this mode of tachycardia, paranoid behaviour or other alterations administration is acceptable; otherwise, administer in mentation, rhabdomyolysis, myocardial infarction by nasogastric tube and stroke (CVA), hepatic necrosis, liver and renal –– 30% of clients will vomit after administration failure.24 of charcoal; in this case, charcoal can be administered again For treatment, see section “Management of Specific –– May cause constipation and charcoal impaction24 Overdoses and Toxidromes” in this chapter, including the management specific to cocaine.

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Gastric Lavage Naloxone produces acute withdrawal from opiates Discuss with physician first. A poison control centre and may precipitate shock, seizures, arrhythmias, should also be consulted. hypertensive crisis, pulmonary edema and intractable ventricular fibrillation.24 –– Lavage alone is not adequate for gastric emptying and delays administration of charcoal Petroleum Distillates –– Not usually indicated especially if benzodiazepines, phenytoin or antibiotics have –– Do not perform lavage or induce vomiting been ingested because minimum lethal doses if swallowed of these agents is so high24 –– If no symptoms within 6 hours, no need for further –– Not effective beyond 1.5 hours after ingestion, observation but can be tried in severely ill clients in selected Tricyclic Antidepressants situations –– Use largest nasogastric tube or orogastric tube –– There is no specific antidote for an overdose –– Instil 300 mL aliquots of saline, then remove until of tricyclic antidepressants saline is clear on removal or until 5 L of fluid has –– Avoid emesis (client may aspirate) been used for irrigation –– Supportive therapy; charcoal may be used –– Airway protection is recommended (client should on the advice of a poison control centre (see be fully conscious and cooperative) “Gastrointestinal Decontamination” in this section) –– Aspiration is a common, serious complication –– Client may appear fine and then rapidly deteriorate of up to 10% of patients –– Client should be admitted to a monitored unit –– Be prepared to manage client’s airway MANAGEMENT OF SPECIFIC –– If client is asymptomatic 6 hours after ingestion, OVERDOSES AND TOXIDROMES he or she should still be admitted to hospital for psychiatric evaluation and care Opioids –– Cardiac complications: prolonged QRS, Naloxone is a specific antidote for opiate poisoning. QT interval, other arrhythmias Toxic dose varies with the specific drug and an –– Neurologic complications: agitation, seizures individual’s prior history of opioid use. –– Seizures usually brief and self-limited; treat as Use naloxone with caution in those who are narcotic outlined in “Status Epileptic (Acute Grand Mal addicts, as it may precipitate acute opiate withdrawal. Seizure)” (see section “Status Epileptic (Acute If this is a concern, the client’s airway must be Grand Mal Seizure)” in the adult Chapter 8, supported until the narcotic wears off. “Central Nervous System”) Always observe the client until there is no chance –– If hypotension occurs, treat initially with IV fluids of further respiratory depression. This is especially (see section “Shock” in this chapter) important with naloxone, which has a relatively short Salicylates (for example, Aspirin [ASA]) elimination half-life (1.1 hours) and an even shorter clinical effect (10–30 minutes).24 This means that –– There is no specific antidote for an overdose patients must be monitored closely should naloxone of salicylates successfully reverse the effects of an opiate overdose. –– Toxic dose: > 300 mg/kg is associated with mild symptoms; ingestions of 300–500 mg/kg Naloxone (Narcan), IV (usually start with 0.4–2 mg in moderately toxic and ingestions of > 500 mg/kg adults); dose may be repeated if needed, at 2 to 3 min are otentially lethal30 intervals. –– IV administration of normal saline to maintain If no response after 10 mg IV, re-evaluate diagnosis blood pressure (see section “Shock” in this chapter) of narcotic overdose. –– IV glucose24 Client may have recurrent narcotization when –– Sodium bicarbonate and hyperventilation to naloxone wears off. correct metabolic and respiratory acidosis (moderate toxicity)24 –– Sodium bicarbonate also results in urine alkalinization which promotes excretion of salicylates

