Forensic Science, 6 (1975) 241-247 0 Elsevier Sequoia S.A., Lausanne - Printed in the Netherlands

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MEDICOLEGAL PROBLEMS IN DETERMINING CAUSE OF DEATH IN MOTOR VEHICLE ACCIDENTS

JOSHUA A. PERPER and CYRIL H. WECHT

Allegheny County Coroner’s Office, Allegheny County, Pittsburgh, Pa. (U.S.A.)

(Received November 14,1975; accepted December 22, 1975)

INTRODUCTION

Fatalities associated with traffic accidents may generate an impressive number of medicolegal problems of vital importance to the families of victims, insurance companies, compensation boards, prosecuting attorneys, traffic regulating authorities, and the public at large.

The medical and legal causality of death, the determination of the role played by the victim in the accident, the responsibility of the victim in initiating the accident, the estimation of the postaccident survival incurring legal compensation for pain and suffering and problems of survivorship related to inheritance, are only some of the more important motives in the medicolegal potpourri of traffic accidents.

Obviously, the pivotal medicolegal problem is the determination of the causality of death: did the demise occur before or after the accident, and is any causal relationship present between the traffic accident and the death?

TABLE I

Comparison between the medical and legal approaches to causality of death

Medical view Legal view

Immediate or basic cause of death Causes of death Precise scientific cause of death Key role of pre-existing disease

Proximate cause of death Legally effective cause of death Probable cause of death Question of aggravation (not degree)

Adapted from E. L. Sagall, Trial, 5 (1969) 60.

Causality is a wondrous prism of endless facets, and the medical and legal viewpoints may be quite far apart (Table I). The medical emphasis of causality is more complex, implicating multiple effective factors and mecha- nisms, more rigid and strict in its requirements of undisputable proof, and aiming toward the understanding of pathogenetic processes culminating in death. The legal emphasis on causality [l] is more empirical and practical, focusing on the probable and legally effective cause of death, even if tan- gential in nature, and vies towards the determination of legal responsibility.

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The legally imposed certification of death resolves the issue by requiring the physician to list the medical cause(s) of death (e.g. pneumonia, sub- dural hematoma) and the legal cause of death or the manner of death (e.g. accident, homicide, natural).

The proper certification of death in general and in traffic associated fatalities in particular is, therefore, not only related to the medical compe- tence of the physician but also to his knowledge and understanding of the related medicolegal issues.

One may stress the obvious in mentioning that not every traffic associated fatality is accidental. Natural death, and even homicides and suicides have to be considered as possibilities [ 2, 31.

The following elements are to be considered in the determination of medical and legal causality of death: (i) autopsy findings; (ii) immediate circumstances of death, (iii) explicit or implicit mental intent of the victim and (iv) psychologic profile and pattern of the victim.

While implicit mental intent of the victim and his psychologic profile and pattern may be important in understanding the genesis of the accident [4, 51, their legal value is highly questionable. Legal demonstration and proof of these elements is extremely difficult and uncertain. Major determinants of medicolegal causality remain the autopsy findings and the factual reconstruc- tion of the accident.

CAUSATION IN IMMEDIATE TRAFFIC DEATHS

The forging of the causation chain between the autopsy findings and the traffic associated death is ‘only partly determined by the type, location, pattern, and severity of the injuries. The chronologic age of the pathologic process in relation to the postaccident survival is also very important.

In most instances in which the death occurs immediately or very close to the time of the traffic accident, causality is relatively easily determined. Presence of severe blunt force injuries alone or in association with minor natural disease obviously affirms a traumatic cause of death (e.g. skull frac- tures, subdural hematoma, laceration of internal organs). The pattern of injuries and the circumstances of death will indicate if the manner of this traumatic death is really accidental or otherwise (homicide or suicide) [3,6]. On the other hand, presence of severe natural disease alone or in conjunction with insigificant trauma will indicate a natural manner of death.

Incidentally, minor and insignificant trauma are not synonymous entities. Minor trauma in an area of vital physiologic importance, such as the nervous centers of the brain or the conduction system of the heart, may well be significant and potentially fatal. One should also note that while the courts are not bound by, but usually respect, a well-grounded medical causality of death, they are quite contemptuous of the certification of the manner of death. The latter is considered to be, and not without reason, a personal and highly disputable medicolegal opinion. Quite often workmen’s compensation

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boards will recognize a clear sudden natural death at the wheel of a car as an accidental death related not to a vehicular accident per se, but to an unexpected or unusual occupational driving or traffic strain [6].

