Death, Bolus (See "Obstruction, acute airway.")

Death, Crib (See "Death, sudden unexpected, of infant.")

Death due to Child Abuse or Neglect (See "Infanticide.")

Death, Intrauterine (See "Stillbirth.")

Death, Postoperative

NOTE: For special autopsy procedures, see p. 4. In some instances, procedures described under "Death, anesthesia-associated" may be indicated. For a thorough review of investiga-tional procedures and autopsy techniques in operating-room-associated deaths, see ref. (1). In patients who developed a cerebral infarct after open heart surgery, arterial air embolism should be considered as a possible cause. The diagnosis often must be based on excluding other causes because the air has been absorbed prior to death. If a patient bled to death despite attempted repair, e.g., of hepatic lacerations, hospital records may not suffice to reach competent opinions but personal accounts from the surgeon and anesthesiologist may be needed.


1. Start RD, Cross SS. Pathological investigations of deaths following surgery, anaesthesia and medical procedures. J Clin Pathol 1999;52: 640-652.

Death, Restaurant

(See "Obstruction, acute airway.")

Death, Sniffing and Spray

Related Terms: Glue sniffing; sudden sniffing death syndrome.

NOTE: No anatomic abnormalities will be noted at autopsy. Sudden death may occur after cardiac dysrhythmia or respiratory arrest.

Organs and Tissues


Possible or Expected Findings



Other organs

If poison had been inhaled at the time when death occurred, tie main bronchi. Submit lungs in glass container for gas analysis.

Submit samples of small bronchi for histologic study.

For removal and specimen preparation, see p. 65. Submit samples of fresh or frozen brain for toxicologic study.

Submit samples in glass containers (not plastic) for toxicologic study.

Trichloroethane, fluorinated refrigerants, and other volatile hydrocarbons are most often involved in the "sudden sniffing death syndrome."

Spray death may occur in asthma sufferers using pressurized aerosol bronchodilators. Freons and related propellants may also be responsible for sudden death. Toxic components of glue—such as toluene—accumulate in the brain of glue sniffers. Also present in various glues are acetone, aliphatic acetates, cyclohexane, hexane, isopropanol, methylethyl ketone, and methylisobutyl ketone. Aerosols may occlude the airway by freezing the larynx. Carbon tetrachloride sniffing may cause hepatorenal syndrome (see also under "Poisoning, carbon tetrachloride").

Death, Sudden Unexpected, of Adult

NOTE: Medicolegal autopsies are usually indicated, and appropriate procedures should be followed (p. 8). If anaphylactic death is suspected, see also under that heading. A history of recent drinking (e.g., among college students) or of chronic alcoholism may be an important clue. The list of "Possible or Expected Findings" below is not complete. For general toxicologic sampling, see p. 16.

Organs and Tissues


Possible or Expected Findings

Abdomen Chest cavity

Blood Heart



Pancreas Adrenal glands

Neck organs

Submit sample of blood or exudate. Record volume and character of contents of pleural and pericardial cavities.

Submit samples for microbiologic (p. 102) and toxicologic (p. 16) study. Submit samples of myocardium (p. 30) with the conduction system (p. 26) for histologic study. For coronary arteriography, see p. 118.

Dissect all pulmonary arteries (p. 45). Submit samples for histologic study.

Procedures depend on grossly identified abnormalities as listed in right-hand column.

Photograph adrenals if hemorrhages are noted.

Remove carefully to avoid dislodging food or other objects from larynx.

Hemoperitoneum; peritonitis.* Hemothorax may occur—for instance, after rupture of aortic aneurysm. Hemopericardium usually occurs after rupture of myocardial infarction or of aortic dissection.*

Meningococcal disease* or streptococcal septicemia may cause sudden death. Coronary atherosclerosis, thrombosis, or arteritis; myocardial infarction, with or without perforation; myocarditis;* valvular heart disease, such as aortic stenosis or ballooning posterior leaflet syndrome.* Anatomic conduction system defects may indicate presence of arrhythmia (p. 34). Pulmonary thromboembolism; tumor embolism. Pulmonary intravascular (arterial and arteriolar) platelet aggregates may be cause of sudden death. Ruptured aneurysm;* aortic dissection.*

Islet cell tumor.

Hemorrhage may indicate presence of meningococcal disease.* Occlusion of larynx by bolus (see "Obstruction, acute airway"). Laryngeal edema may be cause of anaphylactic death.*

Organs and Tissues


Possible or Expected Findings

Brain and spinal cord


For removal and specimen preparation, see pp. 65 and 67, respectively. For cerebral arteriography, see p. 80.

Submit samples for possible chemical and toxicologic study (pp. 85 and 113).

Intracranial hemorrhage after trauma or rupture of aneurysm or—occasionally—with no apparent reason. Changes suggestive of epilepsy* may be present. Increased glucose concentrations may indicate the presence of hyperglycemia in undetected diabetes mellitus.*

Death, Sudden Unexpected, of Infant

Synonyms and Related Terms: Sudden infant death syndrome; SIDS; cot death; crib death.

NOTE: The autopsy alone does not suffice as an adequate investigation of sudden death of an infant. A thorough medical history, as well as complete information regarding the scene and circumstances of death must also be conducted. It should be recorded whether the infant was found in a prone position.

Photographs of the scene should be taken. The environmental and the infant's body temperature should be recorded as close to the time of death as possible. Cases of infanticide have been disguised as SIDS; a high level of suspicion should be maintained, particularly if more than one SIDS case reportedly occurred in the same family. Thus, while some of the "Possible or Expected Findings" in the table refer to typical cases of SIDS (1), other refer to possible infanticide (2).

