Autopsy – Sudden Death

World Health Organization defines sudden death as ‘death within 24 hours from the onset of symptoms’, but most clinician accept sudden death to be death within one hour from the onset of symptoms.

Death can be attributed to the lack of functionality of the tissues. The state of death is conferred by absent electro chemical intercellular communication in the brain and heart. This electro-physiological disturbance leaves no anatomical traces or records except in cases where the individual had been monitored before death. Therefore, one should consider the circumstances before death as well as the surroundings of the body another important medical tool that should be availed at the time of postmortem examination. These can help in determining the cause of death in cases where there are no anatomical abnormalities.

Some common mechanisms for functional deaths are

  • Increased excitability of the myocardium causing propagation of ectopics. These ectopic beats cause ventricular tachycardia or premature ventricular contractions. In the presence of circus pathways, these ectopics may lead to development of ventricular fibrillation causing ineffective circulation with lead to rapid death.
    • Ventricular excitability can be enhanced by myocardial hypertrophy, Ethanol intoxication, Ischemia, Sympathetic discharge, Hyper-thyroids.
    • Ventricular excitability is also enhance by Drugs like Caffeine, Sympathomimetic drugs, Epinephrine, Norepinephrine, Theophylline, Mono-Amine Oxidase inhibitors, Tri-cyclic Anti-depressants,
  • Depression of the myocardial contractility causing failure of the propagation of impulses. In case of failure of propagation of electrical impulse from the SA node, the ectopic pacemakers start producing impulses. The failure of this safety mechanism will lead to cardiac asystole and death.
    • Myocardial depression can be caused by Parasympathetic discharge, Myxedema, Hypothermia, Hyperkalemia

In addition to the causes mentioned above, the nervous system itself can produce strong electrochemical discharges that cause death by causing cardiac asystole, ventricular fibrillation or vascular redistribution. These are controlled by the vasomotor and the respiratory centers in the brain.

The important vasomotor centers are present in the mid-brain, around the third ventricle and in the medulla oblongata. The centers influence the heart through the sympathetic and the parasympathetic pathways. The sympathetic pathways involve the intermedio-lateral columns of the spinal cord from where fibers pass to the sympathetic ganglia (especially the stellate ganglion) and finally via the sympathetic branches passing along the base of the heart to supply the heart. The parasympathetic fibers pass via the vagus nerve, passing through the mediastinum to supply the heart

The important respiratory centers are present in the medulla and are under the influence of the dorsal pontine centers. The respiratory center exert their influence via fibers in the upper spinal cord and the phrenic nerves originating from C3, C4 and C5, passing along the neck and through the pericardial sac to supply the diaphragm. Any abnormal discharge could cause either increased excitability or depression of the myocardium.

Following cessation of circulation due to whatever cause, consciousness is lost within 15 seconds, and cerebral function becomes irreversibly ceases within 5 minutes. In case of respiratory arrest, cerebral function is the same in that consciousness is lost in 15 seconds and death occurs with 5 minutes. However, cardiac function is not disturbed initially so that there is initial tachycardia followed by bradycardia and then complete electromechanical dissociation with presence of electrical activity but no circulation until death occurs.

Other biochemical changes that could lead to cessation of vital functions including electrolyte disturbances, diabetic ketoacidosis, drug overdoses and poisoning which might produce alterations of the intracellular composition causing death.

Death may appear sudden and unexpected to an uninformed or misguided outsider, but may not only be expected but may also not be so sudden to medical personnel. For example, a patient reporting to the emergency department with complaints of rigidity of the neck would appear apparently normal except for fever and pain over the neck to an outsider. However, a doctor would immediately elicit Kernig’s sign and diagnose meningitis. Subsequent death within a few hours may appear sudden to the family members. Similarly, the deceased may have been suffering from chronic disease, symptomless or unaware of the risks. The deceased may also not have shared any knowledge with other individuals. Hence, these deaths may not be sudden, may not be unexpected but are certainly unexplained. As a result, medico-legal investigation is advised to protect the medical doctor from future liabilities.

In some cases, even after complete autopsy examination as well as all appropriate investigations, the cause of death remains unclear. These deaths are known as functional deaths where the death was a result of a functional derangement and so may not have left any anatomical, gross or histological, proof behind.

Sudden death can be divided into 2 groups: those with functional abnormality and those with structural abnormality. In cases of sudden death due to functional disturbance, the cases can again be divided into those that have a significant anatomic alteration for which functional disturbance can be attributed or referred and those in which no anatomic alteration is evident at autopsy.

Those cases where there is no anatomic alteration are designated functional death. Examples of functional death are:

Vagal Cardiac Inhibition – Sudden death that occurs within seconds to within a minute or two after minor trauma or peripheral or internal stimulation of a relatively simple and ordinarily innocuous nature. These cases are often categorized as accidental in nature. E.g. Blow to the larynx, Blow to the solar plexus, Kick in the scrotum, Carotid sinus pressure, Cannulation of the cervix

Spontaneous ventricular fibrillation – history of non-suspicious circumstances surround death associated with pre-mortem exertion, exercise or intense emotional situation. On complete autopsy, including toxicology and microscopy, no abnormalities are noted. Studies have shown that these cases are associated with patients with electrically unstable hearts that suffer a fatal dysrhythmia following adrenergic discharge.

Sudden Nocturnal Cardiac Death – There is a particular type of sudden cardiac death that was prevalent in East and South Asia that has now been discovered to have occurred in the US as well following migration of Hmongs to the US. This syndrome is called by various names, in Japan, it is called Pokkuri, in Philippines, it is called Bangungut, and in the Thailand, Vietnam, Laos and Cambodia it is called laitai and nonlaitai. It is a case of sudden nocturnal cardiac death where ventricular dysrhythmias are demonstrated. This could be attributed to the night terrors occurring in non-REM sleep or due to the increased adrenergic discharge during the nocturnal cycle. These cases show negligible gross changes.

Another group of functional death are the ECG syndromes. These syndromes may clinically show evidences on ECG but are not associated with any gross abnormalities. Three common variants of this group are: Pre-excitation syndromes – most importantly Wolf-Parkinson-White syndrome. Long Q-T syndrome and lastly Sick sinus syndrome.

Wolf Parkinson White syndrome – In this syndrome, there are extra pathways communicating between the atria and ventricles. This leads to re-entry of impulses, which is recirculated,thereby causes ventricular tachycardia and ventricular fibrillations. The ECG findings are Wide QRS complex and Delta wave with a short P- δ interval.

Long Q-T syndrome – This is characterized by prolonged recovery phase from depolarization of the cardiac muscles. This leads to a tendency to syncope and could lead to death due to ventricular tachydysrhythmias. They are of two types: Congenital and acquired. Congenital long Q-T syndrome is seen in Romano-Ward syndrome and Jervell and Lange-Nielsen syndrome. Acquired cases are seen with drugs, electrolyte abnormalities, anorexia nervosa, Hypothermia, Toxic substances, Liquid diet.

Sick sinus syndrome – This can be seen in cases of surgical manipulation in the region of the SA node. May lead to spontaneous sinus bradycardia, syncope and rarely sudden death.

The most common mechanism of sudden death is dysfunction of the cardiovascular system. Other causes include cerebral hemorrhage, spontaneous subarachnoid bleeding, ruptured ectopic pregnancy, hemoptysis, hematemesis and pulmonary embolism.