ASTHMA DEATHS

Scene – presence of inhalers

History – may be absent/ incorrect; any allergen exposure?; Iatrogenic cause of attack e.g. bronchoscopy, B blockers etc

External – exclude trauma/ subcutaneous emphysema

Internal

Lungs – hyperinflation; outlines of ribs present on surface; lungs may resist pressure to collapse them; petechial haemorrhage beneath visceral pleura; airway plugging (occlusive, tenacious, viscid); congested/ oedematous mucosa

Histology

Mucus plugging of airways (increased bronchial gland secretions, up regulation of mucin gene MUC 5AC; goblet cell hyperplasia)

Epithelial loss (desquamation at level of columnar cells leaving intact basal layer. Clumps of epithelial cells (creola bodies) seen in sputum of asthmatics, especially during exacerbations. May be due to damage from eosinophil granule proteins; selective down-regulation of intercellular adhesions or viral infection. May contribute to hyper responsiveness due to exposure of underlying sensory nerves, a loss of epithelium derived relaxing factors and a reduced muco-ciliary clearance)

Neutrophilia of airway walls (neural sensitivity and sudden airway narrowing)

Bronchial gland duct ectasia/ goblet cell metaplasia around necks of glands (due to raised intra-bronchial pressure during acute asthma attacks; obstruction of mouths of mucus glands by viscid mucus plugs and weakening of duct walls secondary to peri-ductal inflammatory infiltrate

Inflammation of bronchial walls – predominantly eosinophils and lymphocytes (CD8+ cytotoxic T cells); higher number of basophils (which can release histamine, leukotrienes and cytokines which may contribute to poor disease outcome)

Remodelling of airways (increase total wall area due to increased smooth muscle thickening, cartilage/ basement membrane thickening and increase in mucus gland area)

Airway blood vessel dilatation/ permeability (increase inflammatory exudate)

Cause of death determination

Asthma on its own not enough – need evidence of disease severity (severe inflammation/ mucus plugs; inadequate treatment history/ compliance problems/ known severe disease)

Differential Diagnosis

PE – can cause recurrent wheeze and reactive outpouring of mucus (but not tenacious; no plugging; not infiltrated with inflammatory cells)

COPD – may co-exist; microscopic features of emphysema may be visible; presence of Right Ventricular Hypertrophy should alert one to COPD)

Sickle Cell – crises may be precipitated by severe asthma/ hypoxia

Anaphylaxis – can get edema/ plugging/ hyperinflation; no airway remodeling (nb. Serum B-tryptase (marker of mast cell degranulation) may be of help, but not very sensitive)