CHAPTER IX
Shock Therapy (957 Casualties)
Beverly T. Towery, M. D., and John D. Welch, M. D.
From the standpoint of the therapy of traumatic shock,1soldiers with major wounds of the abdomen presented more serious problems thanany other group of casualties. There were a number of reasons:
1. Hemorrhage was frequently massive.
2. Contamination of the peritoneal cavity and retroperitoneal tissues carriedthe threat of fulminating infection.
3. Concomitant transdiaphragmatic injury of the thorax frequently causedserious disturbances of cardiopulmonary function.
4. These same injuriesrendered the pleura liable to contamination by gastrointestinal contents orbile.
5. Multiple visceral and vascular injuries, which werecommon, often created surgical problems of great technical difficulty, with theresult that the duration of anesthesia and operation was necessarily prolongedand further blood losses were likely to occur.
The problem of traumatic shock is considered in detailelsewhere in these volumes.2 Resuscitation therapy, however, played such animportant role in the management of casualties with abdominal injuries that itmust be discussed in some detail here. Furthermore, the important causes ofshock deserve careful consideration in relation to therapy and therapeuticfailure in these injuries.
The background of this discussion is a series of 957 casualties selected for thispurpose from the whole series of 3,154 casualtieswith abdominal wounds who were treated by surgeons of the 2d Auxiliary SurgicalGroup during 1944 and 1945. Selectionwas on two grounds: (1) That all the injuries included perforations of hollowviscera and therefore carried the threat of fulminating peritonitis, and (2)that in all cases data relative to shock therapy were complete. The figures forreplacement therapy, as well as the case fatality rates, must be interpretedwith the reservation that the selected series perhaps contains an undueproportion of poor-risk cases, the explanation being that the data were morelikely to be complete in such cases than in cases in which the surgical risk wasbetter.
1The term "shock" throughout this discussion should be understoodas synonymous with the term "traumatic shock." An attempt todistinguish between traumatic and hemorrhagic shock would serve no usefulpurpose.
2Medical Department, United States Army, Surgery in World War II. ThePhysiologic Effects of Wounds. Washington: U. S. Government Printing Office,1952.
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The initial care of casualties in World War II fell intothree phases: (1) Preoperative resuscitation or the therapy of traumatic shock,(2) definitive surgery, and (3) postoperative care. Care could not be consideredoptimal unless these three phases were closely integrated to insure completecontinuity of effort. The immediate aim of shock therapy was to restore thecirculatory dynamics to a sufficient state of competence to permit a successfuloperation. If a fatal outcome from the deleterious effects of shock, continuingperitoneal contamination, and the establishment of widespread virulent infectionwas to be prevented, it was essential that both resuscitation therapy andsurgery be accomplished with as little delay as possible. Moreover, replacementtherapy frequently had to be continued during operation and throughout the firstdays after operation.
The medical officer responsible for triage and shock therapy played a uniquerole in the care of battle casualties. His chief asset was the ability to judgethe gravity of the situation. His initial examination established the status ofthe patient with respect to the extent of injury and the severity of shock andpermitted tentative decisions as to appropriate replacement therapy and theresponse to be anticipated from it. Thereafter he carefully followed thepatient's progress during transfusion therapy so as to recognize promptly anyfailure of response or actual deterioration. Sound judgment was especiallyneeded in reaching a decision as to the optimal time to operate upon a patientwith continuing intra-abdominal hemorrhage. Often the shock officer had todecide who, among a number of wounded men, was in most urgent need of immediatesurgery, as well as whose chance of survival would be least compromised bydelay.
Intelligent triage during the period of resuscitation was difficult toachieve because it depended upon awareness, experience, and judgment which werenot easily acquired. Nevertheless, skill in this, as in surgical technique, wasan extremely important factor in the successful treatment of the seriouslywounded.
The objective of treatment was thus a continuity oftherapeutic endeavor which afforded optimum coordination of replacement andsurgical therapy and which recognized the fundamental importance of operation inthe resuscitation of the severely wounded. The operation was of specialimportance in resuscitation when, because of continuing intra-abdominalhemorrhage or early fulminating infection, transfusion therapy alone had failedto bring about sustained improvement. Obviously, more than blood replacement wasrequired to correct these conditions. The only hope for a successful outcome-andfrequently the hope was slight-lay in supplementing massive transfusion therapyby prompt and skilled surgery. The care of these casualties thus constituted achallenge to all those responsible for all phases of their management in forwardhospitals.
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CLASSIFICATION OF SHOCK
The classification of shock into categories for statisticalpurposes is never entirely satisfactory, since the objectivity of differentobservers naturally varies considerably and their interpretations varyaccordingly. For purposes of comparison and reference, however, four degrees ofshock (table 18) were recognized in the 957 instancesof traumatic perforation of the gastrointestinal tract upon which thisdiscussion is based: (1) No shock, or incipient shock, in which the lower levelof the systolic blood pressure was 101 mm. Hg; (2) moderate shock, in which thesystolic blood pressure was 71 to100 mm. Hg; (3) severe shock, in which the systolic blood pressure was 41 to 70 mm. Hg; and (4) profound orpreterminal shock, in which the systolic blood pressure ranged downward from 40mm. Hg to 0. More than half of the 957 patientsin this series (table 18) exhibited degrees of shock ranging from moderatethrough preterminal, and more than a quarter exhibited severe or profound shock.
Degree of shock | Cases | Proportion | Deaths | Case fatality rate | Timelag (average) | Replacement therapy (average) | |||||
Preoperative | During operation | Total | |||||||||
Plasma | Blood | Plasma | Blood | Plasma | Blood | ||||||
Percent | Hours | cc. | cc. | cc. | cc. | cc. | cc. | ||||
None or incipient (101 to 120 mm. Hg.) | 446 | 46.6 | 81 | 18.2 | 10.4 | 492 | 619 | 178 | 962 | 670 | 1,581 |
Moderate (71 to 100 mm. Hg.) | 250 | 26.1 | 95 | 38.0 | 11.6 | 602 | 873 | 261 | 1,063 | 863 | 1,936 |
Severe (4 to 70 mm. Hg.) | 121 | 12.7 | 61 | 50.4 | 10.7 | 687 | 1,271 | 311 | 1,278 | 998 | 2,549 |
Profound (0 to 40 mm. Hg.) | 140 | 14.6 | 93 | 66.4 | 10.8 | 713 | 1,745 | 311 | 1,617 | 1,024 | 3,362 |
| 957 | 100.0 | 330 | 34.5 | 10.7 | ||||||
The chief shortcoming of a classification based on the level of the bloodpressure lies in the fact that the blood pressure was often maintained atrelatively normal levels for a considerable period of time following injury. Asa result, the soldier's condition might seem better than it really was (cases 1through 4).3 Oligemia and reduction of the peripheral blood flow inthe patients classified as not in shock or in incipient shock were likely to bedisproportionately greater than the level of the systolic pressure wouldindicate. This was not true, however, of the other categories. All theexperience in forward hospitals indicated that when once the blood pressure hadfallen below normal levels, certain therapeutic and prognostic implications wereinherent in the initial reading.
3For the protocols on these cases and the other cases referred to in thischapter, see a Clinicopathologic Study of Abdominal Wounds, at the end of thechapter.
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TIMELAG AND CHARACTER OF WOUND
The average timelag between wounding and operation in these957 casualties with traumatic perforations of the gastrointestinal tract variedfrom 10.4 to 11.6 hours (table 18). Aside from the fact that it was slightlyless in patients with no shock and with incipient shock than in those in othercategories, there was no correlation between timelag and the severity of shockas indicated by the level of the blood pressure. Obviously, in wounds of equalseverity, the total amount of blood lost and the severity of shock wouldincrease with the passage of time (case 4). A patient admitted 10 hours afterinjury, for example, might exhibit signs of severe shock, whereas if he hadbeen admitted 4 hours after injury, only moderately severe shock might have beenobserved.
The correlation between the degree of shock and the severityof the wound is borne out by an analysis of the cases in this series. Not onlydid the patients in the deepest shock consistently exhibit more severe injuriesthan those whose blood pressure approached normal, but multiple visceralinjuries were also more common in the categories of severe shock (cases 5through 8). The high case fatality rate in patients with combined gluteal andabdominal wounds was almost certainly related to the frequency in such injuriesof massive hemorrhage from the iliac and femoral vessels (cases 1, 5, 6, and 9).Lacerations of the spleen and major vascular injuries furnished otherillustrations of the relation of vascular injuries to the degree of shock. Ofthe 140 patients with gastrointestinal perforations in the category of profoundor preterminal shock, 43 (30.7 percent) had associated injuries of this sort, asdid 21 of the 121 patients (17.4 percent) in the category of severe shock. Incontrast, this type of injury was present in only 39 of the 250 patients (15.6percent) in moderate shock, and in only 37 of the 446 patients (8.3 percent) inincipient shock or not in shock.
ROLE OF HEMORRHAGE AND OTHER FLUID LOSSES IN PATHOGENESIS OFSHOCK
Massive hemorrhage was frequently present in injuries of theabdomen, as the result of disruption of a major vessel or a laceration of thespleen or the liver. Even in the absence of such major injuries, widespreaddamage of smaller vessels could account for a considerable blood loss. Bloodloss was undoubtedly the most important factor in the production of traumaticshock in patients with abdominal injuries. It was also chiefly responsible forthe depression of the hematocrit frequently observed in battle casualties. Onthe other hand, it had to be remembered, in the appraisal of severe shock, thatthe administration of plasma also tended to reduce the hematocrit and theoxygen-carrying capacity of a given volume of blood. If an excessive amount ofplasma had been given after hemorrhage, the total volume of the circulatingblood might be only moderately reduced; yet a marked anemia might be present,with a hematocrit reading of only 15 to 18 percent. This observation,incidentally, furnishes additional proof of the superiority of whole blood overreconstituted plasma in the resuscitation of battle casualties (p. 22).
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In addition to hemorrhage, the loss of plasma or of plasma components intothe traumatized or contaminated area of the abdomen contributed materially tothe production of shock. This loss occurred as the result of transudation orexudation of fluid from inflamed peritoneal surfaces and into visceral tissuesunder the influence of mechanical and chemical trauma and beginning infection.While the precise importance of fluid loss from this source has been disputed,certain observations made by the surgeons of the 2d Auxiliary Surgical Groupcaused them to be inclined to regard it as significant. An extremely high casefatality rate was observed when the pleura was widely contaminated by gastric orintestinal contents, and the shock present in this type of case was apt to beespecially severe (cases 4 and 10). Similarly, diffuse peritoneal contaminationconsistently increased the severity of the circulatory collapse associated withevisceration of the intestines (case 11). When, on the other hand, eviscerationoccurred without appreciable peritoneal soiling, shock was often surprisinglymild, and the response to replacement therapy was more favorable than in thepresence of diffuse contamination of the peritoneum.
Changes in the splanchnic capillary bed produced by irritation and infectionalso appeared to be of some importance in reducing the effective circulatingblood volume, though there was no agreement concerning the quantitativeinfluence exerted by these alterations. Mann4had noted in 1915 thatmechanical trauma to the bowel was associated with an increased capacity of thesplanchnic vascular bed. Similar observations were made by the surgeons of the2d Auxiliary Surgical Group who found that, in patients with perforations of thegastrointestinal tract, a considerable volume of blood was likely to be pooledin dilated and engorged venules and capillaries and that the accumulation wasincreased when the bowel was manipulated at operation.
Another source of fluid loss was dehydration, which existed in some degree inall patients with gastrointestinal perforations, whether or not vomiting hadoccurred. Because of paralytic ileus, which was a natural consequence ofperitoneal contamination or infection, small-bowel contents did not reach thecolon, and the normal reabsorption of water did not occur.
Although the loss of plasma or its components into the contaminatedperitoneal cavity resulted in a rise in the hematocrit of the circulating blood,hemorrhage, which was an almost universal sequela of penetrating wounds of theabdomen, ultimately had the opposite effect. The hemodilution which followshemorrhage would seem to account for the fact that even in severe shockassociated with widespread soiling of the peritoneum, hemoconcentration wasseldom observed and was, in itself, a factor of negligible significance in thepathogenesis of shock in battle injuries.
Furthermore, a patient who showed clinical evidence of severe shock mightoccasionally present no significant decrease in the hematocrit level, and therewas frequently little apparent correlation between the hematocrit reading andthe severity of peripheral circulatory failure. On the other hand, con-
4Mann, F. C.: Shockand Haemorrhage: An Experimental Study. Surg., Gynec. & Obst. 21: 430-441, October 1915.
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siderable hemodilution was often found in association withsevere shock. These low hematocrit levels, as already mentioned, were usuallyobserved in cases in which the initial blood loss had been severe and in whichlarge amounts of plasma had been used to prevent death within a short time afterinjury. The subsequent management of these patients was always difficult, a factthat was not always readily apparent at the time of the initial examination.
The maintenance of a normal or slightly elevated hematocritlevel in a patient with a penetrating wound of the abdomen did furnish someevidence that the effects of peritoneal contamination had equaled or exceededthe effects of hemorrhage. So many factors, however, influenced the hematocritin wounds of the abdomen that its usefulness as a means of quantitativeassessment of the loss of blood or of plasma components from the circulation wasquite limited.
REPLACEMENT THERAPY
Aside from any theoretic considerations, increasing experience led thesurgeons of the 2d Auxiliary Surgical Group to emphasize the important role oflocal loss of fluid, particularly blood, in the initiation of the traumaticshock which followed penetrating wounds of the abdomen. Undeniable support fortheir position was furnished by the proved efficacy of plasma and whole-bloodreplacement in the resuscitation of these severely wounded men.
Replacement therapy was frequently begun in the battalion aid station withthe administration of reconstituted plasma. Whenever severe shock was apparentsoon after injury, plasma was usually given, occasionally in excessive amounts.Plasma received under these circumstances is included in the calculation of theaverage figures for replacement therapy in this series (fig. 25; table 18).
The total amounts of blood and plasma used for resuscitation wereproportionate to the severity of the shock exhibited by the casualties.Furthermore, the volume required in each category of shock agreed fairly wellwith the estimate of blood loss made by the Board for the Study of the SeverelyWounded.5 These facts lend support to the contention that the level of theblood pressure is, in spite of its shortcomings, an important criterion in theevaluation of the degree of shock and the extent of blood loss in severelywounded casualties.
Although application of average data to individual casualtieswould naturally be expected to reveal discrepancies, nevertheless the valuescalculated as average for this relatively large series may be taken as a generalguide to the requirements which had to be met in preoperative resuscitation.Patients suffering from severe shock often had to be given extremely largequantities of plasma and blood. The administration of 5,000 to 6,000 cc. was notunusual. Uncontrollable hemorrhage during operation also called for the
5Medical Department, United States Army, Surgery inWorld War II. ThePhysiologic Effects of Wounds. Washington: U. S. Government Printing Office,1952, pp. 21-74.
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use of very large amounts of fluid. One patient in thisseries, for example, received a total of 8,250 cc. (1,750 cc. of plasma, 6,500cc. of whole blood), chiefly because intra-abdominal bleeding could not beeffectively controlled during the early phase of the operation.
Adequate replacement therapy was not available in World WarI, and surgeons quickly recognized the futility of attempting operation in thepresence of severe traumatic shock. Had the same lack of replacement therapyprevailed in World War II, the severity of shock would have precluded operationin many of the 261 patients in this series whose systolic blood pressures were70 mm. Hg or less (table 18). Operation was attempted in the field hospital inevery instance, however, after adequate replacement therapy, and 107 (41percent) survived to be evacuated to the rear, after the usual period ofconvalescence.
Accurate data are not available concerning deaths before operation inpatients in severe shock after perforation of the gastrointestinal tract.Presumably the number was small. During a 4-month period in 1944-45, a singleshock team lost only 6 patients (2.1 percent) of the 285 it was attempting toprepare for operation.
During World War I, Maj. J. W. Vaughan, MC, consultingsurgeon, 32d Division, recorded that of 256 patients sent from the triage to anoperating station for seriously wounded, 41 died in spite of attempts to combatshock
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by various methods, leaving only 215 who received operative treatment.6In marked contrast, under similar circumstances in a field hospital platoon in 1943,there were no preoperative deathsamong 297 consecutivepatients admitted for surgery.
