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Chapter II

TIME OF DEATH AND CHANGES AFTER DEATHPart 1

ANATOMICAL CONSIDERATIONS

JOSHUA A. PERPER

DEFINITION OF DEATH

THE DEFINITION OF death is important to boththe medical and legal professions. While it

is true that for the clinician the demise of apatient signals the unfortunate end to the medi-cal effort, the very determination of death maycarry secondary therapeutic implications re-garding transplantation of organs. Obviously,the occurrence of a death is the starting pointin the professional involvement of the forensicpathologist. Similarly for attorneys, the death ofan individual generates a great number of legalchallenges related to inheritance rights, estatemanagement, criminal liability and tortual injur-ies.

Until the 1960s, the cessation of circulation andrespiration was the unchallenged definition ofdeath. For example, the 1968 edition of Black'sLaw Dictionary defined death as: the cessation oflife; the ceasing to exist; defined by physicians as thetotal stoppage of the circulation of the blood, and cessa-tion of vital functions consequent thereon, such asrespiration, pulsation, etc.

As a matter of fact, even today in most deaths,particularly in those which occur outside hospi-tals or are unwitnessed, the criteria used are stillthe cessation of circulation and respiration.

However, the classical definition of death hasbeen challenged in recent times by two medicaladvances1. Advanced resuscitation techniques (cardio-

pulmonary resuscitation [CPR], mouth tomouth, heart massage, electric shock) capa-ble of effectively reviving many of the clini-cally dead.

2. Advanced life-sustaining equipment capableof maintaining blood pressure, circulation

and respiration in individuals with severebrain injury.

Though the first instance of mouth-to-mouthresuscitation was recorded long ago in the bibli-cal story of the Prophet Elijah resuscitating achild (II Kings 4:32-36), modern cardiac mas-sage, electric shock and routine CPR came intouse only three decades ago.

These developments necessitated, in manycases, the obvious revision of the definition ofdeath from just cessation to irreversible cessation ofrespiratory and heart activity following modernresuscitation attempts. The reversibility of thedeath process is dependent on the capability oftissues to recover from the effects of ischemia/anoxia occurring between the advent of clinicaldeath to the initiation of effective resuscitation.The resistance of various organs to ischemia/anoxia is variable, with the central nervous sys-tem displaying a particularly high sensitivity.The classic literature indicates that a four- to six-minute period of cerebral anoxia from a delayin effective resuscitation will commonly result inirreversible and extensive brain damage. How-ever, more recent experimental and clinical evi-dence points to instances where the reversibleinterval may be as long as fifteen to sixteen min-utes.1

Young children and hypothermic individualsare known to resist cerebral hypoxia for thirtyminutes or more with no ill effects. In a casereported by Kvittingen and Naess,2 a five-year-old boy fell into a partly frozen river and recov-ered fully following a presumed submersiontime of twenty-two minutes.

The development of life-sustaining equip-

14

Time of Death and Changes After Death 15

ment has also changed the definition of deathby permitting a dissociation between a severelyhypoxic or dead brain (incapable of sustainingspontaneous respiration and circulation) andthe peripheral organs which can be kept aliveartificially. Therefore, the definition of death ina person with severe and irreversible brain in-jury, incapable of sustaining spontaneous respi-ration and/or circulation, had to be revised toinclude what is now defined as brain death.

The clinical definition of brain death was firstadvanced in 1968 by the Ad Hoc Committee ofthe Harvard Medical School.3 The committee,which consisted of physicians, a theologian anda lawyer, defined the following conditions fordetermining irreversible brain death:1. Unreceptivity and unresponsitivity, including a

total lack of response to the most intensepainful stimuli.

2. No movement or spontaneous respiration,defined as no effort to breathe for three min-utes off the respirator with the patient's car-bon dioxide tension normal and room airbeing breathed for ten minutes prior to thetrial.

3. No reflexes fixed, non-reactive pupils, and alack of cranial nerve reflexes (corneal, pha-ryngeal, ocular movements in response tohead turning and irrigation of ears with icewater, etc.).

4. Isoelectric electroencephalogram.The committee suggested that all tests be re-

peated in twenty-four hours and emphasizedthat the determination of the irreversibility ofcerebral damage should be made only after theexclusion of potentially reversible conditions,such as hypothermia (temperature below 90° F[32.2° C]) and central nervous system depres-sants such as barbiturates.

In subsequent years, the list of reversiblecauses of coma has been expanded to includemetabolic neuromuscular blockade, shock andyoung age (less than five years of age).

Also, additional objective tests besides electro-encephalogram were added to the determina-tion of brain death, such as cerebral angiographyand radionuclide studies, in order to confirmthe absence of cerebral blood flow.

In 1977, the National Institute of Neurologi-cal Diseases and Stroke conducted a collabora-tive study which somewhat refined the Harvardcriteria. The criteria of brain death proposed bythe collaborative study were as follows:1. Coma and cerebral unresponsiveness.2. Apnea.3. Dilated pupils.4. Absent cephalic (brainstem) reflexes.5. Electrocerebral silence.These criteria were to be present for thirty min-utes at least six hours after the onset of comaand apnea, and all appropriate diagnostic thera-peutic procedures were to be performed. Con-firmatory tests of cerebral blood flow were neces-sary if one of the standards was doubtful orcould not be tested.

Starting with Kansas in 1968, increasing num-bers of states have adopted the definition ofbrain death. In 1980, representatives of theAmerican Bar Association and the NationalConference of Commissioners of Uniform StateLaws agreed upon a model legislative definitionof death: An individual who has sustained either,(1) irreversible cessation of circulatory and respiratoryfunctions or, (2) irreversible cessation of all functionsof the entire brain, including the brain stem, is dead.A determination of death shall be made in accordancewith accepted medical standards.

It has been pointed out that in spite of somedifferences between the legal definitions ofbrain death in various states, physicians can meetthe requirements of all of them by:1. Using the commonly accepted criteria of

brain death.2. Having two physicians, one of whom is a neu-

rologist, make the brain death determina-tion.

3. Avoiding a conflict of interest in having physi-cians separate from the transplant team, cer-tifying the brain death of a potential donor.

4. Determining brain death before removingany organs or disconnecting life-support sys-tems.4

As a matter of fact, a number of states haveformally incorporated such provisions into theirlaws.

16 Medicolegal Investigation of Death

The Pathology of Brain Death andPersistent Vegetative State (PVS)

The brain findings of brain death or so-calledrespirator brain are characteristic on gross exami-nation. The brain has a dusky, grayish appear-ance, with marked swelling and evidence oftranstentorial hippocampal and tonsillar hernia-tion. Depending on survival time, the cerebralparenchyma shows a variable spectrum ofanoxic/ ischemic damage from minimalchanges to severe encephalomalacia and lique-faction, and generally cannot be satisfactorilyexamined prior to fixation.

Microscopic findings in respirator brains arevariable, non-specific, non-diagnostic and corre-late poorly with gross findings.

Brain death changes generally become appar-ent approximately twelve to sixteen hours aftercessation of the cerebral circulation, though insome cases they may be evident after only sixhours, and in others they may be delayed fortwenty-four hours longer.

Rapid respirator brain changes may be observedin cases with acute onset, such as severe headtrauma, large parent hemorrhages or suddencardiac arrest with delayed resuscitation. De-layed manifestations of brain death are seen inchronically ill persons with brain tumors or met-abolic problems.5

Sometimes identification of true antemortemhemorrhages or contusions may be substantiallyobscured or hampered by respirator brain relatedhemorrhages.

Agonal changes in the microcirculation, suchas petechiae in leptomeninges and cerebral pa-renchyma, may be dramatically accentuated incases of brain death. Stagnant or stasis thrombiin veins and arteries may also be present andshould be distinguished whenever possible fromnon-agonal clots.

It is important to distinguish between braindeath and the irreversible brain injury knownas Persistent Vegetative State (PVS). Patients witheither condition are clinically, irreversibly coma-tose and show severe brain injury with neuronaldeath. However, the diagnosis of brain death isbased on brain stem death determination, while

PVS involves only permanent and total destruc-tion of frontal lobe function.

Disconnection of life-support equipment ispermissible following a determination of braindeath, while it is much more problematic incases of PVS, where a living will or specific courtapproval is required.

One should emphasize that premature or ille-gal discontinuation of life-supporting systemsfor an irreversibly unconscious but not braindead patient may result not only in civil liabilitybut also in criminal charges.

The Medicolegal Implications of theDetermination of Death

The practical major medicolegal implicationsrelated to the new definition of death are:1. The earliest determination of death for

prompt harvesting of organs for transplanta-tion purposes.

2. The legality of discontinuation of life-sup-porting equipment.

3. The determination of the time of death incriminal and civil litigation.

In medicolegal cases the transplantation pro-cedures require not only a prior authorizing do-nation by the deceased and/or his family butalso the specific consent of the medical exam-iner or coroner.

