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Finding the Cause of death – The cause of death is the disease or injury responsible for starting the sequence of events, which are brief or prolonged and which produce death. It may be divided into:

IMMEDIATE CAUSE, i.e., at the time of terminal event, e.g., bronchopneumonia, peritonitis, trauma, etc.

BASIC CAUSE, i.e., pathological processes responsible for the death at the time of the terminal event or prior to or leading to the event, e.g., gunshot wound of abdomen complicated by generalized peritonitis.

CONTRIBUTORY CAUSE, i.e, the pathological process involved in or complicating, but not causing the terminal event. In some cases, the basic and the immediate cause may be identical.

The MANNER OF DEATH is the way in which the cause of death was produced. If death occurs exclusively from disease, the manner of death is natural. If death occurs exclusively by injury or is hastened due to injury in a person suffering from natural disease, the manner of death is unnatural or violent.

Violence may be suicidal, homicidal, accidental or of undetermined or unexplained origin. The manner of death is established mainly by the investigational information and also by the pathological findings.

MECHANISM OF DEATH is the physiological or biochemical disturbance, produced by the cause of death which is incompatible with life, e.g., shock, sepsis, toxemia, severe metabolic acidosis and alkalosis, ventricular tibrillation, respiratory paralysis, etc.

AGONAL PERIOD is the time between a lethal occurrence and death.

Determination of the cause of death following autopsy is an interpretive and intelligent procedure, and depends upon sound evaluation of all data, circumstances surrounding the death, morphological evidence of disease and injury and additional laboratory investigations. In fact, the more a forensic pathologist knows about the total investigation, the more he can contribute from his autopsy.

The effectiveness of the doctor would be greatly diminished if he had to work alone, and receives bodies for autopsy without clothing, or a knowledge of the circumstances surrounding death. The recognition of the structural organic changes or chemical abnormalities, which cause stoppage of the vital functions is the first step.

Understanding the mechanism by which the anatomical and chemical deviations from normal actually caused death, i.e. how they produced or initiated the sequence of functional disturbance which were sufficient to cause respiratory or cardiac arrest, which are the two ultimate lethal processes, is the second step.


According to the autopsy findings, the cause of death may be grouped as follows.


(a) where a lesion is found at autopsy which is incompatible with life.

(b) Where a lesion is found at autopsy which is known to cause death.


(a) where a lesion is found at autopsy which is incompatible with life.

(b) Where a lesion is found which may have caused death or which may have precipitated death, but which is also known to be compatible with continued life.

OBSCURE CAUSES: Where no lesion is found at autopsy, or if a lesion is found it is of a minimal or indefinite nature.

NATURAL CAUSES: WHERE A LESION IS FOUND AT AUTOPSY WHICH IS NOT COMPATIBLE WITH LIFE: In this category, the structural abnormalities establish beyond any doubt the identity of the disease which caused death. It is apparent that the lesions observed are incompatible with life because of its nature, site or extent, and they are antemortem in origin. The examples are : massive pulmonary thromboembolism, spontaneous intracerebral hemorrhage, ruptured myocardial infarct, rupture oI an aortic aneurysm.


This category includes deaths in which some lesion is fund at autopsy which may have caused death, but which is also compatible with continued life, e.g., arteriosclerosis of the coronary arteries, advanced chronic heart diseases, lobar pneumonia, etc. The autopsy does not reveal any other reasonable explanation for death, and the location, nature, severity and extent of the anatomical changes are sufficient to cause death, but it is not a conclusive proof.

In such cases, the clinical history is important. In the case of coronary arteriosclerosis, if the deceased had several attacks of angina pectoris before his death, it can be reasonably assumed to be the cause of death. If the clinical history is unusual, the possibilities suggested by the history should be excluded before the death is attributed to the lesion.

Stenosing coronary atherosclerosis can cause sudden death, in which the autopsy may reveal a few scattered foci or only a single site of significant luminal narrowing, and there may be no recent vascular occlusive lesion. In most cases of sudden coronary death, a fresh thrombus or a recent myocardial infarct is not found at autopsy.

In these cases, correlation of the morbid anatomy with the suddenness of death must be based on hypotheses. Emotional stress, e.g., anger, fear, joy, apprehension, etc., can precipitate acute failure in persons with organic heart disease, especially of the coronary atherosclerotic type. Emotional excitement significantly increases the workload of the heart which can overtax the limits of tolerance of damaged, labouring heart.

In a normal person sudden release of adrenaline due to extreme terror can initiate ventricular fibrillation and death. Sudden deaths following assaults or even threats may occur due to existing heart disease.

