DOCSLIB.ORG

Respiratory Patient Pathway

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Respiratory Patient Pathway BWCCG – MOT’s Shortness of Breath Event Thursday 5th November 2020 from 12:00pm – 14:00pm via Microsoft TEAMS • Please note, the webinar will be recorded & by attending the session you are giving consent • Kindly switch off your video & microphone to help avoid interruptions • Lastly, kindly type in your questions clearly in the Chat box ( Symbol). A moderator will read them out at the end of each session. BWCCG – MOT’s Shortness of Breath Event Thursday 5th November 2020 from 12:00pm – 14:00pm Via Microsoft TEAMS 12:00 - Winter Respiratory Pathway Introduction (Dr Heike Veldtman, LTC GP Chair) 12:10 - SOB: Review and Management of Non COVID related Respiratory Conditions (Dr. Anne McGown, Respiratory Consultant – RBFT) 12:50 – Q & A session 13:00 - SOB: Review and management of Heart Failure (Dr Lindsey Tilling, Consultant Cardiologist – RBFT) 13:50 - Q & A Session 14:00 - CLOSE Respiratory Patient Pathway Patient Presents NHS 111 OR GP GP Triage Treat and Safetynet (Enquire about Covid Admit to Secondary Care test) Need F2F MDT Refer to BHFT Primary Care Review Community Respiratory Case Finding – CM input Seen in Primary Care Service Anticipatory Care Respiratory Hub (Care Planning, Planning Virtual Monitoring) MDT Admit to Secondary Care GP webinar – respiratory update Anne McGown November 2020 Summary • Managing exacerbations/deterioration in known respiratory disease – COPD – Asthma – Bronchiectasis – ILD • Other causes of chronic breathlessness • Pulse oximetry and exertional desaturation • CAP during COVID • Breathlessness following covid COPD – gradual deterioration -Deconditioning • Unfit people get more breathless. • Early onset of lactic acidosis in unfit muscles stimulates chemoreceptors to increase ventilation. • One of the reasons pulmonary rehab works. • Unless accompanied by exercise; education or symptom management programs don’t help dyspnoea in COPD. Vicious circle 1 Deconditioni ng Breathless ness on exertion Reduce Perceived as exertion to potentially avoid harmful breathlessness Breathlessness in context Vicious circle Sensations associated with breathlessne Interpret ss ed as dangero us Increased Increased physiological anxiety/distress awareness/aro usal Pulmonary rehab – RBH and community service Physios are accepting referrals for PR. Please complete the attached referral form and email to: [email protected] Patients are currently assessed face to face and enrolled onto a virtual programme (by telephone or via Microsoft TEAMS) Hoping to bring back face to face pulmonary rehabilitation in the New Year Community also up and running – refer through the hub. Takes place in Tilehurst and WBCH. NICE 2019 summary COPD exacerbations – NICE 2018 - steroids • In the absence of significant contraindications, consider oral corticosteroids for people in the community who have an exacerbation with a significant increase in breathlessness that interferes with daily activities. [2004] • Encourage people who need corticosteroid therapy to present early to get maximum benefits. [2004] • Offer 30 mg oral prednisolone daily for 5 days. [2019] • Develop an individualised exacerbation action plan in collaboration with each person with COPD who is at risk of exacerbations. [2018] COPD exacerbation – NICE 2019 - antibiotics COPD exacerbations – self management /rescue pack – NICE 2018 • Offer people rescue pack or steroids and antibiotics if - they have had an exacerbation within the last year, and remain at risk of exacerbations they understand and are confident about when and how to take these medicines, and the associated benefits and harms they know to tell their healthcare professional when they have used the medicines, and to ask for replacements. [2018] Action plan may include adjusting their short-acting bronchodilator therapy to treat their symptoms oral corticosteroids if increased breathlessness interferes with activities of daily living oral antibiotics if their sputum changes colour and increases in volume or thickness beyond their normal day-to-day variation telling their healthcare professional. [2018] Community team contact details • Referral through hub • Exacerbation of Spirometrically diagnosed COPD • Local ABX guidelines are amoxyl for infrequent exacerbators, doxy for frequent. 