Asthma and COPD in the Emergency Department

Sa’ad Lahri Registrar

Department of Emergency Medicine UCT / Stellenbosch University

Synopsis

• Focus on ED management with emphasis that Emergency Medicine is a : “Prevention, Resuscitation, Stabilization and appropriate disposition”1 specialty.

1. The Emergency Medicine Consultation : revisited : letter to the editor South African Family Practice 2006 – Sa’ad Lahri

What is Asthma?

• Chronic inflammatory disorder of airways

• Inflammation causes airway hyper - responsiveness often associated with symptoms (wheeze, cough, SOB).

• Obstruction is reversible

What is the Pathophysiology of Asthma?

• Pathological changes found in asthma are the 3 “S”s:

• 1. Spasm of smooth muscle hypertrophy which

contracts during an attack• 2. Swelling or oedema of bronchial mucosa• 3. Secretions from hypertrophy of mucus glands

leading to thick & tenacious mucus

• All the above cause bronchial narrowing

What is an Asthma Exacerbation?

• Episodes of progressive increase in shortness of breath, cough, wheezing, or chest tightness, or some combination of these symptoms.2

2. Global Strategy for Asthma Management and Prevention

www.ginaasthma.org

Cont… What is an Asthma Exacerbation?

• Represent an exaggerated lower airway response to an environmental stimulus.

• Respiratory viral infection - main trigger of severe exacerbations of asthma.

• Airway inflammation is a key pathogenic feature

Which aspects of asthmatics history are important to current exacerbation?

Other Q’s3

• Prior hospitilizations• ICU admissions• Recent ED visits• Current meds• Co-morbid conditions

3. Emergency Medicine Secrets 4th Edition

How to assess Asthma severity?

Due to be updated 2007

Indicators of Severe Asthma: Clinically

• Anxious & diaphoretic appearance• Breathlessness at rest; inability to speak in full sentences• PaCO2 normal or increased• PEFR < 150 L/min or <50% predicted• Pulse oximetry < 91% on room air• Tachycardia (HR>120) and tachypnea (RR>30)

• Expert Panel Report 2: Guidelines for the diagnosis and management of asthma. National Institute of Health- National Heart, Lung and Blood Institute 1997; NIH publication number 97-4051

Key objectives of management

Global Strategy for Asthma Management and Prevention

www.ginaasthma.org

• Aim: - To relieve airflow obstruction and hypoxaemia - To prevent relapses • Repetitive administration of rapidly acting

bronchodilators.• Early systemic corticosteroids.• Oxygen • Complications - (pneumothorax)

Oxygen Assessment Tests

• Pulse oximetry - in all severe asthmatic patients.

• Arterial desaturation and hypercarbia occur concurrently and normally only develop in life-threatening asthma.

• As result, pulse oximetry is a suitable means for routine assessment of ventilatory status.

Blood Gas?

• Analysis of arterial blood gases can be selectively reserved:

• oxygen saturations on room air of < 92%• do not respond to initial treatment, with the FEV1 remaining 30%.

In interpretation of arterial blood gases, attention focuses• primarily on PaCO2 with normal value in breathless asthmatic being

a warning sign of impending hypoventilation.• values above 6 kPa (45 mm Hg) indicating a life threatening attack

and probable need for transfer to a high dependency unit (HDU) or intensive care unit (ICU).

CXR, Bloods and other investigations?

• Chest radiograph is not routinely needed, being reserved for: 1. those who do not respond to initial treatment 2. or in whom alternative diagnosis such as pneumothorax or pneumonia is suspected.

• The serum potassium concentration should be measured, particularly in patients with prior corticosteroid or diuretic treatment.

• Hypokalaemia caused primarily by high dose b-agonist therapy is not uncommon in severe asthma and may require potassium supplementation.

• Microbiological investigations are seldom required, although purulent sputum should be cultured if present.

Inhaled bronchodilators

• Inhaled b-agonists are the mainstay of bronchodilator therapy

• Metered dose inhalers with a spacer produce outcomes that are at least equivalent to nebuliser therapy in severe asthma

• These finding includes those with life-threatening asthma, with an FEV1 <30% predicted on presentation.

