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Asthma and COPD November 28, 2002 Cass Djurfors Dr. M. Betzner Objectives: Asthma: Definition Epidemiology Pathophysiology Clinical features Diagnostic tests Management Disposition Objectives: COPD Definition Epidemiology Pathophysiology Clinical Presentation Diagnostic Criteria Treatment: Chronic Acute Asthma: definition Chronic inflammatory disease characterized by reversible airflow obstruction, exacerbations and remissions. NAEPP Diagnostic Criteria 1. Intermittent airflow obstruction indicated by a history of nighttime cough, recurrent wheeze or recurrent chest tightness. 2. Reversible airflow obstruction as documented by pulmonary function testing, worsening symptoms in the presence of any of several triggers, or symptoms that occur at night. 3. All other possible diagnoses are excluded. National Asthma Education and Prevention Program. Expert panel report 2: Guidelines for the diagnosis and management of asthma. DHHS pub # NIH 97-4051. 1997 Epidemiology: Affects 4-6% of population in the United States Most common chronic disease of childhood, fourth leading cause of disability in children, increasing in prevalence 30% of children will have persistent symptoms of asthma into adulthood Fatalities are real: 4657 in U.S. in 1998 Etiology: Currently believed that asthma is the result of a combination of genetic predisposition and environmental exposures Common Triggers: Tobacco smoke, air pollutants, animal allergens, dust mites, viral respiratory infections, cockroach allergens, weather changes, molds, outdoor allergens, gerd… Pathophysiology: Acute and chronic inflammation and airway hyperresponsiveness Partially reversible airflow obstruction results from bronchial smooth muscle constriction, airway edema and inflammation, and mucus plugging; bronchoconstriction is superimposed in the acute setting Permanent changes can eventually be seen at the microscopic level…including collagen deposition and fibrosis below the basement membrane from mast cell activity and inflammatory cell migration History: Symptoms: Cough, wheeze, SOB, chest tightness, sputum, fever, poor feeding Pattern of disease: Course, onset, duration, seasonal variation, frequency Aggravating factors/triggers Usual triggers, current trigger History of disease: previous hospitalization previous intubation/ICU previous ED visits typical episode Age at onset and method of diagnosis Present management, meds and history of steroid use History: Family History Social History: Home environment (smoking, pets, allergens) Identification of precipitating cause Exacerbation profile: Usual exacerbation pattern and outcome Past best spirometry measures Medical history, allergies, anaphylaxis Treatment: Medications at home and timing of last dose Treatment before arrival Physical Exam: Vital signs: RR increases HR-tachycardia from anxiety, increased work of breathing, and hypoxia BP-hypotension may be present in patients with impending resp failure due to decreased venous return and increased pleural pressures. Pulsus paradoxus may be present Physical Exam: Accessory muscle use Indrawing: subcostal, intercostal, supraclavicular Paradoxical abdominal and chest wall movements Nasal flaring in young children Physical Exam: Mental status Prolonged expiratory phase Lung findings: Wheeze “Silent chest” Diagnostic Tests: Pulse Oximetry: Continuous monitoring <91% may be a predictor of hospital admission in kids (Geelhoed et al, BMJ, 1988) PEF: An approximation of FEV1 Should be measured in all but the sickest of patients or those younger than 5 years Compare with predicted age/size appropriate value and with personal best Diagnostic Tests: CXR: Of limited utility Useful in those with concern for complications of asthma (pneumothorax) or those patients in whom another diagnosis is suspected Recommended for children with first episode of wheeze to rule out foreign bodies, congenital anomalies (Scarfone, Emergency Asthma, 1999) Diagnostic Tests: ABG: Useful as supportive evidence for the clinical diagnosis of respiratory failure Asthma Severity: CAEP Mild