Synonyms and Related Terms: Acanthocytosis; Bassen-Kornzweig syndrome.

NOTE: Autopsies on patients with this rare genetic disease (1,2) should be considered research procedures. Possible Associated Conditions: Hemolytic anemia;* malabsorption syndrome.*

Organs and Tissues Procedures

External examination Record body weight and length.

Prepare chest roentgenogram (frontal and lateral view). Blood Submit for serum lipid analysis.

Small bowel

Large bowel Liver

Other organs Spine

Brain, spinal cord, peripheral nerves



1. Case records of the Massachussetts General Hospital. Case 35-1992. N Engl J Med 1992;327:628-635.

2. Rader DJ, Brewer HB Jr. Abetalipoproteinemia. New insights into lipoprotein assembly and vitamin E metabolism from a rare genetic disease [clinical conference]. JAMA 1993;270:865-869.

3. Gorin MB, Paul TO, Rader DJ. Angioid streaks associated with abetalipoproteinemia. Ophthalmic Genet 1994;15:151-159.

Possible or Expected Findings

Below-normal weight in infants. Kyphoskoliosis.

Very low concentrations of cholesterol and triglycerides; serum P-lipoprotein decreased or absent; a-lipoproteins present. Acanthocytosis (spiny red cells). Abnormal shape of villi; vacuolation of epithelial cells.

Fatty stools Fatty changes.

Systemic manifestations of malabsorption syndrome* and of vitamin A deficiency.* Kyphoscoliosis.

Axonal degeneration of the spinocerebellar tracts; demyelination of the fasciculus cuneatus and gracilis (2). Possible involvement of posterior columns, pyramidal tracts, and peripheral nerves. Atypical retinitis pigmentosa (2) with involvement of macula. Angioid streaks (3).


NOTE: If a fetus is present, follow procedures described under "Stillbirth." If no recognizable fetal tissue is found, an indication might exist to submit material for chromosome study as decribed in Chapter 10. If attempts to induce abortion appear to have caused the death of the mother, see "Death, abortion-associated."

Prepare smears of undiluted blood. For preservation of small intestinal mucosa and for preparation for study under dissecting microscope, see Part I, Chapter 5. Submit sample for histologic study.

Submit stool for chemical analysis. Record weight and submit sample for histologic study.

Record appearance of spine (see also chest roentgenogram). For removal and specimen preparation, see pp. 65, 67, and 79, respectively. Request Luxol fast blue stain (p. 172).

For removal and specimen preparation, see p. 85.

Abscess, Brain

Synonym: Cerebral abscess.

NOTE: For microbiologic study of tissues and abscesses, see Part I, Chapter 9. Include samples for anaerobic culture. It is best to study the brain after fixation but if specimen is examined fresh, aspirate and prepare smears of abscess content. Photograph surface and coronal slices of brain. Request Giemsa stain, Gram stain, PAS stain, and Grocott's methenamine silver stain for fungi (p. 172, 173).

Organs and Tissues


Possible or Expected Findings

External examination

Cerebrospinal fluid Brain and spinal cord

Base of skull with sinuses and middle ears


Other organs

Record presence or absence of features listed in right-hand column.

If there is evidence of trauma, see also under "Injury, head." Prepare roentgenograms of chest and skull.

Submit for microbiologic study (p. 104). For removal and specimen preparation, see pp. 65 and 67, respectively. For micro-biologic study, photography, and special stains, see under "Note."

For exposure of venous sinuses, see p. 71. Sample walls of sinuses for histologic study. For exposure of paranasal sinuses, mastoid cells, and middle ears, see p. 71-73.

For removal and specimen preparation, see p. 85.

Procedures depend on suspected lesions as listed in right-hand column.

Skin infections in upper half of face. Edema of forehead, eyelids, and base of nose, proptosis, and chemosis indicate cerebral venous sinus thrombosis.* Trauma; craniotomy wounds.

Skull fracture and other traumatic lesions. For possible intrathoracic lesions, see below under "Other organs."

Traumatic lesions of brain. Foreign body.

Cerebral venous sinus thrombosis* or thrombophlebitis.

Paranasal sinusitis and mastoiditis. Subacute and chronic otitis media.* Osteomyelitis* and fractures of base of skull may be present. Thrombosis of angular and superior ophthalmic veins, associated with cavernous sinus thrombosis.*

Congenital heart disease with right-to-left shunt; infective endocarditis.* Bronchiectasis;* lung abscess;* pleural empyema.* Entamoeba histolytica abscesses in liver and lung.