• As a guide, 400 mg salbutamol via a spacer can be considered equivalent to a 2.5 mg dose of salbutamol via nebuliser. (no spacers ever seen in Casualty!)

• The addition of ipratropium bromide to inhaled b-agonist therapy provides an increase in the bronchodilator response in severe asthma.

• One important indication for the use of anticholinergic bronchodilators is as first-line treatment for b-blocker induced attacks.

Systemic corticosteroids:

• The major issue is the optimal dose and route of administration.

• There is no benefit in using very high intravenous doses in severe asthmatics needing hospital admission.

• In terms of lower doses, the most informative double-blind randomised study has shown that intravenous hydrocortisone 50 mg four times a day for two days, followed by prednisone 20 mg daily, is as effective in resolving acute severe asthma as either hydrocortisone 200 mg or 500 mg four times daily followed by prednisone 40 or 60 mg daily, respectively.

• Prednisone is commonly given po in doses of 40-60mg• Side effects of short term steroid use include rise in glucose, fluid retention,

decrease in potassium, peptic ulcers.

Route of administration• Oral glucocorticosteroids are usually as effective as those administered

intravenously and are preferred because this route of delivery is less invasive and less expensive.

• If vomiting has occurred shortly after administration of oral glucocorticosteroids, then an equivalent dose should be re-administered intravenously.

• In patients discharged from the emergency department, intramuscular administration may be helpful , especially if there are concerns about compliance with oral therapy.

• Oral glucocorticosteroids require at least 4 hours to produce clinical improvement.

Global Strategy for Asthma Management and Prevention

www.ginaasthma.org

What about inhaled steroids?• Potential benefits of reduced side-effects, direct airway delivery and greater

efficacy in reducing airway reactivity and oedema.

• Inhaled glucocorticosteroids are effective as part of therapy for asthma exacerbations. (VERY EXPENSIVE)

• In the studies below , the combination of high-dose inhaled glucocorticosteroids and salbutamol in acute asthma provided greater bronchodilation than salbutamol alone (Evidence B), and conferred greater benefit than the addition of systemic glucocorticosteroids across all parameters, including hospitalizations, especially for patients with more severe attacks

Is there a role for IV aminophylline?

• Has been used for hundred’s of years• Cochrane review included 15 trials and found no

benefit over -agonists, in admission rates, even in severe asthma

• Narrow therapeutic window with may significant side effects.

• Increase in adverse effects (palpitations, vomiting)Parameswaran et al. The Cochrane Library,

Issue 3, 2003• No studies compare outcome in patients with severe

asthma who are unable to tolerate inhaled -agonists• There is no evidence supporting its use

Magnesium Sulphate• Intravenous magnesium now recommended in patients with life-threatening

attacks. Not recommended for routine use in asthma exacerbations• Its use leads to an improvement in lung function and a reduction in hospital

admissions in those who respond poorly to initial treatment, but not those with less severe asthma responding to initial treatment.

• Currently, the evidence relates to a single dose (2 g MgSO4 diluted in 50 ml 0.9% normal saline administered over 30 min) and the efficacy of a continuous infusion or repeated dose has yet to be determined.

• If an intravenous bronchodilator is to be administered, current evidence favours the use of intravenous magnesium rather than intravenous b-agonist or aminophylline.

• Nebulized salbutamol administered in isotonic magnesium sulfate provides greater benefit than if it is delivered in normal saline (Evidence A) contentious !!!

Should IV -agonist therapy be used?

• Meta-analysis evaluated 9 RCTs comparing IV -agonists in addition to, or instead of, inhaled -agonists in severe asthma in adults

• No significant differences were found in multiple outcome measures between the two groups

• If the patient can tolerate inhaled -agonists, there is no evidence to support the use of IV -agonists

Travers et al. The Cochrane Library, Issue 3, 2003.

Does IV ketamine improve outcome?