Organs and Tissues


Possible or Expected Findings

External examination


Cerebrospinal fluid Vitreous

Chest cavity Thymus


Heart and great vessels; ductus arteriosus


Record weight of infant; measure crown-rump and crown-heel length and head, chest and abdominal circumference. For expected values, see p. 554. Test skin turgor and look for "sunken eyes" (signs of deydration). Prepare skeletal roentgenograms. Ophthalmic examination.

If there is clinical or pathologic evidence of infection, submit sample for bacterial and viral cultures (p. 104). Prepare smear. Submit sample for possible electrolyte studies and urea nitrogen and glucose determination (pp. 85 and 113). In suspected child abuse, photograph fundus (see p. 85) before considering an aspiration.

Record weight and submit samples for histologic study.

Submit for culture (p. 102). Submit blood drops dried on filter paper for tests for inborn errors of metabolism. Refrigerate blood samples for toxicologic study (p. 16). Check venous return and origin and course of coronary arteries and great vessels. Submit samples for histologic study (p. 30).

Record weights; culture and Gram-stain areas of consolidation. Submit samples for histologic study.

Growth retardation. Signs of dehydration. Crusts or frothy fluid around nose and mouth. Emaciation indicates organic disease or neglect. Bruises or burns indicative of child abuse. Jaundice; edema. Old or recent fractures due to child abuse. Retinal hemorrhages indicative of "shaken baby syndrome." Conjunctival petechiae may be a sign of strangulation (2).

Increased glucose concentrations may indicate undiagnosed diabetes mellitus.* Manifestations of dehydration.*

Petechial serosal hemorrhages. Accelerated involution indicates stress and/or disease, of prolonged duration. Thymic petechiae.

In SIDS, blood in heart chambers tends to remain fluid.

In rare instances, congenital heart disease, myocarditis, coronary artery aneurysm, or coronary artery arising from the pulmonary artery may explain the sudden death. Congestion; hemorrhage; edema; pleural petechiae; atelectasis. Acute pulmonary emphysema may indicate strangulation (2).

Organs and Tissues


Possible or Expected Findings

Neck organs and trachea

Stomach Intestinal tract

Pancreas Urine

Other organs Brain and spinal cord Middle ears

Bones and bone marrow

Photograph and culture sites of infection. Samples submitted for histologic study should include trachea, larynx, epiglottis, pharyngeal wall, tonsils, submaxillary glands, parathyroid glands, and cervical lymph nodes. Dissect, weigh, and section carotid bodies.

Record character and amount of contents.

Record appearance of serosal surface (exudate? discoloration?). Assess attachment of the mesenteric root, which normally runs obliquely from the left upper quadrant (ligament of Treitz) to the right lower quadrant near the inferior pole of the right kidney. Submit samples for histologic study.

Obtain two samples; one saved in preservative and the other frozen or refrigerated for toxicologic assays (p. 16).

Submit portions of spleen, for culture as a double check for the blood culture. Carefully examine, weigh, and submit samples of organs, including endocrine organs, for histologic study. For removal and specimen preparation, see pp. 66 and 70, respectively. Submit portion of brain for microbiologic study if indicated by clinical history or pathologic findings. Open middle ears and mastoid cells (pp. 71-73).

Submit exudate for microbiologic study. Prepare Gram-stained smears of exudate and histologic sections of middle ears. Submit samples from costochondral junctions. For removal and specimen preparation of bone, see p. 95. For preparation of sections and smears of bone marrow, see p. 96.

Laryngitis;* tracheitis.

Epiglottitis. Infection affecting other neck organs and tissues.

Hypoplasia of carotid bodies (few are hyperplastic).

This may be pertinent to allegations of starvation.

Contusions; malrotation; volvulus; infarction.

Degeneration of islets may indicate presence of undetected diabetes mellitus.* Drug intoxication, increased organic acids with medium chain acyl-coenzyme A dehyrogenase deficiency (3). Extramedullary hematopoiesis in the liver. Congenital adrenal hypoplasia.

Head trauma in abused child. Birth injuries; encephalitis. Astroglial proliferations in brain stem. Retarded myelination of brain stem.

Otitis media.*

Bone changes of vitamin D deficiency* (rickets). Normoblastic hyperplasia of bone marrow. Retardation of the rate of enchondral ossification such that hematopoiesis abuts the transition zone.


1. Valdez-Dapena M, McFeeley PA, Hoffman HJ, et al., eds. Histopa-thology Atlas for the Sudden Infant Death Syndrome. Armed Forces Institute of Pathology Washington, DC, 1993. (Order from American Registry of Pathology Sales Office, AFIP, Room 1077, Washington, DC 20,306-26,000.)

2. Becroft DM, Lockett BK. Intra-alveolar pulmonary siderophages in sudden infant death: a marker for previous imposed suffocation. Pathology 1997;29:60-63.

3. Betz P, Hausmann R, Eisenmenger W. A contribution to a possible differentiation between SIDS and asphyxiation. For Sci Intl 1998;91: 147-152.

Decompression (See "Sickness, decompression.")

Defect, Aortopulmonary Septal

Synonyms: Aortopulmony window; aorticopulmonary window or septal defect.

NOTE: The basic anomaly is a defect between ascending aorta and main pulmonary artery. For general dissection techniques, see p. 33.

Possible Associated Conditions: Atrial septal defect;* bicuspid aortic valve;* coarctation,* hypoplasia, or interruption (type A) of aortic arch; coronary artery from main pulmonary artery; right atrial arch; patent ductal artery;* right pulmonary artery from ascending aorta; subaortic stenosis;* tetralogy of Fallot;* ventricular septal defect.* (In approx 50% of the cases, one or more of these associated conditions are found.)