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Acetaminophen (Tylenol) Carbon Monoxide N-acetylcysteine (Mucomyst) is the specific antidote –– Administration of 100% oxygen (to displace for acetaminophen overdose. carbon monoxide from hemoglobin) Toxic dose:31 –– Even if client seems well when seen or is recovering from the central nervous system (CNS) –– Single ingestions of < 150 mg/kg in a child or insult, hyperbaric chambers have been shown to < 7.5–10 g in an adult are unlikely to be toxic reduce long-term sequelae; therefore transfer client –– Single ingestions of > 250 mg/kg or > 12 g in an to hospital adult over a 24-hour period are likely to be toxic –– Single ingestions of > 350 mg/kg are likely to Cocaine result in serious hepatotoxicity There is no specific antidote for cocaine intoxication. –– Unintentional overdose (for example, from use of –– Cocaine has a relatively short half-life, so most several acetaminophen-containing products), liver symptoms are short-lived unless a serious disease and alcohol use/abuse increase the risk complication such as a CVA or MI occurs of hepatotoxicity32 –– For coronary vasospasm, hypertension or –– An acetaminophen level 4 hours post ingestion tachycardia, observation is probably adequate, is a good predictor of toxicity because of the short half-life If ingestion is in toxic range (or if ingested quantity –– For other cases, treat as for myocardial infarction is unknown or cannot be verified), treat with: –– Myocardial infarction and CVA may occur up to N-acetylcysteine (Mucomyst) 20%, 140 mg/kg PO 72 hours after cocaine use and then 70 mg/kg every 4 hours for 17 doses –– Concurrent use of alcohol increases the likelihood (total duration of treatment = 72 hours) of coronary vasospasm –– Repeat any doses vomited within 1 hour –– Do not administer beta-blockers to treat cocaine- of administration related cardiovascular complications because –– N-acetylcysteine may also be administered by IV the combination can result in unopposed alpha- (especially in patients who cannot tolerate oral adrenergic-induced vasoconstriction and end-organ administration)32 ischemia33 –– Do not withhold N-acetylcysteine even if Not all chest pain represents myocardial infarction 24–26 hours after ingestion; late administration, (for example, pneumomediastinum in crack use, though not as effective as early administration, bronchospasm). still reduces mortality –– Seizures are generally self-limited but will respond –– Charcoal use is acceptable in acetaminophen to normal seizure treatment (see section “Status overdose and only minimally interferes with Epileptic (Acute Grand Mal Seizure)” in the adult N-acetylcysteine; charcoal should be given early Chapter 8, “Central Nervous System”) and N-acetylcysteine at least 4 hours later –– CNS symptoms such as agitation and paranoia can Caustic Materials be treated with diazepam (Valium) or lorazepam (Ativan) –– Do not induce emesis or perform lavage –– Charcoal is not indicated Monitoring and Follow-Up –– If the client has visible oral burns, he or she has a Monitor ABC, level of consciousness, vital signs, 50% chance of distal burns of significance (that is, oxygen saturation, intake and urine output frequently esophageal or gastrointestinal; however, absence of until the client is stable. visible lesions does not rule out significant injury (10% to 30% will have burns beyond the mucosa) Referral Medevac as soon as possible.

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HYPOTHERMIA PHYSICAL FINDINGS Core temperature of ≤ 35°C (95°F). Core temperature In the cold client, rectal temperature is one of the below 32°C predisposes patients to ventricular vital signs. fibrillation, which could be preceded by ECG changes In terms of the ABCs, think A, B, C and D for such as QT-interval prolongation, T-wave inversion hypothermic clients: and atrial fibrillation.23 –– A for airway RISK FACTORS34 –– B for breathing –– Age (pediatric patients related to inability to shiver –– C for circulation and decreased body fat; elderly patients related –– D for degrees (body-core temperature) to high incidence of cardiovascular disease and In the cold client, body-core temperature is an decreased body fat) important sign. Although obtaining the body-core –– Endocrine or metabolic derangements temperature is useful for assessing and treating (for example, hypoglycemia) hypothermia, there is tremendous variability –– Infection (for example, meningitis, sepsis) in individual physiologic responses at specific –– Intoxication temperatures. –– Traumatic injury and shock (head injury, major burns) Assessment of Temperature –– Environmental exposure Axillary and oral measurements are poor measures –– Iatrogenic (cold IV fluids, exposure during of core temperature. Rectal temperature more closely treatment) approximates the core temperature and is a practical method for use in the field. Medications (such as phenothiazine, neuromuscular blocking agents, which interferes with the patient’s For clients with cold skin, rectal temperature should ability to shiver;36 clonidine and antipsychotic agents) be determined with a low-reading thermometer may increase the risk of accidental hypothermia.35 (that is, capable of measuring temperatures as low as 21°C). HISTORY Core Temperature 35°C to 36°C The evaluation and treatment of hypothermia is –– Client feels cold, is shivering essentially the same whether the client is wet or dry, on land or in water. Core Temperature 32°C to 35°C –– One or more of above risk factors –– Slowing of mental faculties –– The hypothermic client should be assessed –– Slurred speech carefully for coexisting injury or illness –– Mild incoordination –– Signs and symptoms of hypothermia may be –– Muscle stiffness mimicked by alcohol, diabetes mellitus, altitude –– Inappropriate judgment sickness, overdose and other conditions; therefore, –– Irritability thorough assessment is imperative –– Shivering apparent –– Associated significant illness or injury may exacerbate hypothermia Core Temperature 32°C –– Shivering stops The hypothermic client may appear “beyond help” because of skin colour, pupil dilatation and Core Temperature ≤ 31°C depression of vital signs. However, people with –– Semi-comatose severe hypothermia have been resuscitated. Therefore, –– Progressive decrease in level of consciousness be cautious about assuming that the client cannot –– Coma likely at temperatures ≤ 30°C be resuscitated. It is also wise to be cautious about –– Cyanosis what you say during the resuscitation. Seemingly unconscious patients frequently remember what is –– Tissue edema said and done.