5 days with the steroids unless underlying bronchiectasis. • Only wean pred in those with v frequent courses – get community team involved in these. • Refer anyone to community team on second exacerbation. Bronchiectasis • UK data in 2013 revealed the prevalence in women was 566/100 000 and in men 486/100 000 • Usually an annoying condition which causes chronic cough and recurrent chest infections rather than progressive disability. May co-exist with asthma/COPD • A minority often with known cause have progressive infection and complications. Microbiology • Progressive bacterial colonisation of lower airways • Staph aureus • Haemophilus influenzae • Moraxella catarrhalis • Pseudomonas species • (AAFB) • Send regular samples for MC&S • Annual sputum AAFB Antimicrobial chemotherapy • Short term, long term • Oral, nebulised, intra venous • Regular sputum surveillance • In vivo and in vitro sensitivity can be different • Need more prolonged antibiotic courses • Pseudomonas colonised patients have more exacerbations and a faster decline in lung function Antibiotics • Amoxycillin 1G TDS 10-14 days • Doxycycline 100mg OD 14 days • Ciprofloxacin 750mg BD 2-3 weeks if previous PsA • First isolate of PsA needs eradication: 4-6 weeks ciprofloxacin with nebulised aminoglycoside • Long term nebulised colomycin reduces PsA exacerbations Refer if • New PsA infection – treat with ciprofloxacin (even if lab resistance) and let us know • No response to 3-4 weeks of high dose oral antibiotics (ideally with known sensitivities) • Significant haemoptysis • Weight loss • Ventilatory failure • Please send sputums – multiple if required! Physiotherapy • Regular, part of daily treatment • Active Cycle of Breathing Technique • Deep breathing, mobilise secretions • Regular exercise • Breathing control • Pulmonary Rehabilitation Other Treatments • Of underlying disease • Self management plan • Bronchodilators • Inhaled steroid – only if coexistent asthma • Nutrition, nutrition, nutrition • Vaccinations • Tranexamic acid • Surgery/transplant BTS 2019 Long term macrolides in bronchiectasis BTS April 2020 • Baseline ECG and LFT. If QTc is >450ms for men and >470ms macrolides contraindicated • Counsel patients about potential adverse effects including gastrointestinal upset, hearing and balance disturbance, cardiac effects and microbiological resistance. • Sputum culture for non tuberculous mycobacteria - avoid if present • Accurate assessment of baseline exacerbation rate should be determined before starting long-term macrolides for bronchiectasis. • Liver function tests should be checked one month after starting treatment and then every 6 months. • An ECG should be performed 1 month after starting treatment to check for new QTc prolongation. If present, treatment should be stopped. • Subsequent follow-up at 6 and 12 months should determine whether benefit is being derived from therapy. If there is no benefit, treatment should be stopped. • Even if benefit is seen, consideration should be given to stopping treatment for a period each year, for example over the summer. Asthma deterioration NICE 2017 – adults >17 1 If infrequent, short-lived wheeze and normal lung function, consider treatment with SABA reliever therapy alone. 2 Add low dose inhaled steroid ( if more than 3 SABA a week or waking at night 3. Add leukotriene receptor antagonist (LTRA) in addition to the ICS and review the response to treatment in 4 to 8 weeks. 