The saving of life in World War II among casualties in severeand profound shock was largely attributable to liberal, and frequently massive,transfusions. In numerous instances operation would have been impossible withoutsuch therapy. The improvement which followed prompt and intensive replacementtherapy was often striking, particularly among patients who had suffered verysevere shock of relatively short duration. Improvement was not observeduniformly in this category, it is true, but it occurred with sufficientfrequency to emphasize the therapeutic potentialities of liberal replacementtherapy in the resuscitation of severely wounded men.
Failures of Replacement Therapy
The fact that significant or sustained improvement did not invariably occurafter replacement therapy suggested that, in spite of the importance of thefluid loss in the pathogenesis of shock and the unique role of replacementtherapy in its management, other factors, which were probably not completelyamenable to this type of therapy, had to be taken into account.
One of the most important of these additional factors wasmassive peritoneal contamination, with early fulminating peritonitis, thedeleterious effects of which were often augmented by severe hemorrhage, aprolonged timelag, or both.
The case fatality rate in the various categories of shock inthis series was directly related to the degree of shock (table 18). The steadilyascending rate emphasized the increasing gravity of the prognosis as the degreeof shock increased. About three-quarters of the deaths in the 3,154 cases in the total seriesoccurred by the end of the second postoperative day. Casualties who died withinthis period often pursued a relentlessly downhill course characterized bypersistent or recurrent shock. It was soon learned that failure of the patientto manifest sustained benefit from adequate resuscitative measures, particularlywhen replacement therapy had been liberal and intensive, was clear evidence thatthe prognosis was grave (cases 8, 9, and 12).
The course of such a patient was characteristic. When he was received at thefield hospital he was in shock, which often was severe. The blood pressure wasextremely low. The pulse was rapid and of poor volume. The extremities werecold. The skin was pale, and if the degree of shock was profound there was oftenmore or less purple-red mottling or cyanosis. Venous filling was apt to be poor, even after a tourniquet had been applied. Therectal temperature was seldom above 100? F. and was frequently subnormal. Thepatient was aware of his extreme weakness, complained little if at all, andwanted
6The Medical Department of the United States Army in the World War.Washington: U.S. Government Printing Office, 1927, vol. XI, pt. 1, pp. 109-110.
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to be left undisturbed. The sensorium was likely to be clouded, but in theabsence of acute morphinism true coma was not common except as a terminalmanifestation. Appraisal of the history often suggested that the timelag,although perhaps not intolerable in itself, had become intolerable because ofthe extent and character of the wound. Considerable transient improvement mightbe attained by liberal transfusion therapy, but the clinical response was likelyto be incomplete or poorly sustained, and increasingly severe shock oftensupervened after operation. In fact, one of the most constant characteristics inthis type of case was the tendency to recurrent shock.
The terminal decline as a rule occurred shortly afteroperation, but in many instances it was sufficiently delayed for widespreadbacterial growth to occur. Death was usually attributable to shock or to shockand peritonitis, but the peritonitis, it must be emphasized, differed from thetype of purulent peritonitis familiar in civilian practice (p. 198). It wascharacterized by massive contamination of the peritoneum and by the grosspathologic changes observed during the early stages of bacterial growth. Inaddition, the circulatory and metabolic changes associated with severe traumaticshock, as well as the overwhelming nature of the peritoneal infection, appearedto be capable of inhibiting to an appreciable degree the local leukocyticresponse. Autopsy revealed edema and discoloration of the intestine, opacity anddullness of the serosal surfaces, a moderate amount of turbid, serosanguineousexudate, and relatively little fibrin (cases 7, 8,10, and 11). A purulent exudate of significant amount was not usually seen,probably because of the brief duration of the inflammatory process.
The peritoneal reaction which was the result of early massive soiling thusdiffered materially from the usual bacterial peritonitis of 4 to 6 days'duration. Early in the war, the deleterious local effects of such soiling werenot always appreciated because the surgeon's judgment was based on knowledgelimited to the classical variety of peritonitis.
Preexisting traumatic shock was undoubtedly the explanation of the promptnessand frequency with which death occurred after wounding in this type ofperitonitis. When massive peritoneal contamination was further complicated bycontinuing intra-abdominal hemorrhage, successful resuscitation and surgery wereoften impossible.
In some cases, in spite of massive transfusion therapy,careful surgery, chemotherapy, oxygen therapy and all other available measures,the fatal outcome was merely delayed for a day or two. Its apparentinevitability, in spite of what seemed to be adequate replacement therapy,introduced the question of the possible role of toxic factors in the productionof so-called irreversible shock. The toxic theory is particularly interestingbecause of the massive peritoneal contamination and the associated circulatoryfailure present in many of these severely wounded men. The analogy to anaerobicmyositis was suggestive, especially because in a few instances pure cultures of Clostridium welchii were obtained from the peritoneal cavity. Similarinfections of the pleural cavity were occasionally observed (case 13). Theseisolated observa-
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tions, however, cannot be construed as valid evidence that the same factorswere responsible for severe shock in the presence of peritoneal contamination.The role of toxicity cannot be denied on the basis of the evidence at hand, buta toxic factor, other than infection per se, remains to be isolated andestablished.
It should be realized that the exigencies of warfare often precluded theaccumulation of data which would fully explain the apparent failures ofreplacement therapy in the management of shock. In the absence of these data,unwarranted conclusions were frequently drawn relative to the effect of whatwere termed toxic factors. When comparatively complete clinical and post mortemdata were critically analyzed, these conclusions usually could not besubstantiated. The protocols found at the end of this chapter (cases 1 to 4,inclusive; 9; 10; 14; and 15) disclose various findings which, regardless oftheir relationship to shock, limited the chance of survival of the seriouslywounded. The investigations of the Board for the Study of the Severely Wounded7afforded no evidence of the existence of toxic agents and led the investigatorsto suggest that the term "irreversible shock" should be abandonedbecause of its implications in this respect.
Excessive prolongation of the period of peripheral circulatory failure wasapparently the most important reason for failure of liberal replacement therapyto accomplish resuscitation in some cases. The importance of the duration ofshock cannot be arrived at by a simple analysis of statistical data (table 18).There was no significant correlation, as already pointed out, between theseverity of shock and the duration of injury before operation. Moreover, it wasfrequently impossible to determine the exact duration of the observed state ofshock from the field medical record.
It was readily apparent, however, that the more severe the peripheralcirculatory failure, the more rapidly did a state of profound or so-calledirreversible shock ensue. A relatively short period of delay in resuscitationmight prove fatal to a patient in severe shock, although it could easily be tolerated bya patient in moderate shock. Traumatic shock, satisfactorily alleviated by theprompt transfusion of 1,500 to 2,000 cc. of whole blood, could constituteirreversible shock in the absence of such therapy. It is a rather general customto label shock as irreversible when the therapy at hand has proved to beunsuccessful, but this is a vague characterization defined by therapeutic trial,not by exact knowledge of the fundamental pathologic physiology.
All the World War II experience indicated that peripheralcirculatory failure is followed, within a variable period of time (the variationdepending upon its severity), by alterations in general cellular metabolismwhich cannot be corrected by transfusion therapy alone. These changes werethought to depend upon the interruption of the supply of oxygen and othernutrients to large groups of cells, as, for example, those of the liver andkidney, rather than upon changes in the capillary endothelium. Shock therapy waseffective only
7See footnote 5, p. 124.
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insofar as it restored adequate circulatory dynamics andalleviated tissue anoxia. Changes in cellular metabolism could thus be preventedor arrested, but they could not be completely reversed. In this respect,replacement therapy was always prophylactic.
If the metabolic changes associated with severe shock werethoroughly understood, the knowledge might serve to resolve the enigma ofso-called irreversible shock without invoking factors other than fluid loss inits pathogenesis. Unfortunately, no simple methods were available during WorldWar II-nor are they available now-by which the clinician could determineaccurately the onset of irreversible cellular changes during the course oftraumatic shock. The only solution of the problem was, therefore, to treatexisting circulatory failure as promptly and as vigorously as possible.
THE TOTAL PICTURE OF SHOCK IN WORLD WAR II
The experience of the 2d Auxiliary Surgical Group withcasualties in shock and in need of resuscitation following abdominal woundsapparently paralleled the total war experience. Local fluid loss undoubtedly wasthe most important factor in the initiation of traumatic shock. The mostefficacious means of resuscitation was prompt and adequate replacement therapy,in which whole blood was the most important component. The nature of battlewounds of the abdomen demanded that prompt and expert surgery constitute anintegral part of resuscitative therapy, in order to arrest hemorrhage andperitoneal contamination with the least possible delay. Many factors, not all ofwhich were completely understood, augmented and perpetuated shock. One, whichwas extremely important, was massive contamination of body cavities. Thecirculatory disturbances of severe shock promptly led to bodily changes whichcould not be completely reversed by replacement therapy. Delay in initiatingsuch therapy, as well as improper utilization of available measures, whether asthe result of military exigencies or for other reasons, resulted in failures ofresuscitation.
Many abdominal injuries were lethal, at least in relation to methods ofresuscitation and surgery then at hand. They remained, at the end of the war, asa challenge for the future. It is in the resuscitation of gravely wounded menthat the therapy of traumatic shock will meet its most severe test. Advanceswill depend upon a more fundamental knowledge concerning the relationship ofmassive peritoneal contamination to traumatic shock and death, as well as upon amore thorough understanding of the cellular derangements produced by severeshock. The failures in replacement therapy which occurred in World War II pointto the need for further study of the problem but must not be interpreted topermit the neglect of available measures of resuscitation in the management ofseverely wounded men with abdominal injuries.
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A CLINICOPATHOLOGIC STUDY OF ABDOMINAL WOUNDS ASSOCIATED WITHSHOCK
Introductory Note
In March 1944, the author of this study (Maj. Beverly T. Towery) had the goodfortune to assume the direction of Shock Team No. 6, 2d Auxiliary SurgicalGroup, which was then engaged in the resuscitation of nontransportablecasualties in the field hospitals of the Fifth United States Army, MediterraneanTheater of Operations. As explained elsewhere, the evacuation of gravely woundedcasualties was always specifically interrupted in a forward medical echelon forthe treatment of shock, followed by surgical intervention, after which thepatient was retained in the field hospital for a period of convalescence.
At this time, almost no post mortem examinations were being carried out uponthe fatal cases in this group of patients, although the high incidence of severeshock and the resulting deaths among these "casualties of immediateurgency" provided a remarkable opportunity for the study of the clinical aswell as of the morphologic characteristics of wound shock. The tissues andclinical protocols which the microscopists received were often too inadequate topermit an intelligent interpretation of the findings. Conversely, reports ofmicroscopic diagnoses usually failed to find their way back to the prosectors.
With the enthusiastic encouragement of the late Lt. Col. Tracy B. Mallory,MC, a systematic program was set up for the clinical and post mortem study ofpatients who died in field hospitals, as follows:
1. The author, with only one or two exceptions, performed the post mortemexaminations.
2. He was responsible for providing the microscopist with a record of thegross anatomic findings.
3. With this report, he also included provisional diagnoses and a briefsummary of the case, based upon the autopsy findings and the clinical dataavailable at the time of the post mortem examination.
4. The microscopists provided histologic descriptions of the tissues, addedmicroscopic diagnoses, and frequently wrote brief comments upon theirobservations.
5. The original observations made by the prosector were retained in theprotocols, and the provisional diagnoses were not amended to conform to thesubsequent reports of microscopic findings. Such inconsistencies as might havearisen were discussed and rectified in the final summarizing statements attachedto the end of each protocol.
During the 13-month period in which this program wascontinued, it was possible to accumulate relatively complete clinical and postmortem data upon 47 men who had been wounded under varying circumstances ofterrain, climate, and tactical situation in Italy, France, and Germany. Thirtyof these casualties (64 percent) had sustained wounds of the abdomen. The 15protocols which follow have been selected from this group of cases, in anattempt to define
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clearly the magnitude of the problem of shock among patientswith abdominal injuries. It is believed that these records constituterepresentative source material.
The author was personally responsible for part or all of the resuscitation inmost of the cases in the total series. As collator, however, he has drawn freelyupon the clinical observations of numerous colleagues in respect to replacementtherapy, anesthesia, surgical management, and postoperative care.
This study clearly showed that hemorrhage and peritonealcontamination were the most important determinants of the outcome ofintra-abdominal trauma. Regardless of the ultimate detrimental effects ofperitoneal contamination, the early onset of severe shock was almost invariablydue to brisk hemorrhage. Widespread peritonitis unquestionably increased thelikelihood of a fatal outcome, though, aside from the attendant local loss offluid, the mechanism of the deleterious effects of this complication remainedunexplained in this study. A morphologic evaluation of these phenomena proved tobe a difficult undertaking and one which, on theoretical grounds, was notparticularly rewarding. From a practical standpoint, however, the demonstrationof a microscopic lesion, such as diffuse pulmonary fat embolism, sometimesprovided crucial data in a fatality which otherwise might have remained obscure.
Resuscitation by means of vigorous replacement therapy removed, at least inpart, the immediate risks of shock but seemed to accentuate certain microscopicchanges contingent upon partial or complete recovery from it. Hemoglobinuricnephropathy was perhaps the most striking of these lesions, and the importanceof post traumatic renal failure will be readily apparent on a perusal of theserecords. It is ironical that the development of this particular lesion seemed todepend upon a measure of success in resuscitation.
One of the major aims of this study was to obtain evidence concerning thefundamental pathogenesis of irreversible shock. The results were illuminating.In effect, it was evident that a careful post mortem examination very oftenrevealed findings which provided some other logical explanation for thefatality. Among these findings were unrecognized perforations of thegastrointestinal tract, the autotransfusion of contaminated blood, unsuspectedinfection, pulmonary edema, and cerebral emboli. On the basis of the experienceobtained in this investigation, one would therefore be inclined to minimize theimportance of shock which does not have a reasonable explanation in terms ofhemorrhage, exudation, and infection.
Protocols8
Case 1
CLINICAL DATA
This patient received a bullet wound of the left hip on 2 June 1944, at 1000hours. When he reached a field hospital at about 1600 hours, after having
8The author gratefully acknowledges the generous assistance in this study ofthe various pathologists whose microscopic studies (sometimes identified byinitials) appear in the protocols. He is particularly indebted to the late Lt.Col. Tracy B. Mallory, MC, and to 1st Lt. Leslie S. Jolliffe, MC, and Capt.Joseph G. Rothenberg, MC. First Lt. Kathryn T. Driscoll, ANC, providedinvaluable clerical assistance.
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received 250 cc.of plasma, his blood pressure was 110/60 mm.Hg. He did not appear to be in shock, but examination of the abdomen revealedgeneralized rigidity. He was given 500 cc.of plasma and 500 cc.of blood before operation, and his condition seemed relatively good. His blood belonged togroup A.
At operation, much blood was found in the peritoneal cavity.The missile had perforated the abdomen by way of the left buttock. Whenexploration was attempted, profuse hemorrhage occurred from the left iliacvessels, and the aorta and inferior vena cava were temporarily ligated withtape. After a great deal of difficulty, it was possible to ligate the leftexternal iliac vein, and the internal iliac vein and artery.
The patient's condition was extremely poor during thisprocedure, and he was given 4,500 cc.of group O blood in an attempt to replace the blood loss. Extensive explorationof the abdomen was not carried out, but there was no evidence of perforation ofthe intestine or of peritonitis. At the end of the procedure, which lastedapproximately 7 hours, the blood pressure was 100/40 mm. Hg; it had risenconsiderably after bleeding had been controlled.
The right leg became moderately cyanotic after operation, and, on both thefirst and second postoperative days, right lumbar sympathetic blocks wereperformed with procaine. Some improvement was noted. On the second postoperativeday, the temperature was 98.6? F., thepulse was 100, and the respiration was 24. Whenthe patient was catheterized, only 60 cc.of dark-brown urine was obtained, although the fluid intake had been adequate.Its specific gravity was 1.025. Thepatient became somewhat confused and died at 2000 hours 4 June 1944,58 hours after wounding.
AUTOPSY
Autopsy was performed 5 June 1944, 12 hoursafter death (Cori, Italy).
Gross observations.-The delay in performingthe autopsy, without benefit of refrigeration, had produced marked changes inthe body. The pericardial cavity contained 30 cc.of pink serous fluid, and 120 cc.of similar hemolyzed blood-stained fluid was present in each of the pleuralcavities. The peritoneal cavity was not remarkable, except for generalized pink(hemoglobin) staining of the serous surfaces.
