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Asthma in the emergency department
Asthma is a chronic inflammatory airway disease characterized by reversible airway obstruction. During an exacerbation, patients experience worsening symptoms such as shortness of breath, cough, and wheezing. The document outlines guidelines for assessing and managing acute asthma exacerbations in the emergency department. Treatment involves administering inhaled bronchodilators, systemic corticosteroids, supplemental oxygen, and magnesium sulfate for severe exacerbations. The document also provides guidance on determining whether patients can be discharged or require hospital admission based on post-treatment lung function.
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Asthma in the emergency department
- 1. Asthma in theEmergency Department BY DR.MAHMOUD ALFEKY Pulmonary Diseases specialist MSc. Chest Diseases and tuberculosis, Faculty of Medicine, Cairo University
- 3. What is Asthma? • Chronic inflammatory disorder of airways • Inflammation causes airway hyper - responsiveness often associated with symptoms (wheezes, cough, SOB). • Obstruction is reversible
- 4. Pathophysiology of Asthma(3Ss) • 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
- 5.
- 6. Asthma Exacerbation •Episodes of progressive increase in shortness of breath, cough, wheezing, or chest tightness, or some combination of these symptoms. • Respiratory viral infection, the main trigger of severe exacerbations of asthma.
- 7. Which aspects ofasthmatics history are important to current exacerbation?
- 9. Others • Priorhospitalizations • ICU admissions • Recent ED visits • Current meds • Co-morbid conditions
- 10. How to assessAsthma severity? Due to be updated 2007
- 11. Indicators of SevereAsthma 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)
- 12. Risk Factors fordeath From Asthma
- 13. Risk Factors forDeath From Asthma ((ccoonnttiinnuueedd))
- 14. Management of severeasthma Aim: 1 -Correction of significant hypoxemia. Oxygen 2- To relieve airflow obstruction Repetitive administration of rapidly acting bronchodilators. Early systemic corticosteroids
- 15. Oxygen Assessment •Pulse oximetry - in all severe asthmatic patients. • Arterial desaturation and hypercarbia only develop in life-threatening asthma. • As result, pulse oximetry is a suitable means for routine assessment of ventilatory status. • Measure PEFR: patients with severe distress if PEFR <50% predicted
- 16. In interpretation ofarterial blood gases • in patients with suspected hypoventilation, severe distress, or with or PEFR <30% predicted after initial treatment • primarily on PaCO2 with normal value in breathless asthmatic being a warning sign of impending hypoventilation.
- 17. • values above(45 mm Hg) indicating a life threatening attack and probable need for transfer to a high dependency unit or intensive care unit (ICU). OXYGEN To achieve arterial oxygen saturation of greater than or equal to 90 percent, oxygen should be administered by nasal cannulae or by mask
- 18. CXR, Bloods andother investigations • Chest radiograph is not routinely needed, for: 1. those who do not respond to initial treatment 2. other diagnosis as pneumothorax or pneumonia. • Microbiological investigations are seldom required, although purulent sputum should be cultured if present.
- 19. Inhaled bronchodilators •Inhaled b2-agonists are the mainstay of bronchodilator therapy • Metered dose inhalers with a spacer produce outcomes that are at least equivalent to nebulizer therapy in severe asthma • The addition of ipratropium bromide to inhaled b2-agonist therapy provides an increase in the bronchodilator response in severe asthma.
- 20. • If PEFR<50%: Inhaled high-dose beta2-agonist and anticholinergic (ipratropium bromide) by nebulization every 20 minutes or continuously for 1 hour. • Repeat assessment (symptoms, physical exam, PEF, O2 saturation, other tests as needed)
- 21. Systemic corticosteroids •There is no benefit in using very high intravenous doses in severe asthmatics needing hospital admission. • 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 P.O in doses of 40- 60mg • Side effects of short term steroid use include rise in glucose, fluid retention, decrease in potassium, peptic ulcers.
- 22. Route of administration • Oral cortisones are usually as effective as intravenous and are preferred because this route of delivery is less invasive and less expensive. • If vomiting has occurred shortly after administration of oral cortisones, then an equivalent dose should be re-administered intravenously. • In patients discharged from the emergency department, intramuscular administration may be helpful. • Oral cortisones require at least 4 hours to produce clinical improvement.
- 23. Is there arole for IV aminophylline • Has been used for hundred’s of years • Narrow therapeutic window, should only be considered as an alternate therapy • Increase in adverse effects (palpitations, vomiting) • Used in severe life threatening asthma • Serum theophylline concentration must be done first.
- 24. 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. • Currently, a single dose (2 g MgSO4 diluted in 50 ml 0.9% normal saline administered over 30 min) . • If an intravenous bronchodilator is to be administered, current evidence favours the use of intravenous magnesium rather than intravenous b2-agonist or aminophylline.
- 25. Should IV b2-agonisttherapy be used? • No significant differences were found in IV b2-agonists in addition to, or instead of, inhaled b2-agonists • If the patient can tolerate inhaled b-2 agonists, there is no evidence to support the use of IV b2-agonists
- 26. Does Pregnancy changethe 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”
- 27. How can Itell if my patient is improving? • Ask them how they feel • Re-examine • Obtain objective measurements (PEFR)
- 28. Who should beintubated? • Endotracheal intubation is not curative, only a very small percentage of patients presenting to the ED with acute severe asthma will require endotracheal intubation and assisted ventilation. • Exhaustion, hypoxaemia, deterioration in clinical features despite optimal therapy, PaCO2 is increasing, and depression of mental status strongly indications for intubation
- 29. How should Idecide if my patient can be discharged? Hospitalize 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. • Patients with post-treatment lung function ≥ 60 % predicted can be discharged.
- 30. Antibiotics in severeasthma • 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.
- 31. SEDATION should bestrictly avoided during exacerbations of asthma because of the respiratory depressant effect of hypnotic drugs.
- 32. ANTIHISTAMINICS and CHEST PHYSICAL THERAPY No established role in the treatment of acute asthma exacerbations.