4. Add a long-acting beta2 agonist (LABA) in combination with the ICS, and review LTRA 5. Convert to a MART regimen with a low maintenance ICS dose. 6. consider increasing the ICS to a moderate maintenance dose (either continuing on a MART regimen or changing to a fixed-dose of an ICS and a LABA, with a SABA as a reliever therapy). If asthma remains uncontrolled - options • increasing the ICS to a high maintenance dose (this should only be offered as part of a fixed-dose regimen, with a SABA used as a reliever therapy) or a trial of an additional drug (for example, a long-acting muscarinic receptor antagonist or theophylline) or seeking advice from a healthcare professional with expertise in asthma. • Mepolizumab is possible add on for severe refractory eosinophilic asthma in adults (sc injection every 4weeks), only if: the blood eosinophil count is 300 cells/microlitre or more in the previous 12 months, and the person has agreed to and followed the optimised standard treatment plan and has had 4 or more asthma exacerbations requiring systemic corticosteroids in the previous 12 months or had continuous oral corticosteroids of at least the equivalent of prednisolone 5 mg per day over the previous 6 months, - REFER (specialist commissioning) Asthma deterioration/exacerbation NICE 2017 • Offer increased dose of ICS for 7 days in a self management plan (can quadruple dose if using ICS in single inhaler and within max licensed daily dose). • If not using ICS regularly explain regular use may enable them to regain control of asthma • Acute severe asthma – Prednisolone 40mg until better, minimum 5 days. • Mepolizumab - 45 patients locally – continue to use even if exacerbating Interstitial lung disease – 2 main groups • Idiopathic pulmonary fibrosis – UIP (usual interstitial pneumonia) pattern
Load more

Recommended publications
  • Allergic Bronchopulmonary Aspergillosis As a Cause of Bronchial Asthma in Children
    Egypt J Pediatr Allergy Immunol 2012;10(2):95-100. Original article Allergic bronchopulmonary aspergillosis as a cause of bronchial asthma in children Background: Allergic bronchopulmonary aspergillosis (ABPA) occurs in Dina Shokry, patients with asthma and cystic fibrosis. When aspergillus fumigatus spores Ashgan A. are inhaled they grow in bronchial mucous as hyphae. It occurs in non Alghobashy, immunocompromised patients and belongs to the hypersensitivity disorders Heba H. Gawish*, induced by Aspergillus. Objective: To diagnose cases of allergic bronchopulmonary aspergillosis among asthmatic children and define the Manal M. El-Gerby* association between the clinical and laboratory findings of aspergillus fumigatus (AF) and bronchial asthma. Methods: Eighty asthmatic children were recruited in this study and divided into 50 atopic and 30 non-atopic Departments of children. The following were done: skin prick test for aspergillus fumigatus Pediatrics and and other allergens, measurement of serum total IgE, specific serum Clinical Pathology*, aspergillus fumigatus antibody titer IgG and IgE (AF specific IgG and IgE) Faculty of Medicine, and absolute eosinophilic count. Results: ABPA occurred only in atopic Zagazig University, asthmatics, it was more prevalent with decreased forced expiratory volume Egypt. at the first second (FEV1). Prolonged duration of asthma and steroid dependency were associated with ABPA. AF specific IgE and IgG were higher in the atopic group, they were higher in Aspergillus fumigatus skin Correspondence: prick test positive children than negative ones .Wheal diameter of skin prick Dina Shokry, test had a significant relation to the level of AF IgE titer. Skin prick test Department of positive cases for aspergillus fumigatus was observed in 32% of atopic Pediatrics, Faculty of asthmatic children.
