A Review of Postmortem Examinations in Combat Casualties*
1st Lieutenant Joseph G. Strawitz, MC, USAR
Captain Robert E. Scully, MC,USAR
Captain Austin Vickery, MC, USAR
Captain John M. Howard, MC, USAR
Because of the clinical responsibilities of medical officers in a combat theater, complete postmortem examinations have seldom been routine. Pathologists are rarely available at a surgical hospital and frequently facilities for postmortem study are not available. Although it is obvious that combat casualties die from wounds received in action, the mechanisms of death are not clear.
During a 10-month period in 1952 and 1953, autopsies were performed routinely by the Surgical Research Team in Korea at the 46th Surgical Hospital on the eastern front. Deaths were investigated which resulted from wounds received in combat, vehicular accidents, burns, medical illnesses, and self-inflicted injuries.
This report deals only with 35 patients who died in the hospital after being wounded in combat. Analyses of the other traumatic deaths have been deleted in an effort to emphasize the problems encountered in treating the combat casualty. Because of the relatively small number of autopsies presented, statistical significance cannot be ascertained; however, definite trends can be observed and some generalizations can be made.
Most of the autopsies were performed by the same prosector. Clinical histories were recorded in considerable detail and frequently the prosector had observed the clinical course of the patient prior to death. Therefore, it was possible to be consistent in both the examination and the interpretation of results. Microscopic review was carried out by several members of the Pathology Department of the 406th Medical General Laboratory.
Table 1 summarizes the causes of death in 35 combat casualties. There is considerable overlapping between the first three groups: irreversible shock, vital organ damage, and uncontrolled hemorrhage. Some patients having vital organ damage and others having uncon-
*Previously published in Archives of Surgery 70: 260, 1955.
trolled hemorrhage showed changes consistent with those seen in irreversible shock. On the other hand, a few classified as irreversible shock exhibited uncontrolled hemorrhage during some period of their clinical course. Despite this overlapping, the chief cause of death, as determined by evaluating all known factors, formed the basis of this classification. The causes of death in the remaining patients were quite definite.
Table1. Causes of Death in 35 Combat Casualties
The clinician attending six of these patients observed that hemorrhage had been controlled. After operation, however, the patients remained refractory to massive transfusions. These six patients died in a state of unreversed, recurrent shock.
An additional five patients-after prolonged, profound shock- demonstrated a gradual response to transfusion, but died shortly thereafter. The histologic picture in these two groups was similar. Although the clinical course of the latter five patients was not marked by as profound a terminal hypotension as the first group, the autopsy findings suggested that death was due to irreversible ischemic changes secondary to the initial shock.
Table 2 gives the mean for the evacuation time, survival time, and blood-volume replacement in the 11 patients having irreversible shock.
The morphologic changes in irreversible shock which were found in various combinations were: (1) petechial hemorrhages-serosal, mucosal gastrointestinal); (2) dilation and engorgement-vessels in abdominal and thoracic viscera, brain, striated muscle; (3) pul-
Table2. Mean of Evacuation Time, Survival Time, and Blood-Volume Replacement in Eleven Patients Having Irreversible Shock
monary edema; (4) pulmonary atelectasis-focal and diffuse; (5) dilatation of cardiac chambers with flabbiness of the myocardium; (6) renal tubular changes consistent with post-traumatic renal insufficiency (microscopic); (7) lipoid depletion-adrenal cortical cells (microscopic); and (8) fatty vacuolization-heart muscle, liver, kidney (microscopic).
Petechial hemorrhage involving serous surfaces and mucous membranes were frequent and were believed to be the result of prolonged hypoxemia. Subendocardial hemorrhages were often seen, being peculiarly limited to the right side of the heart. This distribution was also noted in patients who died of hemorrhagic fever. It may be that the differences in anatomy and physiology between the left and right heart explain this peculiar localization of hemorrhages; but to date no positive evidence is available.
A consistent finding was intense congestion of all organs and striated muscles. Fluid blood virtually poured out from the cut surface of the lungs, liver, spleen, and kidneys.
Microscopic examination confirmed the severe dilation and congestion of all blood vessels. The large quantity of blood transfused presumably was needed to maintain an adequate arterial pressure because of an expanded vascular tree.