Such events may be encountered in criminal charges arising out of collapse during fights, in minor assaults upon old persons, in litigation related to death from work stress, etc.

Sufferers from asthma and epilepsy can die suddenly and unexpectedly for no obvious reasons. UNNATURAL CAUSES : (A) WHERE A LESION IS FOUND AT AUTOPSY WHICH IS NOT COMPATIBLE WITH LIFE : In some deaths, injuries may be found at autopsy which are incompatible with life in any person, e.g., decapitation, crushing of the head, avulsion of the heart from the large blood vessels. If they are antemortem, they are the definite cause of death.

(B) A LESION IS FOUND AT AUTOPSY WHICH MAY HAVE CAUSED OR PRECIPITATED DEATH, BUT IS COMPATIBLE WITH LIFE: At autopsy certain injuries may be found which from their nature, site or extent may not appear to be sufficient to cause death in a healthy person. But such injury may be the cause of death due to some complication resulting directly from the injury, but which is not demonstrable at autopsy.

The degree of shock or the extent of hemorrhage following an injury cannot be assessed at autopsy. In such cases, the absence of any other adequate cause of death, and a consideration of the circumstances of the injury and of the symptoms found, may enable the doctor to attribute death to the injury with reasonable certainty.

In some cases, an injury may not appear to be sufficient to cause death, but some natural disease may be present which is known to cause death, e.g., coronary arteriosclerosis. In such cases, the circumstances of death and the symptoms found at the time of collapse may suggest that the death was precipitated by the injury.

NEGATIVE AUTOPSY: When gross and microscopic examination, toxicological analyses and laboratory investigations fail to reveal a cause of death, the autopsy is considered to be negative. Two to 5% of all autopsies are negative. Majority of obscure autopsies are in young adults. A negative autopsy may be due to:

  • Inadequate history: Deaths from vagal inhibition, status epilepticus, hypersensitivity reaction, laryngeal spasm in drowning, etc. may not show any anatomical findings.
  • Inadequate external examination: The presence of fresh and old needle marks may be missed on cursory examination in a drug addict. Death from snake bites and insect bites cannot be explained unless the bite marks are identified. The burn may be missed in electrocution.
  • Inadequate or improper internal examination: Air embolism and pneumothorax are often missed.
  • Insufficient laboratory examinations.
  • Lack of toxicological analysis.
  • Lack of training of the doctor.

Obscure autopsies are those which do not show a definite cause for death, in which there are minimal, indefinite or obscure findings, or even no positive findings at all. They are a source of confusion to any pathologist.

Frequently, these deaths are due to obscure natural causes, but they may be due to certain types of injury or complications of injury, or to poisoning. Mild degrees of natural disease should not be implicated unless other possibilities are most carefully eliminated.

The obscure causes are:

(1) Natural diseases:

  • With obscure or some microscopic findings.
  • Death precipitated by emotion, work-stress, and
  • Functional failure, such as epilepsy, paroxysmal fibrillation.

(2) Biochemical disturbances:

  • Uraemia, diabetes, potassium deficiency.
  • Respiratory pigment disorders, such as anaemic anoxia, porphyria.

(3) Endocrine dysfunction:

  • Adrenal insufficiency.
  • Thyrotoxicosis or myxoedema.

(4) Concealed trauma:

  • Concussion.
  • Self-reduced neck injury.
  • Blunt injury to the heart.
  • Reflex vagal inhibition.

(5) Poisoning: Without microscopic change:

  • Delayed suboxic or narcotic poisoning.
  • Anaesthetic overdosage or maladministration.
  • Neurotoxic or cytotoxic poisons.
  • Plant poisoning.

(6) Miscellaneous: Allergy, drug idiosyncrasy.

Non-medical persons believe that the cause of death can always be determined by autopsy. The police may press the doctor for giving a positive statement with regard to the cause of death. In such cases, the doctor should admit his inability to give a positive opinion. Such obscure cases require clinical and laboratory investigations and interview with persons who had observed the deceased before he died, to know the signs and symptoms shown by the deceased before his death. Laboratory investigations may be bacteriological, virological, histological, biochemical and toxicological.

In the absence of positive findings from these sources, a careful assessment of possible functional causes of death must be made, before any cause of death is given as undetermined. The presence of infectious, malignant, occupational and other diseases are also excluded. Even in these disappointing cases, the negative morbid anatomical and chemical examination is of great value in excluding injuries or poisons, which may have been alleged to have caused or played some part in the death.

Though the pathologist cannot establish the cause of death, he can exclude many conditions which have been incorrectly attributed to have caused death.