exertional dyspnea/cough ± nocturnal symptoms. Increased use of ß agonist for symptom control. Good response to ß agonist FEV1,PEFR > 60% predicted or best. (FEV1 > 2.1L; PEFR > 300L/min) Asthma Severity: CAEP Moderate dyspnea at rest, cough, congested, chest tightness, nocturnal symptoms. Partial relief from ß agonist and or ß agonist needed more often than Q4h FEV1 PEFR 40%-60% predicted or best. (FEV1 1.6-2.1L, PEFR 200-300L/min) Asthma Severity: CAEP Severe laboured respirations agitated, diaphoretic difficulty speaking tachycardic, no prehospital relief with ß agonist FEV1,PEFR - unable or <40% predicted or best (FEV1 <1.6L PEFR <200L/min O2 saturation <90%) Asthma Severity: CAEP Near Death exhausted, confused, diaphoretic, cyanotic, silent chest, decreased resp. effort falling heart rate FEV1,PEFR not appropriate O2 saturation <90% (despite supplemental O2) Treatment Goals: Correct hypoxia Reverse airflow obstruction Treat underlying inflammatory response Management: CAEP Mild: O2 ß agonist (MDI* ± chamber**) *MDI (Metered Dose Inhaler) - MDI adapters available for ET tube **Chamber (valved spacer device) - use of chamber is recommended Management: CAEP Moderate: O2 ß agonist (MDI* ± chamber**) systemic corticosteroids anticholinergics may be helpful in some cases Frequent FEV1 /PEFR to evaluate response to treatment Management: CAEP Severe: 100% O2 anticipate the need for intubation frequent/continuous ß agonist and anticholinergic (nebulized or MDI* with chamber**) Management: CAEP Severe: Systemic corticosteroids Cardiac monitoring Oximetry, ABG's, CXR Frequent reassessment Spirometry when possible Physician and nursing supervision until clear signs of improvement UNRESPONSIVE: Consider near death management Management: CAEP Near Death: 100% O2 paralysis, intubation: modified RSI technique Intubation is a clinical decision continuous ß agonist and anticholinergic (nebulized or MDI* + ETT adaptor) UNRESPONSIVE Rule out pneumothorax or upper airway obstruction consider alternative drugs: I.V. ß agonists, inhalational anesthetic agents Management: CAEP Near Death: Systemic corticosteroids Cardiac monitoring Oximetry, ABG's, CXR Frequent reassessment Spirometry when possible Physician and nursing supervision until clear signs of improvement Ventilatory Strategies: Cautious CO2 reduction with permissive hypercapnea until lung function improves “Controlled mechanical hypoventilation” Bicarb as needed to keep pH>7.2 Slow RR (6-8 breaths/min) to reduce barotrauma and volutrauma Low I:E ratios Low tidal volumes (6-8 mL/kg) Frequent suctioning of mucous secretions as required OXYGEN Will not suppress respiratory drive in acute asthma Start high: FiO2 40-100% Achieve O2Sat 92-95% ß agonists: first line therapy titrate to response (adults and children) e.g. inhaled salbutamol: 100 µg/puff Relaxes bronchial smooth muscle and promotes mucociliary clearance MDI 4-8 puffs q15-20 min X 3 is usual, increase to 1 puff q 30-60 sec (4-20 puffs) prn wet nebulizer 5.0 mg ( 1 ml/3ml ns) q 15-20 min. X3; continuous if necessary administer with oxygen Increase dose for intubated patients ß agonists: first line therapy Several RCT’s have shown equivalent efficacy between MDI + spacer and nebulizers in the emergency treatment of acute asthma Rodrigo et al, American Journal of Emergency Medicine, 1998 Schuh et al, J Pediatr, 1999 For outpatient ß agonist use, MDI’s are equivalent to all other hand held inhaler devices, and remain the most cost effective delivery system. Ram et al, BMJ, 2001 Anticholinergics e.g. inhaled ipratropium bromide (20 µg/puff) Inhibits acetylcholine-mediated bronchoconstriction and decreases mucous production. Not systemically absorbed Peak effect in 60 minutes Indicated for moderate and severe asthma in both adults and children Anticholinergics Zorc et al, Pediatrics, 1999: 427 children>12 months were randomized in a blinded fashion to either ipratropium (250 mcg/dose) or normal saline with each of the first three nebulized albuterol doses. The addition of the ipratropium to a standard ED treatment protocol for acute asthma was associated with reductions