Asthma deaths; persistent and preventable mortality

Sidebotham H.J., Roche W.R. (2003), Histopathology 43: 105-117

Epidemiology

	Affects 20% children; 5% adults in western world
	Increasing prevalence
	1272 deaths in 200 (E&W)

Risk Factors

	increasing age
	increasing disease severity (previous admissions; low FEV1; peripheral blood eosinophilia; high degree of reversibility of bronchospasm with bronchodilator)
	low socio-economic group
	inner city living
	black ethnicity
	smoking
	no spouse
	lack of prescription of inhaled steroids
	poor compliance/ symptom denial
	overlooking nocturnal symptoms
	alcohol/ drug abuse
	use of psychotropic medication

Autopsy in suspected 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)

Asthma histopathology (YouTube)

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 RVH should alert one to COPD)
	Sickle Cell – crises may be precipitated by severe asthma/ hypoxia
	Anaphylaxis – can get oedema/ plugging/ hyperinflation; no airway remodelling (nb. Serum B-tryptase (marker of mast cell degranulation) may be of help, but not very sensitive)

Forensicmed.co.uk book store T-shirt store

This site aims to provide educational resources for medical students in the fields of forensic pathology, clinical forensic medicine, forensic psychiatry and forensic science. All illustrations used are believed to be in the public domain, and royalty free. However, if this is not the case, and you are the copyright holder, I apologise, and will remove the relevant illustrations if required.