The lungs showed bilateral and symmetrical edema and deeppurple-red discoloration, with considerable reduction in crepitus. No bronchialobstruction was present nor were any emboli present in the carefully dissectedbranches of the pulmonary artery.
Two perforations were observed in the retroperitoneal portion of theascending colon. They were caused by passage of the bullet through this viscusabout 8 cm.distal to the ileocecal valve. There was also extensive retroperitonealhemorrhage in this region, with a rather scanty fibrinopurulent exudate.
The kidneys were swollen and moderately increased in size. The cut surfacebulged above the edge of the capsule. The cortex was rather pale, but
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its pallor was modified by hemoglobin staining of all the tissues.Hydroureter and renal-vascular occlusion were not present.
The finer detail of the pelvic vessels was greatly obscured by extensivesuffusion of tissues by markedly hemolyzed blood.
Sections of muscle taken from the upper thigh on the left were not grosslyremarkable except for moderate pallor.
Gross anatomic diagnosis-(1) Penetrating gunshot wound of left buttock,with two perforations of retroperitoneal portion of ascending colon and earlyretroperitoneal abscess; lacerations of left common iliac vein, external iliacvein, and internal iliac artery and vein, all secondarily ligated; and (2)severe, exsanguinating hemorrhage, secondary to these lacerations.
Comment.-Deathmay be ascribed to shock, secondary to severe and prolonged hemorrhage.Since death occurred on the second postoperative day, the perforations of thecolon may have had relatively little to do with the fatality. Theseperforations, however, served to contaminate the wound track with anaerobicorganisms, and clinical manifestations would probably have supervened shortly,had the patient survived. How important this contamination was in causing deathmust remain conjectural. The oliguria present before death suggested a renallesion, but in all probability the inadequate renal blood flow (hypotension)during the postoperative period was alone responsible for the decreased urinaryoutput.
Microscopic observations-Histologic examination of thekidney showed the lower nephron segments to be extensively plugged withpigmented casts. In the cortex, some tubules contained masses of intenselyblue-staining granules and spherules suggesting calcareous material. Thesemasses were not found in the pyramid. There were many bacilli in theinterstitial tissues, and fixation was too poor to judge epithelialdegeneration.
Examination of the bowel showed much of the mucosa to benecrotic. All layers of the wall were infiltrated with leukocytes, and theserous surface was covered by a thick fibrinopurulent membrane.
Comment-The severe lower nephron nephrosis of the hemoglobinuric type issuggestive of a transfusion reaction. The story of the administration of 4,500cc. of group O blood to a group A recipient within a period of a few hours isinteresting and may have been the responsible factor. The clostridial infectionwas evidently only agonal and cannot be held responsible for the fatality. Therewas no massive necrosis of voluntary muscle which could have producedmyohemoglobinuria. The calcareous masses in some of the tubules are assumed torepresent past history; they could be remnants of a previous sulfonamidereaction. (T. B. M.)
SUMMARY
Death probably was due to a combination of factors in thiscase: (1) Severe shock during a prolonged operation; (2) perforation of thecolon with contamination of the retroperitoneal tissues; and (3) renal failure,with consequent
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pulmonary edema. Of these factors, the first seems to be ofgreatest importance, since death occurred within a relatively short time afteroperation. Uremia per se was probably not of primary importance in causingdeath; under the conditions at hand it is extremely difficult to assess theimportance of infection in this case.
Case 2
CLINICAL DATA
This patient received shell-fragment wounds of the left thigh and rightcostal margin 19 March 1945 at 0230 hours. A tourniquet was appliedto the left leg at 0300 hours.When the patient reached a field hospital at 0630 hours,after having received 500 cc.of plasma, the blood pressure was 110/70 mm.Hg, and the pulse was 80. Beforeoperation, he was given 600 cc.of plasma and 500 cc. of whole blood. His blood belonged to group AB.
Anesthesia was begun at 1105 hours 19 March.Laparotomy revealed a laceration of the right lobe of the liver and severedestruction of a 10-cm. portion of the transverse colon. A spur colostomy wasmade through the right upper quadrant, and drains from the hepatic lacerationwere brought out through the wound at the right costal margin. The operationrequired 3? hours,and during it the patient received 2,000 cc.of whole blood.
In addition to his abdominal wound, this patient had afracture of the lower third of the left femur, with severe comminution andposterior angulation of the distal fragment.
The day after operation, the patient was semistuporous. The blood pressurewas 84/50 mm.Hg and the pulse 140. He received 500 cc.of plasma. Medium rales were heard in both lungs. Moderate cyanosis was relievedby the administration of oxygen. There was profuse drainage of bile-stainedfluid from the drains at the right costal margin. During the first 12 hours afteroperation, the patient excreted 275 cc.of urine. His respirations were quite shallow, and he coughed only occasionallyand ineffectually. He died at 1630 hourson the second postoperative day, 62 hoursafter wounding.
AUTOPSY
Autopsy was performed 4 hours after death (St. Avold, France).
Gross observations-The abdomen was moderately distended,in spite of the presence of several drains. The peritoneal cavity containedabout 300 cc. ofblood-tinged, purulent fluid, which was present chiefly above and posterior tothe colostomy spur; a moderate amount of yellow-gray purulent exudate was alsofound in this area. There was considerable dilatation of the stomach and of theupper bowel down to the point at which the small bowel was partially obstructedas it lay posteriorly and lateral to the proximal segment of the colostomy.Distal to this point, the bowel was not distended, though the loops
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were lightly bound together by fibrinopurulent exudate. Therewas no leakage into the peritoneal cavity from the colostomy, the transversespur of which appeared to be under slight tension.
The right auricle was considerably distended by blood. Thetricuspid valve appeared slightly dilated. There were petechial hemorrhages overthe surface of the posterior aspect of the heart, particularly along thecoronary sulcus. On section, the myocardium appeared paler than normal.
There were severe partial atelectasis of both lungs; the aeration of alllobes except the left upper lobe was moderately to markedly decreased. There waswell-established nodular consolidation of the entire right lower lobe, the hilarportion of the right middle lobe, and the posterior portion of the right upperlobe. Near the hilus of the right lower lobe there appeared to be beginningabscess formation.
The spleen was of usual size and was covered by a thin layer offibrinopurulent exudate. On section, it was purple red and moderately firm, butthe pulp scraped away readily.
There was a small laceration of the lateral margin of the right lobe of theliver, but no appreciable collection of bile was present within the peritonealcavity. In the dome of the right lobe was a large, irregular area of yellow mottling. There was no evidence of suppuration in the tissue adjacent to thelaceration.
The kidneys were somewhat smaller than normal, and thecapsular surfaces were smooth and pale pink, with small irregular patterns ofvascular congestion. The cut surface was not remarkable. The adrenals werenormal.
Gross anatomic diagnosis-(1) Perforating shell-fragment wound ofabdomen, via upper right flank, with exit just to right of umbilicus, withmoderately severe laceration of right lobe of liver, and severe perforation andlaceration of right transverse colon, with spur colostomy; (2) acute,moderately severe, fibrinopurulent peritonitis, secondary to perforation oftransverse colon; (3) severe pulmonary atelectasis, involving all lobes, withearly acute bronchopneumonia of right lung and left upper lobe, and possibleabscess of right lower lobe; dilatation of right auricle and subepicardialpetechial hemorrhages probably due to atelectasis and asphyxia (possiblyterminal); (4) perforating shell-fragment wound of left lower thigh, withcomplete, compound, comminuted fracture of lower third of left femur andlaceration of capsule of left knee joint and of suprapatellar bursa; and (5)lacerating shell-fragment wound of left chest wall near 12th rib.
Comment-The immediate cause of death in this caseappears to have been atelectasis and bronchopneumonia. The post mortem findingssuggest that these complications began soon after operation. The semistuporousstate and the diffuse peritonitis and distention of the stomach and upper smallbowel were probably responsible for the poor respiratory exchange andineffectual cough. In the presence of severe bone trauma, stupor and pulmonaryrales suggest the possibility of fat embolism.
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Microscopic observations.-In thealveoli of the lungs were large amounts of eosinophilic coagulum and varyingdegrees of polymorphonuclear infiltration into the coagulum. A second sectionrevealed dissolution of the alveolar walls with extreme infiltration andaccumulations of polymorphonuclear leukocytes. In the central portions of theseaccumulations were bacterial groups and necrotic debris. Some alveolar wallswhich were still present appeared necrotic. Thrombi were seen in the vessels inthese areas. On the pleural surface was a thin, fibrinoid material with enmeshedpolymorphonuclear leukocytes. Large amounts of eosinophilic coagulum were seenin alveoli along with polymorphonuclear leukocytes.
In the section studied from the liver, small vacuoles wereseen throughout the parenchyma. About the central vein, which was slightlydilated, slight sinusoidal congestion was observed.
The sinusoids of the spleen were dilated and congested.
The tubular cytoplasm of the kidney was granular. Many of thenuclei were indistinct or absent. The glomeruli were not remarkable.
Vacuolation of cortical cells was most noticeable in the zona glomerulosa ofthe adrenal glands.
Microscopic diagnosis-(1) Lobular pneumonia with abscessformation, (2) moderate fibrinopurulent pleuritis, (3) severe acute purulentperitonitis, (4) edema of small intestine, and (5) traumatic necrosis of liver.
SUMMARY
This case is an instance of severe abdominal injury. After arelatively short delay, the patient reached the field hospital in surprisinglygood condition. In spite of the many favorable circumstances, however, he diedof pulmonary atelectasis and bronchopneumonia on the second postoperative day.Peritonitis was probably also a contributory factor in the fatality. It isunfortunate that microscopic studies of the lung were not sufficient to excludepulmonary fat embolism.
Case 3
CLINICAL DATA
This patient received a bullet wound of the left abdomen 18 April 1945 at 1800hours. When he was admitted to a field hospital at 2215 hours, his blood pressure was130/80 mm. Hg. He received 500 cc. of group A (his blood group) blood before operation.His condition during the preoperative period was relatively good.
As the peritoneal cavity was being opened, the blood pressure fell abruptlyto 0/0 mm. Hg. The systolic pressure rose to 90 mm. Hg when 1,500 cc. of whole blood were given rapidly. As abdominalexploration was continued, a large quantity of blood was found in the peritonealcavity. There was a severe laceration of the proximal jejunum; a smallsegment was resected and an end-to-
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end anastomosis was performed. A lacerated segment of the colon was exteriorized through a stab wound in the left upper abdomen. Operation was completed19 April at 0220 hours.
Immediately after operation, the systolic blood pressure was170 mm. Hg, which was attributed to a mild transfusion reaction during theoperation. The blood pressure then progressively declined; it was 100/66 mm. Hgat 0830 hours 19 April and only 22/0 mm.Hg at 1200 hours.At this time, the patient appeared moribund. He had vomited large quantities ofblood, and it was thought that the fall in blood pressure was caused by bleedingin the upper gastrointestinal tract.
In an attempt to control this bleeding, a second operation was undertaken at1400 hours 19 April.At this operation, no blood was found in the peritoneal cavity. The originaljejunal anastomosis was examined through an opening made in the bowel justdistal to it. At this time, although he had had 3,000 cc. ofblood just before the operation and during its course, the patient was in severeshock. No point of bleeding could be found along the line of resection. Theanastomosis was, nevertheless, reenforced by an additional row ofthrough-and-through sutures, and the jejunotomy was closed. A gastrotomy was thenperformed, and a large volume of clotted blood was removed from the stomach.There was no evidence of gastric bleeding from the mucosal surface, which wasexamined as completely as possible through the incision.
After the second operation, the blood pressure was 80/0 mm. Hg. By 1830 hours, it had fallen to20/0 mm. Hg, and it did not againexceed this level. The patient expired in profound shock at 2220 hours 19 April 1945, 28hoursafter wounding.
During his brief hospitalization, this patient received 5,500cc. of whole blood, all group Aand all carefully crossmatched with his blood.
AUTOPSY
Autopsy was performed 13 hours after death (Poxdorf, Germany).
Gross observations-The body was not remarkable except for considerabledependent lividity.
The lungs showed only post mortem hypostasis.
The abdominal cavity was not remarkable except for the thin,opaque, fibrinous exudate which covered several loops of small bowel. Thisportion of the bowel was not distended, and there was no appreciable collectionof purulent exudate.
The spleen was moderately enlarged and rather soft and appeared somewhat lesscongested than is usual after massive transfusion therapy.
The gastrotomy, jejunotomy, and jejunal anastomosis 8 cm.distal to the ligament of Treitz were all snugly sutured, and there was noevidence of leakage of bowel contents. When the gastrointestinal tract wasopened, about 300 cc. of old blood were found in the stomach, and a small amountof similar blood was also found in the loop of jejunum at the site ofanastomosis. The duo-
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denum, which was free of blood, was deeply bile stained. In an attempt tolocate a possible source of bleeding, the mesenteric vessels leading to thejejunojejunostomy were cannulated and infused with water, but no vascular leakwas disclosed. Since no blood was present distal to the jejunostomy, the upper gastrointestinal tract was examined minutely. No source of hemorrhagewas present. A small, shallow excoriation of the distal esophagus and another inthe first portion of the duodenum showed no evidence of tissue reaction, and novessels were exposed. No varices were present in the lower esophagus.
Thekidneys were somewhat smaller than usual but were not remarkable on section. Theleft kidney and adrenal were partly surrounded by the blood in theretroperitoneal area.
Gross anatomic diagnosis-(1) Penetrating bullet wound of abdomen withsevere laceration of proximal jejunum, secondary resection and jejunostomy,jejunotomy; perforation of transverse colon, colostomy; and (2) exsanguinatingpostoperative hemorrhage from upper jejunum secondary to lacerating wound ofjejunum, with the operations described.
Comment-A very careful examination of the uppergastrointestinal tract failed to reveal any source of hemorrhage. The mostlikely sequence of events, therefore, is that the patient bled extensively fromthe initial jejunojejunostomy. It may be that no bleeding was found at thesecond operation because of the very low blood pressure at the time. The failureof response to transfusion therapy before and during the second operation isprobably related to the considerable time during which the blood pressureremained at a very low level. From the evidence obtained at autopsy, the secondrow of sutures about the jejunum was apparently successful in preventing furtherhemorrhage, but fatal hemorrhage had already occurred.
The histologic picture of the kidneys will be of interest in this case, inview of the massive therapy with type-specific blood. During the 10 hours thepatient was on the ward between operations, there was no recorded output ofurine. During most of this time, the blood pressure was below the levelnecessary for renal filtration.
Microscopic observations-The sections from the lungs showed confluentpatches of bronchopneumonia. The exudate was hemorrhagic in a few foci butchiefly showed polymorphonuclear leukocytes. In another section, scattered,small areas of atelectasis were seen. Two small vessels were thrombosed. Thealveolar septa were hyperemic.
Sections from the liver showed the centers of the lobules to be congested.The liver cells in these regions contained granular brown pigment (lipochrome).
The pulp of the spleen was moderately congested. The malpighian bodies werelarge and conspicuous, with active secondary follicles, in some of which muchfree and phagocytized nuclear debris was present.
The only change noted in a section from the gastroesophageal junction wasautolysis of the gastric mucosa.
The epithelium lining some of the collecting tubules andHenle's loops in
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the kidney showed degeneration and desquamation. With this exception, bothglomeruli and tubules appeared normal.
Comment-The degenerative changes in the kidney in thiscase were not pronounced and may be entirely post mortem changes. One would bemore inclined, however, to attribute them to the prolonged, severe shock whichthis patient sustained.
The fact that this patient received 5,500 cc. of bloodwithout histologic evidence of incompatibility is a tribute to those responsiblefor the transfusions. In similar cases, the experience has been quite thecontrary, especially when group O blood has been given to a group A patient. (J.G. R.)
SUMMARY
In this case, postoperative hemorrhage from a jejunalanastomosis was responsible for prolonged, severe shock and eventual death.Microscopic examination of the kidneys failed to reveal the presence of pigmentnephropathy, which might have been expected because of its frequency undersimilar circumstances. The following factors may offer a partial explanation forthe absence of such a lesion: (1) The use of group-specific blood instead of thecustomary low-titer group O blood in the resuscitation of a group A patient, and(2) the failure of the blood pressure to reach the glomerular filtrationpressure throughout the prolonged period of shock. Presumably, pigment casts donot appear unless some degree of glomerular filtration is resumed or ismaintained after the initial insult.