Medicolegal offices are major source of or-gans for transplantation purposes, and theirstanding policies may substantially advance orimpede the transplantation program of a partic-ular community. The humanitarian value oftransplantation procedures notwithstanding isincumbent on the forensic authority to insurenot only that the harvesting of organs is dulyauthorized but also that it does not substantiallyinterfere with the medicolegal autopsy.

We have recently seen, for example, two casesof shaken baby syndrome with no external injuriesin which the abusing parents authorized tissuedonation. It is unclear whether the motivationof the parents was purely altruistic or an attemptto cover up a possible homicide. Regardless ofthe motive, when the cause and manner ofdeath are unclear, postmortem harvesting of or-


gans may substantially interfere with the medi-colegal autopsy.

If one wishes to approve the harvesting oforgans under such circumstances, it is stronglyrecommended that a forensic pathologist bepresent during the procedure. Such presence isrequired to insure proper documentation andinterpretation of findings of medicolegal signifi-cance and to avoid the interference of confusingartifacts.

The Determination of Death and Survivorship

When two individuals who previously desig-nate each other as mutual heirs die together ina single incident, the legal question of whetherthey died at the same time or not is of para-mount importance in determining who will bethe ultimate inheritor.

This question, known as survivorship, is oftenposed to the forensic pathologist who will haveto weigh the specific circumstances of each case,including the age of the deceased, the state ofhealth, the extent of injuries and the corres-ponding reactive changes, the level of alcoholand toxic substances, and the nature and stateof postmortem changes.

One should critically evaluate the various pa-rameters in order to ensure that they are compa-rable under similar conditions. For example,two individuals showing marked differences inthe development of postmortem changes maystill have died simultaneously if one was moreprone to accelerated death (e.g. excessivelyobese, septicemic or close to a hot radiator).

The Death Certificate and the Determination ofthe Cause and Manner of Death

Though the laws of many states are unclearin regard to who should make the actual deter-mination of death, all legislatures require thatevery deceased be issued a certificate which isto be signed by the last attending physician orby the coroner/medical examiner.

The central medicolegal requirement of thedeath certificate is the determination of thecause and manner of death. The cause of deathis the medical finding or findings responsiblefor the death, and the manner of death is the

legal classification of death, whether it be natu-ral, suicide, homicide, accident or undetermin-able.

The death certificate has two major groupingsfor the cause of death: the primary or immediatecause of death and the secondary cause of death.The primary cause of death is subdivided into athree-link sequential chain, for example:1. Primary cause of death:

—Hypoxemic necrosis of brain (brain death)due to

—Exsanguinationdue to

—Gunshot wound (GSW) of abdomenThe secondary cause of death includes condi-

tions which are not related to the primary causeof death but are substantially contributory to theindividual's demise (e.g. emphysema of lungs,hypothermia, arteriosclerotic cardiovascular dis-ease) .

In cases of sudden unexpected death, suspi-cious death or unnatural death (suicide, acci-dent or homicide) the coroner/medical exam-iner is the exclusive authority who has thejurisdiction to issue the death certificate. Whenthe death follows shortly after a catastrophicevent (e.g. traffic accident, suicide, accidentaloverdose, homicidal gunshot wound), the re-porting is generally accurate and prompt.

Problems arise when the injured individualsurvives a longer period of time and dies of ei-ther predictable or unexpected complicationsor when death is a result of a combination ofpre-existing natural disease and the initial in-jury. It is not uncommon that the last physicianto treat the patient is unaware of, or forgets, theinitial traumatic or toxic event which triggeredthe chain of complications. Furthermore, manyphysicians are unaware of the medicolegal ap-proach to the determination of the manner ofdeath when both natural and unnatural causesof death coexist. A simple rule of thumb statesthat if an unnatural cause of death (trauma,drug overdose, electrocution, drowning, etc.)plays a contributory role in the death, then themanner of death is unnatural (i.e., accidental,suicidal or homicidal), and, therefore, the case


falls under the jurisdiction of the coroner/medi-cal examiner.

It is immaterial whether the unnatural factor(i.e., trauma) was a direct, indirect, complicat-ing or aggravating element, or whether it was amajor or minor factor in the causation of death.The same is true for the unnatural physical orchemical injury which occurs long before thepatient's demise, providing that the death canbe traced back to the initial physical or chemicalinjury. A continuous chain of symptoms and/or findings must be demonstrated, however, inorder to link the initial injury to its later compli-cations and the death.

For example, the case of a seventy-year-oldwoman who dies of pneumonia or pulmonaryembolism after being confined to bed for severalweeks following a hip fracture sustained in a fallis clearly a case to be reported to the coroner/medical examiner. The accidental hip fractureand the subsequent immobilization can beviewed as the triggering elements of the bron-chopneumonia or embolism. This obviously col-ors the manner of death as accidental and im-plicitly makes it a reportable forensic case.

The lack of clinical continuity of symptomsbetween an injury (e.g. trauma) and a subse-quent, apparently natural death does not neces-sarily classify the death as purely natural and un-related to the trauma. A physical or chemicalinjury may trigger subclinical but neverthelesspotentially fatal complications which may besubstantiated only at autopsy.

A fifty-five-year-old man who dies four to fivedays following a symptom-free interval from thetime of a physical assault is to be considered aforensic case if the autopsy demonstrates a recentinfarction, subclinical cardiac contusions orother fatal complications related to the time ofthe incident.

Difficulties also occur when the death is intra-operative, peri-operative or related to the pa-tient's care, and the question arises whether thisis or is not a reportable case. When a substantialactive medical misadventure occurs, the case isclearly a prima facie coroner/medical examinercase.

Such active misadventures include both physi-

cal and chemical injuries, such as perforationand/or laceration of blood vessels or other or-gans, disconnection of anesthetic equipmentcausing asphyxia, administration of the wrongtype of blood, burns or electrocution by themedical equipment, overdose of anesthetics orother medications, administration of mistakenmedication, and anaphylactic reactions.

The jurisdiction of the coroner/medical ex-aminer in unexplained deaths may be exercisedonly when the manner of death is unexplained. Ifa diagnostic determination was reliably madethat the death is natural, no jurisdiction exists.The precise cause or mechanism of death, in anatural death, may be medically tantalizing andmay have public health significance, but its mys-tery cannot prompt the forensic jurisdiction un-less specific authority is granted under state law.Therefore, the failure to know the precise causeof mechanism of death in an otherwise naturaldeath does not activate the coroner/medical ex-aminer's jurisdiction.

The same approach applies to suspiciousdeaths. It is only when reasonable and reliableinformation indicates that the death is suspiciousthat the forensic jurisdiction may be assumed.In such situations, the presence of a potentiallyfatal natural cause of death is not incompatiblewith the coroner's assumption of jurisdiction,as the natural condition may well be only thebackground on which a subtle unnatural fatalinjury occurred. Obviously, only a forensic au-topsy may confirm or exclude, in such cases, thepossibility of poisoning, hidden time or otherunnatural causes of death.

Embalmment and Exhumation

Postmortem embalming is an extremely wide-spread custom on the North American conti-nent of which most religious denominations ap-prove. The embalming procedure usuallyincludes the application of cosmetic cream tothe face and hands of the deceased, coveringof the eyes under the eyelids with plastic cups,fixation or wiring of jaws, injection of em-balming fluids in the neck (carotid), axilla (axil-lary) and groin (iliac and femoral) arteries, and


FIGURE II-l. Embalmed five-month-old child, (a) Cosmetic cream covering the face of embalmed child, successfullyconcealing extensive bruising of the face, (b) Face after removal of cream.

injection through trocars of cavity fluid into theabdomen and thorax.

Autopsies performed after embalming and/or exhumation require special techniques. Em-balming artifacts may conceal or mimic real in-juries.

The sticky embalming cosmetics placed onthe face and hands of the deceased may effec-tively mask substantial bruises and abrasions ofthe skin and, therefore, should be carefully re-moved with an alcoholic solution or scrapedaway (Fig. II-l). The injection of embalming flu-ids into the body cavities will obviously affect thecomposition, appearance and amount of anypreviously present fluid. Perforations of the in-ternal organs by the embalmer's trocar may bedifficult or impossible to differentiate from gen-uine lacerations.

Perhaps the most intrusive artifactual compli-cation of embalming is the chemical alterationof the blood and tissues by the injected em-balming fluid. Embalming fluids contain variousmixtures of formaldehyde, glutaraldehyde, alco-hols and other preservatives (e.g. hexylresor-

cinol, phenol, methylsalicylate, sodium benzo-ate, sodium and calcium oxalates, quaternaryammonium compounds, EDTA).6 The use ofmetallic salts (e.g. arsenic, mercury, lead, cop-per, silver, etc.) in embalming fluid is now pro-hibited to prevent concealing of heavy metalpoisoning. However, embalming still interfereswith the chemical analysis of many compounds.Some compounds, such as ethanol, opiates, car-bon monoxide and cyanide, are destroyed orcannot be reliably tested.