Abscess, Epidural

Synonym: Epidural Empyema.

NOTE: Procedures are the same as those suggested under "Empyema, epidural." Abscess, Lung

Synonym: Pulmonary abscess.

NOTE: For microbiologic procedures and related suggestions, see also under "Pneumonia."

Organs and Tissues


Possible or Expected Findings

External examination

Chest cavity

Prepare chest roentgenogram.

Record appearance of oral cavity. If peripheral veins contain potentially infected catheters, see below under "Central veins." Before chest is opened, puncture pleural cavity and submit exudate for microbiologic study (p. 102).

Prepare smears of exudate and request Gram, Kinyoun, and Grocott methenamine silver stains (p. 172).

Pulmonary cavities and infiltrates; foreign body.

Periodontal infection. Infected intravenous catheter.

Empyema;* pleural effusion or exudate.*

Bacteria or fungi in exudate.

Organs and Tissues


Possible or Expected Findings

Central veins

Heart Lungs

Other organs

If a metastatic abscess from an infected intravenous catheter is suspected, ligate appropriate vein proximal and distal to catheter tip and submit for microbiologic study. See "Endocarditis, infective."

For bronchography and pulmonary arteriography, see Part I, Chapter 5. If abscess contents are aspirated or microbiologic studies are not crucial, perfuse intact lung with formalin (p. 47).

Procedures depend on expected sources of infection.

Infected intravenous catheter.

Infective endocarditis* of tricuspid or pulmonary valve.

Tumor of lung,* foreign body, or other obstructive bronchial lesion.

Manifestations of possible underlying conditions such as acquired immunodeficiency syndrome.*

Abscess, Subdural (See "Empyema, epidural.")

Abscess, Subphrenic (See "Empyema, subphrenic.")

Abuse, Child (See "Infanticide.")

Abuse, Drugs or Other Chemicals (See "Abuse, hallucinogen(s)," "Abuse, marihuana," "Dependence,..." "Poisoning,..." See also "Alcoholism and alcohol intoxication.")

Abuse, Hallucinogen(s)

Related Terms: Diethyltryptamine (DET); dimethyltrypt-amine (DMT); lysergic acid diethylamide (see "Poisoning, LSD"); marihuana;* mescaline; psilocin; psilocybin ("magic mushrooms"); psychedelics; psychotomimetics; and others (1).

NOTE: See also under "Dependence, drug(s), all types or type unspecified." For routine toxicologic sampling, see p. 16. There are no specific morphologic findings related to hallucinogen intake.


1. Baselt RC, Cravey RH. Disposition of Toxic Drugs and Chemicals in Man, 4th ed. Chemical Toxicology Institute, Foster City, CA, 1995.

Abuse, Marihuana

Synonyms: Cannabis; hashish.

NOTE: The tissues at autopsy show no specific changes. Tetrahydrocannabinol is routinely detected by the EMIT screening procedure (see Part I, Chapter 2) in urine, and is confirmed and quantitated by specific assays on a variety of body fluids, including blood. However, these latter procedures are rarely needed. If abuse of other drugs is suspected, see under "Dependence, drug(s), all types or type unspecified."

Accident, Aircraft

In the event of a major catastrophic air carrier accident, the local police should be called and then The Federal Aviation Administration (FAA) in Washington, DC.* The FAA will notify the National Transportation Safety Board (NTSB). Most fatal air crashes are investigated by the NTSB.** The FAA investigates crashes in which the gross weight of the craft is less than 12,500 pounds (1). The investigations are conducted by a team of federal and other specialists. Local police, firemen, or other officials will seal off the area of the crash, and no one should be allowed to approach the bodies or any objects until the identification teams and the medical examiner or coroner have taken charge.

Several medical examiner and coroner offices have published accounts detailing their approaches to managing mass fatality disasters (2-6). The sudden influx of bodies after a commercial air carrier accident and the request for speedy identification of the victims and for detailed autopsy reports of the crew members would overburden almost any institution. Managing such a disaster requires an efficient organization, and it seems advisable to devise a plan before the necessity arises. Temporary morgue facilities may have to be established near the scene of the crash. Refrigerated trucks may serve as storage space. A practical approach is to deal first with those bodies that seem to be the easiest to identify, in order to narrow the field for the more difficult cases.