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Core Temperature 29°C –– Client frozen (for example, formation of ice –– Respiratory activity slow, may be difficult to detect in airway) –– Heart rate slow; pulse may be difficult to palpate –– Chest wall so stiff that compression is impossible –– Rescuers are exhausted or in danger Core Temperature ≤ 28°C –– Vital signs absent Rise in core temperature may lag behind change –– Pupils dilated and unresponsive in skin temperature and may continue to drop, so monitor rectal temperature frequently. –– Respiratory arrest –– Ventricular fibrillation Basic Treatment for All Cases of Hypothermia MANAGEMENT Prevent further heat loss: insulate from the ground, protect from the wind, eliminate evaporative heat Goals of Treatment loss by removing wet clothing or by covering client with a vapor barrier (such as a plastic garbage bag), –– Rewarm core slowly cover the head and neck, and move the client to a –– Minimize heat loss35 warm environment; consider covering client’s mouth –– Prevent or manage complications and nose with light fabric to reduce heat loss through respiration. Maintain supine position and avoid General Principles unnecessary manipulation.35 The client with severe hypothermia must be handled very gently. The cold heart is highly prone to Mild Hypothermia cardiac arrest, and even cautious movement of the Rewarm passively and gradually: client may induce cardiac arrest. Resuscitation and Step 1: Place client in as warm an environment rewarming are the mainstay of treatment. Rewarming as possible. takes precedence once initial resuscitation has been initiated. The three progressive modalities of Step 2: Increase heat production through exercise rewarming are passive external rewarming, active (without sweating) and fluid replacement with high- external rewarming and active core rewarming.35 calorie, warm, sweet fluid; this method of adding heat is particularly important when emergency care is not –– Carefully remove all wet garments readily available, as in remote or prolonged-transport –– Ensure that any items, oxygen or fluids (both oral environment. and IV) coming into contact with the client are warmed beforehand Step 3: Rewarm passively through application of –– Oxygen should be heated to 40.5°C to 42.2°C insulated heat packs to high heat transfer-loss areas (105°F to 108°F) and humidified, if possible such as the head, neck, underarms, sides of the chest wall and groin; apply heavy insulation to the same –– Because cold skin is easily injured, avoid direct areas to prevent further heat loss (goal is to increase application of hot objects or excessive pressure temperature by 1°C to 2°C per hour). (for example, uninsulated hot water bottles) –– The inside of a vehicle and any rooms where Step 4: Consider warm shower or bath if the client hypothermic clients are treated should be warm is alert. enough to prevent further heat loss (ideally above Do not leave client alone. 26.7°C [80°F]) –– Splinting should be performed, when indicated Severe Hypothermia with Signs of Life and with caution, to prevent additional injuries (for example, Pulse and Respiration) to frostbitten tissues Treat the client as outlined in steps 2 and 3 above, –– Do not give caffeine or alcohol with the following exceptions: Cardiopulmonary resuscitation (CPR) has no –– Do not put a severely hypothermic client in a significant effect on survival of hypothermic clients shower or bath in the following situations and should not be initiated: –– Do not give a client fluids by mouth unless he or she –– Cold-water submersion for > 1 hour is capable of swallowing and protecting the airway –– Core temperature < 15.5°C (60°F) –– Treat hypothermic clients very gently (do not rub or manipulate or apply direct heat to extremities) –– Obvious fatal injuries

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In addition, the following measures should be taken: –– Clients with moderate-to-severe hypothermia may have large amount of fluid sequestration and may –– Reassess ABC and vital signs frequently need aggressive fluid resuscitation; an initial bolus –– Give warm, humidified oxygen at 10–12 L/min or of 1–2 litres is indicated; repeat as necessary more by non-rebreather mask –– Rewarm passively as outlined above –– Administer warmed (to 37–40°C) normal saline by IV –– Clients with moderate-to-severe hypothermia may No drugs are used in resuscitation unless core have a large amount of fluid sequestration and may temperature > 30°C and drugs are ordered by need aggressive fluid resuscitation; an initial bolus a physician. of 1–2 litres is indicated; repeat as necessary, but do not overload with IV fluids Consultation If resuscitation has been provided in conjunction Severe Hypothermia with No Signs of Life with rewarming techniques for more than 60 minutes –– If no pulse (after checking for up to 45 seconds), without the return of spontaneous pulse or respiration, no respiration and no contraindications, start CPR continue efforts but contact the physician for unless contraindicated recommendations. –– Ventilate with Ambubag with 50% warm, humidified oxygen; aim for 12–15 ventilations and Referral 80–100 compressions; continue as long as you can Medevac as soon as possible. –– Administer warmed (to 37–40°C) normal saline by IV

