Sudden Natural Death PDF

Sudden Natural Death Dr. Isam ELHASSAN Definition:- WHO: Death within 24 hours from onset of symptoms. Usually within one hour. 80% of the routine autopsy load consists of cases of sudden death. Medico-legal Aspects:- Can present as:- Natural death presenting as suspicious case...

Sudden Natural Death Dr. Isam ELHASSAN Definition:- WHO: Death within 24 hours from onset of symptoms. Usually within one hour. 80% of the routine autopsy load consists of cases of sudden death. Medico-legal Aspects:- Can present as:- Natural death presenting as suspicious cases. Unnatural death mimicking natural death. Natural death caused or aggravated by unnatural act. Natural disease causing or contributing unnatural death  Causes of sudden death can be discussed under the following titles: Cardiac causes. Cerebral causes. Pulmonary causes Other causes. Cardiac causes of sudden death: Coronary artery disease – Coronary artery atheroma – Non atherosclerotic coronary artery disease. (Coronary artery vasculitis) – Anomalies of the coronary circulation Myocardial Diseases – Cardiomyopathies – Myocarditis Valvular Heart Diseases, Including Congenital Heart Diseases  Anterior descending branch supplies most of the septum, apex, anterior wall and part of the lateral wall.  Coronary artery atheroma (coronary atherosclerosis): – Ischaemic heart disease refers to any form of deprivation of blood supply to the myocardium – although occlusive disease of the coronary arteries is the most common cause, other frequent causes include hypertension, aortic valve disease and some forms of congenital heart diseases.  Atheroma is paste like material consists of intimal thickening of variable proportion of – fragmented elastic fibers – foam macrophages – lipid – cholesterol crystals – collagen – calcium – chronic inflammatory infiltrate. Ulceration of surface of plaques leads to loss of intimal lining with thrombus formation. Common Sites of Occlusion (whether Atheromatous or Thrombosis):- – The first 2 cm of the anterior descending branch of the left coronary artery (AD. LCR). – Distal part of the right coronary (when it bends around the (RT) margin of the heart). – Proximal part of the circumflex. – The left main trunk. Complication of atheroma Progressive narrowing of lumin Rupture plaque Sub-intimal haemorrhage Thrombosis  After occlusion of a coronary vessel. No definite naked-eye changes can be seen within the first 24 hours (12-18 hours).  At the end of the first day into the second, infarct appeared. there is a yellowish background with red streaks. 1-2 weeks formation of mucoid grayish zone (autolysis)  Histologically – No definite histological signs can be observed during the first half-day. – there is swollen fibres, granularity and eosinophilia. – Loss of striations, loss of muscle nuclei (variable) – Leukocytes infiltrate appear from 2 days onwards. – By the end of the first week: disintegration of muscle fibres and appearance of new capillaries. Non-atherosclerotic Cronory Artery Diseases Coronary causes of sudden death in addition to atheroma formation include the followings: Coronary Artery Vasculitis:- that is localized primarily in the heart and adjacent great arteries:- – Kawasaki Disease:- in children T-cell activation by an unknown antigen. Pancarditis with formation of epicardiac coronary aneurysms and thrombosis. – Takayasu’s Disease:- in adults. The most common form of vasculitic syndrome with symptomatic coronary involvement in adults. Involves coronary ostia with stenosis occurs in about 10-20% of patients  Giant Cell Arteritis:- – Causes ischemic heart disease and sudden death. – The inflammation begins at the level of the internal elastic lamina. – Giant cells are not necessarily present but, granulomatous inflammation rich in macrophages is present in areas of destruction of the elastic lamellae. Lupus Arteritis Rheumatoid Arteritis Polyarteritis Nodosa Myocardial Diseases:- Cardiomyopathies:- – Hypertrophic cardiomyopathy asymmetrical, mainly (Lt) ventricle. histological features : Bizarre pattern deformities of fibre length, thickness, nucleation. – Restrictive cardiomyopathy obliteration of ventricular lumen by fibrosis and mural thrombosis – Dilated cardiomyopathy Dilated globular heart (alcoholic myopathy). due to thiamine or other mixed dietary deficiency. Myocardial fibers contain fatty drops with triglycerides dehydrogenase enzyme activity. – Arrhythmogenic right ventricular cardiomyopathy. In which the muscle fibers are replaced by fatty tissue Myocarditis Myocarditis is non-ischemic myocardial inflammation of known or unknown causes. It most often results from – Viruses are the most common cause of infectious myocarditis acquired in the community. – hypersensitivity responses – immune related injury  Causes of Myocarditis:- – Viral Infection: Coxsachie A and B echoviruses Influenza viruse, Epistein-Bar viruse Herpes virus and HIV. – Recheitsiae : Chlamydia (psyttacosis) Coxiela (Q fever) – Bacteria : suppurative myocarditis due to pyogenic infection. Toxin mediated-diphtheria Typhoid fever. – Other Microrganisms: Trypansoma cruzi (chagas disea) T. plesmosis, Weil’s disease Bornellia bugdorfer (Lyme disease). Trychinella. Various fungi (Candida,Asperigillus) – Hypersensitivity : Acute rheumatic fever Rheumatoid arthritis, Viral Myocarditis:- Cases occur in infants but young adults particularly males are most often affected. Mild condition with complete recovery is the rule. It may be severe with fatal cardiac failure.  