If bodies are scattered, the exact locations should be identified by stakes in the ground or spray paint on pavement; only then should these bodies (or remaining parts) and all objects that might belong to them be collected. For this, plastic bags with paired tags are generally used. One tag is used as a marker for the stake; the other stays with the bag. Or, if the stakes are numbered, one tag can be used and the stake number is put on the tag, in addition to the bag number. Proper records and diagrams of the relative positions of victims are prepared during this phase. If the victims are still within the airplane, their exact positions within the wreckage must also be recorded, and appropriate photographs should be taken.

For the identification of the victims, the airline will provide a list of the passengers and the Federal Bureau of Investigation (FBI) disaster team will take fingerprints and aid in the acquisition of other identifying data such as age, race, weight, height, and hair color and style. If dental records can be obtained, this provides one of the most certain methods of identification. A medical history indicating amputations, internal prostheses, or other characteristic surgical interventions or the presence of nephrolithiasis, gallstones, and the like will be helpful. Fingerprints (and footprints of babies) should be taken in all instances. Wallets with identification cards, jewelry, name tags in clothing, or other personal belongings may provide the fastest tentative identification.

The medical examiner may elect to autopsy only the flight crew but not the passengers of an aircraft crash. However, the grossly identifiable fatal injuries should be described, photographed, and x-rayed. This may reveal identifying body changes. If comparison of somatic radiographs, dental records, fingerprints, or photographs do not identify the victim, DNA comparison must be considered. Burned or fragmented bodies of passengers and the bodies of crew members, and particularly the pilots, must have a complete autopsy, including roentgenographic and toxicologic examinations, which must always include alcohol and carbon monoxide determinations. Internal examination might reveal a coronary occlusion, or roentgenograms may disclose a bullet as evidence that violence preceded the crash. In some airplane crashes, particularly in light airplane accidents, suicide must be considered and a suicide note should be sought. Some authors recommend performing autopsies on all deceased occupants of aircraft crashes, including passengers, and cite the need to distinguish among blunt impact trauma, smoke inhalation, and flash fires as causes of death, in order to answer future questions concerning pain and suffering, intoxication, and sequence of survivorship.

After a crash victim has been identified, the coroner or medical examiner will issue a death certificate. If remains of a decedent cannot be found, a judge can, upon petition, declare a passenger dead and sign a death certificate prepared by a medical examiner.

*Phone # of FAA Command Center: 202-267-3333 **Phone # of NTSB Command Center: 202-314-6290.


1. Wagner GN, Froede CH. Medicolegal investigation of mass disaster. In: Medicolegal Investigation of Death, 3rd ed. Spitz WU, ed. Charles C. Thomas, 1993.

2. Clark MA, Hawley DA, McClain JL, Pless JE, Marlin DC, Standish SM. Investigation of the 1987 Indianapolis Airport Ramada Inn incident. J Forens Sci 1994;39:644-649.

3. Clark MA, Clark SR, Perkins DG. Mass fatality aircraft disaster processing. Aviation Space Environm Med 1989;60:A64-A73.

4. McCarty VO, Sohn AP, Ritzlin RS, Gauthier JH. Scene investigation and victim examination following the accident of Galaxy 203: disaster preplanning does work. J Forens Sci 1987;32:983-987.

5. Randall B. Body retrieval and morgue operations at the crash of United Flight 232. J Forens Sci 1001;36:403-409.

6. Wagner GN. Aerospace pathology. In: Handbook of Forensic Pathology. Froede RC, ed. College of American Pathologists, Northfield, IL, 1990.

Accident, Automobile (See "Accident, vehicular.")

Accident, Diving (Skin or Scuba)

NOTE: Skin diving fatalities are usually caused by drowning,* and autopsy procedures described under that entry should be followed. Usually, the circumstances that led to drowning are not apparent from the autopsy findings but can be reconstructed from reports of witnesses and the police. Because the reflex drive to seek air is triggered by hypercarbia, not hypoxia, loss of consciousness and drowning can ensue after hyperventilation and breath-holding by experienced swimmers who then drown without a struggle. There are no specific autopsy findings. A search for trauma, including a posterior neck dissection (see p. 67), should be made in all instances. Head and cervical injuries may be responsible for loss of consciousness and drowning, usually in individuals diving into shallow water with the head striking the bottom. Toxicologic examination as described below for scuba diving accidents is always indicated.