MAJOR TRAUMA SITUATIONS

HEAD TRAUMA –– Brain injuries: –– Concussion: no significant injury to brain, Head injury is often associated with motor vehicle brief period of unconsciousness then return accidents, falls, violence and sports injuries. Severe to normal; short-term retrograde amnesia, head injury can lead to secondary brain damage dizziness, headache, nausea, ringing in ears from cerebral ischemia resulting from hypotension, –– Cerebral contusion: prolonged unconsciousness hypercapnea and raised intracranial pressure.35 It can or serious alteration in level of consciousness; also be defined as blunt, forceful injury to the soft may have focal neurologic signs. Usually related tissues or bony structures of the scalp, skull or brain. to acceleration-deceleration injuries resulting The initial response of the bruised brain is swelling. in hemorrhage into the superficial parenchyma, Bruising causes vasodilation through increased blood often the frontal and temporal lobes36 flow to the injured area; because there is no extra –– Intracranial hemorrhage: bleeding into brain space within the skull, an accumulation of blood takes tissue up space and exerts pressure on the surrounding brain –– Acute epidural hematoma: bleeding between the tissue. This pressure results in deceased blood flow to dura and the skull (collection of blood between uninjured areas of the brain. Cerebral edema does not the inner table of the skull and the outermost occur immediately but develops over 24–48 hours. layer of the dura). Most often associated with Early efforts to decrease the initial vasodilation in the skull fractures, meningeal artery lacerations injured area can save the person’s life. or skull fractures and venous bleeding38 –– Acute subdural hemorrhage: bleeding between TYPES OF HEAD INJURIES the dura and arachnoid associated with –– Scalp wounds (lacerations) underlying brain injury. Most often related –– Skull injury (fracture) to a rupture in the bridging veins between the cerebral cortex and the dura. Also caused by acceleration-deceleration and rotational forces38

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HISTORY AND PHYSICAL FINDINGS Other Aspects

Low-Risk Injuries The initial neurologic assessment is critical as a baseline. –– Criteria: Minor trauma, scalp wounds, no signs of intracranial injury, no loss of consciousness. –– Head injury is frequently associated with other Glasgow Coma Scale (GCS) score of 13 to 15 with severe trauma a loss of consciousness that lasts up to 15 minutes38 –– Hypotension in adults is never caused by an –– Treatment: Observation for any sign or symptom isolated head injury, except if the client is near of rain injury; must discharge to a reliable observer death; look for other injuries, including spinal who will continue observation at home cord injuries –– Physical examination should include a complete Moderate-Risk Injuries neurologic exam, as well as inspection for evidence of basilar skull fracture (for example, –– Criteria: Symptoms consistent with intracranial CSF rhinorrhea, Battle’s sign, raccoon eyes, injury, including vomiting, transient loss of hemotympanum) consciousness, severe headache, post-traumatic seizures, amnesia, evidence of basilar skull fracture –– Assume injury to the cervical spine in all cases (cerebrospinal fluid [CSF] rhinorrhea, Battle’s of head trauma sign, raccoon eyes, hemotympanum, non-focal –– Remember that multiple trauma may be present neurologic signs), GCS score of 9 to 12 with a In cases of head injury, the clinical picture will evolve. 38 loss of consciousness for up to 6 hours The client is either improving or deteriorating over –– Patients are at a high risk for deterioration from time; frequent reassessment is therefore critical. increased cerebral edema and intracranial pressure and as such serial clinical assessments are Glasgow Coma Scale necessary38 The Glasgow Coma Scale is used to assess the severity of coma (see Table 2, “Scoring for the High-Risk Injuries Glasgow Coma Scale”). –– Criteria: Depressed level of consciousness, focal neurologic signs and penetrating injury of skull or –– Assess client frequently palpable, depressed skull fractures. GCS score of –– Monitor for a drop in the score 8 or less after resuscitation or those who deteriorate –– Any drop in the score is a danger sign to that level within 48 hours

Table 2 – Scoring for the Glasgow Coma Scale* Eye-Opening Best Motor Response Best Verbal Response Response Score Response Score Response Score Obeys commands 6 Localizing response to pain 5 Oriented 5 Spontaneous 4 Withdrawal response to pain 4 Confused 4 Abnormal flexion Inappropriate To voice 3 3 3 (decorticate rigidity) words Abnormal extension Incomprehensible To pain 2 2 2 (decerebrate rigidity) sounds None 1 None 1 None 1 *Score is obtained by determining the score for each of the three criteria (eye-opening, best motor response, best verbal response) and summing them. Record scores individually, for example E2M4V3 for a total score of 9. Sources: Young B. (2009). Stupor and coma in adults. Available by subscription: www.uptodate.com Jarvis C. Physical examination and health assessment. 3rd ed. Philadelphia, PA: W.B. Saunders; 2000. p. 732.

