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A Review of Postmortem Examinations in Combat Casualties

Medical Science Publication No. 4, Volume 1

THURSDAY MORNING SESSION
22 April 1954

MODERATOR
LIEUTENANT COLONEL GEORGE J. HAYES, MC


A REVIEW OF POSTMORTEM EXAMINATIONS IN COMBAT CASUALTIES*

FIRST LIEUTENANT JOSEPH G. STRAWITZ, MC

During a 10-month period in 1952 and 1953 a pathologist was assigned to the Surgical Research Team of Korea operating at the 46th Army Surgical Hospital. His mission was to supplement research activities of the team with information gleaned from postmortem examinations performed on victims of traumatic death previously treated at the hospital. Autopsies were also done routinely when death resulted from vehicular accidents, burns, medical causes and suicide.

This report deals only with 35 cases in which death followed treatment of wounds received in combat. Analyses of other traumatic deaths are deleted in an effort to bring emphasis to those cases which pose the greatest problems in management. Because of the relatively small number of cases presented, statistical significance cannot be attached to them. However, definite trends can be observed and some generalizations made.

The large majority of casualties were examined by the same prosector. Microscopic review and interpretation were carried out by several members of the Pathology Department of the 406th Medical General Laboratory. Clinical histories were recorded in great detail and frequently the prosector had observed the clinical course of the patient prior to death. Consequently, considerable consistency in examination and interpretation was possible.

Results

Table 1 lists the causes of death in 35 combat casualties. There is considerable overlap between the first three groups-irreversible shock, vital organ damage, and uncontrolled hemorrhage. Some cases with vital organ damage and others with uncontrolled hemorrhage showed changes consistent with those seen in irreversible shock. On the other hand, in a few cases classified as irreversible shock the patients exhibited uncontrolled hemorrhage during some period of their clinical course. Despite this overlap, the single major cause of death


*Presented 22 April 1954, to the Course on Recent Advances in Medicine and Surgery, Army Medical Service Graduate School, Walter Reed Army Medical Center, Washington, D. C.


378

Table 1. Causes of Death in 35 Combat Casualties

Cause of death

Number of cases

Irreversible shock

11

Vital organ damage

9

Uncontrolled hemorrhage

6

Bronchial obstruction

2

Cardiac standstill

1

Myocardial infarction
(traumatic coronary thrombosis).

1

Blast injury (lungs)

1

Fat embolism (cerebral)

1

Uremia (lower nephron nephrosis)

1

Subdural hematoma

1

Cause undetermined

1

35

was determined by considering all factors. The causes of death in the remaining cases were quite specific.

Irreversible Shock. Over the years there has been a great deal of controversy regarding the disturbed state of physiology called irreversible shock. Some investigators have even denied that such a syndrome exists. Recent thinking on the problem has implicated a number of etiologic possibilities. Hypoxia, bacterial invasion, tissue breakdown, psychological stress and other factors have been considered. They are difficult to evaluate in any single case since their nature is not well understood and methods of measurement have not as yet been developed. A complex etiology is suspected in this series, since survival was observed in other cases with equal and greater degrees of tissue destruction and organ damage.

Experiments subjecting dogs to prolonged periods of hypotension have shown that death ensues despite adequate blood volume replacement. Although the period of hypotension required to produce death in humans is not known, there must be a time limit from which there is no return to normal.

Table 2 shows median values for the evacuation time, survival time and blood volume replacement in 11 cases of irreversible shock. On the basis of the prolonged period of hypotension, the severe state of clinical shock and the marked degree of tissue destruction displayed in most instances, the clinical diagnosis of irreversible shock was made.

Table 2. Median Values, Evacuation Time, Survival Time, and Blood Volume Replacement in 11 Cases of Irreversible Shock

Evacuation time, wounding to MASH

Survival time, wounding to death

Total blood volume replacement

4 hours, 45 minutes

17.5 hours

9.5 liters


379

Table 3 shows a tabulation of morphologic findings occurring in various combinations in irreversible shock. Petechial hemorrhages involving serous surfaces and mucous membranes are commonly thought to result from prolonged hypoxemia. Subendocardial hemorrhages are not infrequently seen and are peculiarly limited to the right side of the heart, as in the medical shock of hemorrhagic fever. The many differences in anatomy and physiology between left and right sides of the heart have been seized upon to explain this peculiar localization of hemorrhages. No positive explanation is available to date.

Table 3. Morphologic Changes in Irreversible Shock

1. Petechial hemorrhages-Serosal, mucosal (gastrointestinal).
2. Dilatation and engorgement-Vessels in abdominal and thoracic viscera, brain, striated muscle.
3. Pulmonary edema.
4. Pulmonary atelectasis-Focal and diffuse.
5. Dilatation of cardiac chambers with flabbiness of the myocardium.
6. Renal tubular changes consistent with lower nephron nephrosis (microscopic).
7. Lipoid depletion-Adrenal cortical cells (microscopic).
8. Fatty vacuolization-Heart muscle, liver, kidney (microscopic).