Table 3 shows various degrees of pulmonary edema in the patients having irreversible shock. The majority of these patients demon-
Table3. Degree of Pulmonary Edema as Compared with Blood-Volume Replacement in Patients Having Irreversible Shock
strated some degree of edema, and over half exhibited marked edema. There appeared to be more edema in those patients who were most vigorously resuscitated. It must be emphasized again that these patients represent a very small sampling and that most patients requiring large transfusions survived.
It has been suggested that pulmonary edema is a constant and integral part of the pathogenesis of shock.1 Several factors may influence its development. The present study suggests that it follows shock and transfusion rather than ischemia alone. It is a frequent complication of post-traumatic renal insufficiency following shock. Cardiac failure must play a considerable role in the formation of pulmonary edema, as evidenced by gross flabbiness of the myocardium, dilatation of cardiac chambers, and fatty degeneration of myocardial fibers. In a review of a large number of traumatic deaths,2 fat embolism did not predispose to this complication.
Varying amounts of pulmonary atelectasis were seen in several patients having irreversible shock. In some lungs, the areas of atelectasis were patchy, while in others the greater part of a single lobe was involved; this was usually basilar in distribution. These pulmonary findings may have represented agonal changes. In one of the 11 patients, diffuse atelectasis was thought to be principal factor contributing to the fatality.
Congestion of striated muscle is listed as a morphologic finding in irreversible shock. This is particularly true of casualties resuscitated with a considerable amount of whole blood and fluids. Striated muscle composes a large part of the human body; but it is seldom studied at the postmortem table. A great part of the vascular tree, however, is found in these large masses of muscle. A typical finding in examining large, avulsive wounds was severe congestion with outpouring of blood and fluids at autopsy incision. Further studies are necessary to correlate this observation with the theory of blood sludging and pooling.
Renal damage was a frequent finding in irreversible shock. The principal morphologic changes consisted of heme casts within tubules and varying degrees of degeneration of the tubular epithelium. These changes, when present in a larger series of patients, were found to be demonstrable after the first 24 hours of shock.3 In the present study, each patient demonstrated a decrease in renal function clinically; however, this condition might have been on a functional rather than on an organic basis. Four of the 11 patients showed morphologic changes consistent with post-traumatic renal insufficiency. The remaining patients might also have exhibited these changes if they had survived longer than the mean of 17.5 hours.
In studying postmortem material from shocked patients during World War II, Mallory found a peculiar morphologic change in the viscera when the survival time was over 18 hours.3 With special stains, fat vacuolization was demonstrated in the heart, the central cells of hepatic lobules, and the ascending limbs of Henle`s loops. The doubly refractile lipid became depleted in the adrenal gland after the same time interval. From the fourth day onward, a tendency to a return to normal could be demonstrated in patients with wounds not complicated by infection.
Special stains were not performed in patients presented in this report. However, Mallory`s finding is another morphologic demonstration of an intracellular response to injury and shock.
Vital Organ Damage. Nine patients died of damage to vital organs to a degree incompatible with life. Seven showed extensive brain damage, and two had direct cardiac involvement by shell fragments. The majority of these patients survived for several hours.
Uncontrolled Hemorrhage. Table 4 gives information concerning six patients whose deaths were attributed to uncontrolled hemorrhage. All showed profuse bleeding from lacerated, large vascular channels. It appeared in most instances that, if early control of profuse hemorrhage could have been achieved, death might have been prevented. The average evacuation time from injury to admission to a hospital was considerably shorter than that seen in irreversible shock. Pulmonary edema was found less frequently.
Bronchial Obstruction. Two patients died of bronchial obstruction. One patient had a simple amputation of a lower extremity which was technically uncomplicated. He died 15 minutes following operation due to aspiration of vomitus. The second patient suffered a perforating wound of the lung with bleeding into the bronchial tree. Obstruction and death occurred shortly after admission.
Cardiac Arrest. One patient with multiple avulsive and perforating wounds of all extremities expired unexpectedly during operation. Cardiac massage was performed, but without benefit. A moderate number of fat emboli were visible microscopically in small myocardial blood vessels. it is not known what influence they may have had on cardiac function.
Myocardial Infarction (Traumatic Coronary Thrombosis). In one patient, myocardial infarction resulting from coronary thrombosis was a surprising finding. Following a wound of the left lung from small arms fire, this patient developed progressive cardiac failure during operation. At autopsy, an ante-mortem thrombus was found in the lumen of the circumflex branch of the left coronary artery. Histologically, the myocardium exhibited degenerative changes. Although there was no myocardial laceration in the region of the left coronary artery, diffuse subepicardial and perivascular hemorrhages
Table4. Patients Having Uncontrolled Hemorrhage
suggested that contusion and arteritis may have occurred from the marked pressure changes when the missile passed through the thorax.
