A physician with specialized training and certification in forensic pathology, which is the branch of pathology that deals with the understanding, preservation and use of evidence in order to determine cause, manner and mechanism of death. The training of a forensic pathologist generally entails a complete five-year residency in anatomic and clinical pathology, followed by one or more years of fellowship training. A completely credentialed forensic pathologist is certified by the American Board of Pathology as both a general pathologist and as a subspecialist, following successful completion of the Board examinations in anatomic, clinical, and forensic pathology.
- What is Forensic Pathology
The good forensic pathologist is an amalgamation of pathologist, detective, politician, and public relations person. Not only must one know the technical aspect of the discipline, but he/she needs to have the communication skills to acquire supportive information from law enforcement officers and explain the results of medical examinations to juries and other lay people.
Forensic determinations go beyond those of patient-oriented medicine, as they involve legal as well as medical considerations:
- Role of a Forensic Pathologist:
A. Cause of death
This is a specific medical diagnosis denoting a disease or injury (e.g., myocardial infarction, strangulation, gunshot wound). In particular,
1. Proximate cause of death. The initial injury that led to a sequence of events which caused the death of the victim.
2. Immediate cause of death. The injury or disease that finally killed the individual.
Example: A man burned extensively as a result of a house fire dies two weeks later due to sepsis. The proximate cause of death is his burns, leading to sepsis, which is the immediate cause of death.
B. Mechanism of death
This term describes the altered physiology by which a disease or injury produces death (e.g., arrhythmia, hypoventilatory hypoxia, exsanguination).
C. Manner of death
This determination deals with the legal implications superimposed on biological cause and mechanism of death:
1. Homicide. Someone else caused the victim's death, whether by intention (robber shoots convenience store clerk) or by criminal negligence (drunk driver, going 55 mph on Fondren, runs red light at Bellaire and strikes pedestrians in crosswalk). After the forensic determination is made, it may of course be altered as a result of a grand jury or other legal inquiry. For instance, when one child shoots another, the forensic examination may conclude from the body that homicide was the manner of death, but after considering all evidence, a grand jury may conclude that the gun discharged accidentally.
2. Suicide. The victim caused his/her own death on purpose. This may not always be straightforward. For instance, a victim may strangle himself accidentally during autoerotic behavior. If the examiner were not to consider all of the evidence (such as erotic literature found near the body), an incorrect determination of "suicide by hanging" might be made. This error may be financially disastrous for the victim's survivors, since many life insurance policies do not award benefits when the insured is a suicide. Also, in some cultures suicide is a social stigma or a sin against its deity.
3. Accidental. In this manner of death, the individual falls victim to a hostile environment. Some degree of human negligence may be involved in accidental deaths, but the magnitude of the negligence falls short of that reasonably expected in negligent homicide. Whereas the negligence of the speeding drunk, above, would be considered gross by a reasonable observer, a pedestrian killed at the same intersection by a sober driver, not speeding or running a red light, would be reasonably considered a victim of accidental death.
4. Natural causes. Here, the victim dies in the absence of an environment reasonably considered hostile to human life. Most bodies referred for forensic examination represent this manner of death. We will consider the major diseases producing sudden death below.
These are important to be familiar with, as they may otherwise mislead the examiner into thinking trauma or other foul play led to the victim's death.
- "Normal" Postmortem Changes:
A. Rigor mortis, familiar to any aficionado of horror films, begins earlier in small muscles and muscles exercised vigorously prior to death. An extreme example is "cadaveric spasm," a great literary/cinematic device, in which a person dying following extreme exertion "freezes" in place virtually in a photographic pose of the moment of death. I would imagine that this occurs a lot more often in movies than in reality. Rigor mortis passes as muscle decomposition begins and is usually gone in 36 hours. It can also be mechanically "broken" by stretching the rigid muscles by force.