• Ketamine is a bronchodilator, potentiates catecholamines• 44 consecutive patients with severe asthma attacks

received IV ketamine (0.1 mg/kg bolus and 0.5 mg/kg/hour infusion) for 3 hours

• Ketamine was used in conjunction with other standard therapies

• No difference in PEFR or hospital admission

Howton. Randomized, double-blind, placebo-controlled trial of IV ketamine in acute asthma. Annals of Emergency Medicine. 27(2). 1996.

What about Adrenalin?

• Non selective Beta agonist that requires (IV/sub cut) admin.

• Effective bronchial smooth muscle dilator with rapid onset of action.

• Use for very severe and life threatening asthma.

• “If you hesitate to give epinephrine to a severely distressed asthmatic, you should consider the fact that if the patient deteriorates further and suffers cardiorespiratory arrest the first drug you will administer is epinephrine 1mg IV”

• ACLS for experienced providers AHA 2003

Does Pregnancy change the management of acute asthma?

• NO! • Treat Aggressively

• Prevent Maternal Hypoxia

• Fetal Morbidity/Mortality• “Risks from respiratory failure and severe acute

asthma are greater than from therapy with standard medications”

Emergency Medicine Secrets 4th Edition

Non-invasive positive pressure ventilation (NIPPV)

• Well established role in the management of exacerbations of COAD, its role in the management of severe asthma is less clearly defined.

• May be useful in patients with hypercapnic respiratory failure as long as they are protecting their own airways

• NIPPV can reduce the work of breathing and respiratory muscle fatigue, thus buying time for transfer to ICU.

• There is concern that it may delay intubation in deteriorating patients.

DO not use NIPV in Asthma

How can I tell if my patient is improving?

• Ask them how they feel

• Re-examine

• Obtain objective measurements (FEV/PEFR)

Who should be intubated?

• Endotracheal intubation is not curative, is associated with significant morbidity, and can increase the degree of airway narrowing and inflammation. Only a very small percentage of patients presenting to the ED with acute severe asthma will require endotracheal intubation and assisted ventilation.

• With the exception of apnoea, or coma no other indications for intubation.

• Exhaustion, hypoxaemia and depression of mental status strongly argue for intubation

• ( if they are distressed and tiring – intubate as with all other patients)

Rapid Sequence Intubation in the Asthmatic

• Oxygenate

• Premedicate ( disagreement – intubate like any other

propofol/etomidate etc)

– Lidocaine

(2mg/kg) reduce bronchospasm induced by larngoscopy

– Induction with ketamine (preferred agent)

• Paralysis with succinylcholine

• Intubation with large ETT(larger tube less airway resistance)

How should I decide if my patient can be discharged?

• Hospitalise Patients with a pre-treatment

FEV1 or PEF < 25% percent predicted or personal best, or those with a post-treatment FEV1 or PEF < 40% percent predicted or personal best, usually require hospitalization.

• Discharge• Patients with post-treatment

lung function of 40-60% predicted may be discharged, provided that adequate follow-up is available in the community and compliance is assured.

• Patients with post-treatment lung function ≥ 60 % predicted can be discharged.

Global Strategy for Asthma Management and Prevention

www.ginaasthma.org

For patients discharged from the emergency department:

• At a minimum, a 7-day course of oral glucocorticosteroids for adults

• The bronchodilator can be used on an as-needed basis, based on both symptomatic and objective improvement, until the patient returns to his or her pre exacerbation use of rapid-acting inhaled 2-agonists.

• Use of peak flow meter to monitor therapy at home should be reviewed.

• Patients discharged from the emergency department with a peak flow meter and action plan have a better response than patients discharged without these resources

Global Strategy for Asthma Management and Prevention

www.ginaasthma.org

Antibiotics?

• Purulent sputum may not indicate infection, and is usually a result of eosinophils in respiratory secretions

• Antibiotics should not be routinely prescribed as bacterial infections seldom provoke exacerbations (in contrast to viral respiratory tract infections), and their routine prescription does not influence outcome in exacerbations of asthma.

Key points

• Reverse airway obstruction

• Reduce the likelihood of recurrence

• Relieve significant hypoxaemia

• Check for objective measurement of improvement

• Adequate discharge includes education, Medications and follow –up.