Defect, Atrial Septal

NOTE: The basic anomaly is a defect of the atrial septum, usually at the oval fossa (in 85%). Possible complications in unoperated cases include atrial arrhythmias, congestive heart failure; paradoxic embolism; plexogenic pulmonary hypertension (<10%), and pulmonary artery aneurysm. Possible surgical interventions include surgical and transcatheter closure of defect. For general dissection techniques, see p. 33.

Possible Associated Conditions: With secundum type: Often isolated; may occur with conotruncal anomalies, patent ductal artery,* valvular atresia,* and ventricular septal defect.* With primum type: Cleft in anterior mitral leaflet. With sinus venosus type: Anomalous connection of right pulmonary veins. With coronary sinus type (unroofed coronary sinus): Left atrial connection of a persistent left superior vena cava. With absent atrial septum or multiple large defects (common atrium): Complete atrioventricular defect;* asplenia syndrome.*

Defect, Complete Atrioventricular Septal

Synonyms and Related Terms: Complete atrioventricular canal; complete AV canal; endocardial cushion defect.

NOTE: The basic anomaly is a large combined atrioven-tricular septal defect and a common atrioventricular valve, with displacement of the atrioventricular conduction tissues. For possible surgical interventions, see complete repair, "mitral" valve replacement in Chapter 3 Appendix 3-4, p. 41. For general dissection techniques, see p. 33.

Possible Associated Conditions: Aortic coarctation; (35%); asplenia or polysplenia syndrome;* atrial septal defect;* common atrium; discrete subaortic stenosis;* double outlet right ventricle;* Down's syndrome;* patent ductal artery;* persistent left superior vena cava; pulmonary stenosis;* tetralogy of Fallot.*

Defect, Partial Atrioventricular Septal

Synonyms and Related Terms: Endocardial cushion defect; primum atrial septal defect with cleft mitral valve.

NOTE: The basic anomaly is a primum atrial septal defect and a cleft in the anterior mitral leaflet. Possible surgical interventions consist of surgical repair of both malformations. For general dissection techniques, see p. 33.

Possible Associated Conditions: Mitral regurgitation.

Defect, Ventricular Septal

Synonyms: Inlet (subtricuspid, AV canal type); membranous (paramembranous, perimembranous, infracristal); muscular (persistent bulboventricular foramen); and outlet (sub-arterial, supracristal, conal, doubly committed juxta-arterial).

NOTE: The basic anomaly is a defect of the ventricular septum, usually at the membranous septum (in 75%). Possible surgical intervention consists of surgical closure of the defect. Late postoperative death may be sudden and related to residual pulmonary hypertension or ventricular arrhythmias. For general dissection techniques, see p. 33. If hypertensive pulmonary artery disease is suspected, perfuse one lung with formalin (p. 47) and request Verhoeff-van Gieson stain (p. 173).

Possible Associated Conditions: With membranous type: Often isolated; may occur with atrial septal defect,* conotruncal anomalies, or patent ductal artery.* With outlet type: Conotruncal anomalies such as double outlet right ventricle,* persistent truncal artery,* or tetralogy of Fallot.* With inlet type: Atrioventricular septal defect* or atrioventricular discordance. With muscular type: Isolated or with tricuspid atresia* or double inlet left ventricle.

Deficiency, alpha1-Antitrypsin

Possible Associated Conditions: See below under "Possible or Expected Findings."

Organs and Tissues


Possible or Expected Findings

Skin and subcutaneous tissue Blood (serum)



Sample normal and abnormal appearing areas for histologic study.

Submit frozen sample for determination of alpha1-antitrypsin concentrations (1 mL is required).

Perfuse lungs with formalin (p. 47). See also under "Emphysema."

If cirrhosis or tumor is present, follow procedures described under those headings. Request PAS stain, with diastase digestion (p. 56).

Characteristic accumulations of alpha1-anti-trypsin can be shown in routine paraffin sections with PAS-D or immunostains.

Panniculitis (1).

Decreased arantitrypsin values. Many genetic alleles can be determined by starch-gel electrophoresis. Panlobular pulmonary emphysema,* primarily of lower lobes; chronic bronchitis and, rarely, brochiectases; interstitial pulmonary fibrosis. Cirrhosis in infants and adults; cholangiocellular or hepatocellular carcinoma; paucity of intrahepatic bile ducts; neonatal (giant cell) hepatitis; periportal hepatitis or cirrhosis and hepatocellular carcinoma in adults (2,3). PAS-positive, diastase-resistant globular inclusions, primarily in periportal hepatocytes or in the periphery of regenerative nodules.

Organs and Tissues


Possible or Expected Findings

Small and large intestine Extrahepatic bile ducts

Pancreas Kidneys

For cholangiography, see p. 56. Dissect bile ducts in situ.

See under "Glomerulonephritis."

Inflammatory bowel disease (rare) (3). Biliary atresia.* Generally no abnormalities in adults.

Chronic pancreatitis; fibrosis of pancreas. Membranoproliferative glomerulonephritis* in childhood (4).


O'Riordan K, Blei A, Rao MS, Abecassis M. Alpha 1-antitrypsin deficiency-associated panniculitis: resolution with intravenous alpha 1-antitrypsin administration and liver transplantation. Transplantation 1997;63:480-482.