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Interpretation of Score Step 1 –– Score < 9: severe head injury –– Secure the airway and provide supplemental –– Score 9–12: moderate head injury oxygen at 10–12 L/min by non-rebreather mask –– Score 13–15: minor head injury –– Hyperventilate the client at 24 breaths/min with The Glasgow Coma Scale is not useful for the a bag-valve mask device41 to maintain adequate diagnosis of coma and may be unreliable in children. oxygenation and reduce intracranial pressure However, it has good interobserver reliability and is –– Once airway and breathing are secure, assess easy to use. The GCS on admission to a tertiary care and manage any uncontrolled hemorrhage using centre has been linked to prognosis prediction for a direct pressure41 number of conditions including traumatic brain injury, –– Assess neurologic status41 subarachnoid hemorrhage and bacterial meningitis. Step 2 Intubation and use of sedating drugs interfere with its utility; for this reason, it is useful to obtain a GCS –– Stabilize client on a spine board prior to these interventions.21 –– The neck should be immobilized in a rigid collar 41 Coma by definition has no eye-opening, no ability and a padded head immobilization device to follow commands and no word verbalization. –– Nurse in head-up position unless contraindicated (for example, in cases of shock or back injury) COMPLICATIONS –– Avoid tight cervical collar (any pressure on the –– Seizures external jugular veins will increase the intracranial pressure) –– Vomiting –– Shock Step 3 –– Record baseline observations DIAGNOSTIC TESTS –– Record blood pressure, respirations, PERRLA None. (pupils equal, round, reactive to light; accommodation normal), sensation and voluntary MANAGEMENT motor activity Minor Head Trauma Step 4 –– Characteristics: No signs of intracranial injury, –– Do serial Glasgow Coma Scale assessments no loss of consciousness Step 5 –– Treatment: Observe for 12–24 hours for any sign or symptom of brain injury; discharge to a reliable –– Monitor and record the above observations observer who will continue observations at home frequently Step 6 Major Head Trauma –– Start IV therapy to keep vein open, unless client In the pre-hospital setting, a major head trauma is hypotensive will require the critical tasks of an examination to recognize severe injuries with potential to cause –– Fluids are generally restricted in clients with rapid decompensation, stabilization for transport closed-head trauma to a tertiary care centre and triage if multiple –– Maintain normal cardiac output victims are involved.37 The principles of assessment –– If hypotensive, suspect hemorrhage or spinal injury and management for trauma apply (see “Primary (see section “Shock” in this chapter) Survey” and “Secondary Survey” under the section Step 7 “Responding to General Emergencies and Major Trauma” in the pediatric Chapter 20, “General –– Insert Foley catheter if client is unconscious Emergencies and Major Trauma”). –– Monitor urine output hourly Remember, ABC (airway, breathing and circulation), Step 8 in addition to D (disability [neurologic status]) and –– Consult a physician as soon as able E (exposure), need to be addressed.37 The order is important.

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Step 9 incontinence, paralytic ileus, immediate loss of all sensation and reflex activity below the level –– Medevac as quickly as possible of the injury. –– Review recommended precautions for flight for a person with head injury (see the “ Emergency CAUSES Medical Transportation Guidelines for Nurses in Primary Care” in chapter 4 “Primary Care During –– Motor vehicle accident Transport”, section “CNS”, “Head Trauma” –– Falls [Medical Services Branch, 1985]) –– Sports –– Acts of violence Increased Intracranial Pressure –– Elevate head of bed by 30° HISTORY –– Hyperventilate, as above Traumatic Event and Mechanism of Injury38 –– Prevent hyperthermia in the patient using antipyretics and cooling (to prevent an increase In a traumatic spinal cord injury (SCI), the history, in cerebral metabolic rate related to increased body including the mechanism of injury, can provide clues temperature)38 to the pathophysiology of the injury. A detailed history eliciting elements suggestive of the force of impact, –– Maintain blood pressure control (must keep blood time of injury or presence or absence of pain at onset pressure high enough to ensure cerebral perfusion can be valuable. The following causes present the but not too high to increase ICP)38 epidemiology of spinal injuries, from more to less –– Anticonvulsant medication may be given (on common. physician’s order) to reduce the risk of secondary ischemic insult associated with seizures38 –– Motor vehicle or bicycle accident –– Control environmental/noxious stimuli that –– Fall may increase ICP (pain, environmental irritants, –– Sporting accident (diving and contact sport) lighting)38 –– Blunt trauma above the clavicles –– Osmotic diuretics such as mannitol may be given –– Stabbing or impalement near the spinal column (on physician’s order) to reduce brain edema in –– Shooting or blast injury to the torso cases of severe brain injury Mannitol, 1 g/kg IV –– Sudden onset of symptoms of neck or back pain, over 20 minutes numbness or tingling in the limbs, weakness or paralysis of the limbs CERVICAL SPINE AND SPINAL CORD TRAUMA PHYSICAL FINDINGS –– Tachycardia CERVICAL SPINE INJURY –– Tachypnea Cervical spine injury occurs in up to 3% of trauma –– Blood pressure may be low if in shock patients; this proportion increases to 10% among –– Pulse oximetry may be desaturating if in shock patients with significant head injury. –– Tenderness on palpation or movement of the Initial care of the client who may have spinal injury spinal column is based on the suspicion of injury, stabilization of –– Obvious deformity of the back or spinal column the spine and prevention of further neurologic injury. –– Loss of sensation Close observation is required. –– Weakness or flaccidity of muscle groups –– Loss of bladder or bowel control SPINAL CORD INJURY –– Priapism (sustained penile erection) Types of injury sustained depends on the mechanism –– Spinal neurogenic shock leads to vasomotor of injury, which can include: hyperflexion, instability from loss of autonomic tone and may hyperextension, rotation, axial loading (vertical lead to hypotension or temperature instability compression) and missile or penetrating injury.38 –– Client may have hypoxia or hypoventilation Look for paralysis and other signs of cord injury, if fracture or compression occurs above C5 including priapism, urinary retention, fecal