With scuba diving fatalities, investigation of the equipment and circumstances is far more important than the autopsy. Scuba fatalities should be studied by or with the aid of diving experts—for instance, members of the nearest diving club or the U.S. Navy. Careful investigation of the scene and study of reports of witnesses and the police are essential. Records should state the site of diving (currents and other underwater hazards), the estimated depth, the water temperature (exposure to cold), and a description of water clarity. Water of the area should be sampled, particularly if it seems heavily polluted. Records should also state whether there were electric underwater cables (if electrocution might have occurred, see "Injury, electric") and whether explosives had been used in the vicinity (blast injury). The method of recovery of the body (injuries by grappling hooks) and the type of resuscitation efforts should be noted. The medical history of the diving victim should be reviewed (for example, evidence of seizure disorders or drug use).

The most frequent cause of death ascribed to scuba diving accidents is drowning. Although drowning may be the terminal event in many scuba deaths, the investigation should be focused on the adverse environmental and equipment factors that place a capable swimmer at risk of drowning (see "Embolism, air" and "Sickness, decompression"). If exhaustion, panic, or cardioin-hibitory reflexes were responsible for loss of consciousness, autopsy findings will only be those of drowning. Gas bubbles should be documented at autopsy, but their interpretation is problematic. Bodies recovered immediately are subjected to resuscitation efforts, which can by themselves produce extraalveolar air artifacts. Bodies not recovered immediately tend to be found in a putrified condition, full of postmortem gas. In the remaining cases, the pathologist must consider the potential of introducing artifactual gas bubbles by the forcible retraction of the chest plate and by sawing the calvarium. The following procedures apply primarily to scuba diving accidents (1-4).

Organs and Tissues


Possible or Expected Findings

External examination

Eyes and ears

Head (skull and brain)

Middle ears


Photograph victim as recovered and after removal of wet suit and other diving gear. Record condition of clothing and gear. Impound all diving equipment for study by experts, particularly scuba tank, breathing hoses, and regulators. Residual air in tank should be analyzed.

Record color of skin (including face, back, soles, palms, and scalp).

Palpate skin and record presence or absence of crepitation.

Record extent and character of wounds. Prepare histologic specimens.

Record appearance of face (including oral and nasal cavities) and of ears.

Prepare roentgenograms. If air embolism must be expected, as in the presence of pneumomediastinum, follow procedures described under "Embolism, air." For evaluation of findings, see also above under "Note."

Otoscopic examination.

Funduscopic examination.

Save vitreous (p. 85) for possible toxicologic and other studies.

For removal of brain, see pp. 65 and 71. Record contents of arteries of the circle of Willis and its major branches and basilar artery.

Blood (from heart and peripheral vessels)

Strip dura from base of skull and from calvarium.

For removal and specimen preparation, see p. 72.

For demonstration of pneumothorax, see p. 430.

If gas is visible in coronary arteries, photograph. Photograph and aspirate gas in heart chambers. (For procedures, see p. 290.)

Mask, fins, weight belt, life vest, scuba tank and regulator, watch, depth gauge, or other gear may be missing. Clothing may be torn. Quick-release mechanisms of scuba tank or of weight belt may have been improperly adjusted and may not work. Mask, mouthpiece, regulator, or exhalation hose may contain vomitus. Air supply may be contaminated.

Cyanosis after hypoxia,* cherry-red color after CO poisoning,* or marbling after air embolism.*

Crepitation from subcutaneous emphysema.

Antemortem and postmortem abrasions, lacerations, contusions, bites, or puncture wounds (marine life—for instance, coelenterate stings). Electrocution marks, blast injuries.

Froth on mouth and nares. Facial edema and edema of pinnae. ("Facial squeeze" and "external ear squeeze" occur during descent.) Vomitus in mouth and nose. Fractures—for example, of cervical spine in skin diving accidents (see above); bone necroses (see below); foreign bodies. Pneumothorax,* pneumoperitoneum, pneumopericardium, and mediastinal and subcutaneous emphysema (all indicating rapid ascent).

Otitis externa. Rupture of tympanic membrane.

Gas in retinal vessels after air embolism. For interpretation of other studies, see p. 115.

Gas bubbles in cerebral arteries after air embolism* (after rapid ascent). Nitrogen bubbles in cerebral vessels are found in victims who had "staggers." Subdural and subarachnoid hemorrhages. Cerebral edema, with ischemic necroses and focal hemorrhages, after air embolism. Skull fracture.

Edema and hemorrhage. ("Middle ear squeeze" occurs during descent; hemorrhage occurs in drowning.) Ruptured tympanic membranes.

Pneumothorax; pneumomediastinum. Petechial hemorrhages of serosal surfaces. Air embolism.*

Organs and Tissues


Possible or Expected Findings

Blood (from heart and peripheral vessels) (continued) Heart

Tracheobronchial tree and lungs

Other organs

Neck organs and tongue

Spinal cord Bones and joints

Submit samples of heart blood and peripheral blood for toxicologic study and drug screen (p. 16).

