Causes of Sudden Natural Death

Sudden Natural Death

• WHO defines sudden natural death as death within 24 hours of symptom onset, usually within one hour.
• 80% of routine autopsies involve cases of sudden death.
• Sudden natural deaths can appear as suspicious natural deaths, unnatural deaths mimicking natural deaths, natural deaths aggravated by an unnatural act, or a natural disease contributing to an unnatural death.

Causes of Sudden Death

• Cardiac causes
  • Coronary artery disease (CAD)
    • Coronary artery atheroma (coronary atherosclerosis)
    • Non-atherosclerotic coronary artery disease (e.g., coronary artery vasculitis)
    • Coronary anomalies
  • Myocardial diseases
    • Cardiomyopathies (e.g., hypertrophic, restrictive, dilated)
    • Myocarditis
  • Valvular heart diseases (including congenital)
• Cerebral causes (almost always vascular)
  • Ruptured intracranial aneurysm (SAH)
    • Ruptured berry aneurysm
  • Intracerebral hemorrhage
    • Most common site: internal capsule anteriorly
    • From leniculo-striate vessels (branch of middle cerebral artery)
      • Stroke
      • Hypertension
  • Cerebral tumors
  • Infections
  • Epilepsy
• Pulmonary causes
  • Pulmonary thromboembolism (in 20% of cases without predisposing factor)
  • Bronchial asthma (risk of sudden death, not necessarily from asthma itself)
  • Sponatneous pneumothorax
  • Massive pulmonary hemorrhage
    • Hemoptysis
    • Tuberculosis (T.B.)
    • Lung tumor ulceration
  • Influenza virus infection
• Other causes
  • Gastrointestinal
    • Perforated peptic ulcer
    • Massive gastrointestinal bleeding
    • Acute intestinal obstruction
    • Peritonitis
    • Postoperative bleeding (e.g., after tooth extraction or tonsillectomy)
    • Portal hypertension with esophageal varices
    • Massive hemorrhage from a duodenal ulcer
  • Ion channel disorders
    • Mutations in cardiac potassium channels leading to prolonged QT interval, ventricular tachycardia, syncope, and sudden death
    • Romano-Ward syndrome (autosomal dominant)
    • Jervell and Lange-Nielsen syndrome (autosomal recessive)
      • Sudden death, sensorineural deafness
    • Brugada syndrome (RBBB, ST segment elevation, ventricular arrhythmias, syncope, sudden death)
    • Bangungut, Nonlaiti, Laitai and Pokkuri
  • Sudden infant death syndrome (SIDS)
    • Unexpected death in infants with no identifiable cause from post-mortem.
  • Sudden adult death syndrome (SADS)
    • Unexpected deaths in young adults, commonly males.
    • Often during sleep.
    • No prior warning signs.
    • Often attributed to cardiac arrhythmias.

Cardiac Causes of Sudden Death

• The anterior descending branch supplies most of the septum, apex, anterior wall, and part of the lateral heart wall.
• Common sites of occlusion (atheromatous or thrombosis):
  • First 2 cm of the anterior descending branch of the left coronary artery
  • Distal part of the right coronary artery (when it bends around the right margin of the heart)
  • Proximal part of the circumflex artery
  • Left main trunk

Coronary Artery Atheroma (Coronary Artherosclerosis)

• Atheroma is a paste-like material consisting of intimal thickening of fragmented elastic fibers, foam macrophages, lipids, cholesterol crystals, collagen, calcium, and chronic inflammatory infiltrate.
• Ulceration of plaque surfaces leads to loss of intimal lining with thrombus formation.

Complication of Atheroma

• Progressive narrowing of the lumen
• Plaque rupture
• Sub-intimal hemorrhage
• Thrombosis

Histological Findings (after occlusion)

• No naked-eye changes are visible in the first 24 hours (12-18 hours) after occlusion.
• After the first day, the infarct appears yellowish with red streaks.
• A mucoid grayish zone forms in 1-2 weeks (autolysis).
• No definite histological signs observed in the first half-day, but swollen fibers, granularity, and eosinophilia are present
• Loss of striations and muscle nuclei (variable)
• Leukocyte infiltrate appears after 2 days
• Disintegration of muscle fibers and appearance of new capillaries by the end of the first week

Non-Atherosclerotic Coronary Artery Diseases

• Coronary Artery Vasculitis: Primarily in the heart and adjacent great vessels
  • Kawasaki Disease (in children):
    • T-cell activation by unknown antigen
    • Pancarditis (inflammation of all heart layers), epicardial coronary aneurisms (and thrombosis)
  • Takayasu's Disease (in adults):
    • Most common form of vasculitic syndrome causing coronary involvement
    • Coronary ostia stenosis (blockage) in 10-20% of cases
  • Giant Cell Arteritis:
    • Causes ischemic heart disease and sudden death.
    • Inflammation begins at the level of the internal elastic lamina
    • Granulomatous inflammation rich in macrophages in areas of elastic lamina destruction
  • Less common causes:
    • Lupus arteritis
    • Rheumatoid arteritis
    • Polyarteritis nodosa

Myocarditis

• Non-ischemic myocardial inflammation caused by known or unknown factors.
  • Most common cause: viral infection
    • Coxsackie A and B echoviruses
    • Influenza
    • Epstein-Barr
    • Herpes virus
    • HIV
    • Chlamydia (psittacosis)
    • Coxiella (Q fever)
  • Bacterial Infections
    • Suppurative myocarditis
    • Toxin-mediated (diphtheria)
    • Typhoid fever
  • Other microorganisms
    • Trypanosoma cruzi (Chagas disease)
    • T. plesmosis (Weil's disease)
    • Borrelia burgdorferi (Lyme disease)
    • Various fungi (Candida, Aspergillus)
  • Hypersensitivity reactions
    • Acute rheumatic fever
    • Rheumatoid arthritis
  • Histologically:
    • Small foci of coagulative necrosis
    • Inflammatory infiltrate (macrophages, lymphocytes, and polymorphs)
    • Necrotic muscle fibers are replaced by fibrous scars.

Valvular Heart Diseases

• Aortic stenosis
  • Enlargement of the left ventricle
  • Reduced diastolic pressure in the aorta, reducing coronary blood flow
  • Calcification of the aortic valve causing coronary ostia blockage.
• Mitral valve prolapse
• Other aortic diseases
  • Aortic aneurysms
    • Atherosclerotic aneurysms (most below the diaphragm, due to media damage and rupture)
    • Dissecting aneurysms (medial necrosis affecting both elastic fibers and muscles)
    • Syphilis-related aneurysms

Dating of Postmortem Thrombi

• Partial endothelialization of the thrombus surface starts in 3 days and is complete at 1 week.
• Hemosiderin first appears on day 8, peaking at about 3 weeks

Causes of death in women of childbearing age

• Complications of pregnancy
• Pulmonary embolism
• Subarachnoid hemorrhage