Asthma and COPD

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 • Intermittent airflow obstruction indicated by a history of nighttime cough, recurrent wheeze or recurrent chest tightness. • 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. • 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 agonistfor 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 agonistand or ß agonist neededmore 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 reliefwith 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 agonistand anticholinergic (nebulized orMDI* with chamber**)

Management: CAEP • Severe: • Systemic corticosteroids • Cardiac monitoring • Oximetry, ABG's, CXR • Frequent reassessment • Spirometry when possible • Physician and nursingsupervision until clear signsof 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 andanticholinergic (nebulized orMDI* + 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 nursingsupervision until clear signsof 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 outpatientß 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 500-1000mg 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 maintenanceof paralysis only

Alternative Drugs • (Not usually required) May be Associated With More ToxicityPatients 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/minKids: 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 isusually necessary

Asthma and COPD

Télécharger la présentation

Plus de contenu associé