Perlmutter DH. Clinical manifestations of alpha 1-antitrypsin deficiency. Gastroenterol Clin North Am 1995;24:27-43. Elzouki AN, Eriksson S. Risk of hepatobiliary disease in adults with severe alpha 1-antitrypsin deficiency (PiZZ): is chronic viral hepatitis B or C an additional risk factor for cirrhosis and hepatocellular carcinoma? Eur J Gastroenterol 1996;8:989-994. Yang P, Tremaine WJ, Meyer RL, Prakash UB. Alpha 1-antitrypsin deficiency and inflammatory bowel disease. Mayo Clin Proc 2000;75: 450-455.

Elzouki AN, Lindgren S, Nilsson S, Veress B, Erisksson S. Severe alpha1-antitrypsin deficiency (PiZ homozygosity) with membrano-proliferative glomerulonephritis and nephrotic syndrome, reversible after orthotopic liver transplantation. J Hepatol 1997;26:1403-1407.

Deficiency, alpha-Lipoprotein (See "Disease, Tangier's.") Deficiency, beta-Lipoprotein (See "Abetalipoproteinemia.") Deficiency, Congenital Transferrin (See "Hemochromatosis.") Deficiency, Folic Acid (See "Anemia, megaloblastic.")

Deficiency, Myeloperoxidase (See "Disorder, inherited, of phagocyte function.")

Deficiency, Vitamin A

Synonyms and Related Terms: Hypovitaminosis A; kerato-malacia; xerophthalmia.

Organs and Tissues


Possible or Expected Findings

External examination Other organs Eyes

Record extend and character of skin lesions and appearance of eyes; prepare sections of skin.

For removal and specimen preparation, see p. 85.

Sebaceous glands covered with keratin; keratomalacia; enlarged meibomian glands of eyelids.

For conditions that may produce vitamin A deficiency, see under "Syndrome, malabsorption."

Bitot's spots (keratinized epithelium and air bubbles at corneal rim); keratomalacia.

Deficiency, Vitamin B1 (Thiamine) (See "Syndrome, Wernicke-Korsakoff.")

Deficiency, Vitamin B6 (See "Beriberi.")

Deficiency, Vitamin B12 (See "Anemia, megaloblastic.")

Deficiency, Vitamin C

Synonyms: Hypovitaminosis C; scurvy.

Organs and Tissues


Possible or Expected Findings

External examination and skin

Record extent and character of skin lesions; prepare sections of skin.

Describe appearance of gums, and prepare sections.

Hyperkeratotic hair follicles with perifollicular hemorrhages (posterior thighs, anterior forearms, abdomen); petechiae and ecchymoses (inner and posterior thighs); subcutaneous hemorrhages. Gingivitis.

Organs and Tissues


Possible or Expected Findings

Other organs

Bones, joints, and soft tissues

Record evidence of bleeding.

For removal, prosthetic repair, and specimen preparation of bones and joints, see p. 95.

In rare instances, gastrointestinal or genitourinary hemorrhages. Hemorrhages into muscles and joints. Subperiosteal hemorrhages occur primarily in distal femora, proximal humeri, tibiae, and costochondral junctions (scorbutic rosary).

Deficiency, Vitamin D

Synonyms: Hypovitaminosis D; rickets.

NOTE: Features or rickets may be found in familial hypophosphatemia (vitamin D-resistent rickets; Fanconi syndrome).

Organs and Tissues


Possible or Expected Findings

External examination

Vitreous or blood (serum) Other organs


Prepare skeletal roentgenograms.

In infants with suspected rickets, record size of anterior fontanelle and shape of head; state of dentition; and shape of costochondral junctions, wrists, long bones, and spine. Submit samples for calcium, magnesium, and phosphate determination (p. 85). Procedures depend on expected findings or grossly identified abnormalities as listed in right-hand column.

Weigh parathyroid glands and submit samples for histologic study.

Submit samples of intestine for histologic study. For removal, prosthetic repair, and specimen preparation, see p. 95.

In infantile rickets, diagnostic sites for histologic sampling are costochondral junctions, distal ends of radius and ulna, and proximal ends of tibia and humerus. For adults, see under "Osteomalacia."

In infants, rachitic changes at costochondral junctions; in adults, osteoporosis* and osteomalacia*—with or without pseudofractures (Milkman's syndrome). Craniotabes; delayed dentition and enamel defects; protrusion of sternum; rachitic rosary; swelling of costochondral junctions and of wrists.

Hypocalcemia, hypomagnesemia, hypophosphatemia.

Possible causes of vitamin D deficiency include diseases associated with malabsorption syndrome,* biliary atresia,* and primary biliary cirrhosis. Parathyroid hyperplasia (hyperparathyroidism*) secondary to hypocalcemia and impaired absorption of vitamin D. Conditions causing malabsorption. Osteomalacia.*

Characteristic abnormalities of osteochondral growth plates in infants. Abundant osteoid in osteomalacia.*

Deformity, Klippel-Feil

Synonym: Congenital fusion of cervical vertebrae.

Organs and Tissues


Possible or Expected Findings

External examination

Neck organs Skull, spine, brain,

Prepare roentgenograms of chest, neck (lateral view), and head.

For removal and specimen preparation of brain and spinal cord, see pp. 65 and 67, respectively.

Short neck; low posterior hairline. Disorders with dysraphia (see below). Fusion of cervical vertebrae. Congenital elevation of the scapula (Sprengel's deformity). Malformed larynx (1). Arnold-Chiari malformation;* basilar impression; meningomyelocele; platybasia; spinal cord compression; syringomyelia.* Intracranial or spinal cord tumors (2).


