Ena le ALLAH wa ena elaih rage3oon...ba3d khabar wafat la3eb el ahlee ra7emaho ALLAH olt a7o6 asbab el wafa el mofage2a ...
Sudden Unexpected Death: Causes and Contributing Factors
In the world of medical examiners, coroners, and pathologist involved in forensic autopsies, "sudden death" does not mean instantaneous death. This outline is an outgrowth of the category referred to as SIDS (sudden infant death syndrome). I suppose one could say "in less than 24 hours". But the implication is of a rapid and unexpected death...mostly unwitnessed...and without obvious cause when the body was found.
PRIMARILY CARDIAC-ABNORMALITY DEATHS: Keep in mind that trauma or metabolic vacillations of acute and chronic illness superimposed on significant cardiac lesions can trigger acute or chronic electrical or mechanical decompensation and death.
Epicardial Coronary Artery Abnormalities:
Chronic...segmental or pipestem stenosis.
Acute myocardial infarction, atherogenic.
Chronic atherosclerosis with chronic changes in myocardial parenchyma.
Constriction of artery ostia.
Congenital abnormalities of coronary arteries:
Anomalous origin from pulmonary artery.
Other type of coronary AV fistula.
Origin of left coronary artery from right sinus of Valsalva.
Origin of right coronary artery from left sinus of Valsalva.
Hypoplastic or aplastic coronary arteries.
Transmyocardial coronary-intracardiac shunt.
Coronary artery embolism or thrombosis from:
Thrombosis over an artery lesion.
Aortic or mitral endocarditis.
Prosthetic aortic or mitral valves.
Abnormal native valves or left-sided mural thrombus.
Polyarteritis nodosa, progressive systemic sclerosis, giant cell arteritis.
Mucocutaneous lymph node syndrome (Kawasaki's disease) with arteritis, then aneurysms.
Syphilitic coronary ostial stenosis.
Focal/segmented arteritis, NOS (A80-547, FA84-115).
Miscellaneous mechanical obstruction of coronary arteries:
Ulceration of an atherosclerotic plaque.
Coronary artery dissection in Marfan's syndrome.
Coronary artery dissection in pregnancy.
Prolapse of aortic valve myxomatous polyps into coronary ostia.
Dissection or rupture of sinus of Valsalva.
Coronary vasospasm: especially if on cocaine; even transmural infarcts without apparent coronary lesions (Am.J.H. 88:219, 1974).
Occult trauma to a normal-appearing coronary artery.
Mural thickening due to metabolic deposits or intimal proliferation (JAMA 231:952, 1975):
Juvenile intimal sclerosis (idiopathic arterial calcification of infancy).
Intimal hyperplasia associated with contraceptive steroids or with postpartum state.
Coronary fibrosis associated with radiation therapy.
Hypertrophy of Ventricular Myocardium:
Left ventricular hypertrophy associated with chronic stenosing coronary atherosclerosis.
Hypertensive heart disease without significant coronary atherosclerosis (be especially careful to view heart weight in view of the body weight).
cardiomyopathy of morbid obesity: (relative cardiomegally [heart to total body wt. ratio normal], LV dilation, and myocyte hypertrophy in absence of interstitial fibrosis); 50% die of sudden cardiac death.
Hypertrophic myocardium secondary to valvular heart disease.
Hypertrophic cardiomyopathy: by late 2001, some 10 genes have been noted in association with HCM...afflicting 1/500 adults.
Primary or secondary pulmonary hypertension (remember, they can be found dead before there is that much increase in RV thickness; so need lots of lung sections to rule this out):
Advanced chronic right ventricular overload.
Pulmonary hypertension in pregnancy.
Myocardial Diseases and Heart Failure:
Chronic congestive heart failure:
Idiopathic cardiomyopathy (A90-893, FA91-640).
Post-myocarditis cardiomyopathy (FA91-640).
Chronic CHF, NOS: and don't overlook additional causes of high-output failure such as occult shunts (Pagett’s disease of bone can do it., e.g.).
Dilated cardiomyopathy: Do to practically any of the above or below influences on the heart muscle, the heart enlarges, then the chambers dilate (etiologies: idiopathic, inflammatory, metabolic,genetic, toxic, peripartum, infiltrative, hypersensitivity, arrhythmogenic, and rheumatologic).
Acute cardiac failure:
Massive acute myocardial infarction.
Acute alcoholic cardiac dysfunction.
Ball-valve malfunction in aortic stenosis prosthesis.
Mechanical disruptions of cardiac structures:
Rupture of ventricular free wall.
Disruption of valvular apparatus:
Acute pulmonary edema in noncompliant ventricles.
Myocardial bridging - is supposedly fairly common at autopsy, being mostly in the left coronary, the first 10 to 20 mm. Deaths ascribed mostly when also involves the posterior circulation (average death is a 31 year old, with or without associated physical activity or excitement) or associated with some other lesion in the (anterior versus posterior) opposite coronary system. The thicker the bridge, the more likely its significance.
Infarction associated primarily with oxygen “supply-demand” disproportion (JAMA 231:952, 1975):
Aortic stenosis, all forms.
Incomplete differentiation of the aortic valve.
Carbon monoxide poisoning.
Miscellaneous odd infarctions (JAMA 231:952, 1975):
AMI with normal coronaries.
Inflammatory, Infiltrative Neoplastic, and Degenerative Processes:
Acute viral myocarditis with or without ventricular mechanical dysfunction.
Myocarditis associated with the vasculitides.
Progressive systemic sclerosis.
Idiopathic giant cell myocarditis.
Senile myocardium: usually a small heart & myocardium soft (elderly person found dead of "old age")
Arrhythmogenic right ventricular (fatty) dysplasia (ARVD) [as opposed to more ordinary fatty infiltration; ARVD tends to be fatty change out of all proportion to the body weight and involving even into the interior...focally transmural...myocardium] (A79-451, FA-94-57, FA-95-9, FA-95-36, A-01-2, FA-01-72).
Neuromuscular diseases (e.g., muscular dystrophy, Friedreich's ataxia, myotonic dystrophy) (FA-94-113).
Primary benign or malignant.
Obstructive intracavitary tumors:
Neoplastic - benign or malignant.
Thrombotic - enlarging chronic thrombus.
Chronic lymphocytic myocarditis: this can be very subtle and may require numerous cardiac sections in order to locate at least several microscopic foci of lymphocytic infiltrates (FA86-261, FA91-605, FA91-631, FA92-23).
Myxoid heart syndrome: mucosubstances in conduction system, valves, etc. (See I,5,c.); a forme frust Marfan's [Nat'l Marfans Foundation]
Intramural arteritis, NOS (A82-655) or other arterial occlusions.
Hurler's (and other similar storage disease) syndrome (gargoylism): accumulation of mucopolysaccharide in RES cells.
Fabry's disease: foamy accumulation in smooth muscle, endothelial and perithelial cells.
Pompe's disease: excessive glycogen storage in heart muscle.
Look for signs of other storage disorders.
Diseases of the Cardiac Valves:
Valvular aortic stenosis/insufficiency.
Mitral valve disruption, see above.
Prolapse of myxoid, floppy mitral valve having accumulation of acid mucosubstances.
Prosthetic valve dysfunction.
Congenital Heart Disease:
Congenital aortic or pulmonic valve stenosis.
Right-to-left shunts with Eisenmenger’s physiology:
During labor and delivery.
After surgical repair of congenital lesions; e.g., tetralogy of Fallot.
CHARGE Syndrome (the Foundation) [note the coloboma...abnormal eye pupil shape...plus various cardiac defects]