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