Examine lungs in situ. Save bronchial washings for analysis of debris. Fresh dissection is recommended.

Complete toxicologic sampling should be carried out (p. 16). Record nature of gastric contents.

Remove neck organs toward end of autopsy. For posterior neck dissection, see p. 67. Incise tongue.

For removal and specimen preparation, see p. 67.

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

Alcohol intoxication (see "Alcoholism and alcohol intoxication"); carbon monoxide poisoning.*

Ischemic heart disease;* patent oval foramen.

Foam, aspirated vomitus, or other aspirated material in tracheobronchial tree. Pulmonary lacerations, bullae, and atelectases. Pulmonary edema and hemorrhage. "Pulmonary squeeze" develops during descent; nitrogen bubbles in pre-capillary pulmonary arteries develop during rapid ascent ("chokes").

Interstitial emphysema. Aspiration (see above).

Trauma to cervical spine.

Mottled pallor of tongue after air embolism.

Contusion of tongue after convulsive chewing.

Nitrogen bubbles in spinal cord arteries may occur after rapid ascent. Aseptic necroses (infarcts, "dysbaric osteonecrosis"), most often in head of femur, distal femur, and proximal tibia. Infarcts indicate repeated hyperbaric exposures. Nitrogen bubbles in and about joints and in periosteal vessels ("bends") occur during rapid ascent.


1. Gallagher TJ. Scuba diving accidents: decompression sickness, air embolism. J Florida Med Assoc 1997;84:446-451.

2. Blanksby BA, Wearne FK, Elliott BC, Blitvich JD. Aetiology and occurrence of diving injuries. A review of diving safety. Sports Med 1997;23:228-246.

3. Arness MK. Scuba decompression illness and diving fatalities in an overseas military community. Aviation Space Environm Med 1997; 68:325-333.

4. Hardy KR. Diving-related emergencies. Emerg Med Clin North Am 1997;15:223-240.

Accident, Vehicular

Related Terms: Automobile accident; motorcycle accident. NOTE: A visit to the scene can make the interpretation of the autopsy findings easier. The vehicle can also be inspected in a more leisurely fashion at the impound lot. This is particularly useful for correlating patterned injuries with objects in the vehicle. Most vehicular crashes occur as intersection crashes or because a vehicle with excessive speed left a curved road.

The medical examiner or coroner should gain a basic understanding of the crash mechanism so that informed descriptions can be rendered, e.g., "Impact to the B pillar of the decedent's automobile by the front of a pickup truck which failed to stop for a stop sign at an intersection, resulting in a 2-feet intrusion into the cabin; restraint belts not employed; air bag deployed; extrication required which took 15 minutes."

Police are responsible for determining mechanical and environmental risk factors for the crash and for determining some human risk factors such as suicidal or homicidal intent. The pathologist determines other risk factors for crashes such as heart disease, a history of epilepsy, and intoxication by carbon monoxide, drugs, and alcohol.

Suicide as a manner of death should be considered when a single-occupant vehicle strikes a bridge abutment or a large tree head-on, with no evidence of evasive action or braking. In such a situation, the standard police traffic investigation should be supplemented of interviews of the victim's family and friends.

The ambulance run sheet is an invaluable source of observations that often are not available from the police. This document should be acquired in all instances, even if the paramedics determined that death occurred and did not transport.

The basic autopsy procedures are listed below. Most traffic victims who die at the scene or who are dead on arrival at the hospital died from neurogenic shock caused by wounds of the head or vertebral column, or from exsanguination from a torn vessel or heart. As such, they have little lividity, and little blood is found in the vehicles. Presence of intense lividity may indicate suffocation or heart disease as a cause of death.

If postural asphyxia is suspected, the first responders to the scene should be interviewed to determine the position of the decedent in the vehicle, and the vital signs, if any, of the decedent from the time of the crash to the time of extrication. Posterior neck dissection (p. 67) is indicated in these instances.

If manifestations of heart disease, intense lividity, and absence of lethal wounds suggest that a crash occurred because the driver was dead, other drivers on the road may have observed that the victim was slumped at the wheel before the crash. The determination of heart attack at the wheel is usually simple, because most such victims realize that something is wrong, and bring the vehicle to a stop at the side of the road, or coast gently into a fixed object. In such instances, damage to the vehicle is minor, and wounds to the decedent are usually trivial.