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Spinal Shock and Transient Paralysis39 –– Immobilize neck in neutral position and restrain Immediately after a spinal cord injury, there may chest to properly immobilize the cervical spine be a physiological loss of all spinal cord function (sand bags are not a good tool for this purpose below the level of the injury, with flaccid paralysis, because if you later want to move the client onto anesthesia, absent bowel and bladder control and loss a spine board, the bags may fall against the neck of reflex activity. In males, priapism may be observed. and cause further injury; instead, use soft rolled This finding is more frequent in cervical cord injuries. supports at the sides of the head, for example, There may also be bradycardia and hypotension not rolled blankets) due to other causes than the spinal cord injury. This The primary assessment of a patient with trauma altered physiologic state may last several hours to in the field follows the ABCD prioritization scheme: several weeks and is referred to as spinal shock. airway, breathing, circulation, disability (neurologic status). If the patient has a head injury, is unconscious A transient paralysis with complete recovery is most or confused, or complains of spinal pain, weakness often described in younger patients with athletic and/or loss of sensation, then a traumatic spinal injury injuries. These patients should undergo evaluation should be assumed. for underlying spinal disease before returning to play. Stabilization of Cervical Spine COMPLICATIONS –– All multitrauma clients should be placed on a spine –– Autonomic dysreflexia38 board with cervical spine immobilization. Extreme –– Neurogenic shock38 care should be taken to allow as little movement of –– Permanent paralysis the spine as possible to prevent more cord injury. –– Respiratory arrest Techniques to minimize spine movement include –– Spinal shock the use of log-roll movements and a backboard for –– Death transfer and placement of a rigid cervical collar.40 A light cervical collar is ideal, allowing rapid DIAGNOSTIC TESTS access to the anterior neck if surgical access to None. the airway becomes necessary –– The collar is useless if it does not fit the patient, MANAGEMENT so any collar must be sized correctly –– To complete immobilization of the cervical spine, Goals of Treatment the client must be fixed as a “package” to the –– Stabilize spine spine board; tape should be placed from board –– Administer treatment in timely fashion to forehead and back to the other side of the board –– Prevent further damage –– It is important not to use the head alone as a –– Prevent complications fixation point, as this allows the cervical spine to act as a fulcrum for movement; restraints Initial Treatment should therefore also be placed across the client’s shoulders –– Assess and stabilize ABCD (airway, breathing, –– Taping across the chin forces the mandible circulation, disability [neurologic status]) posteriorly and may obstruct the airway –– Life-threatening injuries associated with spinal –– Consider the relationship of the axial skeleton to injuries must be addressed first, but the spine must the spine board: in adults, the head is relatively not be put at risk during these maneuvers smaller anteroposteriorly than the body, and the –– If there is penetrating neck trauma, do not remove cervical spine may be in extension without some foreign body form of occipital padding –– Adults and older children may require 1–2 inches (2.5–5 cm) of padding under the head to approximate a neutral position

2011 Clinical Practice Guidelines for Nurses in Primary Care General Emergency and Major Trauma 14–21

Prolonged immobilization (even < 30 minutes) The force necessary to produce this injury also bruises on a spine board will cause occipital headache and the underlying lung tissue, and this contusion will lumbosacral pain in most people, regardless of contribute to hypoxia. The client is at great risk for underlying trauma, and unfortunately predispose pneumothorax or hemothorax (or both) and may the patient to pressure ulcers. be in marked respiratory distress. Also consider the possibility of cardiac contusion and tamponade Adjuvant Therapy if there has been trauma to the anterior chest wall. –– Give oxygen 10–12 L/min by mask; keep oxygen HISTORY saturation > 97% to 98% –– Start IV therapy with normal saline to keep –– Multiple trauma (motor vehicle or other accident) vein open, unless there is evidence of shock –– Severe chest wall pain (see section “Shock” in this chapter) –– Pain aggravated by movement and respiration –– Shortness of breath Nonpharmacologic Interventions –– Impaired cough38 –– Nothing by mouth –– Hypoventilation38 –– Insert nasogastric tube unless there is suspicion of associated basilar skull fracture or facial trauma PHYSICAL FINDINGS –– Insert Foley catheter if there are no The physical findings depend on the severity of contraindications, such as pelvic fracture or blood damage to the underlying lung tissue and the presence in scrotum or at urethral meatus of associated injuries. Pharmacologic Interventions –– Perform primary survey (see “Primary Survey” under the section “Responding to General As directed by the emergency medical service director Emergencies and Major Trauma” in the Pediatric or the on-call physician. Chapter 20, “General Emergencies and Major Monitoring and Follow-Up Trauma”) –– Carry out emergency interventions as necessary Monitor ABCD, vital signs, oxygen saturation, level –– Perform secondary survey (see “Secondary of consciousness, respiratory status and sensory motor Survey” under the section “Responding to General deficits frequently. Emergencies and Major Trauma” in the Pediatric Chapter 20, “General Emergencies and Major Appropriate Consultation Trauma”) Consult a physician as soon as possible, when client’s condition is stabilized. Vital Signs –– Heart rate elevated Referral –– Respirations rapid, shallow Medevac as soon as possible. –– Blood pressure decreased or normal –– Oxygen saturation, if available FLAIL CHEST Inspection Unstable segment of the bony chest wall. –– Acute respiratory distress CAUSES –– Sweating Chest wall trauma with fracture of three or more –– Cyanosis may be present adjacent ribs in at least two places. The result is a –– Chest wall bruising segment of the chest wall that is not in continuity with –– Abnormal chest wall motion (paradoxical the thorax. Lateral flail chest or anterior flail chest movement of chest wall) easily seen in unconscious (sternal separation) may occur. The flail segment client, less apparent in conscious client moves with paradoxical motion relative to the rest of the chest wall.