Case 4
CLINICAL DATA
This patient received an accidental bullet wound on 4 May 1945, at 0945hours. The wound of entrance was located at the right costal margin in themidclavicular line, and the wound of exit was just lateral to the inferior tipof the left scapula. When he was received in a clearing station immediatelyafter injury, the blood pressure was 120/60 mm. Hg, and the pulse 130. He wasgiven 125 cc. of plasma, and the 5th to 12th intercostal nerves on the rightside were blocked with procaine. The patient was then moved forward with thefield hospital which was in convoy at the time. Upon his arrival at the newinstallation, the blood pressure was 90/50 mm. Hg, and the pulse was 140.
A right thoracentesis was not productive, but 635 cc. of blood were removedfrom the left chest. The patient complained of extreme pain in the abdomen,right chest, and both shoulders. The response to the administration of 750 cc.of plasma and 635 cc. of blood by autotransfusion was poor.
Epidural block with procaine was performed, with good results, but severebilateral pains in the shoulders persisted. When the patient was turned on hisside before this procedure, there was a transitory fall in the blood pressure,but the block was accomplished without difficulty. Just before operation, theblood pressure was 84/50 mm. Hg. The patient's blood belonged to group B.
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Gas-oxygen-ether endotracheal anesthesia was begun at 1815 hours. The woundof exit was debrided, and a thoracotomy was performed through the left ninthintracostal space, with resection of a fragment of the ninth rib. Splenectomyand suture of a laceration of the greater curvature of the stomach were carriedout through a transdiaphragmatic incision. Laparotomy was then performed, withclosure of a perforation in the upper portion of the lesser curvature of thestomach. The missile track had traversed the left lobe of the liver.
Just before thoracotomy, when the patient was turned on his right side, therewas a marked fall of blood pressure. Within a short time, he was given 1,500 cc.of whole blood and 250 cc. of plasma. The agglutinin titers of the blood whichhe received at this time were not known; no blood with known agglutinin titerwas available.
On 5 May, the day after wounding, the patient's condition was poor, becauseof atelectasis of the left lung. After tracheal aspiration, there was anincreased density of breath sounds on the left side and a lessening of cyanosis.The abdomen was flat. There was considerable drainage of bile. Approximately 600cc. of bloody fluid drained from the left chest. The hematocrit was 37 and thehemoglobin 13 gm. percent; the plasma protein was 5.8 gm. percent. The systolicblood pressure was 85-90 mm. Hg. Intravenous fluids consisted of 500 cc. of plasma and 500 cc. of blood. The urine outputsince operation was 700 cc. The serum showed no evidence of hemolysis.
On 6 May, the patient was somewhat improved after tracheal aspiration, withremoval of dark, blood-tinged mucus. Aeration of the left chest was better, buta beginning pneumonitis was suspected. The temperature was 101?-102? F. byrectum. The urinary output was 200 cc.; albumin 1 plus was present. The bloodpressure was 100/60. The patient was irrational and required sedation, for whichparaldehyde was used. He perspired profusely, and venous distention was pronounced. All fluids were discontinued.
On 7 May, the left chest was clearing. Bronchial breath sounds were heardover the right base. Oxygen was administered by mask.
At 1300 hours, the patient was moved to the X-ray table. Here he rapidlybecame cyanotic, in spite of continued oxygen administration, and failed torespond after endotracheal suction. The superficial veins were greatly distended. He died 7 May 1945 at 1400 hours, about 76 hours after wounding.
AUTOPSY
Autopsy was performed 1 hour and 15 minutes after death (Adelstetten,Germany).
Gross observations-There was considerable evidence of dehydration. Theveins of the arms and neck were quite distended. In addition to the healingsurgical incisions, the wound of entry lay just inferior to the right costalmargin, and the wound of exit was at the level of the ninth rib just lateral tothe tip of the left scapula.
The peritoneal cavity contained a small amount of clotted blood. The surfaceswere smooth and glistening and there was no general fibrinopurulent
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exudate. Along the drainage tracks to the posteroinferioraspect of the liver and the anterior portion of the stomach was a moderatedeposit of yellow, fibrinopurulent exudate. There was no fluid or bile in thesubhepatic space. The diaphragm was at the level of the fifth rib bilaterally.
The right chest contained about 75 cc. of clotted blood. Amoderate amount of air escaped from the left chest when the cavity was openedand pressure was applied to the sternum. The chest on this side contained 400cc. of bloody, turbid fluid, which was enmeshed in fibrinous strands and whichcompressed the lung more or less uniformly. Anteriorly, a fibrinopurulent-linedpocket was present, with a capacity of approximately 250 cc.; it appeared tohave contained air. The left diaphragm was sutured without leakage.
The pericardial cavity contained about 40 cc. of clear,straw-colored fluid. The heart appeared considerably distended, especially onthe right. The right auricle was distended by blood, which brought thetrabeculae into sharp relief. The tricuspid valve measured 13.0 cm. in circumference. Therewere scattered subepicardial petechiae, chiefly over the posterior cardiacaspect along the coronary sulcus.
The left lung was moderately reduced in size and air content. The surface wascovered by a shaggy, yellow-pink, fibrinopurulent exudate in which were embeddedforeign particles with the appearance of food. Both lungs were greatly congestedand edematous, particularly in the dependent portions. Edema was more severe onthe right, and the right lung was somewhat heavier than the left. Both, however,were considerably increased in weight. Section of the right lung revealed it tobe practically airless. Dark, serosanguineous fluid oozed freely from the cutsurface. The right lower lobe contained no areas of consolidation, but smallareas of early consolidation were present in the subpleural portion of the rightupper lobe. There was no consolidation of the left lung, but all bronchicontained a copious, blood-tinged, serous fluid streaked with purulent exudate.No demonstrable isolated bronchial obstruction existed; rather, obstruction wasgeneralized. There was moderately severe contusion of, and hemorrhage into, theparenchyma of the inferior portion of the left lower lobe.
The liver was not generally remarkable. The missile had entered the left lobeat the falciform ligament anteriorly and had emerged near the lesser curvatureof the stomach. There was the usual degree of infarct necrosis along the missile track. There was no gross evidence of suppuration.
There were two sutured perforations of the fundus of the stomach; no leakagewas noted along either suture line.
The kidneys, which were similar in appearance, were both considerablyswollen, particularly in the anteroposterior diameter. The smooth corticalsurface was pale yellow gray and faintly mottled. On section, the bulging cortexappeared pale and opaque. The pyramidal striations were moderately increased.The renal pelves and vessels were negative.
Gross anatomic diagnosis-(1) Bullet wound of left thoracoabdominal area,with moderately severe perforating wound of left lobe of liver; severe
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perforating wound of stomach with acute fibrinopurulentperitonitis localized to subhepatic region; laceration of spleen, splenectomy;healing perforation of left posterolateral diaphragm; severe contusion of lowerlobe of left lung; complete compound fracture of left ninth rib; (2) severe leftfibrinopurulent pleuritis, secondary to perforating wound of stomach andperforation of left diaphragm; (3) moderate partial left pneumothorax secondaryto contusion of lower lobe of left lung and complete compound fracture of leftninth rib; (4) possible hemoglobinuric nephropathy or shock kidney, asmanifested by severe bilateral pulmonary congestion and edema; acute congestiveheart failure, predominantly right sided; clinical oliguria; and (5) acutepurulent early bronchopneumonia of upper lobe of right lung.
Comment-No group O blood in which the agglutinin titerhad been determined was available for this patient. The only blood which couldbe used did not fall into the category of low-titer blood. Under such circumstances, autotransfusion would ordinarily have been particularly desirable, butin this case, because of the injury of the stomach with soiling of the leftpleura, it was incorrect.
This patient appeared to have been extremely sensitive to changes inposition. On two separate occasions, the blood pressure fell sharply when he wasturned on his side. Before thoracotomy, the blood pressure remained atexcessively low levels for a period of about 80 minutes, in spite of liberaltransfusion therapy. During such periods, the renal blood flow must be markedlyreduced, and it is suggested that this was a crucial factor in the production ofpigment nephropathy in this case.
The delay before operation was unusually long. Part of it wascaused by the fact that the field hospital was in process of moving when thepatient reached the clearing station. During the delay, his conditiondeteriorated considerably, and liberal replacement therapy was necessary beforeoperation. Unfortunately, however, operation was not urged at the earliestpossible moment because of the mistaken belief that there had been noperforation of a hollow viscus. Obviously, the optimum time of operation wouldhave been when the patient first reached the clearing station, only a short timeafter injury.
Microscopic observations-In one section of the lungs, the tissue waspacked with red blood cells. Several vessels contained thrombi. In anothersection, the congestion was almost as severe, and the bronchiolar walls contained a purulent exudate. In a third section, which was free from congestion,the alveolar walls showed patchy approximation and stretching. There was afibrinopurulent exudate on the pleura.
Rare round cells were found beneath the epicardium. No myocardial changeswere noted.
In one section of the liver was a large zone of infarctnecrosis, bordered by a region of inflammatory exudate, beyond which wasnormal-appearing liver tissue. The peritoneal surface showed a thick, purulentexudate. Both in the infarcted area and in the exudate were masses of bacteria.
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Sections from the kidneys showed amorphous material and lightly stainingspherical bodies in capsular spaces and proximal convoluted tubules, which weremoderately dilated. Brown, granular casts were present in the distal tubules andloops of Henle. Nuclear pyknosis and cell shrinkage were noted in relation tothese casts. There was moderate swelling of the capsular and convoluted tubularepithelium. A few cysts filled with pink-staining coagulum were present.
One zone of cortical necrosis was noted in the adrenalglands. Otherwise, there was a decrease in the usual vacuolar appearance of thecortical cells. Adjacent fat tissue showed regions in which cells had lost theirvacuolated structure.
Microscopic diagnosis-(1) Focal necrosis of the adrenal gland; and (2)moderately severe, early hemoglobinuric nephrosis.
Comment-The microscopic findings are in generalagreement with the gross findings. Although the kidney lesion was classified ashemoglobinuric nephrosis, death appears to be related to trauma, peritonealinfection, and pulmonary circulatory obstruction rather than to uremia.
SUMMARY
This patient affords an example of a severe thoracoabdominal wound in whichthe military exigency afforded an opportunity to observe the steadydeterioration which can be caused in a wounded man's condition by the delay inoperation. Resuscitation and operation were made much more difficult in thiscase by the passage of a relatively short period of time. Failure to realizethat a wound of the stomach was present was partly responsible for the delay andwas also responsible for the use of autotransfusion in the presence ofcontamination of the pleura by gastric contents.
Microscopic examination confirmed the presence of pigment nephropathy, whichaccounts for the oliguria and gross anatomic changes in the kidneys. Pulmonaryedema and mild congestive heart failure were again noted as a terminalmanifestation of the renal failure which follows severe traumatic shock.
Case 5
CLINICAL DATA
This patient received a bullet wound of the left buttock 1 June 1944, at 0300hours. He was given 15 mg.of morphine tartrate at 0305 hoursand was brought to the collecting station at 0600 hours. Here his wound wasre-dressed, in preparation for evacuation to the rear. The record indicates thathe seemed in relatively good condition, but at 0630 hours, while he was urinating, helapsed into deep shock and stopped breathing. After the use of artificialrespiration and the administration of 1,750 cc. of plasma, supplemented bytwo large doses of caffeine sodium benzoate, breathing was resumed. At this time(0815 hours), it was noted that the left pupil was dilated and that there was
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weakness of the face on the left side, with equivocalaphasia. At 0900 hours, improvement was continuing, and at 0930 hours thepatient was sent to the rear. He reached the clearing station at 1000 hours andwas taken at once to the field hospital. At 1005 hours, his blood pressure couldnot be obtained by auscultation or palpation. In spite of a plasma transfusionand oxygen inhalations, he continued poorly oriented. Death occurred at 1200hours. The left pupil was notably larger than the right.
This patient had received a total of 500 cc. of plasma in the fieldhospital. He expired just as whole blood was obtained. His blood pressure wasnot obtainable at any time after he reached the field hospital.
AUTOPSY
Autopsy was performed 2 hours after death (Cori, Italy).
Gross observations-Externally the body was not remarkable except forextreme pallor.
The brain was negative, except that the cerebral vessels wereexceedingly pale. There was no gross area of infarction. The lungs werenegative, except for some patchy atelectasis.
The peritoneal cavity contained an enormous quantity of blood, estimated at4,000 to 5,000 cc.The source was the left hypogastric artery, which was transected at the point atwhich it crosses the brim of the pelvis. There was a large hematoma in theareolar tissue of the retroperitoneal space and along the course of the missile,which was through the medial aspect of the ramus of the ischium. A secondfragment of the bullet lay free in the left upper quadrant of the abdomen. Themesentery of the sigmoid colon and a loop of the mesentery of the small bowelwere perforated, and there were two perforations of the jejunum. It wasimpossible to judge the amount of fecal contamination of the peritoneum with anyaccuracy because of the large amount of blood present in the peritoneal cavity.Contamination, however, was not thought to be great.
Gross anatomic diagnosis-Bullet wound of abdomen,entering by way of left buttock, with laceration of left hypogastric artery andexsanguinating intraperitoneal hemorrhage; two perforations of jejunum; compoundcomminuted fracture of ramus of left ischium.
Comment-There is no reasonable doubt in this case thatdeath was caused by massive intraperitoneal hemorrhage. The cerebral changeswere due to the severe degree of cerebral anoxia. It is regrettable that wholeblood was not available at the time this man reached the field hospital,although its liberal use might not have changed the outcome in the face oflongstanding and profound shock.
Microscopic observations-Examination of sections fromthe lung showed extensive alveolar atelectasis with overdistention of therespiratory bronchioles. This finding is consistent with a story of prolongedartificial respiration. A
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few fat droplets were found in small arteries and arterioles, but the numberwas not sufficient to make them of functional significance.
The choroid plexus appeared edematous. The kidney and brain were negative.
SUMMARY
This case illustrates several important points in connection with shock amongbattle casualties.
1. It may be exceedingly difficult to detect the fact that severe circulatorycollapse is about to occur, particularly when hemorrhage is in progress.
2. Once the blood volume has reached a critical level, arelatively minor happening, in this instance the act of sitting up to urinate,may be followed immediately by the onset of profound shock.
3. It is almost impossible to treat shock caused by severe and progressivehemorrhage with plasma alone.
4. Laparotomy to control hemorrhage offers the only hope ofsuccess in such a case as this, and yet, as in this case, it may be impossibleto prepare the patient adequately for operation in the face of severe bleeding.
Case 6
CLINICAL DATA
This patient, who was 22 years of age, received a shell-fragment wound of theleft buttock 3 October 1944, at 2230 hours. After a delay of unknown duration,he was brought to a field hospital in profound shock. Even after he had received250 cc. of plasma and 2,500 cc. of group O blood (it is believed that his bloodbelonged to group AB), the blood pressure was only 98/60 mm. Hg and the pulsewas 130, but operation was begun without further delay because intra-abdominalhemorrhage was suspected. The patient received 50,000 units of penicillinintramuscularly, but no sulfonamides were given in the field hospital.
Exploration of the abdomen revealed multiple perforations of the small andlarge bowel. In the peritoneal cavity, there was an estimated 1,000 to 1,500 cc.of blood which was found to have come from the region of the bladder on the leftside posteriorly. The retroperitoneal space was opened, and, after considerabledifficulty, the bleeding was brought under control by the ligation of twobranches of the left internal iliac vein. The perforations of the small bowelwere sutured, and a sigmoid colostomy was performed through the left lowerquadrant of the abdomen. The gluteal wound was debrided.
The patient was in a critical state throughout the operation.In spite of the administration of 4,000 cc. of group O blood and 750 cc. ofplasma, his blood pressure was often as low as 40/0 mm. Hg, and at the end ofthe operation, which took 4 hours, the blood pressure was only 90/48 mm. Hg.
On the first postoperative day, the blood pressure was 100/50mm. Hg. The urine was deep red brown and contained 2 to 3 red blood cells perhigh-power field.
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The second day after operation, the blood pressure was 120/70 mm. Hg. Thepatient was moderately dyspneic. Examination of the abdomen revealed no evidenceof peritonitis. Catheterization produced only 10 cc. of urine. Isotonic glucosesolution and 500 cc. of a 2-percent solution of sodium bicarbonate were givenintravenously.