While patterned wounds can often be matched to objects (see below), patternless wounds usually cannot be visually matched to specific objects, although an opinion can sometimes be given as to what object was struck, based on the direction of motion and position of the body with respect to the vehicle. Impacts with the A-pillar produce narrow vertical zones of facial laceration and fractures extending from forehead to jaw. Tempered glass shatters into small cubes on impact, and leaves so-called "dicing" wounds, which are abraded cuts arranged in a somewhat rectilinear pattern. Windshield glass leaves shallow, abraded, vertically oriented cuts on the face or scalp.

With pedestrians, the lower extremities are of particular forensic interest, to determine the height and direction of impact from vehicles that left the scene. Scalp hair and blood should be collected from such "hit and run" victims and from occupants of a suspect car if police have a question as to which occupant was the driver; these exemplars can be compared to fibers and tissue recovered from the vehicle in question. Likewise, foreign material in wounds can sometimes be matched to suspect vehicles, and should be sought and retained as evidence. For pedestrians, the distance between the impact point on the lower extremities and the soles of the feet should be recorded. The legs should be opened to inspect tibial fractures; cortical fractures initiate propagation opposite to the side of impact, where they usually have a pulled-apart appearance, and then splinter the cortex at the side of impact. Abrasions are better impact markers than contusions, because subcutaneous blood extravasation can be caused not only by impact to the skin, but also from blood extravasating from underlying fractures. If no cutaneous abrasions or fractures of the leg bones are found, the skin of the legs should be incised to expose contusions.

Fracture descriptions should include location in the bone (e.g., proximal metaphysis or shaft), whether the fracture is complete or incomplete, and whether the fracture is displaced or distracted. Lacerations of intervertebral disks, facet joint capsules, and ligamenta flava should not be loosely termed "frac tures." The presence or absence of blood extravasation in soft tissue adjacent to the fractures should be recorded, and its volume estimated if it appears severe enough.

Venous air embolism from torn dural sinuses cannot be diagnosed without a pre-autopsy chest radiograph or an in situ bubble test. If an X-ray machine is readily available, an anterior-posterior chest radiograph should be obtained in every traffic victim who dies at the scene or after a failed resuscitation attempt.

If a hemothorax is shown by the pleural window technique (p. 13), the rib cuts should be placed further lateral and the chest plate reflected so that the internal mammary vessels can be inspected before the chest plate is removed. After measuring and removing the bloody effusion, the underlying serosal surfaces should be inspected for defects. Lacerations of the heart and aorta will be obvious. Tamponaded lacerations of the aorta, around which the adventitia still holds, must be noted as such. If no lacerations are found at the usual sites, lacerations of the azygous veins must be considered, especially in association with fracture dislocations of the thoracic vertebral column; other sites are the internal mammary arteries, especially with fractures of ribs 1 and 2 or of the sternum, and intercostal arteries with displaced rib fractures. Only after the serosal defect is identified should the organs be removed, because that procedure creates many more holes in the serosa. For that reason, as much information as possible should be gained by in situ observation.

The only evidence of concussion of the heart may be a cardiac contusion or a sternal fracture. The usual clinical history suggests cardiovascular instability that is not associated with craniocerebral trauma and which does not respond to the infusion of intravenous volume agents.

The autopsy assistant may saw but should not retract the skull cap and remove the brain. The pathologist should observe in situ whether shallow lacerations of the pontomedullary junction with stretching of the midbrain are present; these lesions cannot be distinguished from artifact by examining the brain later. Thus, only after appropriate in situ inspection should the pathologist remove the brain.

A posterior neck dissection is required if no lethal craniocerebral or cardiovascular trauma can be found, or if suffocation is suspected; neck trauma must be ruled out to diagnose suffocation in a traffic fatality. Sudden death in a patient with seemingly trivial wounds may be caused by undiagnosed trauma of the craniocervical articulation. A posterior neck dissection (p. 67) is required in these instances.

The diagnosis of diffuse axonal injury of the brain in victims with no appreciable survival interval requires that suffocation was ruled out and that no resuscitaion from a cardiac arrest had been attempted. Clinicians are quick to apply the label "closed head injury" when a victim of a traffic crash has cerebral edema on a computerized axial tomogram of the head, even if no cerebral contusions, scalp contusions, or skull fractures are evident. This may be a misinterpretation, because cerebral edema can be caused by hypoxic encephalopathy made evident after resuscitation from a cardiac arrest, or by hypoxia caused by suffocation.

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