Real difficulties in the determination of causality of death arise mainly in the presence of concomitant moderate or severe, traumatic and natural conditions [7]. The following case is a common and representative illustra- tion of such a situation (ACCO A73-313).

A 52-year-old driver with no prior history of natural disease died in an unwitnessed collision with a tree. The accident occurred in the early morning, in good weather, on a well maintained, functional road. The autopsy revealed, in addition to severe head injuries and fractures of the extremities, an advanced degree of coronary arteriosclerosis with pinpoint lumina, and cardiac dilatation and hypertrophy. Toxicologic tests were negative.

Either the natural condition or the trauma by themselves were considered to be sufficient and satisfactory explanations for the death. It is conceivable that the cardiac condition was responsible for a sudden unexpected death preceding the accident [S, lo]. Equally possible is the assumption that the cardiac condition could have led to sudden unconsciousness, with subsequent loss of car control and the fatal crash.

However, even if loss of consciousness had actually occurred and had been witnessed by other car occupants prior to the crash, the death would still have to be certified as accidental. The reason for this approach is that in no way can we exclude the possibility that the potential fatal head injuries occurred in a living, though unconscious or comatose, individual. People having “heart attacks.” or for that matter, any natural condition leading to unconsciousness, do not invariably die and may recover with or without medical treatment. Therefore, with combined severe trauma and marked natural disease in very rapid traffic-related death, the manner of death should almost invariably be listed as accidental.

A similar line of reasoning should apply to trauma initiating, precipitating, or aggravating a severe natural disorder. The legal emphasis on causality as outlined previously is clearly concerned with the bare fact of aggravation and not its extent. “You take the victim as you find him” (at the time of the accident). This is the legal maxim of causation, and it is not an unreasonable one.

A fatal rupture of a weakened blood vessel, such as an anuerysm of the cerebral arteries or aorta, associated with a traffic accident, cannot be con- sidered a natural cause of death unless the topographic and circumstantial evidence of the accident together with the autopsy findings clearly eliminate any reasonably likelihood of substantial traumatic impact. Unquestionably, blood vessels weakened by pre-existing disease are capable of rupturing spontaneously. Nevertheless, they are more prone to disrupt with trauma even though it may be minor. Even evidence of previous bleeding from such a “leaky” vessel does not exclude the role of trauma in reactivating or aggravating the original hemorrhage.

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Minor trauma may be sufficient to result in death not only by affecting diseased organs but also, as previously mentioned, by affecting critical anatomic areas in the brain or heart.

A most difficult situation may occur in isolated cases in which the autopsy findings are minimal or absent, toxicologic analysis negative or non- contributory, and a pertinent medical history (such as diabetes or epilepsy) lacking or unavailable.

The danger in such cases is that instead of recognizing the diagnostic failure, the pathologist may be tempted to overcome his frustrations by either: arbitrarily assigning the death to an insignificant pathologic finding with impressive title but little weight (such as coronary arteriosclerosis even if minimal); incorrectly labeling and, thereby, upgrading a minor degree of disability or disease to the rank of moderate; or by assigning the death to some pathologically undetectable, unprovable, or hazy, physiologic mecha- nism (e.g. central hypoxia, cardiac arrest, concussion).

This approach is very unfortunate and objectionable on more than moral grounds. These cases are prime candidates for pitfalls in the determination of medicolegal causation and, therefore, should be subjected to extremely careful and intelligent analysis within the complex pattern of the whole circumstantial and psychiatric data.

CAUSATION IN DELAYED TRAFFIC DEATH

Causal relationship in delayed traffic death can be successfully proved, both medically and legally by a continuous chain of symptomatology from the accident to death (so-called “bridging symptoms”), and morphologic proof that the changes of natural disease complicating the trauma can be traced to the time of the accident. The courts and allied quasijudicial bodies have consistently accepted such criteria, and in particular the bridging symptomatology, as reasonable and valid indices of causality [ 131. On this basis, the courts have not hesitated to recognize as a fatal accident product, mental anguish or suffering, precipitating or aggravating a cardiac organic condition, a psychosomatic disease, or a catastrophic mental illness.