in duration and amount of treatment before discharge Anticholinergics MDI 4-8 puffs q15-20 min X 3 is usual, increase to 1 puff q 30-60 SEC (4-20 puffs) prn Wet nebulizer .25. - .5 mg ( 1 -2ml/3ml NS) q 15-20 min. X3; continuous if necessary Decrease frequency in recovery phase May be mixed with ß agonists Corticosteroids All patients seen in ER for asthma should be considered for oral or IV steroids Associated with rapid resolution of airflow obstruction and decreased relapse rate Oral and IV are equally efficacious No good evidence regarding best dose Accepted doses are 100-200 mg of methylprednisolone or equivalent or 5001000mg of hydrocortisone or equivalent, oral doses should be in the range of 40mg of prednisone or equivalent Corticosteroids at d/c: Patients discharged from the ED who require steroid therapy should be given 30-60 mg of prednisone orally for 7-14 days (CMAJ, Guidelines for the emergency management of asthma in adults, 1999) Children: 1-2 mg/kg per day for a total of 5 days Decadron has not been widely used or studied but may be an alternative in children Inhaled Corticosteroids Should be prescribed at discharge but not a component of emergency management CMAJ, Guidelines for the emergency management of asthma in adults, 1999 Dose-related systemic adverse effects, especially at doses >0.8mg/d of fluticasone or equivalent Lipworth, Systemic Adverse Effects of Inhaled Corticosteroid Therapy, Arch Intern Med, 1999. Intubation agents: Induction: Ketamine 1.5 mg/Kg I.V. Add atropine in kids Paralysis: Succinylcholine 1.5 mg/Kg I.V. Roc/vec/pavulon for maintenance of paralysis only Alternative Drugs (Not usually required) May be Associated With More Toxicity Patients unresponsive to treatment may benefit from I.V. ß agonists or inhalational anesthetic agents. These forms of therapy may require consultation with respirology, ICU, anesthesia or internal medicine. Alternative Drugs Adrenaline (1:1000) S.C. 0.3 - 0.5 ml q 15 - 20 min prn (1 ml 1:1000 in 250 D5W = 4 µg/ml) I.V. Infusion: 4-8 µg/min Kids: 0.01mL/kg of 1:1000 S.C. Alternative Drugs Salbutamol (I.V. solution only) Load: 4µg/Kg (over 2-5 min) I.V. Infusion: 0.1 - 0.2 µg/Kg/min Methylxanthines (Aminophylline) Load: 3 - 6 mg/Kg I.V. over 30 min (1/2 if already taking) infusion: 0.2 - 1 mg/Kg/Hour (follow levels). Not usually recommended as Bronchodilator in the first 4 hours of treatment. Alternative Drugs Magnesium: Controversial: Some evidence for IV use in severe asthma Smooth muscle relaxant Adults (AMA guidelines): Severe / Near Death Asthma sats<90%, PEF/FEV1<40% consider 2gm MgSO4 IV over 20 mins Peds: Severe / Near Death Asthma (sats<92%,PEF/FEV1<50% of pb/predicted consider 25mg/kg MgSO4 IV over 20 mins Alternative Drugs Heliox: Mixture of helium and oxygen Low-density gas mixture which is thought to reduce turbulent airflow Must be at least 60% helium which presents a problem in hypoxic patients Evidence is limited Can be considered in a limited group of nonhypoxic severe asthmatics Alternative Drugs Leukotriene Modifiers: Potent bronchodilator with additive effect to B2-agonists Direction for the future May have a role in acute treatment of asthma, but that remains to be investigated Disposition: CAEP guidelines Pretreatment < 25% predicted or best (FEV1 < 1.0 L; PEFR < 100 L/min)* Admission is usually necessary Disposition: CAEP guidelines Post Treatment 1. < 40% predicted or best (FEV1 < 1.6 L; PEFR < 200 L/min)* Admission recommended 2. 40-60% predicted or best (FEV1 < 1.6-2.1 L; PEFR < 200-300 L/min)* Discharge Possible 3. > 60% predicted or best (FEV1 > 2.1 L; PEFR > 300 L/min)* Discharge likely Patients at Risk for Relapse 1. Previous near death episode. 2. Recent E.D. visits. 3. Frequent hospitalizations. 4. Steroid dependent or recent use. 5. Sudden attacks. 6. Allergic/anaphylactic triggers. 7. Prolonged duration of recent attack. 8. Poor compliance or understanding. 9. Returning to same environmental triggers. Discharge instructions: MEDICATIONS A. ß agonists: 1. Regular use often required for 48 hours (24 puffs Q4h). 