Other chemicals (such as barbiturates, tricy-clic compounds and benzodiazepines) can bequalitatively tested if only a few weeks or monthshave elapsed since embalming. However, aquantitative evaluation of these compounds islargely unreliable because of dilution and otherfactors. In some cases, analysis of more pro-tected biological fluids (such as vitreous of theeye and cerebrospinal fluid) may give a fairlygood quantitative estimate.

Metallic compounds and metalloids (e.g. arse-nic) may be recovered from the embalmed bodyafter many years. However, their elution into the


environment or diffusion from the environmentif the soil has a higher concentration, makesone doubt the reliability of their quantitation.

When testing embalmed tissues for metalsand metalloids, it is recommended that the em-balming fluid be analyzed as well in order toexclude the possibility that it contains relatedcontaminants.

The situation becomes more complex whenthere is a need to examine an embalmed bodyafter exhumation. In cases where the death isdue to trauma, it is advantageous that a forensicpathologist be present during the exhumationto ensure that the coffin did not collapse, andthat the body was not otherwise physically dam-aged in the process.

Similarly, if poisoning is suspected, the foren-sic pathologist should collect samples of the soilaround the coffin (above, below and sides) aswell as any water which may have leaked intothe coffin which may contain increased amountsof the chemical suspected in the poisoning. Atypical poison which may be present in in-creased amounts in the soil is arsenic, but obvi-ously, other toxic substances and metals may bepresent as well.

Following exhumation, most bodies show sig-nificant fungal growth on the face and exposedskin areas which may severely disfigure the de-ceased and practically obliterate bruised orabraded areas. Areas of bruising are especiallydifficult to evaluate because of the black, grayor greenish discoloration due to the combina-tion of fungus and decomposition changes. Usu-ally, fungal growth is maximal in areas of pre-mortem injury and bleeding. Aspergillus nigrans,which is black, and flaky white mildew, is espe-cially common on the body surface (Fig. II-2).Interestingly, decomposition is usually reducedin areas with fungal growth because of the bacte-riostatic effect of most strains of fungi.

Furthermore, if fluid is present in the coffin,the skin may become very soggy and slipperyand develop adipocere (see below). The preser-vation of the internal organs varies considerablywith the quality of embalming. In some cases,we have seen excellent preservation after tenor more years; in others we observed advance

FIGURE II-2. Extensive mildew on the face of a recluse. Aleak in the roof had caused water to accumulate on thefloor and soak the furniture. The death was due to alcohol-

internal decomposition in a few weeks followingburial.

Incineration and Cremation

Close to seventy percent of the human bodyis composed of water, twenty-five to twenty-sixpercent of combustible organic tissue and lessthan five percent of fireproof inorganic com-pounds. Most of the latter are present in thebones in the form of calcium salts, mainly ascrystalline hydroxyapatite and partly as amor-phous calcium phosphate. Upon exposure totemperatures in excess of 1000° C, the soft tis-sues of the body and the organic componentsof the bone literally go up in smoke, leaving onlya minimal amount of ash.

In most fires, temperatures do not reach suchlevels, and variable amounts of soft tissue in dif-


ferent stages of carbonization are still present.In rare instances where temperatures are sohigh that the bones burn extensively, inciner-ated bones which may remain appear as white orwhite-gray, porous, friable, calcinated fragmentsof various size.

Careful sifting through incinerated bones re-veals, in most cases, fragments which are largeenough to be recognized as human by an experi-enced examiner, particularly by an anthropolo-gist.

The funeral disposition of human remains byfire is known as cremation. In some parts of theworld, such as India, this is the common funeralmethod. In the United States, the incidence ofcremations has increased in recent years.

In the past, most cremations involved paupersand unclaimed bodies, fetuses and body parts.Recently, increased numbers of upper-middle-class professionals are opting for the method ofpostmortem disposal. In most states, cremationrequires a special permit by the local depart-ment of health or the coroner/medical exam-iner and a mandatory twenty-four-hour post-mortem waiting period.

Cremation is by open flame or oven heating(calcination) at temperatures between 1600° Fand 2200° F. Cremation at these temperaturesand subsequent grinding of the cremated bonesresults in a mixture of small calcinated frag-ments of various color (brown, light-brown, grayand blackish) which cannot be diagnosed bycurrent methods as being specifically human.The total volume of these cremated remains de-pends not necessarily on the weight of the indi-vidual but on the mass of skeletal bones, as mostsoft tissue incinerates with very little trace.

In a personal study of the cremated remainsof two hundred and forty-six males and one hun-dred and forty-eight females, the weight gener-ally varied between 1,500 and 5,510 grams, witha mean in men of 3,035 grams and in women of2,508.3 grams, and a standard deviation of 538.6grams and 598.4 grams, respectively. If the totalweight exceeds 6,000 grams, it is likely that thecremated remains consist of more than one per-son. A few legal suits have indeed alleged thatnegligent funeral directors have, on occasion,mixed the ashes of several people.

POSTMORTEM CHANGES AND THE DETERMINATION OF THE TIME OF DEATH

Following death, numerous physicochemicalchanges occur which ultimately lead to the dis-solution of all soft tissues. The medicolegal im-portance of these postmortem changes is re-lated primarily to their sequential nature whichcan be utilized in the determination of the timeof death and the related destructive and/or arti-factual changes which may simulate premorteminjuries or modify toxicological findings.

The determination of the time of death isgenerally based on the principle of using se-quential changes as a postmortem clock. The evalu-ation may include:1. Physicochemical changes evident upon di-

rect examination of the body, such aschanges in body temperature, livor, rigor anddecomposition. These changes are routinelyreported in a protocols and are most com-monly used in postmortem timing.

2. Changes in the chemical composition of

body fluids or tissues (e.g. postmortem potas-sium concentration of vitreous fluid). Thesechanges are not routinely evaluated and aregenerally recorded when the determinationof the time of death is in doubt and is per-ceived as crucial in the medicolegal investiga-tion.

3. Postmortem residual reactivity of muscles toelectrical or chemical stimuli (e.g. electricalstimulation of the masseter muscle and reac-tion of the iris to chemicals.) The recordingof these changes, primarily popular in Euro-pean medicolegal center, is exceedingly un-common, if at all practiced, in the UnitedStates.

4. Evaluation of physiological processes with es-tablished starting time or progress rate andcessation at death (e.g. presence of gastriccontents as affected by time of digestion andthe gastric emptying time). Recording of the


amount, nature and appearance of gastriccontents is routine in any adequate autopsy.

5. Survival time after injuries, particularly whenthe time of infliction is known. The nature,extent and severity of injuries as well as thequantitation of associated complications(e.g. the amount of bleeding, early tissue re-action to injury) are often useful in determin-ing the time of death.

The major problem encountered when rely-ing upon the results of these methods is thevariation in the environmental and individualfactors on the magnitude and kinetics of post-mortem phenomena.

For example, the physicochemical changesfollowing death are greatly dependent on envi-ronmental conditions and the metabolic statusof the individual prior to death. Therefore, thedeceased must be considered in view of environ-mental factors (temperature, ventilation, hu-midity) and his characteristics (body build, pre-mortem exercise, state of health). Because ofsignificant variation of kinetics of postmortemphenomena, the time of death cannot be pin-pointed exactly but is estimated within a variabletime frame. Furthermore, the longer the timeinterval since death, the wider the estimatedrange.

Because of inherent inaccuracies in timing ofindividual postmortem changes, the followingapproach is usually effective:1. An initial determination of a wide window

of death which is subsequently narrowed andrefined by using variable parameters. Thewindow of death is defined as the time intervalprior to which one may assert with confi-dence that the individual was alive. The win-dow of death should be established accordingto the most reliable testimony or evidenceas to when the individual was last alive (e.g.witnesses, verified signed documents, lasttime newspapers were brought in the house,last time of withdrawal on bank accounts).

2. Conservative determinations of time of deathas a range utilizing individual postmortemchanges.

3. An algebraic integration of all postmortemtiming changes.

Postmortem Cooling (Algor Mortis)

Postmortem body temperature declines pro-gressively until it reaches the ambient tempera-ture. Under average conditions, the body coolsat a rate of 2.0° F to 2.5° F per hour during thefirst hours and slower thereafter, with an aver-age loss of 1.5° F to 2° F during the first twelvehours, and 1° F for the next twelve to eighteenhours. Careful studies under controlled condi-tions have shown that the decrease in the post-mortem body temperature is not rectilinear butsigmoid in shape with a plateau at the beginningand at the end of the cooling process.7

The initial plateau, which rarely lasts morethan three to four hours, is generally explainedon the basis of heat generated by the residualmetabolic process of dying tissues and by themetabolic activity of intestinal bacteria. A recentstudy by Hutchings8 reports elevations of thetemperature rather than a plateau within thefirst hours following death, with a return to base-line within four hours. The final slowing of therate of cooling is attributed to the reduced gra-dient between body temperature and ambienttemperature.

