Asthma and COPD November 28, 2002 Cass Djurfors Dr. M. Betzner.
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Transcript of Asthma and COPD November 28, 2002 Cass Djurfors Dr. M. Betzner.
Asthma and COPDAsthma 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 exposuresCommon 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 hyperresponsivenessPartially reversible airflow obstruction results from bronchial smooth muscle constriction, airway edema and inflammation, and mucus plugging; bronchoconstriction is superimposed in the acute settingPermanent 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 HistorySocial History: Home environment (smoking, pets, allergens) Identification of precipitating cause
Exacerbation profile: Usual exacerbation pattern and outcome
Past best spirometry measuresMedical history, allergies, anaphylaxisTreatment: 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 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 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 orMDI* with chamber**)
Management: CAEP
Severe: Systemic corticosteroids Cardiac monitoring Oximetry, ABG's, CXR Frequent reassessment Spirometry when possible Physician and nursing
supervision 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 and
anticholinergic (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 nursing
supervision 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>7.2Slow RR (6-8 breaths/min) to reduce barotrauma and volutraumaLow I:E ratiosLow 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/puffRelaxes bronchial smooth muscle and promotes mucociliary clearanceMDI 4-8 puffs q15-20 min X 3 is usual, increase to 1 puff q 30-60 sec (4-20 puffs) prnwet nebulizer 5.0 mg ( 1 ml/3ml ns) q 15-20 min. X3; continuous if necessaryadminister with oxygenIncrease 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, 1998Schuh 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) prnWet nebulizer .25. - .5 mg ( 1 -2ml/3ml NS) q 15-20 min. X3; continuous if necessaryDecrease frequency in recovery phaseMay be mixed with ß agonists
Corticosteroids
All patients seen in ER for asthma should be considered for oral or IV steroidsAssociated with rapid resolution of airflow obstruction and decreased relapse rateOral and IV are equally efficaciousNo good evidence regarding best doseAccepted 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 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/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
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:
MEDICATIONSA. ß agonists:
1. Regular use often required for 48 hours (2-4 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 patients1. Prednisone: 30-60 mg/day for 7-14 days taper or
discontinue based on asthma control/physician advice
2. Individual plans based on past treatment/recent symptoms
3. 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 (non-steroid)
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 controlShort-acting B2-agonists on demandRegular 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 medicationsSevere 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 yrsRare in those under age 40Men>women, but this is changing as more women smokeMortality for patients hospitalized with a COPD exacerbation is estimated at 5-14%
Pathophysiology
Smoking accounts for 80-90% of riskEnvironmental factors have been suggested: occupational exposure, air pollution, second hand smoke
Genetic factors:α1-antitrypsin deficiencyEarliest 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 bronchiolesAirway secretions, mucosal edema, bronchospasm, and bronchoconstriction from decreased airway elasticity are all responsible for airflow obstructionIncreased 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 CAPSymptoms of CAP are similar to those of AECOPD: sputum, fever, coughStrep pneumo is most common, followed by H flu, and Moraxella CatarrhalisLegionella and Pseudomonas should always be consideredPneumovax 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 oneNoninvasive 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