    [Show full text]
  • Asthma Exacerbation Management
    CLINICAL PATHWAY ASTHMA EXACERBATION MANAGEMENT TABLE OF CONTENTS Figure 1. Algorithm for Asthma Exacerbation Management – Outpatient Clinic Figure 2. Algorithm for Asthma Management – Emergency Department Figure 3. Algorithm for Asthma Management – Inpatient Figure 4. Progression through the Bronchodilator Weaning Protocol Table 1. Pediatric Asthma Severity (PAS) Score Table 2. Bronchodilator Weaning Protocol Target Population Clinical Management Clinical Assessment Treatment Clinical Care Guidelines for Treatment of Asthma Exacerbations Children’s Hospital Colorado High Risk Asthma Program Table 3. Dosage of Daily Controller Medication for Asthma Control Table 4. Dosage of Medications for Asthma Exacerbations Table 5. Dexamethasone Dosing Guide for Asthma Figure 5. Algorithm for Dexamethasone Dosing – Inpatient Asthma Patient | Caregiver Education Materials Appendix A. Asthma Management – Outpatient Appendix B. Asthma Stepwise Approach (aka STEPs) Appendix C. Asthma Education Handout References Clinical Improvement Team Page 1 of 24 CLINICAL PATHWAY FIGURE 1. ALGORITHM FOR ASTHMA EXACERBATION MANAGEMENT – OUTPATIENT CLINIC Triage RN/MA: • Check HR, RR, temp, pulse ox. Triage level as appropriate • Notify attending physician if patient in severe distress (RR greater than 35, oxygen saturation less than 90%, speaks in single words/trouble breathing at rest) Primary RN: • Give oxygen to keep pulse oximetry greater than 90% Treatment Inclusion Criteria 1. Give nebulized or MDI3 albuterol up to 3 doses. Albuterol dosing is 0.15 to 0.3mg/kg per 2007 • 2 years or older NHLBI guidelines. • Treated for asthma or asthma • Less than 20 kg: 2.5 mg neb x 3 or 2 to 4 puffs MDI albuterol x 3 exacerbation • 20 kg or greater: 5 mg neb x 3 or 4 to 8 puffs MDI albuterol x 3 • First time wheeze with history consistent Note: For moderate (dyspnea interferes with activities)/severe (dyspnea at rest) exacerbations you with asthma can add atrovent to nebulized albuterol at 0.5mg/neb x 3.
    [Show full text]
  • Management of Acute Exacerbation of Asthma and Chronic Obstructive Pulmonary Disease in the Emergency Department
    Management of Acute Exacerbation of Asthma and Chronic Obstructive Pulmonary Disease in the Emergency Department Salvador J. Suau, MD*, Peter M.C. DeBlieux, MD KEYWORDS Asthma Asthmatic crisis COPD AECOPD KEY POINTS Management of severe asthma and chronic obstructive pulmonary disease (COPD) exac- erbations require similar medical interventions in the acute care setting. Capnography, electrocardiography, chest x-ray, and ultrasonography are important diag- nostic tools in patients with undifferentiated shortness of breath. Bronchodilators and corticosteroids are first-line therapies for both asthma and COPD exacerbations. Noninvasive ventilation, magnesium, and ketamine should be considered in patients with severe symptoms and in those not responding to first-line therapy. A detailed plan reviewed with the patient before discharge can decrease the number of future exacerbations. INTRODUCTION Acute asthma and chronic obstructive pulmonary disease (COPD) exacerbations are the most common respiratory diseases requiring emergent medical evaluation and treatment. Asthma accounts for more than 2 million visits to emergency departments (EDs), and approximately 4000 annual deaths in the United States.1 In a similar fashion, COPD is a major cause of morbidity and mortality. It affects more than 14.2 million Americans (Æ9.8 million who may be undiagnosed).2 COPD accounts for more than 1.5 million yearly ED visits and is the fourth leading cause of death Disclosures: None. Louisiana State University, University Medical Center of New Orleans, 2000 Canal Street, D&T 2nd Floor - Suite 2720, New Orleans, LA 70112, USA * Corresponding author. E-mail address: [email protected] Emerg Med Clin N Am 34 (2016) 15–37 http://dx.doi.org/10.1016/j.emc.2015.08.002 emed.theclinics.com 0733-8627/16/$ – see front matter Ó 2016 Elsevier Inc.