Clinical Practice Guidelines for Nurses in Primary Care 2011 14–22 General Emergency and Major Trauma

Palpation Nonpharmacologic Interventions –– Tenderness in injured area Priority is ABC. –– Crepitus may be felt –– Control airway –– Abnormal movement of chest wall may be palpable –– Ensure adequate ventilation Percussion –– Protect cervical spine –– Control pain by gently splinting chest with a pillow –– Hyper-resonance and absent vocal and tactile –– Do not splint aggressively fremitus (if pneumothorax present) –– Dull (if hemothorax, pulmonary contusion present) In the traumatized client with an injury above the clavicle, assume fracture of the cervical spine. Auscultation Adjuvant Therapy –– Air entry reduced in injured area –– Crackles may be present due to the presence –– Give oxygen 10–12 L/min by mask of fluid –– Start two large-bore IV lines (16-gauge or larger) with normal saline DIFFERENTIAL DIAGNOSIS –– Replace blood losses –– Chest wall contusion –– Adjust IV rate according to heart rate, blood –– Simple rib fractures pressure and clinical response See section “Shock” in this chapter for further details. COMPLICATIONS –– Poor ventilation Monitoring and Follow-Up –– Hypoxia –– Monitor mental status, vital signs, pulse oximetry –– Hypovolemia and heart and lung sounds frequently –– Pneumothorax –– Confusion, agitation may be signs of hypoxia –– Hemothorax Referral –– Pulmonary contusion –– Myocardial contusion Medevac as soon as possible. –– Cardiac tamponade PELVIC FRACTURE MANAGEMENT Disruption of the bony structure of the pelvis. Often Goals of Treatment the result of blunt trauma, pelvic fractures may range –– Ensure patency of airway from benign to life threatening and include pelvic ring and acetabular fractures, and avulsion injuries.41 –– Improve oxygenation –– Replace blood loss Classification of Pelvic Fractures38 –– Identify and treat associated injuries –– Lateral Compression (LC): the most common. –– Provide pain control38 Produces shortening of the pelvis diameter and typically does not involve ligamentous injury. Appropriate Consultation Generally forgiving to pelvic ring vessels, however, Consult a physician as soon as client’s condition localized bleeding may still occur, particularly to is safely stabilized. the posterior pelvis –– Anterior Compression (AC): occurs when force is applied in the anterior-posterior direction and the pelvic diameter widens. The injury can be completely ligamentous and manifests as an open sacroiliac joint or open pubic symphasis. Commonly associated with vascular injury

