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Medical Science Publication No. 4, Volume 1

22 April 1954




During a 10-month period in 1952 and 1953 a pathologist was assignedto the Surgical Research Team of Korea operating at the 46th Army SurgicalHospital. His mission was to supplement research activities of the teamwith information gleaned from postmortem examinations performed on victimsof traumatic death previously treated at the hospital. Autopsies were alsodone routinely when death resulted from vehicular accidents, burns, medicalcauses and suicide.

This report deals only with 35 cases in which death followed treatmentof wounds received in combat. Analyses of other traumatic deaths are deletedin an effort to bring emphasis to those cases which pose the greatest problemsin management. Because of the relatively small number of cases presented,statistical significance cannot be attached to them. However, definitetrends 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 membersof the Pathology Department of the 406th Medical General Laboratory. Clinicalhistories were recorded in great detail and frequently the prosector hadobserved the clinical course of the patient prior to death. Consequently,considerable consistency in examination and interpretation was possible.


Table 1 lists the causes of death in 35 combat casualties. There isconsiderable overlap between the first three groups-irreversible shock,vital organ damage, and uncontrolled hemorrhage. Some cases with vitalorgan damage and others with uncontrolled hemorrhage showed changes consistentwith those seen in irreversible shock. On the other hand, in a few casesclassified as irreversible shock the patients exhibited uncontrolled hemorrhageduring some period of their clinical course. Despite this overlap, thesingle 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.


Table 1. Causes of Death in 35 Combat Casualties

Cause of death

Number of cases

Irreversible shock


Vital organ damage


Uncontrolled hemorrhage


Bronchial obstruction


Cardiac standstill


Myocardial infarction
(traumatic coronary thrombosis).


Blast injury (lungs)


Fat embolism (cerebral)


Uremia (lower nephron nephrosis)


Subdural hematoma


Cause undetermined



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

Irreversible Shock. Over the years there has been a great dealof controversy regarding the disturbed state of physiology called irreversibleshock. 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 andother factors have been considered. They are difficult to evaluate in anysingle case since their nature is not well understood and methods of measurementhave not as yet been developed. A complex etiology is suspected in thisseries, since survival was observed in other cases with equal and greaterdegrees of tissue destruction and organ damage.

Experiments subjecting dogs to prolonged periods of hypotension haveshown that death ensues despite adequate blood volume replacement. Althoughthe 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 andblood volume replacement in 11 cases of irreversible shock. On the basisof the prolonged period of hypotension, the severe state of clinical shockand the marked degree of tissue destruction displayed in most instances,the clinical diagnosis of irreversible shock was made.

Table 2. Median Values, Evacuation Time, SurvivalTime, 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


Table 3 shows a tabulation of morphologic findings occurring in variouscombinations in irreversible shock. Petechial hemorrhages involving seroussurfaces and mucous membranes are commonly thought to result from prolongedhypoxemia. Subendocardial hemorrhages are not infrequently seen and arepeculiarly limited to the right side of the heart, as in the medical shockof hemorrhagic fever. The many differences in anatomy and physiology betweenleft and right sides of the heart have been seized upon to explain thispeculiar localization of hemorrhages. No positive explanation is availableto date.

Table 3. Morphologic Changes in IrreversibleShock

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 consistentfinding. On section of lungs, liver, spleen or kidneys, fluid blood virtuallypoured out.

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

Table 4 shows various degrees of pulmonary edema in 11 cases of irreversibleshock. 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 samplingand should be evaluated in this light.

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

Degree of pulmonary edema

Number of cases

Average blood volume replacement

No edema (below 500 grams)


2.0 liters

Slight (500-700 grams)


4.8 liters

Moderate (700-900 grams)


12.0 liters

Marked (900 grams plus)


13.0 liters


In classical descriptions, it has been suggested that pulmonary edemais a constant and integral part of the shock mechanism. Several factorsmay influence its development. It is certainly a common complication ofrenal insufficiency which frequently accompanies shock. Cardiac failure,as evidenced by gross flabbiness of the myocardium, dilatation of cardiacchambers and microscopic fatty degeneration of myocardial fibers, mustplay a considerable role in the formation of pulmonary edema. In a reviewof a large number of traumatic deaths, fat embolism has been shown notto predispose to this complication. It is difficult to assess the importanceof overenthusiastic intravenous therapy.

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

Congestion of striated muscle is listed as a morphologic finding inirreversible shock. This is particularly true of patients strenuously resuscitatedwith whole blood and fluids. Striated muscle composes a large part of thehuman body but is not often seriously considered at the postmortem tablebecause of its somewhat hidden anatomical location. Yet a great part ofthe vascular tree is found in these large masses of muscle. The typicalfinding in examining large avulsive wounds was severe congestion with outpouringof blood and fluids at autopsy incision. Further studies are necessaryto correlate this observation with the theory of blood sludging and pooling.

Renal failure is a universal finding in irreversible shock. The principalmorphologic findings consist of heme casts within tubules and varying degreesof degeneration of the tubular epithelium. In larger series of cases thesechanges are found to occur after the first 24 hours of shock. In this series,all showed marked renal insufficiency during the clinical courses. Fourof 11 cases showed morphologic changes consistent with lower nephron nephrosis.The remaining cases might have exhibited these changes had the time ofsurvival been longer than the average 17.5 hours.

