Department
Cezar Darwiche FY1
Asthma
Chronic inflammatory disease of the
airways
Episodic cough, wheezing, dyspnea
Type I hypersensitivity reaction (Ag cross
links IgE on pre-sensitized mast cells and basophils triggering release of vasoactive amines) Types
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Extrinsic
- Onset in childhood
-Triggered by inhaled allergen exposure:
Dust mites
Cockroaches
Cat antigen
Molds and pollens
Types
Intrinsic
Early adulthood
• Triggered by viral infections, nonspecific irritants • Obesity risk factor
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Types
Exercise-induced
Bronchospasm lasting 10-20 mins after exercise • Triggered by drying/ cooling of airways
• Requires prophylaxis
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Types
Triad Asthma
Samter’s Syndrome …show more content…
Failure to respond satisfactorily
Requirement for ventilation
Emergency management
If improving
40-60% O2
• prednisolone 40-50mg/ 24hrs PO
• Nebulized salbutamol every 4hrs
• Monitor peak flow
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Emergency management
If not improving after 15mins
Continue 100% O2
• Repeat steroids
• Salbutamol nebulizers every 15min or
10mg continuous per hour
• Ipratropium 0.5mg every 4-6hrs
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Emergency management
If patient still not improving at >30mins
Consider MgSO4 1.2-2g IV over 20mins
• Aminophylline IV
• Transfer to ICU for ventilation
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Emergency management
Monitoring
Repeat PEF 15-30mins after treatment
• Pulse oximetry monitoring maintain SaO2
>92%
• ABG within 2hrs if initial PaCO2 was normal/raised or initial PaO2 <60mmHg
• Record PEF pre and post B2 agonist in hospital at least 4 times
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Emergency management
Patient has improved
Stop Aminophylline over 12-24hrs
• Reduce nebulized Salbutamol and switch to inhaled B2 agonist
• Stop oral steroids and initiate inhaled
• Monitor PEF
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Emergency management
Cardiac Arrest in Acute severe ashtma
Usually PEA
Due to :
• Prolonged severe hypoxia
• Hypoxia related arrythmia
• Tension pneumothorax
• Acidosis and hyperkalemia
• Follow ACLS guidelines