2. PRN use after 48 hours if symptoms controlled 3. If unable to control symptoms with ß agonists return to E.D. or see your physician. Discharge instructions: B. Corticosteroids - indicated for most patients 1. 2. 3. Prednisone: 30-60 mg/day for 7-14 days taper or discontinue based on asthma control/physician advice Individual plans based on past treatment/recent symptoms Inhaled: Continue at previous dose even if taking prednisone. Initiate at 500-1000 ug/day (Beclomethasone/Budesonide or equivalent). Higher doses may be necessary. Consider as integral part of long term management. Discharge instructions: Anti inflammatory medications (nonsteroid) 1. To be continued on discharge. 2. Role in long term management to be assessed by family physician or consultant. PATIENT INSTRUCTIONS Review: 1) Drug Delivery Technique (puffer, spacer device, powder delivery) 2) Role of relievers (ß agonists) and preventers (anti inflammatory) Explain: Treatment failure: indications for emergency assessment or physician advice. This should be based on signs, symptoms and medication requirements, e.g. dose (number and frequency of puffs) of ß agonist required for relief or control of symptoms. PATIENT INSTRUCTIONS Educate: The Lung Association, Asthma and Allergy Information Association and the Asthma Society of Canada has educational materials and some communities have formal education programs. Refer: Consider respirology, internal medicine, allergy/ immunology consultation for high risk patients. Worsening/ persisting symptoms, modify dose and schedule of steroid therapy. Follow up with family MD or consultant in 1-7 days to assess response. Chronic Management Considerations: Environmental control Short-acting B2-agonists on demand Regular inhaled glucocorticoid for all but the mildest of asthmatics (if B2-agonist is needed>3 times per week, other than for exercise, inhaled glucocorticoid should be added) If asthma is not adequately controlled by moderate doses (500-1000mcg/d of beclomethasone or equivalent) additional therapy should be added…consider long-acting B2-agonists, leukotriene antagonists or other medications Severe asthma may require additional treatment with prednisone CMAJ, Canadian Asthma Consensus Report, 1999 COPD ATS Definition: A disease state characterized by the presence of airflow obstruction due to chronic bronchitis or emphysema Progressive Airway hyperactivity, if present, may be partially reversible COPD: Definitions Chronic Bronchitis: Presence of chronic productive cough for 3 months in each of 2 successive years in a patient in whom other causes of chronic cough have been excluded Emphysema: Abnormal permanent enlargement of the airspaces distal to the terminal bronchioles, accompanied by destruction of their walls and without obvious fibrosis Tintinalli, Emergency Medicine, 2000 Epidemiology Sixth leading cause of death in the world in 1990 (WHO) Leading cause of morbidity and mortality among smokers > 55 yrs Rare in those under age 40 Men>women, but this is changing as more women smoke Mortality for patients hospitalized with a COPD exacerbation is estimated at 5-14% Pathophysiology Smoking accounts for 80-90% of risk Environmental factors have been suggested: occupational exposure, air pollution, second hand smoke Genetic factors:α1-antitrypsin deficiency Earliest detectable changes in COPD evolution are evident as small increases in peripheral airway resistance or lung compliance Pathophysiology Disease progression is slow and insidious, spanning decades; may be masked by sedentary lifestyle of most smokers Abstinence from smoking is most advantageous during early course of disease Variability in disease pattern and progression between similar patients…much is still unknown Pathophysiology Airflow impedance (expiratory mostly) results primarily from increased resistance or decreased caliber of the small bronchi and bronchioles Airway secretions, mucosal edema, bronchospasm, and bronchoconstriction from decreased airway elasticity are all responsible for airflow obstruction Increased airway resistance = reduced minute ventilation +/- increased work of breathing Pathophysiology Alveolar