Intense congestion of all organs and striated muscle was a consistent finding. On section of lungs, liver, spleen or kidneys, fluid blood virtually poured out.

Microscopic examination confirmed the severe dilatation and congestion of all blood vessels. It is not surprising that large quantities of blood were used in attempts to maintain adequate arterial pressures in such expanded vascular trees.

Table 4 shows various degrees of pulmonary edema in 11 cases of irreversible shock. The majority show some degree and over half exhibited marked edema. The average blood volume replacement is shown with each grade of edema. There appears to be more edema in those patients most vigorously resuscitated. It must again be emphasized that these cases represent a very small sampling and should be evaluated in this light.

Table 4. Degrees of Pulmonary Edema Compared to Blood Volume Replacement in Cases of Irreversible Shock

Degree of pulmonary edema

Number of cases

Average blood volume replacement

No edema (below 500 grams)

1

2.0 liters

Slight (500-700 grams)

3

4.8 liters

Moderate (700-900 grams)

1

12.0 liters

Marked (900 grams plus)

6

13.0 liters


380

In classical descriptions, it has been suggested that pulmonary edema is a constant and integral part of the shock mechanism. Several factors may influence its development. It is certainly a common complication of renal insufficiency which frequently accompanies shock. Cardiac failure, as evidenced by gross flabbiness of the myocardium, dilatation of cardiac chambers and microscopic fatty degeneration of myocardial fibers, must play a considerable role in the formation of pulmonary edema. In a review of a large number of traumatic deaths, fat embolism has been shown not to predispose to this complication. It is difficult to assess the importance of overenthusiastic intravenous therapy.

Varying amounts of pulmonary atelectasis were seen in many cases of irreversible shock. In some cases, patchy areas were seen, while in others the greater part of a single lobe might be involved; this was usually basilar in distribution. These pulmonary findings may very well have represented agonal changes frequently seen in patients subjected to anesthesia, etc. In one case of the eleven, diffuse atelectasis was thought to be one of the principal factors causing death.

Congestion of striated muscle is listed as a morphologic finding in irreversible shock. This is particularly true of patients strenuously resuscitated with whole blood and fluids. Striated muscle composes a large part of the human body but is not often seriously considered at the postmortem table because of its somewhat hidden anatomical location. Yet a great part of the vascular tree is found in these large masses of muscle. The 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 failure is a universal finding in irreversible shock. The principal morphologic findings consist of heme casts within tubules and varying degrees of degeneration of the tubular epithelium. In larger series of cases these changes are found to occur after the first 24 hours of shock. In this series, all showed marked renal insufficiency during the clinical courses. Four of 11 cases showed morphologic changes consistent with lower nephron nephrosis. The remaining cases might have exhibited these changes had the time of survival been longer than the average 17.5 hours.

Dr. Tracy Mallory, in studying postmortem material from shocked patients during World War II, found a peculiar morphologic change in the viscera when the survival time was over 18 hours. With special stains, fat vacuolization was demonstrated in the heart, the central cells of liver lobules and the ascending limbs of Henle's loops. In the adrenal gland the doubly refractile lipid became depleted after the same time interval. From the fourth day onward in cases not com-


381

plicated by infection, a tendency to a return to normal could be demonstrated. Special stains were not carried out in cases presented in this report. However, Dr. Mallory's finding is an important morphologic demonstration of an intracellular response to injury produced by shock.

Vital Organ Damage. Nine patients died of vital organ damage not compatible with life. Seven showed extensive brain damage and two had direct cardiac involvement by shell fragments. The majority of patients survived for some hours.

Uncontrolled Hemorrhage

Table 5 shows a summary of six patients whose deaths were attributed to uncontrolled hemorrhage. All showed profuse bleeding from lacerated, large vascular channels. It appears in most cases that if adequate control of profuse hemorrhage had been possible early, death may not have occurred. The average evacuation time from wounding to hospital admission is considerably shorter than that seen in irreversible shock. Pulmonary edema is a less frequent finding.

Table 5. Summary of Six Cases of Uncontrolled Hemorrhage

Case No.

Evacuation time wounding to MASH (hours)

Total blood vol. replacement (liters)

Pulmonary edema

Site of bleeding

Survival time (hours)

1

51/2

10.5

None

Laceration of pulmonary vessels.

113/4

2

3

0

None

Splenic rupture, laceration of lung.

3

3

21/2

Total unknown
3.5.

None

Lacerated kidney, retroperitoneal and peritoneal hemorrhage.