B. Livor mortis, or hypostasis, a purplish discoloration of the body and organ surfaces, results when blood settles to dependent parts of the body. It becomes visible between one half hour and two hours after death. Early on, the blood remains in the vessels, so the livor can be blanched by applying pressure to the affected part. Later, the blood hemolyzes, and the hemoglobin breakdown pigment leaches out into the extravascular interstitium. At this point, the livor cannot be blanched by pressure and is said to be "fixed." The period over which livor becomes fixed is so variable that whether it is fixed or not offers little information in trying to determine the time of death.
C. Desiccation occurs most prominently on the mucous membranes, which during life are kept moist (by blinking, lip licking, etc) and are not protective by water repellant keratin in cornified skin. The membranes may look "burned," and the conjunctiva may actually be black ("tache noire").
D. Putrefaction is the sequence of physicochemical events that begins with death and ends with dissolution of the nondurable parts of the body. It begins with a greenish discoloration of the skin and mucous membranes. The epidermis becomes detached from its basement membrane, and flaccid cutaneous bullae form. Overgrowth of bacteria (which normally seed the entire body via the bloodstream at or immediately before the time of death) cause gas production, resulting in gaseous distension of the body cavities, which may then rupture. The soft tissues may also puff up and appear swollen, also as a result of gas release. Finally, autolysis and bacterial lysis hydrolyze proteins and fats, to produce frank liquefaction of the soft tissues. The proteins get broken down into amino acids, which then are decarboxylated and become "biogenic amines" with such memorable and apt names as "putrescene" and "cadaverine." Other protein-derived products of putrefaction are amino acid residues with sulfhydryl (-SH) groups; these are also mighty rank. The sulfhydryl groups are often further cleaved off, then released as hydrogen sulfide, which also has the ability to put your olfactory neurons into overload.
E. Alternatives to putrefaction include mummification, in which the body dries out faster than decomposition takes place, and adipocere formation, in which by some unknown mechanism the adipose tissues become chemically transformed into a waxy substance that acts as a preservative. As might be expected, mummification typically occurs in dry environments. Adipocere formation, which is much rarer, tends to occur in moist environments, such as caves. A good example of adipocere can be viewed at Philadelphia's Mutter Museum, where the "Soap Lady" is on exhibit.
This is the cornerstone of forensic pathology. Terms used to describe traumatic lesions are somewhat more specific than analogous terms used in surgery and internal medicine.
A. Laceration is a tearing injury due to friction or impact with a blunt object. The typical laceration has edges which are ragged, bruised, and/or abraded. Generally, surgeons and ER physicians do not make a distinction between lacerations and incised wounds, calling them both "lacerations."
B. Incised wound is a cutting injury due to slicing action of a blade like object. The wound edges are smooth. Serrated blades produce the same smooth edges as do non serrated blades.
C. Puncture is a penetrating injury due to pointed object without a blade, such as an ice pick.
D. Abrasion is a friction injury removing superficial layers of skin, allowing serum to exude and form a crust. Abrasions may not be visible on wet skin; therefore, an abrasion not apparent when a body is first examined may appear the next day, after the wet body has had a chance to dry out in the morgue refrigerator.
E. Contusion is a bruise due to rupture or penetration of small-caliber blood vessel walls. Contusions may be seen on the surfaces of internal organs (such as the brain or heart) as well as the skin and mucous membranes.
F. Gunshot wounds represent a special form of trauma very important to forensic pathology. The types of determinations made on bodies include 1) type of firearm used (shotgun, handgun/rifle, or high-powered rifle), 2) distance of the gun from the victim at the time of firing, 3) whether a given wound is an entrance wound or an exit wound, and 4) track of the projectile through the body. Wounds may be classified by distance as follows:
1. Contact wound: Muzzle of gun was applied to skin at time of shooting. Classic features include an impression of the muzzle burned around the entrance wound and absence of fouling and stippling (see below). Contact wounds over the skull may have a stellate appearance because of expulsion of hot gases from the barrel which are trapped against the outer table of the skull and blow back toward the exterior, ripping apart the skin around the entrance wound.