hypoventilation = hypoxemia + hypercarbia V/Q mismatching Pulmonary hypertension RV hypertrophy then dilatation Cor pulmonale Clinical Presentation Chronic Stable COPD: Symptoms: Exertional dyspnea Cough Exam: Tachypnea Accessory muscle use “Pursed-lip” breathing Expiratory wheeze Coarse crackles Reduced air entry Clinical Presentation Acute exacerbation of COPD: Patients present complaining of: Worsening dyspnea Increased sputum volume Increased sputum purulence Hypoxemia, tachypnea, cyanosis, agitation, tachycardia, hypertension, acc mm use, pursed-lip exhalation, “sitting up leaning forward” posture Hypercapnea may result in confusion, tremor, decreased LOC Respiratory failure Causes of AECOPD Superimposed respiratory infection Cardiovascular deterioration Smoking Noncompliance with meds Environmental exposures Meds: e.g. β-blockers, benzos, narcotics Misuse of oxygen therapy Metabolic derangements DDX AECOPD: Pneumonia IHD CHF Asthma PE Pneumothorax Etc. Diagnostic Tests Pulse Oximetry: Easy, immediate, noninvasive test that provides information about the severity of respiratory compromise in an acute exacerbation ABG: Provides accurate information about pH, PaO2 and PaCO2 Consider in most if not all patients presenting with an acute exacerbation Diagnostic Tests PFTs: FEV1 as compared to percent predicted is an excellent measure of disease severity As FEV1 falls below 25-30% of predicted, both hypoxemia and hypercarbia usually occur PEF can be used in ED to estimate FEV1, with the understanding that PEF is effort dependent and tends to overestimate lung function in the mid ranges Diagnostic Tests CXR: Almost always abnormal, comparisons with prior exams should be made Helpful in the diagnosis of complications such as pneumothorax, pneumonia, pleural effusions, pulmonary neoplasia Infectious Precipitants Viral infections often implicated in COPD exacerbations: influenza, PAI, RSV Atypical organisms may also be involved: Mycoplasma, Chlamydia pneumoniae, Legionella Chronic colonization also occurs, most often with H. flu, Strep pneumo, and Moraxella…role of these organisms in exacerbations is controversial. CAP in AECOPD COPD patients are at high risk for CAP Symptoms of CAP are similar to those of AECOPD: sputum, fever, cough Strep pneumo is most common, followed by H flu, and Moraxella Catarrhalis Legionella and Pseudomonas should always be considered Pneumovax and yearly influenza vaccines are important prevention Antibiotics in AECOPD Controversial and difficult to study Currently accepted practice based on the best evidence is that patients presenting with infectious symptoms: Fever Increased sputum production Change in character of sputum will have a better outcome with the use of empiric antibiotic therapy Antibiotics in AECOPD Increasing evidence for newer antibiotics as first line therapy: azithromycin, respiratory fluoroquinolones, β-lactamase inhibitors. Antibiotics in AECOPD CHA recommendations: <4 exacerbations/year: Amoxicillin 500mg po tid x 7-10d Doxycycline 200mg po x 1d then 100mg po od x 7-10d TMP/SMX 1 DS tablet po bid x 7-10d Antibiotics in AECOPD CHA recommendations: > or = 4 exacerbations per year or failure of first line agent or Abx last 6 weeks: Cefuroxime axetil 250-500mg bid x 7-10d Amoxicillin-clavulanate 875mg po bid x 7-10 d For pen allergic patients: Azithromycin 500mg x 1d then 250mg po od x 4d Clarithromycin 250-500mg po bid x 7-10d Levofloxacin 500mg po od x 5-10d Moxifloxacin 400mg po od x 5-10d Management of stable COPD Lifestyle modifications: Smoking cessation Regular exercise Weight control Pulmonary rehabilitation Prevention: Pneumovax Influenza Management of stable COPD Oxygen Started after room air ABG’s document PaO2<55 or 56-59 in the face of cor pulmonale Bronchodilators: β-agonists Ipratropium bromide Long acting β-agonists +/- Theophylline Management of stable COPD Steroids: 20-30% are steroid responders Inhaled or oral Management: AECOPD Goals of therapy: Relieve bronchoconstriction Improve oxygenation Approach to treatment: Multi-modal Be cognizant of previous disease pattern Management: AECOPD Oxygen: All patients in respiratory distress should receive supplemental oxygen Target O2sat>90% Be aware that patients known to be CO2-retainers may require controlled oxygen therapy Hypercarbia is likely secondary to the Haldane effect: a shift of the hemoglobin-CO2 binding curve, as well as due to increased CO2 production and changes in physiologic dead space Management: AECOPD β2-agonists: COPD patients will have some reversibility to their airflow obstruction that can effectively be relieved by inhaled short acting β2-agonist therapy Long acting β2-agonist therapy should be reserved for chronic management only No evidence that one specific agent has any greater efficacy than any other Little evidence regarding timing of administration (q60 min vs. q20 min etc.) Management: AECOPD Anticholinergics: Preferentially dilate larger central airways compared to β2-agonists which dilate peripheral airways Slower onset of action than β2-agonists Thought to inhibit vagal stimulation of the bronchi…thereby promoting smooth muscle relaxation Atropine and glycopyrrolate have been used Most common agent is ipratropium bromide q4-6h by neb or MDI Management: AECOPD Theophylline: Controversial Narrow therapeutic window Significant side effects: dysrhythmias, seizures Limited evidence for efficacy Management: AECOPD Corticosteroids: Conflicting results in the literature In acute exacerbation, there is likely a role for systemic steroids, but not for inhaled Steroid response is likely a continuum rather than an “all or none” phenomenon Management: AECOPD Magnesium: Studied mostly in asthma One study showed benefit in COPD, used as 1-2g IV over 20 min Heliox: No large-scale studies Probably should only be considered as a last alternative Mechanical Ventilation: the controversies Widespread fear among healthcare workers that patients will become ventilator dependent Evidence suggests that most patients in fact will be extubated around day 10 but that 1-5 year mortality rate following an episode of respiratory failure is very high Likely a decision that should be addressed by the patient, family, primary health care provider PRIOR to the actual event Mechanical Ventilation Decision to begin assisted ventilation is a clinical one Noninvasive ventilation (BiPAP): BiPAP works by providing nasal, bilevel positive airway pressure. This overcomes the intrinsic PEEP of most COPD patients, and significantly reduces work of breathing, thereby improving gas exchange Response is usually seen within the first hour Should be considered first line before endotracheal intubation unless patient has impaired mental status or cardiovascular instability Mechanical Ventilation Kramer et al Selection criteria for NPPV (any two): Moderate to severe dyspnea with use of accessory muscles and paradoxical abdominal motion Moderate to severe acidosis (pH 7.3-7.35) and hypercapnia (PaCO2 45-60) Respiratory frequency > 25 breaths/min Mechanical Ventilation Kramer et al Exclusion Criteria for NPPV (any one): Respiratory arrest Cardiovascular instability (hypotension, dysrhythmias, AMI) Somnolence, impaired mental status, uncooperative patient High risk of aspiration Viscous or copious secretions Recent facial or gastroesophageal surgery Craniofacial trauma with fixed nasopharyngeal abnormalities Extreme obesity Mechanical Ventilation Indications for invasive mechanical ventilation in AECOPD (Pierson, Respiratory Care, 2002) Severe dyspnea with accessory muscle use and paradoxical abdominal motion RR>35 Life-threatening hypoxemia (PaO2<40) Severe acidosis (pH < 7.25) and hypercapnea (PaCO2 > 60) Respiratory arrest Somnolence or impaired mental status Cardiovascular complications Other complications (sepsis, pneumonia, PE…) Failure of NPPV Disposition Consider Overall respiratory status post-treatment Home environment Mental status Comorbid illness Age Compliance Previous pattern of illness Keep in mind high relapse rate Disposition Treatment at home: O2 if needed Inhaled β2-agonists Inhaled anticholinergic agents Proper inhaler technique (review prior to discharge) Corticosteroids +/- Theophylline +/- Antibiotics