On the third postoperative day, dyspnea was severe. Thepatient was drowsy, and his speech was slurred. The blood pressure was 180/100 mm. Hg. Moist rales were firstnoted throughout both lungs about 2? hours before death. Dyspnea rapidlyworsened, and death occurred at 1830 hours5 October 1944, 44 hours after wounding. The total output of urine from thebeginning of operation until death was about 210 cc.
AUTOPSY
Autopsy was performed 12 hours after death (Elayes, France).
Gross observations-The peritoneal cavity contained 200 cc. of bloodyfluid. There was no exudate other than the generalized matting of loops of smallbowel by fibrin. In the pelvis was a small amount of clotted blood. The lungswere indurated and edematous. Only the kidneys were saved for microscopic study.They were somewhat swollen and appeared to be congested. Small subcapsularhemorrhages were scattered over both renal surfaces, but on section it was foundthat they did not extend into the cortex. The cut surfaces of the kidneys wererather pale.
Gross anatomic diagnosis-(1) Perforating shell-fragmentwound of abdomen with multiple perforations of ileum, multiple perforations ofsigmoid colon, and multiple lacerations of branches of left internal iliac vein;and (2) pigment nephropathy, hemoglobinuric type, possibly due to massivetransfusion of group O blood, with severe pulmonary congestion and edema,manifest clinically by severe oliguria, moderate arterial hypertension, andsevere pulmonary edema.
Comment.-Although the blood group of this patient is notpositively known, it is believed that his blood belonged to group AB. If this betrue, his AB cells were susceptible to agglutination and hemolysis by the anti-Aand anti-B iso-agglutinins found in the plasma of group O blood. The difficultyof providing enough group-specific blood is apparent, as are the shortcomings ofuniversal donor blood under such circumstances.
Microscopic observations-Examination of the kidney tissue revealed thata very large number of collecting tubules, and a smaller number of distalconvoluted tubules, were plugged with pigmented casts. There was slight dilatation of the proximal nephrons. The interstitial tissues were slightlyedematous. In some areas, proliferation of the tubular epithelium was evident,the casts being encapsulated within the tubules. Here and there, smallgranulomas had formed in the interstitial tissues. There were scattered foci oflymphocytic infiltration.
Microscopic diagnosis-Severe hemoglobinuric nephropathy.
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SUMMARY
This case provides another example of posttraumatic renal failure, with themicroscopic finding of pigment nephropathy. Although definite proof is notavailable, it is believed that the transfusion of a large volume of group Oblood contributed to the production of the renal lesion. Perhaps, in thepresence of severe shock, the kidney is particularly liable to injury by arelatively small amount of hemoglobin in the plasma. A moderately severe degreeof hypertension was observed before death; its possible relationship to thepathologic physiology of renal failure is of considerable interest.
Case 7
CLINICAL DATA
This patient, a German prisoner of war with a bullet wound of the abdomen,was first seen 6 March 1945 at 1430 hours.The precise time of wounding was unknown but was probably several hours earlier.He reached a field hospital at 1715 hours,after having received 750 cc.of plasma. At this time, he was in profound shock, and his blood pressure couldnot be obtained. He was stuporous and at times semidelirious, and his appearancewas striking because of a peculiar cherry-red flush of the face and extremitiesand a red mottling of the skin of the trunk. He was moderately dehydrated. Theresponse to 1,500 cc. ofplasma and 1,500 cc. ofblood was poor; the blood pressure rose only to 78/40 mm.Hg, and no clinical improvement was evident. His blood group was O.
Operation was begun 6 March at 2210 hours. Laparotomy revealed extensivecontamination of the peritoneal cavity by 2,000 cc. of bloody fecal material.There were multiple perforations of the jejunum, and the transverse colon wasfound almost completely torn away from its attachments except for a narrow bandof tissue along the mesenteric border. It was necessary to resect about 15 cm. of the small bowel; threeperforations in the jejunum were sutured, and a colostomy was performed. Thepatient received 1,000 cc. of whole blood during the operation.
At the conclusion of the operation, the blood pressure was ata very low level, and there was never any significant rise. Often it wasunobtainable. The patient was stuporous, and death occurred 11 hours afteroperation.
AUTOPSY
Autopsy was performed 4 hours after death (St. Avold, France).
Gross observations-The mottled, pink-gray discoloration of the skin ofthe trunk noted before operation was still present.
The peritoneum showed the effects of severe contamination. Asmall amount of seropurulent fluid was present. The serosal surfaces of thebowel were opaque, dark and congested, and patches of fibrinopurulent exudatewere present.
The heart was rather soft. The right side was distended by blood.
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The pleural cavities were not remarkable, except for an old fibrous pleuritisat both bases.
Both lungs showed considerable hypostatic congestion and partial atelectasisof the dependent and inferior portions.
There was a moderately large laceration of the left lobe of theliver.
The spleen was about three times the usual size and was darkpurple red. The consistency was firm. The pulp, which was uniformly dark purple,did not scrape away easily.
The gastrointestinal tract showed the sutured lacerations and anastomoses ofthe small bowel already described.
The kidneys were of the same size, but the right kidney appeared somewhatmore congested and purple than the left. The cortical surfaces of both kidneysshowed focal punctate hemorrhagic areas, more marked on the right side. Onsection, these hemorrhagic areas were seen to extend varying distances into thecortex in the form of small, blood-suffused columns. On section, the parenchymabulged above the cut edge of the capsule. A few petechiae were present in themucosa of the renal pelvis.
The cortex of the left adrenal gland exhibited several radial hemorrhagicareas in which there was possibly destruction or necrosis of the tissue. Themedullary area was negative.
Gross anatomic diagnosis-(1) Perforating gunshot wound of abdomen, withsevere laceration and avulsion of transverse colon; multiple perforations ofsmall bowel; moderately severe laceration of left lobe of liver; (2) severegeneralized peritonitis, secondary to injuries of transverse colon and smallbowel; (3) extensive hemorrhagic focal necrosis of kidneys and possibly of leftadrenal, causes unknown; (4) moderately severe splenomegaly, possibly secondaryto massive transfusion therapy and peritonitis; and (5) hypostatic pulmonarycongestion and edema, with bilateral partial atelectasis.
Comment-The exact lapse of time between wounding and operation in thiscase was unknown but seems to have been at least 16 to 18 hours.The patient was moribund on admission, as the result of shock and extremeperitoneal contamination.
The case illustrates the difficulty which occasionally was encountered in themanagement of patients with overwhelming contamination of the peritoneum. Oncecontamination of this degree has occurred, effective therapy is difficult eventhough the patient is seen relatively soon after wounding.
The peculiar gray-pink mottling of the skin suggests a considerable degree ofcapillary damage. The pathogenesis of the hemorrhagic columns in the renalcortex is obscure, but is possibly related to the severity of the shock andinfection.
Microscopic observations-There were a few atelectatic patches in thelungs. The alveolar septa were hyperemic. The bronchial walls were infiltratedwith lymphocytes. One small artery was thrombosed. Another section showedscattered small areas of hemorrhage into the peribronchial alveoli.
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The centers of the lobules of the liver were congested. The portal triadswere infiltrated with moderate numbers of lymphocytes.
The malpighian corpuscles had active germinal centers; manycontained foci of degeneration, with nuclear debris. The pulp and sinuses wereengorged with blood.
A moderate number of distal convoluted and collecting tubules in the kidneyscontained pigmented casts. Protein precipitate was seen in many of theconvoluted tubules. Some of the tubules contained hyalin casts. Neitherinflammatory reaction nor edema was present in the interstitial tissues. A smallnumber of basophilic structures, probably sulfonamide crystals, were seen.Vascular congestion was pronounced.
There was pronounced congestion of both the inner zone of the cortex and ofthe medulla. Small foci of lymphocytes were seen in the medulla.
The serosallayer of the intestine was thickened and edematous. It was infiltrated withlymphocytes, histiocytes, and polymorphonuclear leukocytes. The mucosa wascovered with blood, serum, and epithelial debris.
Microscopic diagnosis-(1) Hemoglobinuric nephropathy, moderately severe;and (2) focal necroses in spleen.
Comment-In the absence of other factors which producepigmented casts in the renal tubules, the renal lesion in this case must beattributed to the blood transfusions which the patient received. His blood groupwas O, and he received 1,500 cc. of O bank blood. If the blood typings werecorrect, the crossmatches negative, and the blood free of hemolysis beforetransfusion, there is no evident explanation for the nephropathy. (J. G. R.)
SUMMARY
This patient sustained an extremely severe wound of theabdomen with widespread peritoneal contamination, and his status on arrival at afield hospital reflected the relatively long lapse of time since the injury. Hedied within a short time, in spite of replacement therapy and prompt surgicalcare. Failure to survive such a wound seems to depend upon (1) the severity ofthe hemorrhage and (2) the deleterious effects of massive peritonealcontamination. It seems likely that appropriate bacteriologic studies would haverevealed significant findings in this instance.
Case 8
CLINICAL DATA
This patient received a perforating bullet wound of the abdomen 30 March1945, at 1740 hours. When he reached a field hospital at 1945 hours, he was inprofound shock, with a blood pressure of 42/20 mm. Hg and a pulse of 128. Hisresponse to 500 cc. of plasma and 1,500 cc. of whole blood was not good. At 0030hours 31 March, his blood pressure was only 80/60. His blood group was O.
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Laparotomy was performed about 4? hoursafter the patient was received at the field hospital. The peritoneal cavity wasfull of blood, and there were perforations of the stomach and proximal ileum, aswell as a laceration of the left lobe of the liver. Severe bleeding was inprogress from the gastrohepatic ligament; it was stopped as promptly aspossible. The perforations in the intestine were then sutured, and a largedefect in the transverse mesocolon was repaired. The spleen and the left kidney,both of which were badly lacerated, were removed. The wounds of entrance andexit were debrided. Throughout the operation, the patient's condition wascritical in spite of the administration of 250 cc.of plasma and 2,750 cc.of whole blood.
He failed to improve after operation and died at 0005 hours1 April 1945, about 24 hoursafter operation and 28 hours after injury.
AUTOPSY
Autopsy was performed 15 hoursafter death (Grossostheim, Germany).
Gross observations.-There wasconsiderable post mortem lividity of the neck and face. The abdomen wasmoderately distended.
The left chest contained 600 cc. and the right chest 200 cc. of blood-tingedfluid. The peritoneal cavity contained about 800 cc. of cloudy, blood-tingedfluid. The loops of small bowel were loosely bound together by strands offibrinopurulent exudate, particularly in the vicinity of the suturedperforations of the ileum. No free purulent exudate was present in theperitoneal cavity. The adipose tissue of the colon and omentum exhibitednumerous focal areas 0.5 to 1.5 cm. in diameter, of chalky,gray-white discoloration, particularly in the upper abdomen.
The heart was not remarkable except for the presence of subepicardialecchymosis posteriorly along the coronary sulcus and over the wall of the leftauricle.
The lungs were both markedly increased in weight and showed hypostaticcongestion and atelectasis. The tracheobronchial tree was filled with atenacious, blood-tinged mucoid exudate which was occasionally flecked bypurulent material. Some of the smaller bronchi contained similar material. Therewas no evidence of established pneumonic consolidation.
The left lobe of the liver, which was the site of an extensive laceration, aswell as a portion of the right lobe, was pale, yellow gray, and of abnormallysoft consistency.
The body of the pancreas was partially torn away from its attachments, andthere had been considerable autolysis of the contiguous tissues. The portion ofpancreas adjacent to the bullet track was pale, reddish gray, and extremely softin consistency. Surrounding this area were evidences of old hemorrhage. Nopurulent exudate, however, was present in the pancreatic area.
The gastrointestinal tract showed only healing sutured perforations.
Gross anatomic diagnosis.-(1) Perforating gunshot wound of left abdo-
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men, with severe laceration of left lobe of liver, possiblenecrosis of most of left lobe and of portion of right lobe; two healingperforations of proximal ileum; laceration or contusion of body of pancreas withautolysis of pancreatic tissue and acute fat necrosis throughout peritonealcavity; severe laceration of spleen, surgical removal; severe laceration of leftkidney, surgical removal; (2) severe bilateral pulmonary atelectasis, secondaryto bronchial obstruction by mucus; (3) subepicardial hemorrhage, probably due toasphyxia, secondary to pulmonary atelectasis; (4) acute fibrinopurulentperitonitis, secondary to perforating wounds of intestine and liver; and (5)moderately severe bilateral pleural effusion.
Comment-Aside from the severe trauma to several organs,the insult of extreme pulmonary atelectasis appears to be immediatelyresponsible for the death, which seemed inevitable from the time of wounding.
Microscopic observations-Numerous hemorrhages werepresent in the fat tissue around the adrenal gland. Several small hemorrhageswere also seen in the medullary portion. A portion of the cortex stained a veryfaint pink resembling an area of infarction. The sinusoids were congested.
Numerous hemorrhagic areas were seen in two slides of the lung tissue. Areasof atelectasis were present. Cells of the heart-failure type were present in allareas. In a third slide, the tissue was for the most part normal, but in onearea were alveoli filled with protein-rich fluid in which were manyerythrocytes.
Granules of brown pigment were seen in the muscle bundles of the heart. Somehemorrhage was visible in the fat of the pericardium.
Extensive areas of hemorrhage and necrosis of liver substancewere observed along one side of the first slide examined. In the immediatevicinity of the traumatized area were considerable accumulations of polymorphonuclear leukocytes and lymphocytes. In some areas were evidences of small abscessformation. Numerous lymphocytes were seen in nearly all the periportal areas. Ina second slide, extensive areas of tissue destruction were present. The livercells were dark-staining cords without nuclei.
SUMMARY
The findings in this case are characteristic of the massiveabdominal injuries which are by no means rare among severely wounded men. Woundsof this kind produce profound shock by destruction of tissue, hemorrhage, andmassive peritoneal contamination. Death almost always occurs with little delayin spite of liberal replacement therapy and prompt surgical care. If the patientdoes survive the immediate postoperative period, the renal damage of the periodof profound shock may prove fatal within a few days.
The microscopic observations in this case suggest that therewas widespread necrosis of liver tissue which was not restricted to the missiletrack. Since the kidneys were not examined microscopically, the question of arenal lesion cannot be settled.
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Case 9
CLINICAL DATA
This patient received a perforating bullet wound of the right buttock 30March 1945, at1700 hours. When he was received at the field hospital at 1945 hours, he appeared moribund;neither pulse nor blood pressure could be obtained. In the space of an hour, hewas given 250 cc.of plasma and 2,500 cc. ofgroup O blood, but the response was poor. Laparotomy was undertaken in thebelief that hemorrhage was continuing. Just before operation, the blood pressurewas 50/30 mm.Hg. The patient's blood belonged to group O.
Exploration of the wound track fromthe right gluteal fold to the right iliac fossa revealed (1) a completelaceration of the right external iliac artery and vein, (2) a completelaceration of the right gluteal artery and vein, (3) division of the rightfemoral nerve, and (4) a perforation of the terminal ileum. All the injuredvessels were ligated, and the ileal perforation was closed. During theoperation, an extensive expanding retroperitoneal hematoma was noted. At the endof the operation, the blood pressure was 70/40 mm.Hg; 2,500 cc. of groupO whole blood had been given while it was in progress.
The patient's condition continued critical after operation. On the firstpostoperative day, the hemoglobin was 55 percentof normal; the red blood cells numbered 3,290,000 percubic millimeter. On the second day, the volume of urine was 225cc. On the third day, no urinewas excreted. The right leg was gangrenous, with a line of demarcation justbelow the knee. On the fourth day, no urine was excreted. The blood pressure was160/80 mm. Hg. Venesection was carried out for the relief of pulmonary edema,but dyspnea continued. The patient died 3 April 1945, at 1635 hours, about 96 hours after wounding.
AUTOPSY
Autopsy was performed 1 hour and 25 minutesafter death (Grossostheim, Germany).
Gross observations-The sclerae were slightly icteric.There was considerable brawny edema of the whole of the right leg, with aneffusion into the knee joint and beginning dry gangrene below the knee.