2011 Clinical Practice Guidelines for Nurses in Primary Care General Emergency and Major Trauma 14–23

–– Vertical Shear: a complete disruption of HISTORY45 a hemipelvis associated with hemipelvic The mechanism of a significant blunt trauma should displacement. Typically occurs when people fall prompt consideration of a pelvic fracture. from great height and land on one extremity –– Open Fracture: involves open wound with direct –– Ambulatory at the accident scene communication between the site of the fracture –– Location of pain and a laceration involving the vagina, rectum or –– Bowel and bladder incontinence perineum. Mortality is high because of the resulting –– Symptoms of shock external exsanguination –– Bleeding: rectal, vaginal, hematuria38 –– Peri-anal ecchymosis38 CAUSES –– Lower limb paresis or hypoesthesia38 Pelvic fractures generally require substantial force, –– Last menstrual period such as a motor vehicle collision or a fall from a significant height, but can also be seen in frail Be aware that the amount of force necessary to and elderly patients who sustained low energy cause a pelvic fracture is likely to have caused other mechanisms of impact. Risk factors include: low significant injuries. Investigate for associated intra- bone mass, smoking, hysterectomy, older age and abdominal and intra-pelvic injuries. a propensity to fall.42 PHYSICAL FINDINGS –– Motor vehicle collisions and motorcycle accidents: 43% to 58% of cases –– Tenderness over the pelvis that can be appreciated with pelvic springing, which involves applying –– Pedestrian struck by a motor vehicle: 20% to alternating gentle compression and distraction 22% of cases over the iliac wings –– Falls: 5% to 30%43 –– Palpable instability of the pelvis on bimanual The pelvis consists of the ileum (or iliac wings), the compression or distraction of the iliac wings (it is ischium and the pubis, which form an anatomic ring important to be very gentle when pelvic tenderness with the sacrum. Disruption of this ring requires is appreciated; do not rock or apply great force significant force. Because of the forces involved, until skeletally unstable pelvic fractures have been pelvic fractures frequently involve injury to the organs excluded by x-ray, since an overly aggressive contained within the bony pelvis. In addition, the exam can unnecessarily increase hemorrhage) pelvis is supplied with a rich venous plexus, as well –– Instability on hip adduction (pain on any hip as major arteries; therefore, fractures in this area may motion suggests the possibility of an acetabular produce significant bleeding. fracture, in addition to a possible hip fracture) The rate of complications related to injury to the –– Signs of urethral injury in the male, such as scrotal underlying organs and bleeding is significant. Patients hematoma or blood at the urethral meatus older than 60 with a significant pelvic fracture predicts –– Vaginal bleeding in a female a higher likelihood of bleeding that may require –– Hematuria angiography.44 –– Limb length discrepancy or obvious rotational 46 Because of the tremendous force necessary to cause deformity of the pelvis or lower extremity most pelvic fractures, concomitant severe injuries are –– Rectal bleeding or Earle’s sign which is the common and are associated with high morbidity and appreciation of a large hematoma (swelling) or a mortality rates. The overall mortality rate in adults palpable coccyx or sacral fracture line along with ranges from 10–16%; open fractures are associated tenderness on (careful) rectal exam.48 Digital rectal with a mortality rate of 45% but account for 2–4% of exam has a very low sensitivity for pelvic fractures all pelvic fractures.48 Pelvic hemorrhage is the direct and often misses them47 cause of death in less than half of patients with pelvic –– Destot’s sign, a superficial hematoma above the fractures who die. Retroperitoneal hemorrhage and inguinal ligament, on the proximal thigh or over secondary infection are the main causes of death. the scrotum/perineum

Clinical Practice Guidelines for Nurses in Primary Care 2011 14–24 General Emergency and Major Trauma

–– Roux’s sign, in which the distance measured from Appropriate Consultation the greater trochanter to the pubic spine is less on Consult a physician as soon as possible when a pelvic one side than the other (indicating an overriding fracture is suspected or diagnosed. Hemodynamically fracture of the anterior pelvic ring – a lateral unstable clients (with unstable pelvic fractures) 48 compression fracture) require emergent orthopedic consultation for –– Neurovascular deficits of the lower extremities consideration of external fixation.

DIFFERENTIAL DIAGNOSIS Nonpharmacologic Interventions –– Hip dislocation or fracture –– Priority is to assess and stabilize ABC –– Femur fracture (this is a high-risk situation –– Address acute, life-threatening conditions due to the potential for significant hypovolemia) –– Avoid excessive movement of the pelvis COMPLICATIONS Do not insert a urinary catheter until you have confirmed –– Continued bleeding from the fracture or injury that there is no urethral injury (by physical exam). to the pelvic vasculature Adjuvant Therapy –– Shock –– Genitourinary problems from bladder, urethral, –– Obtain large-bore IV access and administer normal prostate or vaginal injuries saline as needed (see section “Shock” in this chapter) –– Infections from disruption of the bowel or urinary system –– Give oxygen at 10–12 L/min or more by mask; keep oxygen saturation > 97% to 98% –– Deep vein thrombosis –– Death Pharmacologic Interventions A woman in the later stages of pregnancy is at Treat pain with narcotic analgesics: increased risk of complications from pelvic fracture, and there is great risk of placental abruption and morphine 5–10 mg IM or SC uterine rupture. Monitoring and Follow-Up DIAGNOSTIC TESTS –– Closely monitor vital signs and pulse oximetry –– Obtain sample for urinalysis (look for gross –– Monitor the client for signs of ongoing blood or microscopic hematuria) loss and signs of infection –– Pelvic ultrasound, CT scan or x-ray may be –– Monitor for development of neurovascular required. Upon consultation, a routine plain x-ray problems in the lower extremities in patients with a Glascow Coma Scale score of Referral > 13, presenting with no pelvic, abdominal or back complaints and no tenderness in the lower –– Medevac abdomen, lower back, groin or bony pelvis, may –– Achieve hemodynamic stabilization and transfer not be required48 on a spine board

MANAGEMENT

Goals of Treatment –– Stabilize fracture –– Prevent and treat complications –– Prevent or control life-threatening hemorrhage38

2011 (Revised April 2013) Clinical Practice Guidelines for Nurses in Primary Care General Emergency and Major Trauma 14–25

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2011 Clinical Practice Guidelines for Nurses in Primary Care