Histologically: – Small foci of coagulative necrosis surrounded by an inflammatory infiltrate of macrophages, lymphocytes and polymorphs. – The necrotic muscle fibers subsequently undergo absorption and replaced by small fibrous scars.  Hypersensitivity Reactions:- – Myocarditis is a serious feature of Rheumatic fever also found as a less serious form in SLE and Rheumatoid arthritis. Granulomatous Myocarditis:- – 25% of cases of sarcoidosis. Valvular Heart Diseases Including Congenital Heart Diseases:- – Aortic Stenosis:- Enlarge the left ventricle. Reduce the diastolic pressure in the aorta so reduce the coronary blood flow (coronaries fill in diastolic). Calcification of aortic valve may block coronary ostia. – Mitral valve prolapse.  Aortic Disease:- – Aortic Aneurysm:- Atheromatous aneurysm:- – almost present below the diaphragm due to progressive destruction of the media. – when ruptured presented as retroperitoneal haematoma and peri-renal haematoma. – rupture of aortic aneurysms is more common in cold weather. Dissecting Aneurysm. – medial necrosis with degeneration – affect both elastic fibres and muscle. Syphillitic Aneurysm.  Sudden unexpected death syndrome (SUDS) Sudden adult death syndrome (SADS) No anatomical cause of death Functional death Believed to be cardiac arrythmia  Ion channel disorders Mutations resulting in inactivation of the cardiac potassium channel subunits leading to prolonged QT interval, ventricular tachyarrythmias, syncope and sudden death Romano-Ward syndrome, an autosomal-dominant condition with premature sudden death Jervell and Lange-Neilson syndrome, an autosomal recessive disorder with marked prolongation of the QT interval, sudden death and sensorineural deafness  Ion channel disorders…. The Brugada syndrome – RBBB, ST segment elevation, ventricualr arrythmias, syncope and sudden death Bangungut, Nonlaiti, Laitai and Pokkuri- autosomal dominant Sudden Infant Death Syndrome (SIDS) Death of an infant which is unexpected in history and where an adequate postmortem fails to reveal a cause of death Cardiac cause? Sleep apnoea? Functional death Several associated factors Sudden Adult Death Syndrome (SADS /SUDS) Unexpected deaths, in young adults, mostly males The victims are apparently healthy individuals Majority of deaths occur during sleep No premonition prior to death Common in South East Asian region Complete postmortem fails to reveal a cause of death Death is due to cardiac arrythmia (Functional death) / Similar to Sudden Infant Death syndrome(SIDS) Cot death Cerebral Causes:- Almost always vascular in origin. Ruptured Intracranial Aneurysm:- – Ruptured berry aneurysm with subarachnoid haemorrhage (SAH). – SAH is more common in women. Intracrebral Haemorrhage:- – The most common site for a haemorrhage is the internal capsule anteriorly. – It is almost entirely from Artery of cerebral haemorrage (Charcot’s artery), a branch of leniculo-striate vessels from middle cerebral artery (stroke – hypertension). Cerebral Tumours. Infection. Epilepsy. Pulmonary Causes:- Pulmonary Thromboembolism:- In 20% of the cases occur without any predisposing factor. Bronchial Asthma. Athmatics are running the risk of sudden death, not due to status ashmaticus. Spontaneous pneumothorax. Massive pulmonary haemorrhage (Haemoptesis. T. B or ulceration of lung tumours). Infection (Influenza virus). Other Causes:- Gastrointestinal:- – Perforated peptic ulcer. – Massive Gastro intestinal bleeding. – Acute intestinal obstruction. – peritonitis Postoperative bleeding, tooth extraction or tonsillectomy. Portal hypertension with oesophageal varcies. A massive haemorrage from a duodenal ulcer  Ante-mortem Thrombosis:- – Firm (Strong enough to be handled easy), pale and not a cast of the vessel in which it is found Postmortem clot:- – is soft, jelly like, shiny, can not stand still with chicken fat appearance  Dating:- – Partial endothelialisation or coating of the thrombus surface starts at about 3 days, complete at about 1 week. – The first appearance of haemosidein is on the 8th day. Maximum intensity at about 3 weeks.  All sudden deaths in women of child-bearing age likely to be caused by:- – Complications of pregnancy. – Pulmonary embolism. – Subarachnoid Haemorrhage The end