Fat Embolism. Fat embolism has been recognized for many years as a complication of trauma and fractures. Different investigators have ascribed varying degrees of importance to it as a clinical entity. Scully showed that fat emboli were present in the lungs in over 90 percent of the men dying of battle wounds. Occasionally emboli were found in the kidneys. Death resulting from fat embolism was infrequent in his review.2
The criteria for establishing fat embolism as a cause of death are a typical clinical history, abnormal neurologic findings, and the presence of a moderate to a marked degree of fat in the vessels of the lung, kidney, and brain. Parivascular hemorrhages and necrosis in the brain are the usual findings in fatal instances.
The one fatality due to fat embolism presented a classical picture. The patient suffered traumatic amputations of several extremities and numerous avulsive and puncture wounds. Preoperative resuscitation and surgery were uneventful. Recovery, however, from anesthesia was not complete and intracranial hemorrhage was suspected as the patient remained unconscious and displayed muscular twitchings. A craniotomy showed no evidence of hemorrhage. Death ensued several days after injury. Postmortem examination revealed the typical morphologic findings of fatal fat embolism.
Blast Injury. In World War I and World War II, it was observed that injuries to the thoracic and abdominal viscera and to the central nervous system resulted from rapid changes in the environmental pressure, for instance, from an air blast.4 When persons are exposed to the effects of nearby shell or mortar explosions, death may occur with minimal evidence of external injury. Hemorrhages and lacerations may occur in the lungs, abdominal viscera, or brain. One patient in this series was close to an exploding mortar round and died shortly afterwards in severe respiratory distress with hypoxia. Autopsy showed that he had severe pulmonary hemorrhage, congestion, contusion, and edema without perforation of the thorax. A large shell fragment was found in the region of the left kidney.
Post-traumatic Renal Insufficiency. One patient having marked renal insufficiency resulting from multiple perforations of the small intestine was included in this series. The patient died from uremia 6 days following injury. The morphologic findings were compatible with severe, lower nephron nephrosis. There were numerous heme casts in renal tubules and marked degeneration of the tubular epithelium. A fibrinopurulent peritonitis was also present.
Subdural Hematoma. In one instance, a subdural hematoma resulted as a complication of a skull
fracture. A large subdural blood
clot was removed. Death followed shortly thereafter from increased intracranial pressure.
Cause Undetermined. The one patient in whom a cause of death could not be determined suffered a gunshot wound of the abdomen with a laceration of the tail of the pancreas. His postoperative course seemed uneventful and he was ambulated early. On the sixth postoperative day, he suddenly developed severe respiratory distress and died 12 hours later in vascular collapse. The clinical history was suggestive of pulmonary embolism, but the autopsy did not confirm the diagnosis. There were no significant findings to establish the cause of death.
An analysis was made of 35 postmortem examinations in combat casualties dying a short time after injury. Irreversible shock, vital organ damage, and uncontrolled hemorrhage constituted the major causes of death. Bronchial obstruction, cardiac arrest, traumatic coronary thrombosis, blast injury, and subdural hematoma were found less frequently. Although fat embolism was found frequently in the lungs following traumatic death, it appeared to be the principal factor causing death in only one patient. Post-traumatic renal insufficiency was the cause of death in only one patient in this series, as patients with this complication were evacuated to another hospital for treatment.
1. Moon, V. H.: Shock: Its Mechanism and Pathology. Arch. Path. 24: 642 and 794, 1937.
2. Scully, Robert E.: Fat Embolism in Korean Battle Casualties: An Analysis of Its Incidence, Clinical Significance, and Pathologic Aspects. (Chapter 22 of this volume.)
3. Mallory, Tracy B.: The Physiologic Effects of Wounds: Surgery in World War II. (Chairman of the Board, Henry K. Beecher, Editor.) The Board for the Study of the Severely Wounded, North African-Mediterranean Theater of Operations. Office of The Surgeon General, Department of the Army, Washington, D. C., 1952.
4. Zuckerman, S.: Experimental Study of Blast Injuries to Lungs. Lancet 2: 219, 1940.