The pericardial and pleural cavities contained small amountsof straw-colored fluid. There was a large bilateral retroperitoneal hematoma,which was larger on the right. Blood had disseminated upward as high as theperirenal tissue bilaterally and downward to fill the areolar tissue about thebladder. The right external iliac artery and vein and the right gluteal arteryand vein had been ligated.
The heart was pale. Subepicardial petechial hemorrhages weredistributed over the surface. The right ventricle was unusually soft. Thetricuspid valve measured 13.5 cm.,the mitral valve 10.3 cm., and the aortic valve 5.8 cm. Thecoronary vessels were normal.
Both lungs were partially atelectatic. The cut surface was very wet andexuded a large quantity of serosanguineous fluid. The bronchi were filled withedema fluid.
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The liver was apparently slightly increased in size, but on section theparenchyma was not remarkable.
The spleen was moderately increased in size. The consistency was somewhatsofter than normal and the malpighian bodies were prominent.
The gastrointestinal tract was negative, apart from a healing laceration ofthe ileum.
The kidneys, both of which presented the same appearance, were somewhatsmaller than usual. The surfaces were smooth and were deep purple red, with apeculiar, finely mottled, nutmeg appearance. On section, the cortex was somewhatpale in comparison to the color of the renal surface. The peripheral portions ofthe pyramids as seen on section were dark, due to the presence of fine, closelyplaced, red-brown striae. The renal vessels were negative.
Gross anatomic diagnosis-(1) Perforating bullet wound ofabdomen via right buttock, with laceration of right external iliac artery andvein, laceration of right gluteal artery and vein, division of right femoralnerve, healing perforation of terminal ileum, and incomplete fracture of rightilium; (2) severe retroperitoneal hemorrhage, secondary to laceration of iliacvessels; (3) edema and dry gangrene of lower right leg, secondary to ligation ofiliac and gluteal vessels; (4) pigment nephropathy possibly due to shock andischemia of right leg, as evidenced clinically by oliguria, slight hypertension,and pulmonary edema; (5) pulmonary congestion, bilateral, severe, with partialatelectasis, possibly due to uremic pneumonitis and left heart failure secondaryto pigment nephropathy; (6) multiple petechial subepicardial hemorrhage; and (7)icterus, slight.
Comment-This case epitomizes the outcome in manypatients who have suffered severe shock for long periods of time. In suchinstances, the ultimate decline is manifest chiefly as cardiorenaldecompensation with increasing pulmonary edema, particularly when relativelylarge quantities of fluid are given. Ischemic muscle necrosis, massivetransfusion therapy, and the extensive retroperitoneal hematoma present in thiscase may have contributed to the pigment which will almost certainly be found inthe renal tubules on microscopic examination. Whatever may be the source of thepigment, it would appear that in this case the severe degree of shock was themost important factor in the development of the renal lesion.
The blood which this patient received was fresh; it was drawn in the fieldhospital just before it was administered. All flasks were inspected forhemolysis, and none was apparent. Routine crossmatchings showed no incompatibility, and the group of all the blood used was carefully checked just beforetransfusion.
Microscopic observations-A few small areas in thepulmonary alveoli contained fibrin and a few polymorphonuclear and mononuclearcells. The interlobular septa were edematous. On frozen section a large numberof fat emboli were observed in the alveolar capillaries and arterioles.
The portal triads were infiltrated with moderate numbers of lymphocytes andeosinophiles.
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The pulp of the spleen was moderately congested. There were increased numbersof eosinophiles in the malpighian bodies.
A very large number of the distal convoluted and collecting tubules in thekidney sections were plugged with pigmented casts. Sulfonamide crystals wereseen here and there in the tubules. A few small foci of lymphocytes were foundin the interstitial tissues. Epithelial proliferation had occurred about some ofthe casts in the pyramid. No fat emboli were seen on frozen section.
Sections ofthe pancreas showed cystic dilatation of a small number of acini, whichcontained pink-staining material.
Microscopic diagnosis-(1) Severe pulmonary fat embolism; and (2) severepigment nephropathy, hemoglobinuric type.
SUMMARY
Because of his severe vascular injury and the resulting hemorrhage, thispatient remained in shock for a prolonged interval. In spite of the fact thatresuscitation and operation were accomplished with a fair degree of success,postoperative oliguria occurred, and death followed, from pulmonary edema, onthe fourth day after operation. Microscopic examination confirmed the presenceof pigment nephropathy and revealed, in addition, a high degree of pulmonary fatembolism. It is suggested that the fat embolism may have been the more importantfactor in the pulmonary edema which occurred on the fourth day after operation.It seems unlikely, however, that this patient could have survived therenal lesion.
The amount of trauma to the bone appears to have beenrelatively mild in this case, and it may be that injury of gluteal adiposetissue contributed to the pulmonary embolism.
Case 10
CLINICAL DATA
This patient received a perforating shell-fragment wound of the thorax andabdomen 14 December 1944, at 1020 hours. When he reached a field hospital at1245 hours, the blood pressure was 80/34. Hg, the pulse was 140, and he was inmoderately severe shock. He complained of shortness of breath and of right-sidedchest pain. The wound of entry was at the left lateral costal margin and thewound of exit in the fourth interspace in the right anterior axillary line.Right thoracentesis produced 960 cc. of blood. The right 4th to 12th intercostalnerves were infiltrated with procaine, and pain in the chest lessened. At 1525hours, after the administration of 500 cc. of plasma and 1,000 cc. of wholeblood, the blood pressure was 122/64 mm. Hg. A catheterized specimen of urineshowed occasional erythrocytes.
Thoracotomy was begun at 1600 hours, under endotracheal gas-oxygen-etheranesthesia. The thorax was opened in the right fifth interspace, and fragmentsof the fifth costal cartilage were removed. Five hundred cubic centimeters ofblood were aspirated from the right pleural cavity. A small laceration
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of the lower lobe of the right lung was closed with amattress suture. After a 6-cm. laceration of the right diaphragm had beensutured, the thoracotomy incision was closed. The sucking wound of the anteriorright chest was debrided and closed.
Laparotomy revealed much blood in the peritoneal cavity. Thesource appeared to be the severely lacerated and comminuted left lobe of theliver. There was an extremely severe laceration of the left transverse colon,which involved about three-fourths of its circumference for a distance of 7 cm.This portion of the large bowel was exteriorized through a left subcostalincision. No perforations were evident in the remainder of the gastrointestinaltract, and at this time there was no evidence of an acute inflammatory processwithin the peritoneal cavity. The spleen and kidneys were not injured. Duringthe course of the operation, the patient's condition remained poor, although hereceived 1,500 cc. of whole blood, 750 cc. of plasma, and an autotransfusion ofthe 960 cc. of whole blood which had been aspirated from the right chest beforeoperation. The operation required 2 hours.
Immediately after operation, the blood pressure was 40/0 mm.Hg, the pulse 104, and the respiration 24. The respirations were described asgurgling. The patient reacted from anesthesia at 0100 hours 15 December 1944,but respirations ceased at 0625 hours, about 20 hours after wounding.
AUTOPSY
Autopsy was performed 7 hours after death (Meisenthal, France).
Gross observations-The peritoneal cavity contained 300 cc. offoul-smelling, bloody fluid. There was an extensive laceration of the left lobeof the liver. The omentum, which was dirty and hemorrhagic, was displaced aboutthe colostomy. Gentle pressure upon the stomach caused leakage of gas andgastric contents through a small aperture in the midportion of the omentum justinferior to its attachment to the greater gastric curvature. The loops of smallbowel, particularly those in the lower portion of the peritoneal cavity,exhibited evidences of marked peritoneal contamination. The serosa was injected,bright red, and more opaque than normal. No fibrinopurulent exudate wasrecognized.
The right pleural cavity contained 300 cc. of blood, butthere was relatively little fibrinous exudate. There was a defect in the fifthcostal cartilage and a fracture of the sixth costal cartilage on the right.
The heart was somewhat dilated. The myocardium was softer than usual inconsistency.
The appearance of both lungs was the same. They were considerably increasedin weight and exhibited generalized atelectasis and loss of resiliency. Thelaceration of the right lower lobe had been closed, and contusion of thepulmonary parenchyma was not marked. On section, much blood and serous fluiddripped from the cut surfaces. The main bronchi and their smaller branches wereoccluded by a tenacious, mucosanguineous exudate which appeared to beresponsible for the observed atelectasis. There was no evidence
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of bronchopneumonia, but some of the smaller bronchi contained moderateamounts of mucopurulent exudate.
The spleen was small and soft but not otherwise remarkable.
The liver was of normal size. There was marked destruction of the left lobe,but no evidence of suppuration, and little autolysis was observed along thetrack of the missile. No exudate was present, nor was there a discernible zone of leukocytic infiltration. Thrombosis of the hepatic veins was notedonly in the immediate vicinity of the laceration and was not striking. Onsection, the right lobe of the liver was not remarkable.
The stomach was greatly distended by partially digested food.There was a small (8-mm.) unsutured perforation in the greater curvature 10 cm.proximal to the pylorus. The contamination of the lesser peritoneal sac wasminimal, and gastric contents appeared to have been extruded into the mainperitoneal cavity through a small perforation in the omentum. A small (3-mm.)perforation of the ileum was located about 90 cm. from the ileocecal valve.
The kidneys were not enlarged, but the smooth corticalsurfaces were pale, and on section the cortex showed faintly hemorrhagicmarkings through the pale yellow-gray substance. The renal pyramids were faintlystriated by red-brown markings and had a peculiar pale-pink coloration.
Gross anatomic diagnosis-(1) Thoracoabdominalshell-fragment wound, with entrance at left costal margin and exit via rightchest at level of fifth costal cartilage, with small perforation of greatercurvature of stomach; small perforation of terminal ileum; severe laceration oftransverse colon, loop colostomy; severe laceration and comminution of left lobeof liver; sutured perforation of right leaf of diaphragm; moderately severelaceration of lower lobe of right lung, closed; multiple compound fractures ofright fifth and sixth costal cartilages and left sixth and seventh costalcartilages; (2) severe bilateral bronchial obstruction with pulmonaryatelectasis; (3) acute generalized peritonitis, secondary to perforating woundsof stomach, terminal ileum, and transverse colon; (4) moderate right hemothorax,secondary to thoracoabdominal wound; and (5) congestion and edema of lungs,probably secondary to bronchial obstruction and atelectasis.
Comment-The severe laceration of the liver and the extreme peritonealcontamination were ominous findings at operation. It is remarkable, however,that there was so little evidence of peritonitis at this time. A severefibrinopurulent peritonitis was present at autopsy. The difference was perhapsdue simply to the passage of time, though it must be remembered that unclosedperforations of the stomach and ileum had permitted additional contamination ofthe peritoneal cavity.
The large amount of bloodstained mucoid exudate present inthe bronchi at autopsy was remarkable. It did not seem reasonable to try toaccount for it simply on the basis of the contusion of the right lung. Thesevere atelectasis appears to have been immediately responsible for death, andits development may have been favored by the fact that after operation thepatient received two injections (each of 0.008 gm.) of morphine sulfate.
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The use of autotransfusion under the circumstances of thiscase constituted an error of judgment. In the presence of a large wound of thecolon, the blood could scarcely have escaped contamination, and its useundoubtedly contributed to the fatality.
Microscopic observations-The lung tissue showed largeareas of atelectasis. The alveolar septa were hyperemic. Many pigmentedmacrophages were seen within the alveoli.
One section of the liver was essentially normal. The other showed extensivetraumatic infarction.
Examination of the spleen showed the malpighian bodies to be numerous andlarge and the pulp slightly congested.
A few cystic tubules in the kidney were lined with flattened epitheliumcontaining pigmented material. The epithelial cells in some of the collectingtubules contained granules of golden-brown pigment. A single focus oflymphocytes was seen in the interstitial tissues.
One of the interlobular septa seen in the section from the pancreas wasinfiltrated with polymorphonuclear leukocytes and a few histiocytes.
A section of voluntary muscle showed hemorrhage and polymorphonuclearleukocyte infiltration into the tissues between the muscle bundles.
A smallamount of purulent exudate covered a small area in the serosa of the jejunum. Inthe spaces between the valvulae conniventes were desquamated and necroticepithelial cells. The mucosa was infiltrated with a moderate number oflymphocytes and a few eosinophiles.
Section from the stomach showed hemorrhage into the submucosaand many mononuclear cells containing formalin-pigment (formaldehyde pigment)precipitate. In one small area was a collection of polymorphonuclear leukocytes.
SUMMARY
This is an example of a very severe thoracoabdominal wound inwhich death occurred within a relatively short time after injury. Extremedestruction of the liver and widespread peritonitis appear to have been the mostimportant factors in the fatality. The patient's critical state and thewidespread visceral damage explain why two small perforations of thegastrointestinal tract were missed at operation. Other important lethal factorswere undoubtedly the continuing peritoneal contamination, the autotransfusion ofcontaminated blood, and the rather liberal administration of morphine.
Case II
CLINICAL DATA
This patient received a shell-fragment wound of the abdomen 17 October 1944 about 1130 hours.When he reached a field hospital at 1350 hours, his blood pressure was 128/70 mm. Hg, and his conditionappeared surprisingly good. The foreign body had entered the abdominal cavitythrough the right
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upper quadrant and had made its exit through a large defectin the left upper quadrant, with the evisceration of 14 to 16 cm. of thetransverse colon, several loops of small bowel, and most of the omentum. Twohundred and fifty cubic centimeters of plasma were administered rapidly, and atransfusion of group O whole blood was begun. During roentgenologic examination,after he had received about 300 cc. of blood, the patient had a chill. Thetransfusion was stopped immediately, and a second flask of blood was substitutedfor the first. On the operating table, shortly after the chill, the bloodpressure was 90/60 mm. Hg, and operation was deferred until it reached 124/70mm. Hg. This delay amounted to about 2 hours.
Laparotomy revealed a small amount of blood and some bile inthe peritoneal cavity. There was a large laceration of the liver, a perforationof the second portion of the duodenum, a perforation of the midjejunum, andmultiple perforations of the transverse colon. The duodenal perforation wassutured, and posterior gastroenterostomy performed. The jejunal perforation wassutured. A segment of the colon was exteriorized. It was noted that duringoperation bleeding tended to be excessive and hemostasis was difficult. Beforethe abdomen was closed, 50,000 units of penicillin were placed in the peritonealcavity.
The patient's condition was so critical after operation that he wasimmediately given 1,000 cc. of blood. The blood pressure had fallen to 90/60,and shortly afterward it fell to 80/50 mm. Hg. The day after operation, the exteriorized colon was opened; its appearance was not remarkable. Coarse ralesappeared in the chest, and considerable quantities of purulent material wereaspirated from the trachea. Death occurred 19 October 1944, about 48 hours afteroperation.
During this period of survival after injury, this patient received a total of3,000 cc. of plasma and 3,500 cc. of blood. Before the first plasma transfusionwas started, a sample of blood was taken. The group was O, and all the bloodwhich he received was compatible by routine crossmatching.
AUTOPSY
Autopsy was performed 2 hours after death (Lun?ville, France).
Gross observations-The right pleural cavity contained 200 cc. of serousfluid. The peritoneal cavity contained 300 cc. of thin, purulent exudate. Ageneralized fibrinopurulent peritonitis was present. There apparently had beenno appreciable hemorrhage from the liver after operation, and the seroussurfaces were not bilestained. Neither the sutured lesions of the intestine northe gastroenterostomy was remarkable. The colostomy was also not remarkable.There was a large defect of the anterior peritoneum medial to the colostomy inthe left upper quadrant, and there appeared to be an early infection in theproperitoneal tissues of the upper abdomen.
The heart was negative except for slight atherosclerosis of the coronaryarteries.
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There was considerable atelectasis of all lobes of the lungs, particularly inthe lower and posterior portions. The right upper lobe, in addition, was firmand had a slightly nodular consistency. On section, there was earlyperibronchial consolidation. The bronchi contained a moderate amount ofmucopurulent, blood-tinged exudate.
The spleen was three times normal size. It was soft, and onsection the pulp was easily scraped away. The secondary follicles were prominent.
A small laceration of the right lobe of the liver was notremarkable. Although local congestion and focal hepatic vein thromboses werenoted adjacent to the missile track, the hepatic defect was partly filled byplasma clot.
The kidneys were moderately swollen and congested. On section, the cortex wasslightly pale.