Acute rheumatic carditis may cause sudden death in a young adult. In some such cases, naked-eye cahnges may be absent, but typical Aschoff bodies of rheumatic fever are found in the myocardium on microscopic examination. Acute toxic myocarditis of diphtheria may cause sudden death, in which the primary lesion in the nose or throat may be overlooked.

Idiopathic myocarditis may cause sudden death. Brown atrophy of the heart and senile heart may prematurely fail suddenly. Myocarditis, fibrosis, and necrosis of conducting tissue may escape detection. Small coronary thrombosis and easily dislodged emboli may be overlooked.

Acute occlusion of coronary artery may result from thrombosis or hemorrhage within the wall of the artery. Zones of occlusion are usually less than five mm. in length, and most of the occlusions occur within three cm. of the orifices of the vessels.

First part of the anterior descending branch of left coronary artery within two cm. of its origin is commonly affected, followed by the proximal part of the right coronary artery, first part of the circumflex branch of left coronary artery, and the short main trunk of left coronary artery. Fresh thrombi are dark-brown, and attached to the vessel walls. Old thrombi appear as homogeneous yellowish or grey, firm plugs blocking the vessels.

Most infarcts occur in the left ventricle in the anterior wall. Posterior infarcts may be due to blockage of either the right vessel or the circumflex branch of the left artery. Infarction usually occurs when the lumen is reduced to twenty percent or less. Right ventricle is involved in less than ten percent cases. Coronary insufficiency from narrowing of the lumen of major vessels may lead to chronic ischaemia and hypoxia of the muscle distal to the stenosis. Hypoxic myocardium is electrically unstable and liable to arrhythmias and ventricular fibrillation, especially at moments of sudden stress, such as exercise or an adrenaline response, such as anger or emotion.


There is no need for the ischaemia to be severe enough to produce a niyocardial infarct. At autopsy, no naked eye changes are seen for the first 12 to 18 hours. After this period, there is oedema and pallor of the affected area which is the first sign, and the cut surface looks granular and dull. After 24 hours to third day, the area becomes better demarcated, and turns yellow and is surrounded by an area of hyperaemia.

In one to three days there is a progressive softening and thinning of infarcted area, which is maximum about the tenth day, and rupture may occur. With breakdown of myocytes, red streaks appear giving a ‘tigroid’ appearance. From the third week and later, the centre of the infarct becomes gelatinous and the colour becomes grey.

From ten days onwards, the infarct is slowly converted into a fibrous scar, which is completed in three months. During the next month or two, fibrosis replaces the dead muscle to form a scar. Infarcts may be transmural, or may be confined to inner zone. The papillary muscles are usually involved.


Eosinophilia of muscle cytoplasm begins to occur in about 8 to 12 hours. With ultraviolet light, such fibres usually “autofluoresce” as yellow against greenish background. Swelling of the muscle fibres and granularity of cytoplasm appears. Later cell outline becomes indistinct.

By 24 hours, monocytes are deeply eosinophilic and show coagulation necrosis. After 2 days maximum concentration of polymorphs is seen. In 2 to 4 days nuclei disappear. Between 5 to 7 days, periphery of infarct shows phagocytosis of dead muscle by macrophages. Fibroblasts begin to proliferate and collagen formation occurs.

Between 1 to 3 weeks, further collagen is deposited and capillaries are progressively obliterated. By the fourth week early fibrosis is seen, leucoytes diminish and fibroblats and macrophages increase. Firm fibrosis occurs in about three months.

Cardiomyopathies account for the second largest number of sudden death after coronary artery disease.

Immersion of tissue slices in a solution of triphenyl tetrazolium chloride (TTC) gives brick-red colour to intact area (where dehydrogenase enzymes are preserved) and infarcted area appears pale. This is seen in about 4 hours, but the results are variable.

Severe Narrowin2 of Coronary Arteries (at least 75%) without thrombosis or myocardial infarction is the common cause of sudden death. A physical or emotional stimulus may demand sudden increase in cardiac effort, and if the circulation of the deceased is unable to satisfy the immediate need for increased oxygen, death may result (acute coronary insufficiency). Fresh thrombotic lesions are seen in less than 25% of the cases.

Transitory coronary artery spasm can cause death in persons suffering from angina without narrowing of the coronary arteries and without significant atherosclerosis or congenital anomalies. Spasm of the coronaries may lead to cardiac arrhythmia and death. A thrombus or an occlusive lesion in the terminal part of the artery may be overlooked. The ostia of the coronary arteries may be occluded by atherosclerosis of the aorta.