1. Clarke RA, Davis PJ, Tonkin J. Klippel-Feil syndrome associated 2. Diekmann-Guiroy B, Huang PS. Klippel-Feil syndrome in associa-with malformed larynx. Case report. Ann Otol Rhinol Laryngol 1994; tion with a craniocervical dermoid cyst presenting as aseptic menin-

103:201-207. gitis in an adult: case report. Neurosurgery 1989;25:652-655.


1. Clarke RA, Davis PJ, Tonkin J. Klippel-Feil syndrome associated 2. Diekmann-Guiroy B, Huang PS. Klippel-Feil syndrome in associa-with malformed larynx. Case report. Ann Otol Rhinol Laryngol 1994; tion with a craniocervical dermoid cyst presenting as aseptic menin-

103:201-207. gitis in an adult: case report. Neurosurgery 1989;25:652-655.

Degeneration, Cerebellar Cortical

Synonyms and Related Terms: Alcoholic cerebellar degeneration; parenchymatous cerebellar degeneration.

Organs and Tissues Procedures Possible or Expected Findings

Brain and spinal cord For removal and specimen preparation, Cortical atrophy (predominantly loss of see pp. 65 and 67, respectively. Purkinje cells) of dorsal vermis of cerebellum and adjacent anterior lobe.

Other organs Procedures depend on expected findings or Manifestations of chronic alcoholism,*

grossly identified abnormalities as listed in amebiasis,* cirrhosis,* malnutrition, or right-hand column. pellagra.*

Degeneration, Cerebello-Olivary (See "Degeneration, spinocerebellar.")

Degeneration, Hepatolenticular

Degeneration, Spinocerebellar

Related Terms: Familial cortical cerebellar atrophy; Fried-reich's ataxia; hereditary ataxia; Machado-Joseph disease; olivopontocerebellar atrophy.

NOTE: The term spinocerebellar degeneration encompasses a variety of lesions whose classification is controversial.

A new approach has come from linkage analysis and molecular biology. For instance, Friedreich's ataxia, the classic form of hereditary ataxia, is due to an intronic expansion of a GAA tri-nucleotide repeat. Other forms are also identified by their specific gene loci. Neuropathologic examination still is important and ample sampling is suggested, which should include cerebral cortex, basal ganglia (caudate nucleus, putamen, and globus pallidus), thalamus, subthalamic nucleus, midbrain (red nucleus and substantia nigra), pons (pontine nuclei), spinal cord (at cervical, thoracic, and lumbar levels), optic tract, optic nerves with lateral geniculate nucleus, and sensory and motor peripheral nerves.

Organs and Tissues


Possible or Expected Findings

Brain and spinal cord Peripheral nerves

For removal and specimen preparation, see pp. 65 and 67, respectively.

For removal and specimen preparation, see p. 79.

Symmetric neuronal loss with reactive astrocytosis in the affected areas. See also above under "Note."


1. Koeppen AH. The hereditary ataxias. J Neuropathol Exp Neurol 1998;57:531-543.

Degeneration, Spongy, of White Matter

Synonyms and Related Terms: Bertrand-van Bogaert disease; Canavan's disease; familial leukodystrophy. NOTE: The disease is caused by defective asparto acylase activity. The gene has been cloned and mutations found.

Organs and Tissues Procedures Possible or Expected Findings

External examination Record head circumference. Enlargement of head.

Prepare roentgenograms of skull.

Brain and spinal cord For removal and specimen preparation, Poor demarcation between cortex and see pp. 66 and 70, respectively. Request gelatinous white matter. Extensive

Luxol fast blue stain (p. 72). demyelination and vacuolation of white matter, particularly subcortically.

Eyes and optic nerves For removal and specimen preparation, Optic atrophy.

Degeneration, Striatonigral (See "Atrophy, multiple system.")


Related Term: Thirst.

NOTE: Possible underlying conditions not related to inaccessibility of water include burns, exposure to heat, gastrointestinal diseases, recent paracentesis, renal diseases, and use of diuretic drugs. See also under "Disorder, electrolyte(s)."

Organs and Tissues


Possible or Expected Findings

External examination



Prepare histologic sections of blisters, ulcers, or skin abrasions.

Submit sample for sodium, chloride, and urea nitrogen determination (p. 85).

Record volume and specific gravity

Skin turgor may be decreased and eyes may be sunken.

Microscopic changes help to decide whether skin lesions are antemortem or postmortem.

Sodium concentrations more than 155 meq/L, chloride concentrations more than 130 meq/ and urea nitrogen concentrations between 40 and 100 meq/dL indicate dehydration. Absence or minimal amount of urine (p. 115).

Dementia (See "Disease, Alzheimer's.")

Dependence, Amphetamine(s)

NOTE: There are no diagnostic autopsy findings. Follow procedures described under "Dependence, drug(s)."

Dependence, Cocaine

NOTE: Cocaine is spontaneously hydrolyzed by blood esterases, even after death. However, its major metabolite, benzoylec-gonine, is routinely identifiable by EMIT and ELISA screening tests (see p. 17). When cocaine is abused concurrently with heroin or other drugs, it may be difficult to ascribe death to a single agent.

Organs and Tissues


Possible or Expected Findings

External examination



Stomach and colon

Liver and gallbladder

Other body fluids and organs

Record condition of nasal septum.

Submit nasal swab for toxicologic study. Submit sample with NaF added for toxicologic study (see Chapter 2); request drug screen (p. 14).

Record heart weight and thickness of ventricles. For dissection of the heart and coronary arteries, and for histologic sampling, see also Chapter 3.

Save gastric contents for toxicologic study. Sample stomach and colon for histologic study.

Save liver tissue and bile for toxicologic study. Sample liver for histologic study. Save vitreous (p. 16), urine, kidneys, and brain for toxicologic study.