Gross anatomic diagnosis-(1) Perforating shell-fragmentwound of upper abdomen, with evisceration of transverse colon, small bowel, andomentum; multiple perforations of transverse colon; perforation of jejunum;perforation of second portion of duodenum; moderately severe laceration ofliver; (2) generalized severe fibrinopurulent peritonitis; (3) generalizedsevere congestion, edema, and atelectasis of lungs; (4) early acutebronchopneumonia of right upper lobe; (5) acute splenomegaly, secondary toperitonitis and possibly to multiple transfusions; and (6) moderately severepassive congestion of kidneys.
Comment-Death in this case appears to have been causedby severe visceral trauma and the effects of massive contamination of theperitoneal cavity. The chill which occurred during transfusion was attributedeither to chilling of the patient or to the presence of pyrogens in thetransfusion equipment. It was not thought to be due to incompatibility of theblood. The appearance of the urine, however, suggested that hemoglobin-derivedpigment might have been present. Plasma was given in an unusually large volumeduring operation, in an effort to limit the amount of blood needed, and thus tolessen the danger of a transfusion reaction.
Microscopic observations-The heart was negative, except for slightatherosclerotic changes in the coronary arteries.
The pulmonary tissue showed an extensive bronchopneumonia, confluent inplaces. The bronchial and alveolar exudate in some lobules was composed ofpolymorphonuclear leukocytes. In some areas, many red blood cells were mixedwith the leukocytes. In one section in which the alveoli contained protein-richedema fluid, a few hyalin membranes were seen in the respiratory bronchioles.
Sections from the liver showed large areas of hemorrhage andtraumatic infarction. One section showed a moderate degree of vacuolation of theliver cells in all parts of the lobule.
Groups of fat cells were seen in some of the malpighianbodies of the spleen. Considerable nuclear debris was enmeshed in a fibrinousexudate which covered the capsule.
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Sections from the kidneys showed that a moderate number ofcollecting tubules and a small number of distal convoluted tubules containedpigmented casts. Some of the proximal nephrons were dilated. There was noepithelial proliferation, interstitial edema, or inflammatory reaction.
Microscopic diagnosis-Moderately severe hemoglobinuricnephropathy.
Comment.-This case represents another instance ofhemoglobinuric nephropathy in a patient supposedly belonging to blood group O.In the experience of the 6713th Blood Transfusion Unit at Naples, which coveredmany thousands of donors, listings of the blood type on the identification tagwere found to be incorrect in about 10 percent of the soldiers, and one wonderswhether that happened in this case. Unless hemolyzed blood is injected, therewould seem no reason for a transfusion reaction in a group O recipient when Oblood is given. In crossmatching, there is one possible source of error inreading the result if the possibility is not borne in mind. Agglutinationhemolysis may occur, and crossmatching may be reported by an unwary observer ascompatible. (J. G. R.)
SUMMARY
This patient had a very severe abdominal wound, with massiveevisceration of abdominal viscera, and death occurred within a relatively shorttime after injury. The blood pressure remained at a low level during operationand most of the postoperative period. It is thought that the most importantlethal factors were (1) severe abdominal injury with evisceration and consequentperitonitis, (2) prolonged anesthesia and operation, and (3) bronchopneumoniaand pulmonary edema.
Uremia per se probably was not important in producing death so soon afteroperation, and the importance of the renal lesion as a lethal factor isminimized by at least two facts, namely, the moderate renal changes present andthe fact that the patient excreted 300 cc. of urine during a period of 48 hoursin which the blood pressure ranged from 90/60 mm. Hg downward.
It was customary in World War II to disregard the blood grouplisted on the identification tag, for the reasons already stated. This patientwas regrouped in the field hospital, and his blood type was found to be O. Hedid, however, receive blood which had been drawn 6 to 9 days earlier, and smallamounts of free hemoglobin may have been present in the 3,500 cc. of blood whichhe received.
Case 12
CLINICAL DATA
This patient received a shell-fragment wound of the right hip and sacralregion 9 October 1944, at about 0800 hours. He was brought into the fieldhospital at 1700 hours with a rapid, weak pulse and blood pressure of 70/50 mm.Hg. He had received 500 cc. of plasma. Before operation he received
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another 500 cc.of plasma and 2,500 cc.of group O (his blood group) blood, but the blood pressure never rose above 90/60mm. Hg. Through error, he did notreceive penicillin before operation.
Operation was unavoidably delayed until approximately 24 hours after injury. Explorationrevealed an extensive perforating wound of the right buttock with widespreaddestruction of the gluteal muscles and fractures of the right wing of the iliumand the right side of the sacrum. The missile track was filled with semiliquid,necrotic muscle, which was pale pinkish gray. The necrosis evident along thewalls of the missile track seemed to extend for a considerable distance into themuscles of the lumbar region and posterior upper thigh. So extensive was theprocess that complete excision of damaged muscles was impossible. At operation,sections were taken from the right gluteus medius at the base of the wound andwere fixed for microscopic study. At no time during operation were gas bubblesor crepitus noted in the muscle or in the subcutaneous tissue adjacent to thewound.
Laparotomy revealed two small perforations of the terminal ileum, but thesite of entry of the foreign body could not be identified. The right colon wasintact. Small spicules of bone had been driven into the soft tissue, and thesefragments may have been responsible for the injury to the small bowel. Sigmoidcolostomy was performed. No perforations were found on careful examination ofthe intraperitoneal portion of the rectum. Before the abdomen was closed, 10 gm.of sulfanilamide crystals were placed in the abdominal cavity. The wound of thehip was widely debrided, and a fasciotomy was performed along the right lateralgluteal fold. Zinc peroxide, which was sprinkled liberally throughout thegluteal wound, could not be activated because no reliable source of heat wasavailable. Operation was completed at about 1200 hours10 October. During its course, the patient received 1,000 cc. of blood.
Immediately after operation, the patient was given 2.5 gm.of sulfadiazine sodium by vein. On the third day, it was found that thepenicillin which had been ordered intramuscularly in dosages of 25,000 units every3 hours was being given subcutaneously. As soon as the error was discovered,100,000 units were given intravenously.
For the first day or two after operation, the patient looked remarkably well.There was little systemic evidence of severe infection, the pulse remainedwithin the normal range, and the maximum temperature elevation was 99.6? F. On the second postoperativeday, the blood pressure was 126/90 mm.Hg. The patient appeared slightly drowsy and was oliguric. An attempt was madeto render the urine alkaline by placing 4 gm. of sodium bicarbonate in thestomach every 2 hours.An intravenous infusion of 1,000 cc. of 1.25 percentsodium bicarbonate solution also was given daily. Although the total daily fluidintake averaged 3,000 cc., the greatest single volume of urine was about 100cc., and the total output from operation to death, which occurred on the sixthday after wounding, was about 400 cc. The urine was dark amber brown andcontained many granular casts and many erythrocytes. A few
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sulfadiazine crystals were noted soon after operation. Thehemoglobin by the copper sulfate method was 12.7 gm.percent and the plasma protein 5.1 gm. percent.
The patient received an average of 250 cc. of plasma daily, andduring the immediate postoperative period he also received 750 cc. of carefully crossmatchedO-type blood.
On 13 October, the blood pressure was 178/120 mm. Hg, but it declined fromthis level and during the last 3 days of life was in the range 140/80 to 160/85 mm. Hg. On 13 October, theleukocyte count was 6,000 percubic millimeter, with a moderate increase in stab forms. There was alsomoderate pitting edema, and the temperature reached 100.2? F. On the night of the fifthpostoperative day, moist rales were noted throughout the chest, andintratracheal aspiration was performed. The patient died the following morning, 15October 1944, at 0800 hours, approximately 144 hours after injury.
AUTOPSY
Autopsy was performed an hour after death (Lun?ville, France).
Gross observations-Externallythe body showed moderate pitting edemaover the back and sacrum. There was no icterus.
The peritoneal, pleural, and pericardial cavities were negative.
The right side of the heart was greatly distended by blood;the tricuspid valve measured 15 cm.There was a considerable degree of atherosclerosis of the coronary arteries,most marked in the right circumflex artery.
There was complete atelectasis of all lobes of the lungs except the rightupper lobe. There was loss of crepitus, and the involved lobes were rubbery inconsistency. Consolidation was thought to be present but was difficult to detect because of the marked degree of atelectasis. On section,the lung was purple and beefy red. There was only a moderate increase in the amount ofserous fluid which oozed from the cut surface. The bronchi contained a largequantity of hemorrhagic purulent exudate.
The spleen was twice normal size and moderately firm. Onsection, it did not seem remarkable, but the purple-red pulp scraped awaysomewhat more easily than would have been expected from the firmness of itsconsistency.
The liver was moderately enlarged. On section it was not remarkable exceptfor the presence of scattered pinpoint areas of hemorrhage.
The gastrointestinal tract showed the operative changes already mentioned.
Both kidneys were considerably swollen, particularly in the anteroposteriordiameter. Their size was estimated at 1? times normal. The subcapsular surfacewas uniformly homogeneous, yellow gray, and of an opaque, slightly granularappearance. On section, the parenchyma bulged above the edge of the capsule. Thecortex appeared somewhat thickened and was of the same yellow gray as thesurface. The pyramids were gray brown; near their bases the tissue had an opaquegranularity like that of the cortex. The tips of the pyramids were congested andthe mucosa was hemorrhagic, as was the mucosa of the renal pelves generally. Therenal arteries showed early atherosclerosis.
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Examination of the adrenals showed liquefaction and destruction entirely outof proportion to the brief time which had elapsed since death. There was noevidence of medullary hemorrhage.
There was moderate edema of the bladder mucosa.
In the lumbosacral area was an extensive phagedenic wound track extendingfrom the right posterolateral rib margin downward and across the midline to theleft gluteal region. There was considerable undermining of the subcutaneoustissue, with involvement of the adjacent muscle and connective tissue about theperiphery of the track. The odor was foul. The exudate was watery and grayishgreen, except that in many places it was slightly pink, the color suggesting thepresence of blood or muscle pigment. The exposed sacrum and the wing of theilium formed the floor of the wound. There was no evidence that the peritonealcavity had been invaded.
At operation, an attempt had been made to provide drainage for the wound bymaking incisions along the right gluteal fold and in the posterior right flank.The edges of these incisions had the appearance of those of the original wound.Infection had extended upward to the level of the 12th rib along the lumbarmuscles and downward into the posterior muscles of the upper thigh. Grosslythere was no apparent predilection for muscle tissue, and adipose and connectivetissue were extensively involved. In the midst of the wound, however, pale-pink,edematous, and necrotic muscle fibers were present.
Gross anatomic diagnosis-(1) Perforating shell-fragment wound of rightlumbosacral and gluteal regions, with extensive destruction of soft tissue, andcompound, comminuted, incomplete fracture of right ilium; compound, comminuted,incomplete fracture of right posterior aspect of sacrum; two healingperforations of terminal ileum; (2) extensive phagedenic infection of wound ofgluteal region, with necrosis of muscle and connective tissue, bacterial causeunidentified; (3) nephrosis, possibly hemoglobinuric in type, with pulmonarycongestion and edema, moderately severe, manifest clinically by oliguria,uremia, and arterial hypertension, moderately severe; (4) purulent bronchitis,bilateral, severe, with complete atelectasis of left lung, right lower andmiddle lobes, due to bronchial obstruction by exudate; (5) extensive bilateralnecrosis of adrenal medulla, possibly due to overwhelming infection; and (6)moderate, generalized atherosclerosis.
Comment-The clinicaland gross post mortem findings in this case aretypical of pigment nephrosis. In view of the widespread destruction of skeletalmuscle, myoglobin rather than hemoglobin may have been the offending pigment. Whatever the pigment, the kidney always appears to be particularlyvulnerable to it during periods of severe shock.
This type of infection is of considerable interest. Bubbles of gas were neverobserved, but the invasive and destructive properties of the infecting organismswere evidently very great. A mixed infection which includes microaerophilicstreptococci deserves consideration. The delay in effective penicillin therapymay or may not be important. The delay of 24 hours in operation certainly was.
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Microscopic observations.-Sections ofthe lungs showed small patches of atelectasis. Several lobules were filled withexudate composed largely of red blood cells, stringy protein deposits, and smallnumbers of polymorphonuclear leukocytes and mononuclear cells. The character ofthe alveolar exudate varied in different lobules. In some it was chieflycomposed of erythrocytes. In others, the red blood cells were mixed withgranular, pink-staining protein precipitate. In still others, there was anadmixture of these elements with mononuclear cells. A few small bronchicontained polymorphonuclear leukocytic exudate. Slight edema of the interlobular septa and blood were observedin scattered alveoli, but nothing else of note was seen. On frozen section, fatemboli, in moderate numbers, were present in capillaries in the alveolar septa.
The liver cords in the centers of the lobules were atrophic. The cellscontained fat vacuoles and granular brown pigment. A few foci composed ofhistiocytes were seen. The portal triads were infiltrated with moderate numbersof lymphocytes.
The splenic pulp was moderately congested. There was a large amount offormalin-pigment (formaldehyde pigment) precipitate.
A large number of distal convoluted and collecting tubules inthe kidneys were plugged with pigmented casts. The proximal nephrons wereslightly dilated. Some tubules contained epithelial debris mixed with pigment.There was a moderate degree of epithelial proliferation, most evident in themedulla, with the formation of a few granulomas in the interstitial tissues.Only a very slight inflammatory reaction, consisting of lymphocytes, was seen. Asmall number of sulfonamide crystals were identified in the tubules.
The appearance of the voluntary muscle varied in different sections, and evenin different parts of the same section. Many muscle fibers were swollen. Sometook an orange stain. Others had lost striations and nuclei. In places, theinterstitial tissues were edematous. There was a large amount ofpolymorphonuclear leukocytec infiltration in the interstitial tissues in someareas and a small amount in others. In still others, there was an absenceof inflammatory reaction. A few vessels were thrombosed.
Sections examined after straining by the MacCallum-Goodpasture techniqueshowed large numbers of organisms, usually mixed. There were present large, fat,gram-positive bacilli, some of which were comma shaped. No spores were seen. Theother prominent organism was a gram-positive coccus. Some of these cocci weresmall, some large.
Microscopic diagnosis-Moderate pulmonaryfat embolism.
Comment.-Histologically the voluntary muscle lesion in this case appears to be acombination of clostridial and suppurative myositis. Without cultural proof, anexact diagnosis is not possible. One can guess, however, that the germ-positiverods were Clostridium sordellii and that the cocci were streptococci.
Therenal lesion is typical of hemoglobinuric nephropathy. The very destructivemuscle lesion might conceivably have liberated myoglobin, but whether this wouldbe absorbed and then excreted through the kidney, as in the crush syndrome, itis not possible to say. In addition, clostridial organ-
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isms are hemolytic, and, if hemolysis were sufficientlysevere, this process, too, might produce hemoglobinemia and hemoglobinuria. In arecipient belonging to group O and receiving only group O blood, there wouldseem no reason for a transfusion reaction, unless hemolyzed blood had beeninjected. This fact would tend to favor a relationship between the myositis andthe nephropathy.
SUMMARY
This case provides another example of posttraumatic renalfailure and pigment nephrosis. The type of wound infection encountered here,however, was not common, and the myositis per se may have been important in thedevelopment of the renal lesion. In attempting to assess the role of thisinfection in the pathogenesis of the nephrosis, other factors should not beoverlooked, including prolonged and severe shock due to trauma and hemorrhage,massive transfusion therapy, and sulfonamide administration. Probably the singlemost important lethal factor was the prolonged period of shock, and it may wellbe in this regard that the myositis exerted its deleterious effect upon thekidney.
Case 13
CLINICAL DATA
This patient suffered a shell-fragment wound of the right costovertebralregion 18 May 1944 at 1300 hours. After a delay of 38 hours, during which hereceived 1,000 cc. of plasma and several injections of morphine, he arrived at afield hospital 20 May at 0300 hours. The delay in evacuation was due to anoffensive breakthrough; combat units outstripped supporting medical units.
Atthis time, the patient's condition was critical. The blood pressure was 88/52mm. Hg, the pulse 98, and the respiration 26. Hewas dehydrated, febrile, and semistuporous. In 4 hours after he reached thefield hospital, he received 1,400 cc. of plasma and 1,000 cc. of group O wholeblood; 10,000 units of polyvalent gas-bacillus antitoxin; and 100,000 units ofpenicillin by vein and 100,000 units by instillation into the right pleuralcavity, from which 1,000 cc. of bloody, foul-smelling fluid had been aspirated.These measures produced little improvement; at 0600 hours the blood pressure was108/30.