    [Show full text]
  • 2020 GINA Pocket Guide for Asthma Management and Prevention
    POCKET GUIDE FOR ASTHMA MANAGEMENT AND PREVENTION (for Adults and Children Older than 5 Years) DISTRIBUTE OR COPY NOT DO MATERIAL- COPYRIGHTED A Pocket Guide for Health Professionals Updated 2020 BASED ON THE GLOBAL STRATEGY FOR ASTHMA MANAGEMENT AND PREVENTION © 2020 Global Initiative for Asthma GLOBAL INITIATIVE FOR ASTHMA ASTHMA MANAGEMENT AND PREVENTION DISTRIBUTE for adults and children older ORthan 5 years COPY NOT A POCKET GUIDE FOR HEALTHDO PROFESSIONALS MATERIAL-Updated 2020 GINA Science Committee Chair: Helen Reddel, MBBS PhD COPYRIGHTED GINA Board of Directors Chair: Louis-Philippe Boulet, MD GINA Dissemination and Implementation Committee Chair: Mark Levy, MD (to Sept 2019); Alvaro Cruz, MD (from Sept 2019) GINA Assembly The GINA Assembly includes members from many countries, listed on the GINA website www.ginasthma.org. GINA Executive Director Rebecca Decker, BS, MSJ Names of members of the GINA Committees are listed on page 48. 1 LIST OF ABBREVIATIONS BDP Beclometasone dipropionate COPD Chronic obstructive pulmonary disease CXR Chest X-ray DPI Dry powder inhaler FeNO Fraction of exhaled nitric oxide FEV1 Forced expiratory volume in 1 second FVC Forced vital capacity GERD Gastroesophageal reflux disease HDM House dust mite ICS Inhaled corticosteroids ICS-LABA Combination ICS and LABA Ig Immunoglobulin IL Interleukin DISTRIBUTE IV Intravenous OR LABA Long-acting beta2-agonist COPY LAMA Long-acting muscarinic antagonist NOT LTRA Leukotriene receptor antagonistDO n.a. Not applicable NSAID Nonsteroidal anti-inflammatory drug MATERIAL- O2 Oxygen OCS Oral corticosteroids PEF Peak expiratory flow pMDI PressurizedCOPYRIGHTED metered dose inhaler SABA Short-acting beta2-agonist SC Subcutaneous SLIT Sublingual immunotherapy 2 TABLE OF CONTENTS List of abbreviations ........................................................................................
    [Show full text]
  • Global Strategy for Asthma Management and Prevention, 2019. Available From
    DISTRIBUTE OR COPY NOT DO MATERIAL- COPYRIGHTED ASTHMA MANAGEMENT AND PREVENTION GLOBAL STRATEGY FOR Updated 2019 9 Global Strategy for Asthma Management and Prevention (2019 update) DISTRIBUTE OR COPY NOT DO The reader acknowledges that this reportMATERIAL- is intended as an evidence-based asthma management strategy, for the use of health professionals and policy-makers. It is based, to the best of our knowledge, on current best evidence and medical knowledge and practice at the date of publication. When assessing and treating patients, health professionals are strongly advised to use their own professional judgment, and to take into account local or national regulations and guidelines. GINA cannot be held liable or responsible for inappropriate healthcare associated with the use of this document, including any use which is not in accordance with applicable local or national regulations or COPYRIGHTEDguidelines. This document should be cited as: Global Initiative for Asthma. Global Strategy for Asthma Management and Prevention, 2019. Available from: www.ginasthma.org 1 Table of contents Tables and figures ............................................................................................................................................................... 5 Preface ................................................................................................................................................................................. 7 Members of GINA committees (2018) ................................................................................................................................