A ventricle which is overworked and under-nourished may suddenly go into ventricular fibrillation or asystole. This can occur even if the arteries are not completely blocked and is often precipitated by a sudden demand for an increased cardiac output. The lesions of the conducting system of the heart may sometimes cause arrhythmias and death.

Any person with a heart in excess of 420 gm. is at risk of sudden death, even though the coronary arteries are normal. In these cases a state of electrical instability occurs from chronic hypoxia, so that sudden stresses, such as exercise or emotion can suddenly cause the arrhythmias.

Sympathetico-adrenal stimulation causes increased myocardial irritability resulting in ventricular extrasystoles and ventricular fibrillation and death occurs after several minutes. At autopsy, coronary artery sclerosis, fatty heart, chronic valvular disease, etc. may be seen. Lungs are congested and oedematous with pleural petechial haemorrhages.

Primary Cardiac arrest during exercise:

During or immediately after exercise, ischaemia of myocardium, arrhythmias and sudden death can occur. During exercise there is progressive increase of systolic pressure and heart rate, but diastolic pressure is affected very little, and peripheral resistance is decreased. Levels of catecholamine increase, which continue to rise following cessation of exercise, with tenfold increase of epinephrrne. Sudden death occurs with ischaemia sensitising the heart to the arrhythmogenic properties of the catecholamines. Sudden death following assaults or even threats may occur due to existing heart disease.


(a) Cerebral Concussion: This may cause death without any external or internal marks of injury.

(b) NECK INJURY: Cervical spinal fracture- dislocation may occur in diving, fall on head, impact downstair with a wall-facing, from oblique impact or by fall of some object on the head, in such a way as to cause the dislocation especially with the head thrown back. The dislocation may be associated with tears of the. ligaments and with the displacement of the skull from the spine. Sudden movements of the head over the spine with displacement may cause contusion and laceration of the spinal cord and rapid death.

If death is delayed, there may be oedema, softening and necrosis of the cord. Injury to the spinal cord causes spinal concussion and may cause death. Unconsciousness is not seen in all persons, but all get up with residual tingling, numbness, weakness of arms or legs and gait defects. Routine autopsy and X-ray may not show any abnormality.

The dislocation of the cervical segments is often self-reducing, and externally there may not be any injury, or there may be abrasions on the brow or chin. Complete dissection of spine is essential. The spinal cord, cut longitudinally, may show internal bruising. Death may be instantaneous.


Concussion of the chest as in steering-wheel impacts, head-on collisions, from blast or heavy punching, may temporarily or permanently derange the heart without much evidence of trauma. Contusion of the heart may cause death. Trauma may cause arterial spasm and it is likely that a functional inhibition or coronary spasm may cause sudden death that sometimes follow upon blows to the chest.



(1) Deaths due to allergic reactions are rare. Most deaths occur within 1 to 2 hours and are preceded by signs and symptoms suggesting hyperacute bronchial asthma. Sometimes, deaths are delayed for several hours with nervous symptoms, such as coma or with symptoms of circulatory failure resembling traumatic shock.

Aetiology: Allergic reactions may occur due to:

(1) Drugs: penicillin, aspirin, horse-serum products, iodine-containing agents.

(2) Insect bites.

(3) Foods: fish, sehll-fish, eggs, nuts, fruits.

(4) Hormones: insulin, ACTH.

(5) Enzymes: trypsin.

When an allergen is injected into the body, the antibodies formed by plasma cells combine with their antigens to form antigen-antibody complexes (allergens), which stimulate mast cells to release histamine and similar substances. About 75% of patients dying of penicillin anaphylaxis do not have allergic reactions during earlier course of penicillin therapy. Patients should be observed for 30 minutes after receiving the injection of antibiotics.

The anaphylactic syndrome is caused by local and systemic release of endogenous active substances. These include leukotrienes, C, D, E or histamine, eosinophilic chemotactic factor and other vasoactive substances, such as bradykinin and kallikrein. Anaphylactic shock is due to bronchospasm with contraction of the smooth muscle of the lungs, vasodilation, and increased capillary permeability. Death occurs due to laryngeal oedema, bronchospasm and vasodilation. Serum tryptase levels are an indicator of mast cell activation and elevated suggest, an allergic mediator release, particularly in anaphylaxis.