The skin, as the closest organ to the environ-mental air, cools quite rapidly and is not usefulfor sequential temperature measurements .Temperature changes of the inner core are pre-ferred, because the decline is slower and moreregular. Many sites have been tried for takingbody temperatures. The most convenient andcommonly used procedure involves hourly mea-surements of the rectal temperature. Some pre-fer the liver and brain as more representativesites of the inner core temperatures.

The postmortem rate of cooling may be usedfor estimating the time interval since death. Asa matter of fact, literature surveys indicate thatmore than a hundred and fifty years ago post-mortem cooling was used for this purpose inmedicolegal cases. Since then, numerous stud-ies by forensic scientists have attempted to refinethe use of cooling rate as a reliable postmortemclock. A thorough historical review of variousmethods of estimating the time of death frombody temperature by Bernard Knight9 con-


cluded that in spite of the extensive application ofphysical theory and a great deal of direct experimenta-tion, the level of accuracy remains low, even in theartificial venue of a controlled experiment. This doesnot mean that measurements of postmortemtemperatures are worthless in determining thepostmortem interval, but that these data shouldbe cautiously interpreted in view of variables af-fecting postmortem cooling.

Postmortem cooling of the human body atthe skin surface (i.e. loss of heat to the environ-ment) takes place by three major mechanisms:1. Conduction: transferal of heat by direct con-

tact to another object.2. Radiation: transfer of heat to the surrounding

air by infrared rays.3. Convection: transfer of heat through moving

air currents adjacent to the body.Internal organs cool primarily by conduction.

It follows that factors which affect these mecha-nisms are bound to affect the rate of cooling aswell.

For example, body insulators such as clothingand increased body fat will decrease the rate ofheat loss and, therefore, decrease the rate ofcooling. Active air currents increase heat loss byconvection and, therefore, accelerate the rateof cooling. Similarly, immersion in cold waterwill increase the heat loss by conduction andaccelerate the rate of cooling. A larger bodysurface ratio to body mass, such as the case inchildren, will increase relative heat loss andtherefore increase the rate of cooling. Further-more, the rate of cooling is dependent on thetemperature gradient between the body and theenvironment, and its calculation assumes thatthe environment is cooler than the body tem-perature; the higher the gradient, the faster bethe loss of heat.

However, if the environment is warmer thanthe body temperature, the postmortem bodytemperature will be increased. In calculatingback to the time of death, one should not neces-sarily assume that the body temperature at thetime of death was normal (36.5° C to 37° C, or98.6° F). People may die with hyperthermia atmuch higher than normal body temperature be-cause of a variety of factors including sepsis, hy-

perthyroidism, physical exercise, heat stroke,seizures or drugs (cocaine, amphetamines, anti-cholinergic drugs, phencyclidine). Head in-jury, with damage of the hypothalamic area ofthe brain, may cause a terminal body tempera-ture of 105° F or higher. Obviously, postmortemcooling would be significantly affected in suchcases. On the other hand, individuals may diein a state of hypothermia caused by shock, envi-ronmental exposure or drugs (alcohol, sedative-hypnotics, opiates, phenothiazines).

Early Postmortem Ocular Changes

The eyes often exhibit some of the earliestpostmortem changes. An immediate sign ofdeath in the fundi of the eyes is the arrest ofcapillary circulation with settling of red bloodcells, in a rouleaux or boxcar pattern.

When the eyes remain open, a thin film maybe observed within minutes on the corneal sur-face, and within two to three hours cornealcloudiness develops. If the eyes are closed, theappearance of the corneal film may be delayedby hours and that of corneal cloudiness by twen-ty-four hours or longer.

If the eyes are partly open in a dry environ-ment, the exposed areas between the lids maydevelop a blackish-brown discoloration knownas tache noire (black spot). This phenomenonhas been mistakenly interpreted as bruising. Ab-sence of intraocular fluid suggests a time ofdeath of at least four days. (Even in the absenceof fluid within the eyeballs, the interior of theglobes can be rinsed with water or saline andthe fluid submitted for toxicological analysis.)

Postmortem Lividity (Livor Mortis)

Postmortem lividity (livor mortis) or postmor-tem hypostasis is a purplish-blue discolorationdue to the settling of blood by gravitationalforces within dilated, toneless capillaries of thedeceased's skin.

Accordingly, livor is seen in the dependentareas, i.e. on the back if the body was in a supineposition, and on the face and front if the bodyremained prone. Within the circumscribed sitesof livor, one may see pale areas where the skinwas pressed against a hard surface or object pre-


venting postmortem sedimentation (Fig. II-3).Postmortem lividity may be evident as early astwenty minutes after death or may become ap-parent after several hours. The development oflividity is a gradual process which progressivelybecomes more pronounced. However, evenafter a number of hours postmortem lividity maybe difficult to discern in cases of severe anemiaor following extensive blood loss. In a case ofa ruptured aortic aneurysm or severed aorta,postmortem lividity may be so faint as to be prac-tically indiscernible.

In individuals with dark skin pigmentation,lividity in the skin can go unnoticed. At autopsy,finding congestion of internal organs, such asthe kidneys, may assist in determining the pres-ence of lividity.

In the early stages, livor can be blanched bycompression (Fig. II-4) and may shift if the posi-tion of the body is changed. After eight to twelvehours, the blood congeals in the capillaries ordiffuses into the extravascular tissues and doesnot usually permit blanching or displacement.In advanced stages of livor, the skin capillariesoften burst and cause pinpoint hemorrhages

known as Tardieu spots (Figs. II-5 and II-6).Unusual discoloration of postmortem lividity

may serve as a diagnostic clue regarding thecause of death. The pathological mechanism re-sponsible for the abnormal discoloration is usu-ally the presence of an abnormal hemoglobincompound (e.g. carboxyhemoglobin, methe-moglobin). In some instances cherry-red discol-oration may be caused by the poisoning of cellu-lar respiration (inhibition of cytochromeoxidase) resulting in excessive oxygen in thevenous blood, as in cyanide and fluoroacetatepoisoning {see Table II-l).

Cherry-pink livor is also seen in bodies recov-ered from water, wearing or covered with wetclothes, or lying on moist metal trays. Humidityprevents the escape of oxygen, allowing for anexcess of bright red oxyhemoglobin in the skin.

In certain cases it may be difficult to distin-guish between postmortem livor and antemor-tem bruises. Incision of the skin may be re-quired. Postmortem lividity is entirelyintravascular and in its early stages can bedrained. In a bruise, blood diffusely infiltratesthe interstitial tissue and cannot be removedby drainage. With the onset of decompositionblood vessels become permeable and permit theescape of livor-blood into the interstitial tissues.Differentiation of such areas from true bruisesmay be difficult or impossible.

Since scars are devoid of blood vessels, post-mortem lividity does not affect scarred areas.Thus, a scar in an area of lividity is usually easily

TABLE II-l

POSTMORTEM LIVIDITY DISCOLORATION

FIGURE II-3. Livor mortis. Note blanched area where facewas pressed onto floor. This man died of heart disease.The forehead lesions are superficial abrasions sustainedwhen he collapsed.

Etiology

NormalCarbon monoxideCyanide

FluoroacetateRefrigeration/

hypothermiaSodium chlorateHydrogen sulfide

Color of Liver

Blue-purplishPink, cherry-redPink, cherry-red

Pink, cherry-redPink, cherry-red

BrownGreen

Mechanism

Venous bloodCarboxyhemoglobinExcessive

oxygenated blood be-cause of inhibition of cy-tochrome oxidase

Same as aboveOxygen retention in cuta-

neous blood by cold airMethemoglobinSulfhemoglobin

Time of Death and Changes After Death

FIGURE II-4. Livor is blanched by the patterned glove compression seven-and-one-half hours after death.

FIGURE II-5. Tardieu's spots in the feet of a hanging victim. There is also considerableswelling of the ankles as a result of hanging for several hours.

25


FIGURE II-6. Close-up of Tardieu's spots over the abdomen in the area ofintense livor. Note absolute confinement of spots to the area of livor.

noticeable. Also, the absence of blood retardsdecomposition of a scarred area. A cirrhoticliver, for instance, is likely to decompose at asignificantly slower rate than a normal liver.

Postmortem Rigidity (Rigor Mortis)

Following death, the muscles become initiallyflaccid, and the lower jaw and extremities canbe passively moved. The flaccidity is followed byan increasing stiffness or rigidity of the muscularmass, which freezes the joints and is known aspostmortem rigidity or rigor. The rigidity thengradually subsides, and the body becomes flac-cid again.

In temperate climates, under average condi-tions, rigor becomes apparent within half anhour to an hour, increases progressively to a

maximum within twelve hours, remains forabout twelve hours and then progressively disap-pears within the following twelve hours (Fig. II-

Rigor mortis develops and disappears at a sim-ilar rate in all muscles. However, because of alesser volume, small muscles (e.g. masseters,hands) become totally involved by rigor beforethe large volume muscles (e.g. thigh muscles),a phenomenon which formerly led to the mis-leading belief that rigor progresses from thehead downwards. Once fully established, thebreaking of rigor in joints is irreversible and itwill not reappear. However, if the rigor is brokenbefore it is totally completed, a variable extentof rigidity will reappear.