However, problems do exist in cases of delayed traffic death in deter- mining the relationship between the terminal cause of death (usually a natural disease complication) and the original trauma [ll, 121. These problems increase considerably with the lengthening of the postaccident survival period. The most common causes of these problems are: (i) delayed symptomatology, (ii) intervening medical treatment, and (iii) intervening trauma.

When natural complications of traumatic traffic injury lack the continuity element and are both silent in nature and delayed in time, the causal relationship between the terminal complication and the accident can be demonstrated only through the ageing of the natural disease process as men- tioned above. The following case represents a proper illustration of such

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silent and delayed symptomatology, clearly related to the original trauma (ACCO A73-681 cv.f.).

A 4%year-old white male was involved in a two-car accident, when hit head-on by an oncoming driver crossing the center line. The patient was admitted to a local hospital with a fracture of the right patella which involved internal fixation and casting. He was released a week later in good condition. Two weeks after the accident, the patient suddenly developed severe back pain. He was immediately taken to another hospital, where he developed ventricular fibrillation and expired within minutes. An external examination revealed a well-developed individual with a properly healing surgical incision of the right knee. Internal examination disclosed major pulmonary thromboembolism and phlebothrombosis of the deep veins of the right calf. No other significant pathology was evident. The location of the phlebothrombosis and the age of the thrombi clearly indicated that the pulmonary embolism was a delayed complication of the vehicular trauma to the right knee.

The causal relationship between vehicular accidental trauma and delayed death can be severed only by unrelated and independent injurious agents. Blatantly negligent medical treatment, idiosyncracy or adverse side effects to medication for unrelated disease, nontraumatic degenerative disease, and coincidental superimposed trauma (falls, electrocution, drowning, etc. ) leading to death are a few examples of intervening factors severing the causal chain with the original traffic accident.

PITFALLS IN THE DETERMINATION OF CAUSATION OF TRAFFIC ASSOCIATED

DEATHS

Incorrect determination of the causation of traffic associated deaths [14, 151 may result from: (i) faulty reconstruction of accident; (ii) incomplete gross autopsy; (iii) misinterpretation of patterns of injury; (iv) incomplete microscopic examination; (v) improper aging of injuries; and (vi) incomplete toxicological examination.

An incomplete autopsy is obviously a common source of pitfalls in the medicolegal evaluation of causation. The posterior area of the neck includes important organs, such as the upper cervical cord with its vital functional centers. Many deep injuries of the posterior neck are possible in vehicular accidents: (i) hemorrhages in the atlanto-occipital joints; (ii) fractures of the atlanto-occipital joints; (iii) extensive muscular hemorrhage; (iv) epidural or subdural spinal cord hemorrhage; and (v) contusions and lacerations of upper cervical cord.

Severe trauma with extensive contusion hemorrhages may occur in the depth of the back of the neck as a result of sudden overstretching forces with no apparent injury to the overlying skin. The usual anterior surgical approach at the autopsy may, therefore, completely miss such significant lesions. Such deaths may be easily mislabeled as natural or assigned to minor or insignificant findings.

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Microscopic examination of the tissues is also essential in assigning proper medicolegal causation. Autopsies of traffic fatalities often lack microscopic examination; as a result, major but discrete or subtle natural diseases, such as myocarditis, or omnious complications of trauma, such as fat embolism, may again be completely missed, and the manner of death misdiagnosed.

Complete toxicologic analysis is also a crucial element in this context, and not only in relation to the well-known and publicized role of alcohol [6]. Carbon monoxide exhaust gas may seep into the compartment of faulty vehicles, and precipitate a fatal accident or an apparent natural death [ 17, 181. Unfortunately, in some places, the toxicologic analysis is limited to alcohol levels alone, and carbon monoxide determinations are done sporadically or in drivers alone. It should be made clear that negative or low carbon monoxide in one occupant of the car does not preclude low level carbon monoxide poisoning in another occupant more susceptible to death by virtue of pre-existing natural disease (such as coronary arteriosclerosis, chronic lung disease, etc.).

CONCLUSION

The major problems of medical and legal causation in traffic associated fatalities have been reviewed, and the possible pitfalls in relating causation emphasized.

In conclusion, the determination and evaluation of causality in vehicular traffic deaths may be a very complex process, requiring special skills and thorough understanding of medicolegal issues. Proper determination of medicolegal causality is crucial to the financial, legal, and medical interests of many individuals and social groups.

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