Chronic inflammation and perforation of nasal septum after prolonged sniffing of cocaine.

Remnant of cocaine. See above under "Note."

Left ventricular hypertrophy caused by hypertension complicating or aggravated by cocainism. Cardiotoxicity with focal myocarditis and myocyte necrosis (2), contraction bands (3), and coronary occlusion.

Ischemia of gastric mucosa after ingestion of cocaine. Ischemic colitis (4).

Zonal hepatic necrosis (5). See above under "Note."


1. Brody SL, Slovis CM, Wrenn KD. Cocain-related medical problems. Consecutive series of 233 cases. Am J Med 1990;88:325-331.

2. Peng SK, French WJ, Pelikan PCD. Direct cocaine cardiotoxicity demonstrated by endomyocardial biopsy. Arch Pathol Lab Med 1989; 113:842-845.

3. Karch SB, Billingham ME. The pathology and etiology of cocaine-induced heart disease. Arch Pathol Lab Med 1988;112:225-230.

4. Brown DN, Rosenholtz MJ, Marshall JB. Ischemic colitis related to cocaine abuse. Gastroenterology 1994;89:1558-1561.

5. Silva MO, Roth D, Reddy KR, Fernandez JA, Albores-Saavedra J, Schiff ER. Hepatic dysfunction accompanying acute cocaine intoxication. J Hepatol 1991;12:312-315.

Dependence, Drug(s), all Types or Type Unspecified

Related Terms: Cocaine dependence;* crack dependence; heroin dependence; intravenous narcotism; morphinism.

NOTE: If narcotic paraphernalia and samples of the drug itself are found at the scene of the death, they should be submitted for analysis. Helpful information about the nature of a drug may be obtained from witnesses. State crime laboratories may provide much assistance. If name of drug is known, see also under "Poisoning,..." The slang name of a drug may be insufficient for identification because these names often are used for different compounds at different times of places.

Opoid narcotics can be injected intravenously, or subcuta-neously, or snorted. Death may occur with such speed that the bodies may be found with needles and syringes in the veins or clenched in the hands. Drug dependence may be associated with a multitude of local (see below) or systemic complications, including malaria* and tetanus.*

For general toxicologic study, see p. 14. As stated in Chapter 2, for a growing number of analytes, most notably tricyclic antidepressants, peripheral blood is preferred over central blood.

Peripheral blood is aspirated by percutaneous puncture before autopsy, from the femoral vein or the subclavian vein. The authors prefer the femoral approach in order to avoid any question of artifact in the diagnosis of venous air embolism. It may be prudent to add NaF to some of the samples.

Possible Associated Conditions: Acquired immunodeficiency syndrome (AIDS) and many other acute and chronic infections; malnutrition.*

Organs and Tissues


Possible or Expected Findings

External examination and skin






Perihilar lymph nodes



Brain and spinal cord

In suspected homicides or other unusual circumstances, excise fresh needle marks with surrounding skin and underlying tissues and submit for toxicologic analysis. (In routine accidental drug-related deaths, this is not necessary.) Submit samples with needle marks for histologic study under polarized light. If victim has not been identified, follow procedures described on p. 11. Photograph changes that indicate addiction. For toxicologic sampling, see above under "Note.' Submit samples for bacterial, fungal, and viral cultures, study of viral antibodies (hepatitis B and C), and blood alcohol determination. If endocarditis is suspected, follow procedures described under that heading (p. 103).

Bones and joints

Submit portions for toxicologic and micro-biologic study (p. 103). Submit multiple samples for histologic study. Request Verhoeff-van Gieson stain (p. 173). Study sections under polarized light.

Submit sample of bile for toxicologic study (p. 16).

Submit samples for toxicologic and histologic study.

Record weight.

Submit sample for toxicologic study.

For removal and specimen preparation, see pp. 65 and 67, respectively.

Submit samples of grossly abnormal areas for histologic study.

Foam may exude from nostrils. Erosions of the nasal septum occur in heroin sniffers. Needle marks may be found at any accessible site. Scars, "track hyperpigmentation," ulcers, skin abscesses, and subcutaneous hemorrhages may be abundant. Other complications are ischemic crush injuries with acute rhabdomyolysis, myositis ossificans (brachial muscle), and thrombophlebitis.

Septicemia; evidence of acute or chronic viral infection; alcohol intoxication.

Infective endocarditis* that is often on the right side. Expected organisms include

Acinebacter spp., Staphylococcus aureus, Staphylococcus albus, Salmonella spp., enterococci, and Staphylococcus epidermidis.

Pulmonary edema; aspiration; diffuse lobular pneumonia. Septic pulmonary abscesses. Perivascular pulmonary talc granulomas; foreign body emboli; pulmonary necrotizing angiitis; atelectases and fibrosis. Heroin is metabolized to morphine. Morphine accumulates in bile, where it is sometimes easier to detect than in blood. Nonspecific portal hepatitis; acute or chronic viral hepatitis;* alcoholic liver disease.* Foreign body granulomas may be present in the liver.

Chronic lymphadenitis. Splenomegaly with follicular hyperplasia. Detects monoacetylmorphine to distinguish heroin from morphine poisoning. Bilateral symmetric necrosis of globus pallidus; cerebral abscess;* meningitis;* transverse myelitis; mycotic aneurysms; subdural or epidural empyema.* Acute cerebral falciparum malaria.* Infectious spondylitis and sacroiliitis.