2. Close range (6 - 8 inches): The entrance wound is surrounded by fouling, which is soot that travels for a short distance from the gun barrel to be deposited on the skin. There may also be stippling (see below).
3. Intermediate range ( 6 - 8 inches to 1.5 - 3.5 feet): This is too far for soot to travel, so there is no fouling, but hot fragments of burning propellant (gunpowder) follow the bullet to the victim and produce stippling by causing pinpoint burns around the entrance wound. Of the two type of propellant, "ball" and "flake," the former will produce stippling at a greater distance.
4. Distant (greater than 1.5 - 3.5 feet): This is too far for either soot or burning propellant to travel, so the wound margins are clean, with neither fouling nor stippling. Entrance versus exit wounds represents an important distinction for the forensic pathologist to make. A grand jury may look with more favor on an assailant alleging self defense, if the victim has the entrance wound on the front and the exit wound on the back, rather than vice versa. Classically, the entrance wound has a rim of abrasion surrounding the wound, because the projectile "drags" the surrounding skin into the wound a bit, abrading it along the way. The exit wound lacks this abrasion, unless the victim was braced against a wall or other solid object that may secondarily abrade the margin of the exit wound as the projectile penetrates the skin and pushes it into the wall.
Perhaps having a bit more relevance to patient-oriented medicine is the problem of sudden and unexplained death by natural causes. Careful attention to the autopsy and the patient's history usually establish the cause of death, but a few cases remain mysteries indefinitely.
A. Coronary artery disease is the most common cause of non traumatic sudden death. Autopsy typically shows occlusion of at least 60% of the luminal cross-section of one or more of the three major branches of the coronary arterial system. The occlusion may be all atheroma, or thrombus superimposed on atheroma. It is likely that spasm of the coronary artery, which cannot be demonstrated at autopsy, plays a role in a significant proportion of these cases. The myocardium itself may be perfectly normal, death having resulted from ischemia-induced arrhythmia before anatomic changes of infarction have time to develop.
B. Pulmonary embolus, typically a saddle thromboembolus, stops the heart by some type of reflex action. At autopsy all that may be found is the embolus itself, as the patient dies before anatomic changes of pulmonary infarction have time to develop. Emboli may occur in previously normal individuals, but one may find in some cases a history of recent immobilization (like a truck driver on a long haul, or a person recently discharged from the hospital).
C. Myocarditis, typically of viral etiology, may cause sudden death, often in association with vigorous physical activity. There may be history of a recent acute viral upper respiratory infection.
D. Aortic valvular stenosis physiologically resembles coronary artery disease in a patient with essential hypertension. The coronary ostia are poorly supplied due to the marked pressure differential across the aortic valve. Also, the myocardium demands more blood supply as a result of having to pump against that pressure gradient. Most cases nowadays are due to a congenital bicuspid aortic valve, but a history of old rheumatic fever should be sought.
E. Berry aneurysms of the arteries at the base of the brain may rupture, producing fatal subarachnoid hemorrhage. The typical victim is a young or middle-aged female. There may be history of complaints of a very severe headache immediately before the collapse.
F. Intracerebral hemorrhage is usually seen in older, typically hypertensive patients. Embolic or atherosclerotic strokes usually do not produce sudden death
G. Perforated peptic ulcer is common, as about 10% of peptic ulcers present with perforation and no previously documented manifestations. Fortunately, only rarely do they produce sudden death. The mechanism of death is unknown but probably involves some sort of autonomic reflex (which is what is typically invoked when the cognoscenti have absolutely no idea about what the pathogenic mechanism is).
H. Anaphylaxis, better known as Type I Immunologic Hypersensitivity Reaction, may cause sudden death by laryngeal edema, causing asphyxiation. Usually, the inciting stimulus (bee sting, penicillin injection, etc.) is apparent from the history.