The occurrence of postmortem rigor is a phys-


icochemical process following somatic deathwhere the muscles continue their metabolic ac-tivity of glycolysis for a short time. During thisprocess, ATP is hydrolyzed to ADP, and lacticacid is produced, lowering the cellular pH. Thelack of ATP regeneration after death and theincreased acidity result in the formation of lock-ing chemical bridges between the two major mus-cle proteins, actin and myosin. This interlockingconnection is fixed and produces rigor, withoutshortening of the muscle. In physiologic con-traction, in contrast, the actin molecules slideinwards over the myosin, and the muscle short-ens. Animal experiments indicate that in addi-tion to the declining postmortem levels of SATP,a certain concentration of free calcium ions isalso required for the development of rigor mor-tis, and that rigor is inhibited by calcium bindingagents.10

With decomposition of body proteins, thechemical bridges between actin and myosin ofthe muscle in rigor break down, and the musclebecomes flaccid again.

As with other sequential postmortemchanges, rigor mortis can assist in the determi-nation of the postmortem interval. However,one should remember that the progression ofrigor may be substantially modified by a varietyof factors which affect the underlying chemicalprocess. Rigor mortis appearance and disap-pearance is accelerated by prior exercise, con-vulsions, electrocution, hyperpyrexia or hotenvironmental temperature. In a hot environ-ment, for example, the rigor mortis may disap-pear in only nine to twelve hours. Similarly, met-abolic states associated with acidosis and uremiahasten the process. Hypothermia and cold envi-ronmental temperatures slow the chemical reac-tions and, therefore, delay the rigor process.Rigor mortis development is also affected by to-tal body muscle mass and has been shown todevelop poorly in young children, the elderlyand debilitated. Drugs affect postmortem rigoraccording to their physiological actions. Strych-nine poisoning, which is associated with strongtetanic convulsions, accelerates rigor while car-

FIGURE II-7. Rigor mortis, intense enough to support the body as shown. This man had beendead for eighteen hours when the photograph was taken.


bon monoxide poisoning, associated with shockor hypothermia, delays it.

The variability of postmortem rigor makes itsuse as a postmortem clock rather tenuous, tobe considered only in conjunction with othertiming indices. When the appearance of rigidlimbs is inconsistent with gravitational forces,rigor is a reliable indicator of a postmortem shiftin the position of the body. For example, anindividual who is found in rigor with armsraised, defying gravity, was obviously movedfrom his original position after the initiation ofrigor (Figs. II-8 and II-9).

Rigor Mortis of Involuntary Muscles

Rigor mortis affects not only the voluntarymuscles but the involuntary muscles as well, pro-ducing misleading artifacts. Rigor mortis, for ex-ample, may, to a different extent, affect the irisof each eye and produce an artifactual differ-ence between the pupil size which may simulatea significant premortem pupillary disparity. Thearrectores pilorum, the tiny muscles of the hairfollicles, may be strikingly affected by rigor, re-sulting in cutis anserina or gooseflesh (Fig. II-10).Some believe erroneously that gooseflesh is some-how associated with drowning or death in water.Also, some believe mistakenly that hair growsafter death because rigidity of the arrectores pi-lorum muscles causes hair to erect and appearlonger.

Another manifestation of postmortem rigidityis the finding of semen at or near the tip of thepenis. This expulsion of semen is the result ofcontraction due to postmortem rigidity of thelayer of muscle in the wall of the seminal vesi-cles, which function as semen reservoirs.

The heart in rigor mortis may simulate hyper-trophy, while secondary flaccidity may mimicpathologic dilation. It is interesting to note thatfollowing open heart surgery cardiac patientsmay develop an ischemia-related, irreversiblecontraction of the heart resembling rigor, whichhas been graphically described as stoneheart.11-13

Cadaveric Spasm

In rare instances, a forceful agonal contrac-

tion or seizure is converted almost immediatelyinto tight rigor without preceding primary flac-cidity. In such cases, labeled as cadaveric spasm,the clenched fist may be seen tightly holding acigarette, blades of grass, clothing or some otherobject. Cadaveric spasm usually occurs in deathspreceded by great excitement or tension. It isusually seen in cases of drowning, with the de-ceased grasping weeds or other aquatic vegeta-tion, and in cases of homicide where the victimclutches some of the assailant's hair or clothing(Fig. II-11).

Stomach Contents

The presence, appearance and amount ofstomach contents may be helpful in determin-ing the time of death. This determination isbased on the assumption that the stomach emp-

FIGURE II-8. Supine body with rigid forearms and hands inair, defying gravity. The body has been displaced from aprone position while holding a rifle.


FIGURE II-9. Rigidity maintaining the legs against the brick wall. The flexed position of thelegs led to the immediate conclusion that she had died elsewhere and had been moved afterbeing dead at least six hours. Search of the area disclosed bloodstains in the home whereshe had been beaten. Her male friend confessed to having moved her body from the househours later during darkness, concealing it in the court of an adjacent house.

ties at a known rate. However, the emptying ratemay be only approximated, because it changesaccording to various factors, including theamount and type of food, drug or medicationintake, prior medical and emotional conditionof the deceased and other individual variables.

An ideal postmortem evaluation protocol ofthe rate of gastric emptying should include:1. A description of the nature, amount, size and

condition of the stomach contents.2. A microscopic examination of the contents

if the contents are difficult to identify or arepartially liquefied by the digestive process.

3. An examination of the small intestine for un-digestible markers (e.g. corn kernels, tomatopeels) to see how far ahead certain digestedfoods traveled.

4. A toxicological examination of both bloodand stomach contents for drugs and alcohol.

5. An evaluation of the prior medical and psy-

chological status and related medicationsand drugs.

Gastric emptying is a complex process whichdepends on signals originating not only in thestomach but in the intestines and brain as well.14

The stomach's distension by the meal affects theemptying process through reflex relaxation ofthe gastric fundus. Additionally, the meal's pres-ence stimulates the gastric mucosa to secretehormonal substances of a peptide nature (e.g.gastrin) which delay gastric emptying. Osmoticand calcium binding receptors in the duodenalmucosa respond to the composition of the in-coming food and trigger the release of addi-tional hormonal peptides (e.g. cholecystokinin)which have both a direct and indirect neuraleffect on post-prandial gastric emptying. Fur-thermore, additional chemical receptors in thedistal small intestines and colon trigger the re-lease of additional factors, such as peptide VV,


FIGURE II-10. Gooseflesh due to postmortem rigidity of muscle fibers of hair follicles.

which also affect the rate of gastric emptying.Finally, the central nervous system also exerts asubstantial control over gastric emptying.

This complicated array of monitoring stationsis affected by many factors. The rate of empty-ing, for example, is substantially influenced bythe physical state of the food. Solid foods emptyslower than liquid foods.

While the half-emptying time for one hun-dred and fifty grams of orange juice is reportedto average about half and hour, the amount oftime required to digest and empty fifty gramsof solid food may require two hours.15,16 This,however, depends on the type of food and itsnutritive density (isocaloric value). The greaterthe nutritive density and osmolarity of a meal,the slower the meal is transferred from the stom-ach into the duodenum. Starchy and fatty foodsmay delay both the digestive process and empty-ing of the stomach. Light meals are usually pres-ent in the stomach for up to one-and-a-half to

two hours, medium meals up to three to fourhours and heavy meals four to six hours ormore.17,18 The head of the meal usually reachesthe cecum within six to eight hours.

The stomach does not empty instantaneously;neither are large amounts of food expelled peri-odically. Only a small amount of food (a fewgrams) is expelled per minute, only after havingbeen ground to small particles. Therefore, thesize of food particles and the extent of mastica-tion also affect the emptying rate of the stom-ach. Individuals who gulp their food withoutadequate mastication, whether because of lackof dentition or poor habits, have prolonged gas-tric retention of the meal prior to emptying toallow for its digestion.

An increased volume of ingested food acceler-ates only moderately the rate of gastric emptyingwhen the energy density of the meal remainsthe same.

Drugs and alcohol also affect the rate of gas-


FIGURE II- l1. Cadaveric spasm in a case of drowning.

tric passage. The presence of concentrated alco-holic beverages (more than thirty percent) inthe stomach causes constriction of the pyloricmuscle and delays gastric emptying. A variety ofcompounds including narcotics (heroin, meper-idine, etc.), phenothiazines, atropine, beta-ad-renergic drugs, potassium salts and syntheticprogestins also substantially inhibit gastric emp-tying, while others such as diazepam (Valium®),metoclopramide and bulk laxatives accelerate it.