Depressant(s) (See "Dependence, drug(s),...") Dermatomyositis

Related Term: Childhood dermatomyositis (or polymyositis) associated with vasculitis; dermatomyositis (or polymyositis) associated with neoplasia or collagen vascular disease; primary idiopathic dermatomyositis; primary idiopathic polymyositis.

Possible Associated Conditions: Carcinoma (lung, stomach, intestine, and prostate in males; breast, ovary, and uterus in females; miscellaneous sites in both sexes); lymphoma* (rare) and other malignancies (1); lupus erythematosus;* mixed connective tissue disease; progressive systemic sclerosis;* rheumatoid arthritis;* Sjogren's syndrome;* and others. Vasculitis of childhood polymyositis (dermatomyositis).

Organs and Tissues


Possible or Expected Findings

External examination and skin

Heart Lungs

Esophagus and gastrointestinal tract


Other organs

Skeletal muscles

Peripheral nerves Joints

Photograph grossly involved skin.

Prepare sections of involved (anterior chest, knuckles, knees) and grossly uninvolved skin and subcutaneous tissue.

Prepare roentgenograms.

Submit samples from myocardium for histologic study (p. 30).

Perfuse one lung with formalin (p. 47).

Submit samples from all segments for histologic study.

Submit samples of liver for histologic study. For sampling in diabetes mellitus, see under that heading.

Submit samples from deltoid, biceps, cervical, gluteal, and femoral muscles, and also from other muscles that may have been involved clinically (pharynx, tongue), for histologic study. Photograph abnormal gross specimens. For specimen preparation, see p. 80. For removal and specimen preparation, see p. 79.

For removal, prosthetic repair, and specimen preparation, see p. 95.

Erythema; maculopapular eruption; eczematoid or exfoliative dermatitis; ulcerations; calcification. Microscopically, dermatitis and panniculitis with edema and fibrinoid necroses are found. Vasculitis in childhood cases. Lipodystrophy (2).

Pneumomediastinum and subcutaneous emphysema (3). Mycarditis* (rare).

Microscopic changes similar to those in skeletal muscles (see below). Lymphocytic pneumonitis; obliterating bronchiolitis; edema; interstitial pulmonary fibrosis (see "Pneumonia, interstitial"). Vasculitis; myositis, rarely with rupture (4). Features of inflammatory bowel disease may be present.

Arteritis* and phlebitis* with thrombosis, fibrosis, and infarctions. Steatohepatitis and manifestations of diabetes mellitus* may be found (2).

Myositis with muscular atrophy and fibrosis; vasculitis in childhood cases.

Polyneuropathy (rare) (5). Arthritis.


1. Maoz CR, Langevitz P, Livneh A, Blumstein Z, Sadeh M, Bank I, et al. High incidence of malignancies in patients with dermatomyositis and polymyositis: an 11-year analysis. Semin Arthritis Rheum 1998; 27:319-324.

2. Quecedo E, Febrer I, Serrano G, Martinez-Aparicio A, Aliaga A. Partial lipodystrophy associated with juvenile dermatomyositis: report of two cases. Pediatr Dermatol 1996;13:477-482.

3. de Toro-Santos FJ, Verea-Hernando H, Montero C, Blanco-Aparicio M, Torres Lanzas J, Pombo Felipe F. Chronic pneumomediastinum and subcutaneous emphysema: association with dermatomyositis. Respiration 1995;62:53-56.

4. Dougenis D, Papathanasopoulos PG, Paschalis C, Papapetropoulos T. Spontaneous esophageal rupture in adult dermatomyositis. Eur J Cardio-Thor Surg 1996;10:1021-1023.

5. Vogelsang AS, Gutierrez J, Klipple GL, Katona IM. Polyneuropathy in juvenile dermatomyositis. J Rheumatol 1995;22:1369-1372.

Diabetes Insipidus

Organs and Tissues


Possible or Expected Findings

Brain and pituitary gland

Vitreous Other organs

For cerebral arteriography, see p. 80. For removal and specimen preparation of brain and pituitary gland, see pp. 65 and 71, respectively. If infection is suspected, follow procedures described on p. 102. Submit samples from brain and pituitary gland for histologic study.

Submit sample for sodium, chloride, and urea nitrogen determination (p. 85). Procedures depend on expected findings or grossly identified abnormalities as listed in right-hand column.

Head injury* (including birth trauma); Langerhans cell (eosinophilic) granulomatosis;* local infection; metastatic tumor (frequently from carcinoma of breast); neurosurgical procedures; primary neoplasm involving neurohypophyseal system; sarcoidosis.*

Changes associated with dehydration.*

No diagnostic findings.

Nephrogenic diabetes insipidus is caused by renal tubular defect.

Manifestations of histiocytosis,*

sarcoidosis,* and other possible underlying conditions.

Diabetes Mellitus

Synonyms: Type I (insulin-dependent or juvenile-onset) diabetes mellitus; type II (insulin-independent or adult onset) diabetes mellitus; secondary diabetes mellitus (e.g., due to drugs or pancreatic disease).

NOTE: In infants of diabetic mothers, megasoma and congenital malformations of the cardiovascular and central nervous systems must be expected. Record size and weight of placenta and total weight and length, crown to rump length, and crown to heel length of infant. Compare with expected measurements

(pp. 555 and 561). Expected histologic finding include hyperplasia with relative increase of B cells of the islands of Langerhans with interstitial and peri-insular eosinophilic infiltrates, decid-ual changes of the endometrium, enhanced follicle growth in the ovaries, and Leydig cell hyperplasia.