    [Show full text]
  • Respiratory Drug Guidelines ______
    Respiratory Drug Guidelines ______________________________________________ First Edition 2008 Ministry of Health Government of Fiji Islands 2008 "This document has been produced with the financial assistance of the European Community and World Health Organization. The views expressed herein are those of the Fiji National Medicine & Therapeutics Committee and can therefore in no way be taken to reflect the official opinion of the European Community and the World Health Organization.” Disclaimer The authors do not warrant the accuracy of the information contained in these guidelines and do not take responsibility for any deaths, loss, damage or injury caused by using the information contained herein. Every effort had been made to ensure the information contained in these guidelines is accurate and in accordance with current evidence-based clinical practice. However, if the evidence in the medical literature is either limited or not available, the recommendations in these guidelines are based on the consensus of the members of the subcommittee. In view of the dynamic nature of medicine, users of these guidelines are advised that independent pr ofessional judgment should be exercised at all times. ii Preface The publication of the Respiratory Drug Guidelines represents the culmination of the efforts of the National Medicines and Therapeutics Committee to publish clinical drug guidelines for common diseases seen in Fiji. These guidelines are targeted for health care settings. It sets the gold standards for the use of respiratory drugs in Fiji. These guidelines have taken into account the drugs available in the Fiji Essential Medicines List (EML) in recommending treatment approaches. All recommended drug therapies are either evidence-based or universally accepted standards.
    [Show full text]
  • Respiratory Guidelines
    RESPIRATORY GUIDELINES Medicines Used in Respiratory Diseases Introduction This chapter contains brief summaries of the major drugs used in the management of respiratory disease and are recommended in these guidelines. The summaries do not contain comprehensive accounts of the pharmacology of these compounds. The reader is advised to consult standard textbooks and/or the industry product information for more details. It is important to consider the risks and benefits of drugs (particularly corticosteroids) that are used to treat respiratory diseases. As a general principle, the lowest drug doses that achieve best control should be used. For example: Patient adherence to asthma treatment is better if regimens have: fewer devices and drugs fewer adverse effects been understood and agreed between patient and health care professional. Beta2 receptor stimulating drugs (Beta2 agonists) Introduction Stimulation of beta2-receptors on airway smooth muscle relaxes the muscle resulting in bronchodilation. All beta2 agonists may also stimulate beta1-receptors; however, the effects of beta1-receptor stimulation (eg tachycardia) are more likely to occur following systemic absorption or following inhalation of relatively large doses. Under almost all circumstances, the preferred route of administration for beta2 agonists is by inhalation. Administration by inhalation causes bronchodilation with low doses thus minimising systemic adverse effects. Adverse effects: Dose-limiting adverse effects of the beta2 agonists are most commonly tachycardia (which can also lead to paroxysmal tachyarrhythmias, such as atrial fibrillation or paroxysmal supraventricular tachycardia), tremor, headaches, muscle cramps, insomnia, and a feeling of anxiety and nervousness. In high doses (eg tablets,intravenous and emergency nebulisation) all beta2 agonists can cause hypokalaemia and hyperglycaemia.
    [Show full text]
  • Acute Severe Asthma
    - According to consensus guidelines, a severe episode is believed to exist when one or more of the following features are present: (i) accessory muscle activity, (ii) a paradoxical pulse exceeding 25 mm Hg, (iii) a heart rate greater than 110 beats/minute, (iv) a respiratory rate greater than 25–30 breaths/minute, epidemiology (v) a limited ability to speak, (vi) a peak expiratory flow rate (PEFR) or FEV1 <50% of predicted, and (vii) an arterial saturation less than 91–92% - Altered mental status, paradoxical respiration, bradycardia, a quiet chest, and absence of pulsus paradoxus from respiratory muscle fatigue are features of imminent respiratory arrest. - the classic gross anatomic features of those who die from asthma are airway narrowing, extensive plugging of the airways with mucus and inflammatory infiltrates, hyperinflation, and atelectasis - increased airway resistance and dynamic hyperinflation leads to: (i) increased work of breathing (ii) ventilation-perfusion mismatch as a result of airway narrowing & closure (iii) adverse cardiopulmonary interactions - spontaneously breathing patients with acute severe asthma can generate inspiratory pressures as low a -35cmH2O which are sufficient to cause increased left ventricular afterload and promotes egress of fluid into alveolar pathophysiology airspace - right ventricular afterload is increased by hypoxic pulmonary vasoconstriction, acidosis & increased lung volume - patients with severe asthma exacerbation have critical airflow obstruction limiting exhalation. - in severe cases, expiratory flow may not cease for as long as 60 seconds. Because expiratory time is shorter (1 to 5 seconds) during spontaneous or assisted breathing, there is incomplete emptying of gas and dynamic lung hyperinflation (DHI). - Fortunately, DHI is self-limiting because as lung volume increases so do lung elastic recoil pressure and airway diameter-factors that favor expiratory flow.