Natural diseases may also affect the rate ofgastric emptying. For example, diabetes, bu-limia and pyloric diseases (e.g. pyloric stenosisor peptic ulcers) are associated with delayed gas-tric emptying. The final emptying time for anidiopathic functional dyspeptic patient, for ex-ample, was found to be delayed by more thanforty percent as compared to normal.19

Emotional stress (fear, excitement, etc.) alsoaffects the time of gastric emptying by delayingit for many hours. Similarly, individuals in shockmay retain gastric contents for days. Age andbody build also affect the rate of gastric empty-ing, the elderly and the obese shown to have aslower emptying gastric rate. Finally, environ-mental factors such as extreme cold or very hot

weather may also retard gastric emptying.Subtotal gastrectomy with gastroenterostomy

and certain types of moderate exercise, suchas running, have been shown to accelerate thegastric emptying rate. On the other hand, ex-haustive exercise, such as a marathonic run, sub-stantially slows the rate of gastric emptying.

In conclusion, the emptying of the stomachis a complex multifactorial process, and its evalu-ation for determining time of death requirescaution and careful review of all limiting factors.Consideration must also be given to the possibil-ity of one or more close consecutive meals.

It has been found that stomach contentswhich are readily identifiable by naked-eye in-spection were usually ingested within a two-hourperiod.

DecompositionThe disintegration of body tissues after death

is known as decomposition. Decomposition fol-lows the arrest of the biochemical processeswhich preserve the integrity of the cellular andsubcellular membranes and organelles. Duringdecomposition, the tissue components leak andbreak up, hydrolytic enzymes are released from


the intracellular lysosomal sacs, and bacteriaand other microorganisms thrive on the unpro-tected organic components of the body.

Accordingly, two parallel processes of decom-position have been distinguished:1. Autolysis: self-dissolution by body enzymes re-

leased for the disintegrating cells.2. Putrefaction: decomposition changes pro-

duced by the action of bacteria and microor-ganisms.

A third kind of postmortem destruction of thebody occurs as a result of anthropophagy (i.e.attacks by various types of predators) from smallinsects to larger animals, particularly rodents.

Autolytic Changes

The earlier autolytic changes occur in organsrich in enzymes such as the pancreas, gastricmucosa and the liver, Focal autolytic changesof the pancreas are almost invariably seen atautopsy.

Gastromalacia (autodigestion of the gastricmucosa with perforation) has been described tooccur following injuries in the last stages ofcoma or shortly before or after death. We haveobserved it more often in cases of closed headinjury, possibly related to stimulation of the heatregulatory center in the brain and a terminalsurge of body temperature, promoting autolysis.It usually occurs in the area of the fundus ofthe stomach and is devoid of any vital reaction.Esophagomalacia is a similar process which in-volves the lower portion of the esophagus andallows esophageal and gastric contents to burstinto the left chest cavity.

Putrefaction

Putrefactive changes are dependent primarilyon environmental temperatures and the priorstate of health of the individual. Changes whichin temperate climates take days to develop maydevelop within hours in a warm environment.

Furthermore, individuals dying in the samearea may show very different stages of decompo-sition, according to their individual degree ofexposure to the sun or proximity to a source ofheat (stove, radiator, etc.) (Fig. II-12).

Individuals with sepsis usually undergo rapid

decomposition with putrefaction. In some casesof gas-producing Clostridia sepsis, one may wit-ness an amazingly rapid progression of putrefac-tive changes in the liver, from a seemingly nor-mal appearance at the beginning of the autopsy,to a mushy, decomposing mass an hour or solater. The putrefaction gases include methane,carbon dioxide, hydrogen and particularly mal-odorous ammonia, hydrogen sulfide and mer-captans. This gas burns readily when ignited(Fig. II-13).

Fever prior to death, such as encountered insepsis, rhabdomyolysis and cocaine overdose,also substantially accelerates decomposition andputrefaction. In such cases advanced putrefac-tion may be observed in less than twelve hours.Putrefaction is also more rapid in obese individ-uals. The putrefaction process is accelerated inedematous or exudative areas of the body anddelayed in dehydrated tissues or following mas-sive blood loss. On the other hand, in infantsand thin individuals, putrefaction proceeds at asignificantly slower pace.

The rate of putrefaction.also depends on thephysical environment in which the body lies. Itis generally accepted that putrefaction in air ismore rapid than in water, which is more rapidthan in soil. One week in air equals two weeksin water and eight weeks in soil.

Exposure to cold also substantially delays thedecomposition process. In evaluating postmor-tem changes, it is, therefore, important to con-sider any intermittent period of exposure tocold, refrigeration or freezing. A further consid-eration is postmortem rewarming or thawing ofthe body. Experiments have shown that pre-viously frozen and thawed animal tissues decom-pose significantly faster than freshly killed ani-mals. Tissues which are damaged by traumashow accelerated rates of decomposition.20

Decomposition gases may cause tissue arti-facts mimicking softening cysts in the brain (en-cephalomalacia) and elsewhere, although theSwiss cheese pattern of the cavities easily indicatestheir postmortem character.

Similarly, decomposition gases may make dif-ficult the diagnosis of air and fat embolism andcause the lungs of stillborns to float, leading to


FIGURE II-12. The influence of environmental temperatureon postmortem decomposition. This couple was killed atthe same time by a mentally deranged son. The body ofthe mother was found in the cool basement, while thebody of the father was discovered in a warm upstairs room.Outside temperature was 90° F, postmortem interval aboutforty-eight hours.

erroneous determination of spontaneousbreathing at birth.

Under condition that promote putrefaction,especially in hot and humid environments, onemay occasionally see a peculiar red discolorationof the teeth (pink teeth). The red discolorationis due to diffusion of hemoglobin from hemo-lyzed red blood cells into the dentin canaliculi.Some studies have reported a frequency as high

FIGURE II-13. Jet of ignited putrefaction gas (methane) atthe end of a 12-gauge needle inserted into swollen scrotumof a decomposed body.

as twenty percent of pink teeth in sequentialautopsies.21

A rare change caused by decomposition is thepresence of white-gray, pinpoint foci, called mili-aria, which are scattered below the endocar-dium and below the capsules of the liver, kidneysand spleen. The miliaria are easily distinguishedfrom granulomas, fungi or fatty necrosis and arepresumably due to autolytic changes resultingfrom precipitation of calcium and other salts.

In temperate climates, early decompositionbecomes manifest within twenty-four to thirtyhours with greenish discoloration of the abdo-men, due to denaturation by colonic bacteria,of hemoglobin to biliverdin and its reaction withhydrogen sulfide. Such discoloration is moreprominent in the right lower abdominal areabecause of the close proximity of the cecum tothe abdominal wall.

This is followed by gaseous bloating, darkgreenish to purple discoloration of the face andpurging of bloody decomposition fluids from thenose and mouth. The tongue swells and progres-sively protrudes from the mouth, and the eyes


FIGURE II-14. Prominent marbling two days after death.Note swelling and discoloration of face. Marbling is limitedto areas of livor mortis.

bulge because of accumulating retrobulbar de-composition gases.

The greenish and purplish discoloration rap-idly spreads within thirty-six to forty-eight hoursto the chest and extremities, displaying a mar-bling pattern which delineates the decomposi-tion of the blood and formation of sulfhemo-globin and hematin within dilated subcutaneousblood vessels (Fig. II-14).

Postmortem discoloration of the skin may beso dark that white individuals may be easily mis-taken as black (Fig. II-15).

As decomposition progresses, the skin be-comes slippery with vesicles and slippage of theepidermis, and generally, after three days, the

FIGURE II-15. Postmortem discoloration of the face andswelling, mimicking black racial features in a white manwith straight, light-brown hair.

entire body becomes markedly bloated. Swellingis particularly dramatic in areas of loose skin(eyelids, scrotum and penis). The skin of thehands often sheds, together with nails, in glove-like fashion, and the skin of the legs in a stocking-like pattern, a phenomenon which is also seenfollowing prolonged immersion in water and incases of second-degree burns (Figs. II-16 and II-17).

Additional destruction of the body is causedby maggots. Fly eggs initially deposited at thecorners of the eyes, mouth and other mucocuta-neous junctions (Fig II-18) develop into innu-merable crawling maggots which rapidly destroysoft tissues. The maggots concentrate primarilyin areas of body openings and perforationswhere they seek shelter and feed on blood andtissues.

Anytime a decomposed body is found with anunusually large concentration of maggots in aparticular area, it is probable that a wound pre-existed in that location. In the case of a close-range gunshot wound, maggots may remove tis-


sue at the edges of the wound but leave sootdeposited on the bone and gunpowder undis-turbed.

Ultimately, decomposition ends in completeskeletonization. In temperate areas, under aver-age conditions, the minimum period for fullskeletonization is about one-and-a-half years.

The rate of putrefaction is significantly fasterin arid environments. Galloway et al., in re-viewing the earliest time of postmortem changein the hot, dry climate of Arizona, reportedbloating of bodies as early as two days, gasesat three days, advanced sagging of tissue andadvanced intra-thoracic and intra-abdominal ac-tivity of maggots at four days, partial mummifica-tion with leathery change of skin at four days,and skeletonization after six to nine months.22

Under most favorable conditions, particularlywith necrophagous insect activity, skeletoniza-tion may occur even earlier. Stewart23 reportsthe case of a thirteen-year-old Mississippi girl,victim of a homicide, whose body became almostcompletely skeletonized within ten days duringlate summer.