Possible Associated Conditions: Acanthosis nigricans; acromegaly;* amyotrophic lateral sclerosis;* ataxia telangiectasia;* Fanconi's anemia;* Friedreich's ataxia;* gout;* hemochro-matosis;*hyperlipoproteinemia;* hyperthroidism;* obesity;* Turner's syndrome;* and many others, too numerous to mention.

Organs and Tissues


Possible or Expected Findings

External examination and skin



Prepare sections of skin lesions, of grossly unaffected skin, and of subcutaneous tissue.

If there is evidence of mastopathy, sample tissue for histologic study. Prepare sections and smears of intertriginous and other skin infections. Request Gram and Grocott's methenamine silver stains (p. 172). Prepare whole-body roentgenograms.

Submit samples of skin tissue for electron microscopic study (p. 132). Submit sample for bacterial and fungal cultures (p. 102). If diabetic coma must be ruled out or if disease is only suspected, submit samples of blood and vitreous (see below) for biochemical study. For interpretation, see p. 114. Record weight and thickness of walls. For coronary arteriography, see p. 118. For histologic sampling, see p. 30.

Gangrene of lower extremities and other ischemic changes.

Xanthelasmas of eyelids. Diabetic xanthomas on forearms. Diabetic lipoatrophy. Subcutaneous atrophy at former sites of insulin injection. Diabetic mastopathy.

Fungal vulvitis.

Subcutaneous and vascular calcifications. Joint deformities (see below under "Joints"). Diabetic microangiopathy.

Septicemia. Increased concentrations of blood glucose (unreliable for diagnosis) and serum ketones and lipids. Postmortem insulin determination may permit the diagnosis of insulin poisoning. Cardiac hypertrophy;* coronary atherosclerosis;* myocardial infarction.

Organs and Tissues


Possible or Expected Findings










Adrenal glands



Urinary bladder Seminal vesicles, spermatic cords, and testes Ovaries

Lower extremities

If glycogen content is to be evaluated, place specimens in alcohol (p. 129) or Carnoy's fixative (p. 130) or—preferably—prepare for electron microscopic study (p. 132). Submit one lobe for bacterial and fungal cultures (p. 103). Request Gram and Grocott's methen-amine silver stain (p. 172). Sample for histologic study. For special stains, see "Lungs."

Record weight and sample for histologic study.

Record appearance of concrements.

Submit sample for histologic study.

Record size and shape of stomach and appearance of mucosa.

Prepare soft tissue roentgenogram. Dissect pancreas and record weight. Slice organ in 2-mm sagittal sections. Place one slice in alcohol or

Carnoy's fixative (p. 130). Request Best's carmine, Masson's trichrome, Congo red, and

Gomori's chromium hematoxylin phloxine stains

fixed organs should be refixed for 12-24 h in

Bouin's solution (p. 129). Whenever granules are to be demonstrated in beta cells, a slice of fresh tissue should be placed in Bouin's or

Record weights. If abnormalities are noted, sample for histologic study.

Record weights of both organs. For renal arteriography, see p. 59. Submit samples for histologic and electron microscopic study (p. 132). Request PAS-alcian blue and Grocott's methenamine silver stains (p. 172). All sections should include papillae. Submit fresh material for immunofluorescence study.

Prepare sediment and submit sample for protein, glucose, and acetone determination.

Submit samples for histologic study.

Submit samples for histologic study. For arteriography, see p. 120. Submit samples from smaller arteries for histologic study. For decalcification procedures, see p. 97.

Request von Kossa's and Verhoeff-van Gieson stains (p. 172).

Bacterial or fungal (aspergillosis,* candidiasis,* cryptococcosis*) pneumonia.

Intramural pseudodiverticulosis (dilatation of submucosal gland ducts). Fungal esophagitis.

Hepatomegaly; fatty changes; diabetic steatohepatitis or steatohepatitic cirrhosis. Other types of cirrhosis may be a cause of secondary diabetes (Naunyn's diabetes). Cholelithiasis.* Lipoid histiocytosis.

Gastric dilatation; mucosal hemorrhages.

Glycogenosis of beta cells in prolonged hyperglycemia (in type II diabetes); degranulation of islets of Langerhans; lymphocytic or eosinophilic infiltration around islets (in type I diabetes); amyloid-osis or fibrosis of islets. Lesions that may have caused secondary diabetes include pancreatitis, tumors of the pancreas,* cystic fibrosis,* and hemochromatosis.* Focal or diffuse nesidioblastosis in infants of diabetic mothers (may be a cause of hyperinsulinemic hypoglycemia).

Adrenocortical nodules or tumor or pheochromocytoma (see also under "Syndrome, Cushing's" and "Tumor of the adrenal glands").

Diabetic nephropathy and microangiopathy. Arteriolonephrosclerosis; diabetic intercapillary glomerulosclerosis; tubular atrophy and interstitial fibrosis; pyelonephritis* and necrotizing papillitis.

Glomerular capillary and tubular basement membranes stain for IgG and albumin. Abnormal sediment. Proteinuria, glycosuria, and acetonuria. Urocystitis.

Submucosal granular deposits in seminal vesicles; calcification of vas deferens; tubular atrophy of testes. Stromal hyperthecosis. Gangrene. Obliterating arteriosclerosis of anterior and posterior tibial arteries, peroneal arteries, and dorsal artery of the foot.

Monckeberg's sclerosis* of muscular arteries.

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Beat The Battle With The Bottle

Alcoholism is something that can't be formed in easy terms. Alcoholism as a whole refers to the circumstance whereby there's an obsession in man to keep ingesting beverages with alcohol content which is injurious to health. The circumstance of alcoholism doesn't let the person addicted have any command over ingestion despite being cognizant of the damaging consequences ensuing from it.

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