Signs and Symptoms: The onset of symptoms is within 15 to 20 mm. General: malaise, weakness, sense of illness, oedema of face. Dermal: skin rashes, urticaria, pruritus, erythema. Mucosal: periorbital oedema, nasal congestion, angio-oedema, cyanosis. R.S. sneezing, rhinorrhoea, dyspnoea. Upper airway:

laryngeal oedema, hoarseness, stridor, oedema of tongue and pharynx. Lower airway: dyspnoea, acute emphysema, asthma, bronchospasm. G.I: nausea, vomiting, dysphagia, abdominal cramps, diarrhoea C.V.S: tachycardia, palpitation, shock. C.N.S.: anxiety, convulsions.


Search for injection sites or sting marks. The sting area should be excised and frozen at .70°C and submitted for antigen-antibody reactions. Findings are non-specific. There is usually oedema of the larynx (recedes soon after death) oedema of trachea and bronchi, emphysema, cyanosis, petechial haemorrhages, congestion and oedema of the lungs, focal pulmonary distension alternating with collapse and bronchiolar constriction, froth in the mouth and nostrils, visceral congestion, and infiltration of bronchial walls with eosinophils.

History is very important. In cases of insect bites, Ig E antibodies are found in the serum. Ig E binds to the mast cells and basophils. When the cells interact with specific antigens, they release a number of potent compounds, including histamines and an eosinophilic chemotactic factor, which causes an immediate hypersensitivity reaction.


To establish diagnosis of death from allergic shock, the following should be established:

(1) The injected material must be non.toxic to normal persons.

(2) Characteristic allergic symptoms should be present before death.

(3) Autopsy should not reveal the presence of any other lesion capable of causing death.

(4) By the passive transfer technique, a specific cmvsitisiug substance corresponding to the allergen must be demonstrated.

DRUG IDIOSYNCRASY: The administration of drugs in amounts which are known to be harmless to normal person may cause death due to drug idiosyncrasy, e.g., many persons are hypersensitive to cocaine. The diagnosis is based mainly on clinical history.

DIABETES: An elevated vitreous glucose level is an accurate reflection of an elevated antemortem blood glucose level. Glucose levels above 200 mg% are diagnostic of diabetes mellitus even if i.v., glucose infusions were administered. Glucose level in vitreous falls gradually as the time after death increases.

ASTHMA: If airflow obstruction is not relieved, there will be steady progression to elevated C02, metabolic acidosis, exhaustion and death. Asthma can cause sudden death without being in status asthmaticus.

At autopsy, the lungs appear overexpanded, and completely occupy the chest cavity. A sticky tenacious white mucus leposit tills the bronchi. Microscopically, chronic inflammatory infiltrate with numerous eosinophils are seen around the bronchi. The basement membrane of the bronchi is thickened and has a wavy appearance.

EPILEPSY: Very few persons die in status epilepticus. Bite marks in the tongue are seen in about 25% of cases. Death is caused due to postictal respiratory failure.

NEGRI BODIES They are found in the pyramidal cells (ganglion or nerve cells) of hippocampus and uncus and Purkinje cells of cerebellum.


HIV attaches itself to the T-receptor molecule on T-helper lymphocytes in order to infect them. T-helper lymphocytes are found in most body fluids, such as semen saliva, tears and breast milk.

After infection with HIV, blood becomes positive after 2 to 18 months. AIDS is usually communicated by sexual intercourse or from blood transfusion. According to guidelines laid by the Government of India, the status of HIV should not be disclosed to blood donor. The intention is to spare him of the agony of knowing the helplessness of his situation. If the blood drawn is positive, it should be discarded. Once blood sample is drawn, the register of patient identities should be kept quite separate and sample identified only with a code number.

If the donor wants to know the result of HIV test, he should be referred to an accessible HIV testing centre where supplemental tests with counselling will be offered to him. HIV testing requires both pre-test and post- test counselling. Patient has to be informed face to face about the test result and not over the telephone or by a third party. HIV positivity should not be revealed to unauthorised persons.

The Centre for Disease Control (CDC), estimates that 5.5% of all HIV positive persons are employed in the health care field. According to the guidelines issued by CDC, with the exception of health care workers and personal service workers who use instruments that pierce the skin, no testing or restriction is indicated for workers known to be infected with HIV, but otherwise able to do their jobs.

The treating doctor has the duty to inform the paramedical staff involved in the treatment of such patients, the mortuary staff, pathologist and the staff of the crematorium so that due precautions can be taken by these people, who are likely to come in direct contact with the infected biological material. WHO guidelines state that ther is no public health rationale to justify isolation, quarantine or discrimination based on a person’s HIV status.

A person testing positive for HIV cannot be removed from service, if he is physically fit to discharge his duties. If a person suffering from AIDS, knowingly marries or has sexual intercourse with a normal person and thereby transmits the infection to other person, he would be guilty.



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