Post-Skeletonization Weathering Changesand the Time of Death

Once the body is fully skeletonized, the bonesundergo a slow process of weathering and break-ing down, lasting decades or centuries. Typicalweathering of bones includes bleaching, exfolia-tion (desquamation) of cortical bone and de-mineralization. The rate and severity of thesechanges depends on environmental conditions,whether the bones were buried or exposed, theacidity of the soil and extent of humidity. Soilstaining, which is a brown or sometimes tan dis-coloration of the bone surface, is variable butmay occur in as little as one to two years aftercomplete skeletonization. Green discolorationof the bone surface is often caused by contactwith copper or brass and may be seen as earlyas six months after exposure.

In hot, arid climates such as Arizona, bleach-ing of bones has been reported to occur as earlyas two months and exfoliation as early as fourmonths, though usually the former takes sixmonths and the latter as long as twelve to eigh-

teen months. Demineralization is a late process,commonly seen in old bones or those foundin archaeological excavations. It results in verylight, porous and friable bonds. Such bones mayturn to dust on touching. Contact with certainroots may significantly accelerate bone deminer-alization.

FIGURE II-16. Skin stockings and left glove. Bloating of body,especially of the breasts and marked discoloration of theface (three-and-a-half days after death).


FIGURE II-17. Postmortem detachment of the skin in glove form. Note that the nails stay withthe skin. These gloves often yield a full set of fingerprints and should be retained untilidentification is certain. This was a narcotic addict (note stocking around wrist) whose bodywas found in a heated house in November. He was reported missing five days earlier.

Mummification and Adipocere

Two types of postmortem changes, mummifi-cation and adipocere, may counter substantiallythe process of tissue destruction by decomposi-tion. Mummification results from drying of tis-sues under conditions of high environmentaltemperature, low humidity and good ventila-tion.

The conjunctivae of the eyes dry along theopening between the lids, causing a dark-brownhorizontal band across the corneal surfacesometimes referred to as tache noire (Fig. II-19).

The scrotum dries at the sides where exposedand not in contact with the moist skin of thethighs (Fig. II-20). Tightened mummified skindisplays a brownish discoloration and a parch-ment-like appearance, which preserves facialcontour and dries and discolors bent knees (Fig.II-21). Similar drying may be observed in fingersand toes exposed to hot, dry air. Mummifiedfingers and toes are shriveled with wrinkled,firm, brown skin (Fig. II-22). The process beginsat the fingertips which become spindly. Fingersin this condition are unsuitable for fingerprint-


FIGURE II-18. Eggs laid by flies in the moist areas of thecorners of the eyes, nares and angles of the mouth.

ing unless first soaked in warm water to stretchand unfold the skin for the return of its naturaltexture. Shrinkage of the nail beds has occasion-ally misled investigators and mystery book writ-ers to conclude that fingernails and toenailsgrow after death.

The skin around the fingernails and toenailsshrinks as a result of drying and may give theerroneous impression that the nails have grownafter death. Drying of certain parts of the bodymay cause shrinkage of the skin to the extent ofcausing large splits that resemble actual injury.

FIGURE II-19. Postmortem dark discoloration of sclera(tache noire) along the exposed palpebral fissure of the

FIGURE II-20. Drying of the scrotal skin is sometimes mis-taken for bruising.

Such splits are especially common in the groins,neck and armpits.

In mummified bodies in temperate areas, theinternal organs are usually poorly preserved ormay have totally disappeared due to decomposi-

FIGURE II-21. Leathery, shrunken face of mummified bodyfound two months after death. Deceased was found cov-ered by some clothing in a basement.


FIGURE II-22. Mummification of fingers showing shriveling and discoloration oneweek after death.

tion. Once mummification is fully developed,the body remains preserved as a shell for longperiods of time, even years (Fig. II-23). The rateof mummification and its extent depend on thehumidity of the air and the intensity of the envi-ronmental heat, and its full development in tem-perate areas generally requires at least threemonths of postmortem interval.

Adipocere (waxy fat) (Fig. II-24) develops un-der conditions of high humidity and high envi-ronmental temperature and especially involvesthe subcutaneous tissues of the face, extremities,buttocks and female breasts. The chemical pro-cess underlying adipocere consists of hydrationand dehydrogenation of body fats, a processwhich imparts a grayish-white color and soft,greasy, clay-like, plastic consistency to the softtissues of the body.

Recent research has demonstrated that bacte-rial enzymes of both intestinal and environmen-tal sources, particularly Clostridia, are primarilyresponsible for adipocere, by converting unsatu-rated liquid fats (oleic acid) to saturated solidfats (hydroxystearic acid and oxostearic acid).24

The time for the development of adipocere isestimated to be at least three months and usuallyis not observed before six months.

Stillbirths

Human fetuses are generally considered via-ble after twenty-four weeks of pregnancy, atwhich time they reach a weight of six hundredto eight hundred grams and measure twenty-one to twenty-two centimeters from crown torump. (Foot length is the most reliable externalmeasurement parameter for gestational age.) Astillbirth is the delivery of a viable fetus which isnot breathing and shows no sign of life (Apgarscore 0). The term stillbirth is synonymous withdead birth and the word still describes the ab-sence of fetal respiration or other movements.

The determination of stillbirth has importantmedicolegal implications, particularly in in-stances when the death of a newborn is con-cealed. In such instances, it must be determinedwhether the delivery was indeed that of a deadfetus, i.e. a stillborn, whether the fetus was bornalive and died as a result of failure to providerequired care, or whether there was an inten-tional infanticide.

In such cases, the questions which the foren-sic pathologist must address are:1. What is the gestational age of the fetus (by

weight and dimensions)?


FIGURE II-23. Mummification of chest and arms. Note the parchment-like appearance ofthe skin in these areas. The skull is partly exposed by maggots, the surrounding tissuesdecomposed and blackened. The body was found in an apartment in the middle of JulyNewspapers at the door and other evidence indicated that death had occurred one weekearlier.

2. Was the fetus viable by estimated age, weightand size, and alive at birth? (Did the childbreathe air?)

3. Were there traumatic injuries present in thefetus, and what was their significance?

4. What was the cause and manner of death?To fully answer these questions, a thorough

autopsy, including careful examination of theumbilical cord and placenta, should be per-formed. Common histological abnormalities ofthe placenta in stillbirth cases include placentalinfarcts, hemorrhagic endovasculitis, retropla-cental hematomas, acute chorioamnionitis andhydrops.25

Similarly, the examination of the umbilicalcord of the stillborn may reveal significant ab-normalities such as true knots, torsion, arterialagenesis, thrombosis and funisitis.

When intrauterine death has occurred daysor months prior to the delivery, the body of

the fetus shows postmortem changes defined asmaceration. Maceration is an autolytic process,i.e. a decomposition due to self-disintegrationof the body by released cellular enzymes. Thefetus and the bathing amniotic fluid are sterileand, therefore, will not undergo putrefaction ifthe membranes are intact. The macerated fetusinitially shows a reddish, dusky discolorationand an easily peeling skin with fluid accumula-tion beneath the epidermis and formation oflarge bullae. The reddish discoloration is due todiffuse hemolysis and involves both the skin andthe internal organs. Easy separation of the epi-dermis does not occur until the last trimester ofpregnancy. Before this period, the epidermis isless differentiated and is tightly adherent to thedermis.

This is followed, within one to three days, byfurther darkening of the skin, flaccidity, separa-tion and overlapping of the cranial bones, dislo-


FIGURE II-24. Adipocere formation in the face and head of a seaman who had drowned sixmonths before recovery of his body in April in the Chesapeake Bay. During winter the baywas covered with ice for two or three weeks. Water temperature when body was recoveredwas near 60° F. A key with the Norwegian word for cook was found in the pocket of theseaman and helped to establish identification.

cation of the temporomandibular joints and ac-cumulation of hemolyzed blood and fluid in thebody cavities. Rigor is almost never observed inmacerated fetuses. In fetuses which are retainedfor more than seven to ten days, the reddishdark color starts to change into a light greenish-brown. Within a few days, the brain liquifies andthe abdominal tissues decompose, often with

disintegration of the intestinal wall, releasingmeconium into the abdominal cavity. In caseswhere pregnancy continues, the dead fetus maybe gradually resorbed or mummified (papyra-ceous appearance). In rare cases, usually associ-ated with ectopic pregnancy, the dead fetus maycalcify (lithopedion).

It is important to realize that some body mea-


surements, including weight of a macerated fe-tus, may be altered by postmortem changes andbe unsuitable for estimating the gestational age.This makes it difficult, from the pathologist'spoint of view, to correlate the gestational ageof the fetus, to a dire traumatic event to themother.

Decomposition certainly complicates the au-topsy of a macerated fetus, although major de-velopmental anomalies can still be detected.One should be careful not to interpret as trau-matic the subarachnoid or intraventricular hem-

orrhages often observed in stillborns as a resultof hypoxemia.