    [Show full text]
  • EVIDENCE-BASED OUTCOMES CENTER Asthma/Recurrent Wheezing Clinical Guideline Evidence-Based Guideline
    DATE: January 2014 TEXAS CHILDREN’S HOSPITAL EVIDENCE-BASED OUTCOMES CENTER Asthma/Recurrent Wheezing Clinical Guideline Evidence-Based Guideline Definition: (1) Acute asthma exacerbations or “asthma attacks” Physical Examination (2) are episodes of progressive increase in shortness of breath, Evaluate patient’s ability to complete a sentence cough, wheezing, or chest tightness, or some combination of Pulse rate these symptoms. Respiratory distress is common. Respiratory rate Exacerbations are characterized by decreases in expiratory Use of accessory muscles airflow that can be quantified by measurement of lung function Severity of respiratory symptoms using the Clinical (PEF or FEV1). Respiratory Score (CRS) Pathophysiology: (2) Asthma is a complex process that Rhinitis, increased nasal secretions, mucosal swelling, or depends on the interaction of: nasal polyps Bronchoconstriction Exacerbation Severity Assessment Tool Airway hyperresponsiveness Airway inflammation, resulting in edema and mucus Clinical Respiratory Score (CRS) plugging Assess Score 0 Score 1 Score 2 < 2 mos: < 50 < 2 mos: 50-60 < 2 mos: > 60 Inclusion Criteria Respiratory 2-12 mos: < 40 2-12 mos: 40-50 2-12 mos: > 50 Patients ≥2 years with a diagnosis of asthma/recurrent Rate 1-5 yrs: < 30 > 1-5 yrs: 30-40 > 1-5 yrs: > 40 wheezing in whom foreign body or vocal cord dysfunction > 5 yrs: < 20 > 5 yrs: 20-30 > 5 yrs: > 30 Diminished or Good air have been ruled out Depressed air absent breath movement, movement, sounds, severe scattered Exclusion Criteria inspiratory
    [Show full text]
  • Guideline on Management of the Acute Asthma Attack in Children by Italian Society of Pediatrics
    Indinnimeo et al. Italian Journal of Pediatrics (2018) 44:46 https://doi.org/10.1186/s13052-018-0481-1 REVIEW Open Access Guideline on management of the acute asthma attack in children by Italian Society of Pediatrics Luciana Indinnimeo1*, Elena Chiappini2, Michele Miraglia del Giudice3 and The Italian Panel for the management of acute asthma attack in children Abstract Background: Acute asthma attack is a frequent condition in children. It is one of the most common reasons for emergency department (ED) visit and hospitalization. Appropriate care is fundamental, considering both the high prevalence of asthma in children, and its life-threatening risks. Italian Society of Pediatrics recently issued a guideline on the management of acute asthma attack in children over age 2, in ambulatory and emergency department settings. Methods: The Grading of Recommendations Assessment, Development, and Evaluation (GRADE) methodology was adopted. A literature search was performed using the Cochrane Library and Medline/PubMed databases, retrieving studies in English or Italian and including children over age 2 year. Results: Inhaled ß2 agonists are the first line drugs for acute asthma attack in children. Ipratropium bromide should be added in moderate/severe attacks. Early use of systemic steroids is associated with reduced risk of ED visits and hospitalization. High doses of inhaled steroids should not replace systemic steroids. Aminophylline use should be avoided in mild/moderate attacks. Weak evidence supports its use in life-threatening attacks. Epinephrine should not be used in the treatment of acute asthma for its lower cost / benefit ratio, compared to β2 agonists. Intravenous magnesium solphate could be used in children with severe attacks and/or forced expiratory volume1 (FEV1) lower than 60% predicted, unresponsive to initial inhaled therapy.