Dr. Tracy Mallory, in studying postmortem material from shocked patientsduring World War II, found a peculiar morphologic change in the viscerawhen the survival time was over 18 hours. With special stains, fat vacuolizationwas demonstrated in the heart, the central cells of liver lobules and theascending limbs of Henle's loops. In the adrenal gland the doubly refractilelipid became depleted after the same time interval. From the fourth dayonward in cases not com-


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 demonstrationof an intracellular response to injury produced by shock.

Vital Organ Damage. Nine patients died of vital organ damagenot compatible with life. Seven showed extensive brain damage and two haddirect cardiac involvement by shell fragments. The majority of patientssurvived for some hours.

Uncontrolled Hemorrhage

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

Table 5. Summary of Six Cases of UncontrolledHemorrhage

Case No.

Evacuation time wounding to MASH (hours)

Total blood vol. replacement (liters)

Pulmonary edema

Site of bleeding

Survival time (hours)





Laceration of pulmonary vessels.






Splenic rupture, laceration of lung.




Total unknown


Lacerated kidney, retroperitoneal and peritoneal hemorrhage.






Lacerated vena cava






Lacerated dural vessels.






Lacerated mesenteric vessels.



2. 9




9. 6

Bronchial Obstruction. An open airway is always a primary considerationin surgical cases in both military and civilian life. Two patients in thisseries died of bronchial obstruction. A simple amputation of a lower extremitywas performed in one case with excellent chance of recovery. Aspirationof vomitus 15 minutes postoperatively was the cause of death. The remainingpatient suffered a perforating gunshot wound of the lung with bleedinginto the bronchial


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

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

Myocardial Infarction (Traumatic Coronary Thrombosis). The onecase of myocardial infarction resulting from coronary thrombosis was asurprising finding. The patient, who suffered a puncture wound of the leftlung from small arms fire, showed progressive cardiac failure during surgery.At autopsy, an antemortem thrombus was found in the lumen of the circumflexbranch of the left coronary artery. Microscopically the myocardium exhibiteddegenerative changes. Although there was no myocardial laceration in theregion of the left coronary artery, diffuse subepicardial and perivascularhemorrhages suggested that contusion and arteritis may have occurred fromthe marked pressure changes when the missile passed through the thorax.

Fat Embolism. Fat embolism has been recognized as a complicationof trauma and fractures for many years. Different investigators have ascribedvarying importance to it as a death-producing clinical entity. CaptainRobert E. Scully has reviewed a large number of battle casualty autopsiesand has shown that fat is found in the lungs in over 90 percent of casesand is occasionally seen in the kidneys (1). Cases of death resultingfrom fat embolism were rare in his review. The criteria for establishingfat embolism as a cause of death are a typical clinical history with neurologicfindings and the presence of a moderate to marked degree of fat in thevessels of the lung, kidney and brain. Perivascular hemorrhages and necrosisin the brain are the usual findings in fatal cases.

The one fatal case of fat embolism in this series was classical. Thepatient suffered traumatic amputations of several extremities and numerousavulsive and puncture wounds. Preoperative resuscitation and surgery wereuneventful. However, recovery from anesthesia was not complete and intracranialhemorrhage was suspected when the patient remained unconscious and displayedmuscular twitchings. A craniotomy was negative. The patient died severaldays after wounding and postmortem examination revealed the typical morphologicfindings of fatal fat embolism.

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


to occur as the result of rapid changes in the environmental pressurefrom air blast. When persons are exposed to the effects of nearby shelland mortar explosions, death may occur with minimal evidence of externalinjury. Hemorrhages and lacerations of the lungs, abdominal viscera orbrain may occur. One patient in this series was close to an exploding mortarround and showed severe pulmonary hemorrhage, congestion, contusion andedema without perforation of the thorax. This patient was admitted to thehospital but died shortly afterwards with severe respiratory distress andhypoxia. A large shell fragment was found in the region of the left kidney.

Lower Nephron Nephrosis. One case of marked renal insufficiencyresulting from a penetrating abdominal wound with multiple perforationsof the small intestines was seen in this series. The patient died 6 dayspost-wounding in uremia. The morphologic findings were compatible withsevere lower nephron nephrosis. There were numerous heme casts in renaltubules and marked degeneration of the tubular epithelium. A fibrinopurulentperitonitis was found at autopsy.

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

Cause Undetermined. In the one case in which a cause of deathcould not be established, the patient suffered a gunshot wound of the abdomenwith laceration of the tail of the pancreas. The postoperative course wasuneventful and the patient was ambulatory. He suddenly developed severerespiratory distress on the sixth postoperative day and died 12 hours laterin vascular collapse. The clinical history was suggestive of pulmonaryembolism, but the autopsy did not confirm this diagnosis. There were nosignificant findings to suggest a cause of death.


An analysis of 35 postmortem examinations in combat casualties dyingrelatively soon after wounding is presented. Irreversible shock, vitalorgan damage and uncontrolled hemorrhage constitute the major causes ofdeath. Bronchial obstruction, cardiac standstill, traumatic coronary thrombosis,blast injury and subdural hematoma were found less frequently. One caseof 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 traumaticdeath, it rarely is the principal factor causing death.


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