At operation, a laceration of the diaphragm was closed. The chest wasalso closed after a catheter had been inserted in the right pleural cavity.Laparotomy revealed a laceration of the right kidney. The kidney was notremoved, and drainage was provided for the perirenal, subdiaphragmatic, andsubhepatic regions on the right. The patient was apparently in fairly goodcondition throughout the procedure but died suddenly as operation was beingconcluded.
AUTOPSY
The autopsy was performed 1 hour after death (Minturno, Italy).
Gross observations-Theskin and sclerae were definitely icteric. Theabdomen was moderately distended and tympanitic. No bubbles of gas were
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noted in the tissues at the site of entrance of the missile,which was beneath the 12th rib in the right costovertebral region. The shellfragment had passed forward through the reflection of the diaphragm and thenthrough the dome of the liver, coming to lie beneath the skin in the rightmidclavicular line at the level of the sixth intercostal space.
The right pleural cavity was remarkable in that the right lung was almostcompletely collapsed and the entire cavity was lined with a thick, fibrinousexudate. This cavity contained about 200 cc. of bloody fluid. The stomach wasgreatly dilated; it extended downward to a point 3 cm. below the umbilicus. Itwas so distended with gas that it appeared tense and drumlike. The hepaticflexure of the colon was plastered to the anterior surface of the right kidneyby fibrinous exudate. There was moderate bile staining of the lesser peritonealsac and of the retroperitoneal tissues of the right renal region.
There was practically total collapse of the right lung, whichwas bound down by the exudate just described. This exudate covered all exposedsurfaces, and in the thicker portions, which lay posteriorly, there were manybubbles of gas. The amount of gas present was out of proportion to the degree ofsubcutaneous emphysema present, and it was thought that the gas represented theproduct of bacterial growth in the exudate. This lung contained practically noair, and on section it was found to be almost completely consolidated, thecollapsed tissue being suffused with hemorrhagic fluid. There was almostcomplete atelectasis of the left lower lobe and moderately severe patchyatelectasis of the left upper lobe, in which peripheral emphysematous blebs wereobserved. The bronchi contained moderate amounts of serous bloody fluid, butthere was no evidence of obstruction of a major bronchus.
A missile had passed through the dome of the right lobe ofthe liver. Incision through Glisson's capsule at a point of hemorrhagicdiscoloration released bloody fluid containing bubbles of gas. On section, thewound track measured 5 to 6 cm. in diameter. The wallswere made up of pale-yellow, opaque, necrotic liver parenchyma, which containedsmall, irregular bubbles of gas and had the appearance of fermented culturemedia. Bubbles of gas were expelled from the blood vessels of the liver.
Except for the extreme gastric dilatation already described, and thinning ofthe wall by pressure of retained air and gas, the stomach was not remarkable.
The passing missile had caused a severe contusion of the central portion of theright kidney, and on section a spherical hemorrhagic area was seen, which was 4to 5 cm. in diameter. Overlyingthis area was considerable capsular reaction, but the cortex of the kidney didnot appear to be directly lacerated by the missile.
The spleen was moderately swollen and somewhat softer than normal.
Thecapsule overlying the relatively normal portion of the kidney stripped away withsome difficulty and slight tearing of the underlying parenchyma. The renalpelvis on the right was bile stained to a degree not noted on the left.
Grossanatomic diagnosis.-(1) Shell-fragmentwound of right thoraco-abdominalregion, with right hemopneumothorax and extreme atelectasis of
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right lung; empyema of right pleural cavity, possibly causedby clostridia; laceration of right lobe of liver with extensive necrosis due toanaerobic infection; and (2) severe atelectasis of left lower lobe and partialatelectasis of left upper lobe, secondary to right pneumothorax and gastricdilatation; severe acute dilatation of stomach; severe contusion of rightkidney, and moderately severe contusion of hepatic flexure of colon; suturedlaceration of right diaphragm.
Comment-When this patient was received in the field hospital, he wassuffering from overwhelming infection and severe respiratory embarrassment.Gastric dilatation and atelectasis of the left lung may have accounted for hissudden death on the operating table. A roentgenogram taken before operationshowed a large gas bubble in the region of the stomach.
Microscopic observations-Theheart veins were dilated and engorged withblood.
Two sections of the lungs showed massive collapse with patent bronchi. Manydust cells were present. The pleural surfaces were covered with afibrinopurulent exudate which showed no evidence of organization. Exudatestained with the MacCallum-Goodpasture stain showed many gram-positivespore-bearing bacilli morphologically consistent with clostridia.
One section of the liver showed extensive traumatic necrosis. A second showedcentral congestion, acidophilia, and slight vacuolation.
The splenic pulp was very cellular.
One section of kidney tissue showed only moderate diffuse dilatation of allportions of the nephrons. A second showed massive hemorrhagic traumaticnecrosis. Many of the collecting tubules were plugged with casts; some werehyaline, some consisted solely of red blood cells, and others showed all gradesof transition.
The pleural surface of the pericardium was covered with a fibrinopurulentexudate. The pericardial surface was normal.
Comment-This is the first case to come to autopsy in theNaples laboratory with what appears to be a clostridial infection of the pleuralcavity. (T. B. M.)
SUMMARY
Even if this patient had survived operation, it is doubtful that he couldhave tolerated such overwhelming infection. His response to replacement therapybefore operation was slow and incomplete and was in itself indicative of theprofound circulatory changes which characterize clinical gas-bacillus infection.
Case 14
CLINICAL DATA
This patient received a bullet wound of the mid-upper abdomen17 April 1945, at 1800 hours. He reached a field hospital 18 April, at 0130hours, without replacement therapy during evacuation. The blood pressure at this
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time was 80/60 mm. Hg and the pulse 120. Improvement wasprompt after the administration of 500 cc. of plasma and 500 cc. of whole blood,and the blood pressure before operation was 128/80 mm. Hg. The patient's bloodbelonged to group O.
Laparotomy through a left paramedian incision revealed theomentum to be badly lacerated and torn. The proximal jejunum, which wastransected, was repaired by end-to-end anastomosis. The splenic flexure of thecolon, which was badly lacerated, was resected and the loops were brought out inthe left abdomen as a colostomy. The posterior wound of exit in the left flankwas debrided. Exploration showed that the left kidney was lacerated, but it wasnot removed. The perirenal space was drained, and drains were brought outthrough the inferior portion of the abdominal incision. The patient's conditionwas satisfactory during operation, in the course of which he received anadditional 500 cc. of blood.
His condition the day of operation continued fairly good. He voided 600 cc.of urine. The following day, 19 April, his status worsened rapidly; he becamestuporous and was unable to void. The following laboratory values were reported: Hematocrit, 51; hemoglobin, 17.2 gm. percent; and plasma protein, 6.5gm. percent.
On 21 April, the patient's condition was fair, thoughdrainage of small-bowel contents was noted through the posterior wound in theleft flank, and it was thought that the jejunal anastomosis might have brokendown.
On 22 April, the patient was very ill, and there was evidenceof a severe peritonitis. He died on this day at 1000 hours, approximately 112hours after injury.
AUTOPSY
Autopsy was performed 4 hours after death (Poxdorf, Germany).
Gross observations-Externallythe body showeddehydration and moderate weight loss. The abdomen was quite distended.Foul-smelling, watery fluid oozed from the wound in the left flank.
A considerable quantity of gas escaped when the abdominal cavity was opened.The cavity contained about 2,000 cc. of foul, blood-tinged fluid in a largepocket which extended from the left upper abdomen across the midline to theright para-umbilical region. The walls of this pocket were made up offibrinopurulent exudate, and the serosa of the adjacent bowel was opaque anddark in color. Fluid present in the pelvic portion of the peritoneum containedsmall particles of undigested food. Strands of purulent exudate were scatteredthroughout the peritoneal cavity. The diaphragm was elevated to the level of thethird rib bilaterally; both leaves were intact.
There was much old blood in the left perirenal tissues.
The left cardiac ventricle showed moderately severe concentric hypertrophy.
The lungs revealed only slight congestion and atelectasis of the inferiorportions of the lower lobes.
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The spleen was somewhat softer than normal.
In the posterior wall of the stomach were two unclosedperforations. The larger, which measured 4 cm. in diameter, lay near theattachment of the gastrocolic omentum in the midportion of the greatercurvature. The second, which measured 1 cm. in diameter, overlay thetip of the pancreas. The stomach was empty and contained no blood, butapparently considerable bleeding had taken place into the peritoneal cavity fromthe gastric perforations. The jejunojejunostomy was not remarkable.
There was a small area of trauma at the extreme tip of the tail of thepancreas. Two small foci of fat necrosis were present in the interlobularadipose tissue of the pancreas. There was no gross evidence that pancreaticjuices had entered the peritoneal cavity to any appreciable extent.
On the anterolateral aspect of the lower pole of the left kidney was a 3-cm.stellate laceration.
Gross anatomic diagnosis-(1)Perforating bullet wound of abdomen, withtransection of proximal jejunum, healing jejunostomy; severe laceration oftransverse colon, colostomy; two large perforations of posterior wall of stomach; moderately severe laceration of left kidney, with retroperitonealhemorrhage; minimal laceration of tail of pancreas; (2) severe, acute,generalized peritonitis, secondary to unclosed perforations of stomach; and (3)gastric fistula via wound of exit in posterior left flank, secondary to unclosedgastric perforations.
Comment-Thetechnical error of omission in this caseemphasizes the necessity for thorough exploration of the abdomen in anycombat-incurred wound. Unfortunately, the lesser peritoneal sac was not exploredat operation.
Microscopic observations-Onthe pleural surface of the lung, an exudateof polymorphonuclear leukocytes, blood, and fibrinoid material was noted. Thealveolar walls were approximated, and blood or a slight amount of eosinophiliccoagulum was present in some alveoli. The vessels were engorged. Alveolarhemorrhage was most apparent subpleurally. A second section showed approximationof the alveolar walls with foci of intra-alveolar fibrinoid material and clumpsof polymorphonuclear leukocytes; these changes were moderately extensive incertain areas. Several small bronchioles showed ulceration of the epitheliumwith blood and polymorphonuclear leukocytes in the lumens. Other bronchioleswere partly filled by accumulations of polymorphonuclear leukocytes.
A fibrinoid material with intermingled polymorphonuclear leukocytes waspresent on the capsular surface of the spleen. The sinusoids were large andfilled with blood.
There was vacuolation of the liver cells, chiefly about the central vein ofthe lobule. The veins appeared to be slightly dilated.
Hemorrhage had occurred into the interlobular fat of the pancreas, and therewas a focal collection of fibrinoid material with enmeshed leukocytes.
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On the serosal surface of the stomach was an extensive fibrinoid exudate withscattered polymorphonuclear leukocytes. At the attachment adjacent to theserosa, the exudate showed early organization, as evidenced by fibroblastic andcapillary proliferation.
The tubules of the kidney showed degeneration to the point of necrosis, withgranularity of the cytoplasm and loss of nuclear detail. The glomeruli weresmall. Another section showed irregular necrosis and hemorrhage into theparenchyma. About the periphery of these areas were moderate accumulations o?polymorphonuclear leukocytes.
Microscopic diagnosis-(1)Moderate lobular pneumonia; (2)fibrinopurulent pleuritis; (3) severe traumatic renal necrosis and hemorrhage;(4) slight fatty metamorphosis of liver; (5) moderate interlobular pancreatichemorrhage; and (6) pulmonary atelectasis.
Comment-Themicroscopic findings were in essential agreement with thegross diagnosis. The peritonitis was well illustrated by the exudate seen on thecapsular surface of the spleen and the serosal surfaces of the stomach andpancreas. (E. N. B.)
SUMMARY
This case is an example of one of the numerous pitfalls which can occur asthe result of failure to carefully explore all abdominal wounds. In spite of theseverity of the abdominal wound, the patient tolerated operation surprisinglywell. Failure to close two perforations of the stomach, however, led to death onthe fourth postoperative day.
Case 15
CLINICAL DATA
This patient sustained a shell-fragment wound of the right lumbar region 1June 1944, at1510 hours. He reached a field hospital at 1800 hours, after having received1,000 cc. of plasma. The blood pressure at this time was 86/44 mm. Hg and the pulse 120. Remarkableimprovement occurred after the administration of 1,000 cc. of plasma and 500cc. of whole blood. Just before operation, the blood pressure was 120/88 mm. Hg, and there was noexcessive bleeding from the large wound.
At operation, the wound of the right lumbar region was foundto be perforating and very large. The missile had entered the abdomen just tothe right of the third lumbar vertebra and had caused extensive destruction ofthe body of this vertebra and of the cauda equina. There was a massive defect inthe lumbar muscles on the right, with extreme damage to the cecum, whichrequired resection. An ileotransverse colostomy was performed. The wound wasdebrided and drained, and a large pack was placed in the retroperitoneal muscledefect. During operation, in spite of continued transfusion of whole blood, thepatient's condition became critical. He did not rally after operation and died 2June 1944.
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AUTOPSY
Autopsy was performed 4 hours after death (Cori, Italy).
Gross observations-Therewas no apparent invasive infection of the largelumbar wound, which measured 6.0 by 8.0 cm. and which made a gaping defect inthe right paravertebral region. The floor of this defect was formed by theposterior portion of the parietal peritoneum. A large retroperitoneal hematomawas present.
The pericardial and pleural cavities were not remarkable.There was no increased fluid in the peritoneal cavity, although the loops ofsmall bowel were loosely bound together by strands of fibrinopurulent exudate.
The heart showed minimal coronary atherosclerosis, with some increasedthickness of the left ventricular myocardium.
The lungs showed only moderate congestion and edema of both lower lobes.
Theliver, spleen, and adrenal glands were essentially negative. Thegastrointestinal tract showed only a recent healing ileotransverse colostomy.
The kidneys were normal, and the intact right ureter bridgedthe lumbar defect. There was moderate hydroureter and slight hydronephroticdilatation of the right renal pelvis. The orifice of the ureter was partlyoccluded by two blood clots at the level of the wound (third lumbar vertebra).No blood was present in the renal pelvis. The bladder showed somewhat increasedtrabeculations of the mucosal surface.
Examination of the vertebral column showed extensive destruction of the thirdlumbar vertebra, with contusion of the filaments of the cauda equina.
Grossanatomic diagnosis.-(1) Severe shell-fragment wound of right posteriorabdomen, with multiple lacerations and perforations of cecum and ascendingcolon, secondary resection of cecum and ileotransverse colostomy; compoundcomminuted fracture of body and transverse and spinous processes of third lumbarvertebra, with severe retroperitoneal hemorrhage; moderately severe contusion ofright ureter, with moderate hemorrhage into ureter and slight secondaryhydronephrosis; (2) severe, acute, purulent, generalized, early peritonitis,secondary to wounds of cecum and ascending colon; and (3) severe, multiplecontusions and lacerations of cauda equina, secondary to fracture of thirdlumbar vertebra.
Comment-Themassive trauma, blood loss, and severe peritonealcontamination made the outlook in this case very poor from the first. It issurprising that the patient responded as well as he did to 1,000 cc. of plasmaand only 500 cc. of blood. In retrospect, it seems probable that he received toomuch plasma, and, more important, too little blood before operation.
Microscopic observations.-Thelungs showed diffuse partial atelectasis and markedcongestion. A few fat droplets were present in the arterial tree, chiefly inthe arterioles.
The kidney showed a focus of interstitial and intratubularhemorrhage consistent with a traumatic lesion. Scattered through the cortex werespaces lined with very flat epithelium or swollen endothelium which containedorange-
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staining material. No pigment precipitates were found in anypart of the tissues which could be recognized definitely as a nephron. Thenature of the lesion was not apparent, but it was not regarded as important toclinicopathologic correlation.
Microscopic diagnosis-Minimalpulmonary fat embolism. (T.B. M.)
SUMMARY
It is remarkable, in retrospect, that this patient lived aslong as he did, because of (1) extreme tissue destruction and consequent loss ofblood, (2) the difficulty of controlling blood loss during operation, and (3)the overwhelming contamination of the peritoneal cavity. Early postoperativedeaths were not uncommonly seen in severely wounded patients after such a longand tedious operation as this patient underwent.