18

4

4

18

None

Lacerated vena cava

17

5

1

6.5

Moderate

Lacerated dural vessels.

41/2

6

11/2

9.5

Moderate

Lacerated mesenteric vessels.

31/2


Average


2. 9


8.5


-----


-----


9. 6

Bronchial Obstruction. An open airway is always a primary consideration in surgical cases in both military and civilian life. Two patients in this series died of bronchial obstruction. A simple amputation of a lower extremity was performed in one case with excellent chance of recovery. Aspiration of vomitus 15 minutes postoperatively was the cause of death. The remaining patient suffered a perforating gunshot wound of the lung with bleeding into the bronchial


382

tree and obstruction. This patient died shortly after hospital admission.

Cardiac Standstill. Cardiac standstill is a physiologic death which ordinarily is unaccompanied by morphologic changes. One patient with multiple avulsive and puncture wounds of all extremities died during surgery. Cardiac massage was performed without benefit. A moderate number of fat emboli were seen microscopically in small myocardial blood vessels. It is not known what influence they may have had on cardiac function.

Myocardial Infarction (Traumatic Coronary Thrombosis). The one case of myocardial infarction resulting from coronary thrombosis was a surprising finding. The patient, who suffered a puncture wound of the left lung from small arms fire, showed progressive cardiac failure during surgery. At autopsy, an antemortem thrombus was found in the lumen of the circumflex branch of the left coronary artery. Microscopically the myocardium exhibited degenerative changes. Although there was no myocardial laceration in the region of the left coronary artery, diffuse subepicardial and perivascular hemorrhages 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 as a complication of trauma and fractures for many years. Different investigators have ascribed varying importance to it as a death-producing clinical entity. Captain Robert E. Scully has reviewed a large number of battle casualty autopsies and has shown that fat is found in the lungs in over 90 percent of cases and is occasionally seen in the kidneys (1). Cases of death resulting from fat embolism were rare in his review. The criteria for establishing fat embolism as a cause of death are a typical clinical history with neurologic findings and the presence of a moderate to marked degree of fat in the vessels of the lung, kidney and brain. Perivascular hemorrhages and necrosis in the brain are the usual findings in fatal cases.

The one fatal case of fat embolism in this series was classical. The patient suffered traumatic amputations of several extremities and numerous avulsive and puncture wounds. Preoperative resuscitation and surgery were uneventful. However, recovery from anesthesia was not complete and intracranial hemorrhage was suspected when the patient remained unconscious and displayed muscular twitchings. A craniotomy was negative. The patient died several days after wounding and postmortem examination revealed the typical morphologic findings of fatal fat embolism.

Blast Injury. In World Wars I and II injuries to the thoracic and abdominal viscera and to the central nervous system were observed


383

to occur as the result of rapid changes in the environmental pressure from air blast. When persons are exposed to the effects of nearby shell and mortar explosions, death may occur with minimal evidence of external injury. Hemorrhages and lacerations of the lungs, abdominal viscera or brain may occur. One patient in this series was close to an exploding mortar round and showed severe pulmonary hemorrhage, congestion, contusion and edema without perforation of the thorax. This patient was admitted to the hospital but died shortly afterwards with severe respiratory distress and hypoxia. A large shell fragment was found in the region of the left kidney.

Lower Nephron Nephrosis. One case of marked renal insufficiency resulting from a penetrating abdominal wound with multiple perforations of the small intestines was seen in this series. The patient died 6 days post-wounding in uremia. 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 found at autopsy.

Subdural Hematoma. One patient had a subdural hematoma as a complication of a skull fracture. A very large subdural blood clot was evacuated. The patient died shortly thereafter with signs of increased intracranial pressure.

Cause Undetermined. In the one case in which a cause of death could not be established, the patient suffered a gunshot wound of the abdomen with laceration of the tail of the pancreas. The postoperative course was uneventful and the patient was ambulatory. He suddenly developed severe respiratory distress on the sixth postoperative day and died 12 hours later in vascular collapse. The clinical history was suggestive of pulmonary embolism, but the autopsy did not confirm this diagnosis. There were no significant findings to suggest a cause of death.

Summary

An analysis of 35 postmortem examinations in combat casualties dying relatively soon after wounding is presented. Irreversible shock, vital organ damage and uncontrolled hemorrhage constitute the major causes of death. Bronchial obstruction, cardiac standstill, traumatic coronary thrombosis, blast injury and subdural hematoma were found less frequently. One case of lower nephron nephrosis is described in a patient who died 6 days post-wounding. Although fat embolism is found frequently in the lungs of victims of traumatic death, it rarely is the principal factor causing death.

Reference

Scully, R. E.: Fat Embolism in Wartime. (Awaiting publication.)