Microscopic examination of lungs of still-borns frequently reveals some evidence of amni-otic fluid aspiration with keratin squames in thealveoli, a finding which has been related to fetaldistress. Other histological findings seen in fetaldistress are tubulocystic change in the adult cor-tex of the adrenal gland, involution {starry skyappearance) of the thymus and meconium stain-ing of the skin and placental membranes.

POSTMORTEM ARTIFACTS

Distinction of antemortem injuries from post-mortem artifacts is of obvious importance. Prob-lems in differential diagnosis may occur as aresult of faulty autopsy technique, distortingpostmortem changes, and destructive environ-mental factors such as high environmental tem-peratures, postmortem mechanical trauma andanthropophagy, i.e. destructive changes by scav-engers.26

Even examination of fresh bodies may giverise to diagnostic difficulties when fatal injuriesare accompanied by minimal hemorrhage orwhen immediate postmortem trauma opensblood vessels and causes artifactual bleeding.

I. Faulty Autopsy TechniqueFaulty autopsy techniques can create confus-

ing postmortem artifacts. For example, carelessremoval of congested neck organs before ex-tracting the chest and abdominal organs mayproduce artifactual hemorrhages in the strapmuscles of the neck or laryngeal fractures, mim-icking strangulation. Similarly, prying the skullwith a chisel to break any remaining bridge ofbone missed by sawing may produce linear ba-silar fractures simulating fractures sustainedduring life. Removing the chest plate at the au-topsy involves tearing large arteries and veinsand may result not only in bleeding within thechest and abdominal cavities but also in drawingair into blood vessels, mimicking air embolism.

II. Errors in Interpretation ofDecomposition Changes

The following is a non-inclusive list of com-

mon situations in which distortions due to post-mortem changes may be subject to misinterpre-tation:1. Postmortem bloating of the body may create

a misleading appearance of obesity.2. Bloody decomposition fluid purging from

the mouth and nose may be misinterpretedas premortem bleeding due to trauma.

3. The presence of decomposed bloody fluidin the chest cavity may be misconstrued ashemothorax.

4. Agonal or postmortem autolysis and perfora-tion of the stomach may be misinterpretedas a perforated ulcer.

5. Postmortem dilatation and flaccidity of thevagina and anus may produce the appear-ance of a sexual attack or sodomy.

6. Pinpoint foci of extravasated blood fromburst capillaries in areas of intense livor maysimulate premortem petechial hemorrhages.

7. Diffusion of hemolyzed blood into tissues inareas of livor may be difficult to distinguishfrom genuine bruising in cases of moderatelyadvanced decomposition.

8. Focal autolytic changes in the pancreas maybe misinterpreted as focal necrosis or focalhemorrhagic pancreatitis.

Failure to carefully examine areas where de-composition is particularly advanced may resultin missing of significant trauma, particularlysince premortem injuries undergo more rapiddecomposition.

Alterations in blood and tissue levels of pre-mortem toxic substances as a result of postmor-


FIGURE II-25. Anthropophagy: Irregular, bloodless defect under the eye,caused by dog (?) postmortem nibbling.

FIGURE II-26. Postmortem mutilation by rats. Note complete absence of hemorrhage.


FIGURE II-27. Postmortem injury by mice closely resembling that due to roaches. The sceneat first suggested violence, since there was a pool of nearly a pint of blood on the floor whichhad drained out of these lesions as the deceased lay supine on her bed with the feet on thefloor. She had died of chronic heart failure with marked venous hypertension.

tern hydrolysis or decomposition may make adiagnosis of poisoning or overdose difficult ifnot impossible. For example, cocaine disap-pears rapidly from postmortem blood and tissueas a result of hydrolysis, while postmortem levelsof alcohol can substantially increase due to tis-sue decomposition.

A less known toxicological artifact resultsfrom postmortem redistribution of drugs. Post-mortem diffusion of certain drugs, such as pen-todiazepines, barbiturates and digoxin, hasbeen reported to occur from areas of high tissueconcentration into the blood.27

III. Destructive Environmental Factors

Exposure of the body to environmental forcesmay result in pathological changes which mayobscure, modify or mimic genuine premorteminjuries.

Some of the artifactual injuries clearly point

to their etiology, while others are less specificand more questionable. Postmortem thermal ar-

FIGURE II-28. Postmortem mutilation by ants restricted bythe collar line could suggest strangulation.

44Medicolegal Investigation of Death

FIGURE II-29. Postmortem artifact produced by ants. The girl was dumped face-down in awooded area after being raped and strangled. The injuries of the face were first mistakenfor fingernail marks. The fine linear scratches are due to twigs and undergrowth

FIGURE II-30. Postmortem artifact. Skin lesions of arm caused by roaches. These are easilyconfused with antemortem abrasions if the roaches are not observed when the body isdiscovered. Note the similarity with the postmortem injuries produced by ants The latterare somewhat smaller and more discreet.


FIGURE II-31. Postmortem gnawing of flesh by small petdog.

tifacts often seen in fire victims include fracturesof the skull and epidural hemorrhage due tointracranially generated steam, fractures of theextremities due to thermal contractions of ten-dons, and wide splitting of skin and muscles,simulating lacerations, cuts and stab wounds. Itis interesting to note that subdural and suba-rachnoid hemorrhages are not artifactually pro-duced in conflagrations.

Frozen bodies of infants may show artifactualfolding of the skin of the neck, simulating liga-ture strangulation. Drowning fatalities recov-ered from larger bodies of water (rivers, lakes,oceans) may show extensive postmortem mutila-tion due to boat propellers, simulating injuriessustained during life.

Similarly, postmortem injuries caused by vari-ous scavengers (such as flies, ants, beetles,roaches, dogs, rodents, aquatic animals) may

FIGURE II-32. Postmortem gnawing of human femurs, whichwere exposed for some months in a wooded area. Theteeth marks are most likely from dogs, but smaller animals,such as opossums or skunks, may leave similar marks.

cause injuries (anthropophagy) simulating pre-mortem trauma (Figs. II-25 to II-36). Superficial(epidermal) skin defects produced by insectfeeding are sometimes mistaken for cigaretteburns. When in doubt, microscopic examina-tion of such areas readily reveals the true natureof such lesions. We have seen cases where dogsremoved the head from a decomposing body


FIGURE II-33. Confluent superficial (epidermal) defects producedby roaches and ants.

FIGURE II-34. Superficial skin injuries produced after deathby ants and roaches. Injuries resemble abrasions and possi-bly assault.

and gnawed it at some distance away. Outdoorsanimals often take body parts a long distanceaway and sometimes such parts are never recov-ered. It is often possible to determine the sizeof an animal involved in a particular case ofpostmortem mutilation by examining the edgesof the injuries on the body.

Anthropophagy and Postmortem Vegetal Growth

Anthropophagy (Greek: eating of man) is thepostmortem assault of the body by various scav-engers. Identification of the specific scavengerand the stage of its development may assist inestimating the minimal period of time whichelapsed since death.

For example, identification of maggots as be-ing those of a particular fly (e.g. the bluebottlefly) permits determination of the minimumtime elapsing from the deposition of the eggsto the hatching of larvae. Most flies require atleast twenty-four hours for hatching, but knowl-edge of the life cycle of a particular fly permitsa more precise determination of the hatching

Maggot size (length) may permit further eval-uation of the time which elapsed from hatchingto the time of recovery of the larvae. Pupae, thenext stage of larval development, will obviously


FIGURE II-35. Superficial skin defects between the fingersproduced by ants. Moisture and shelter attracted the ants.

indicate an even longer postmortem interval. Itis recommended that larvae by measured, pre-served in a fixative (seventy percent alcohol orfour percent formalin solution) and submittedfor examination by an entomologist.

Similarly, botanists may be helpful in de-termining the minimal time interval since deathby identifying the type and stage of postmortemgrowth of fungi and vegetation on bodies whichwere buried or left exposed to soil.29

Recent Developments for Determinationof the Time of Death

In recent years a number of new methodshave been suggested for determining the timeof death. Some of the methods are based onprogressive postmortem increases in levels of 3methoxytyramine (3MT) in the basal ganglia ofthe brain and on the circadian variations in the

FIGURE II-36. Body recovered from water after several months during the winter. The groupof small defects near the area of the web of the thumb were caused by fly maggots whichburrow in and out through the skin.


levels of betareceptors and melatonin in the pi-neal gland.

Unfortunately, these methods involve quiteintricate and time-consuming chemical or radio-

immune techniques and dedicated expertise,and are as yet insufficiently confirmed andlargely in early experimental stages.

CONCLUSION

In conclusion, none of the methods used inestablishing the time of death are totally reliableand mathematically precise. Dogmatic and pin-point accuracy in this matter is clearly notachievable.

However, careful consideration of environ-mental and individual influences, and the con-

comitant use of as many postmortem clockingdevices as possible, frequently permit determi-nation of a realistic range of the postmorteminterval.

The author thanks Doctor Katherine Jasnosz for her valuableassistance.

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