    [Show full text]
  • Pulmonary Hypertension in Patients with COPD
    EDITORIAL 283 Pulmonary hypertension in COPD with severe COPD.10 11 A degree of pulmo- ................................................................................... nary hypertension was observed in 55% Thorax: first published as 10.1136/thorax.58.4.284 on 1 April 2003. Downloaded from of consecutive respiratory outpatients using Doppler echocardiography.12 The Pulmonary hypertension in patients presence of pulmonary hypertension in patients with COPD is associated with with COPD: NO treatment? increased mortality11 13 and an increase in exacerbation rate and length of hospi- J Pepke-Zaba, N W Morrell tal stay, independent of the degree of air- flow obstruction.14 Although often in- ................................................................................... ferred, the precise contribution of pulmonary hypertension to exercise The application of “pulsed” NO combined with LTOT may limitation or quality of life in stable have a role in treating pulmonary hypertension secondary to COPD patients is unknown. Mean pul- COPD. monary artery pressure in patients with COPD is typically mild (in the region of ollowing the identification of nitric exchange based on low ventilation/ 25 mm Hg) at rest but can rise to abnor- oxide (NO) in 1986 as “endothelium perfusion (V/Q) ratios. This includes the mally high levels on exercise. derived relaxing factor”, there has use of NO in patients in intensive care, At present there are no specific treat- F ments recommended for the reduction of been an exponential growth in our neonates with persistent pulmonary understanding of the physiological role hypertension, and in postoperative set- pulmonary artery pressure in COPD. Although long term oxygen therapy of NO culminating in the award of a tings where NO is used to reduce pulmo- (LTOT) improves survival in hypoxaemic Nobel Prize, and the naming of NO as nary vascular resistance and/or improve patients with COPD, it has a negligible “molecule of the decade”.1 Considerable oxygenation—for example, pulmonary effect on pulmonary haemodynamics.
    [Show full text]
  • Medical Emergencies: Pulmonary Embolism and Acute Severe Asthma
    Anaesthesia 2013, 68 (Suppl. 1), 102–116 doi:10.1111/anae.12051 Review Article Medical emergencies: pulmonary embolism and acute severe asthma K. Somasundaram1 and J. Ball2 1 Specialist Registrar in Anaesthesia and Intensive Care Medicine, 2 Consultant and Honorary Senior Lecturer in General and Neuro Intensive Care, St George’s Hospital, London, UK Summary In this, the second of two articles covering specific medical emergencies, we discuss the definitions, epidemiology, pathophysiology, acute and chronic management of pulmonary embolus and acute severe asthma. ................................................................................................................................................................ Correspondence to: J. Ball Email: [email protected] Accepted: 24 September 2012 In our previous article we covered atrial fibrillation By far, the most common pathological scenario is and myocardial infarction; here we review the man- venous thromboembolism (VTE) from the lower agement of pulmonary embolism and acute severe extremities, originating in the inferior vena cava (IVC) asthma. or below. All of the major risk factors for lower extremity venous thrombosis are ubiquitous in peri- Pulmonary embolism operative and ICU patients, namely immobility and Pathology variable degrees of pro-thrombotic pathologies (surgery, The lungs bring inspired gas into very close proximity systemic inflammatory response syndrome (SIRS) an- with blood to facilitate diffusion of oxygen and carbon d ⁄ or infection, tissue injury, cancer etc.). In addition, dioxide. To achieve this, the lungs have very large localised venous injury (e.g. femoral venous lines [2]) (alveolar) epithelial and (pulmonary capillary) endothe- and a chronic thrombophilic state (drugs, congenital or lial surface areas. This, coupled with in-series pulmonary acquired thrombophilia) may be present. Indeed, so and systemic circulations, results in a secondary, and high is the risk that both mechanical and ⁄ or medicinal arguably neglected, role of blood filtration.
    [Show full text]