Battle Casualties in Korea: Studies of the Surgical Research Team, Volume IV
Observations on the Surgical Care of Patients With Post-traumatic Renal Insufficiency*
Major Henry H. Balch, MC, USAR
Major William H. Meroney, MC, USA
Captain Yoshio Sako, MC, USAR
Acute renal failure following battle injury was noted in Germany in World War I,1 following air raids in England in World War II,2 and was also investigated in the Italian Theater of operations at that time.3 Luckè4 has stated that lower nephron nephrosis is the most frequent form of fatal kidney disorder encountered among military personnel during war. The Second Auxiliary Surgical Group5 reported anuria to be the principal or contributing cause of death in 4.6 per cent of a large series of fatal abdominal cases in World War II. The latter were thought to represent patients in whom early fatality had only just been averted, but nevertheless fatal physiologic or structural changes in the kidney had not been avoided. Renal failure following battle injury is most likely to occur with severe or multiple injury which has been associated with prolonged shock.5
The mechanism of renal damage is not entirely understood. Some of the proposed theories have been reviewed elsewhere 4, 6, 7 and need not be repeated here. Prolonged selective renal vasoconstriction is probably of prime importance resulting in the development of widespread areas of renal tubular degeneration.8
Post-traumatic renal failure is associated with a high mortality rate. Beecher and his associates3 reported an over-all fatality rate of 65 per cent in 78 patients with acute renal failure; this may be separated into a fatality rate of 47 per cent for patients with oliguria and 91 percent for those with anuria.** Uremia was the primary cause of death in 67 per cent of the fatalities. Ninety-four per cent of all deaths occurred within the first 10 days. Luckè4 reported that 74 per cent of the patients in a series of 100 fatal cases of post-traumatic renal failure reviewed at the Armed Forces Institute of Pathology died within 8 days. Overhydration, potassium intoxication, or unknown toxins as-
*Previously published in Surgery, Gynecology and Obstetrics 100: 439, 1955.
**Oliguria=urinary output of 100 to 600 ml. in 24 hours.
Anuria=urinary output of less than 100 ml. in 24 hours.
72
sociated with the syndrome of uremia have been considered to be the most common causes of death.
Since World War II, there have been advances in the therapy of acute renal failure. These have been directed primarily toward the prevention of overhydration and the control of undue tissue catabolism. The latter minimizes the release of potassium into the circulation. In addition, ion exchange resins and artificial hemodialysis are used to lower dangerously elevated serum potassium levels and possibly to eliminate unknown toxins associated with uremia.
A center for the treatment of acute renal failure was established in Korea under the direction of the Army Medical Service Graduate School, Walter Reed Army Medical Center, and operated in collaboration with Eighth United States Army. The treatment of renal failure at the center has been discussed in another paper9 and will be mentioned only briefly here. It is the purpose of this paper to draw attention to some of the surgical problems encountered in the management of these patients.
Clinical Material and Methods
Observations reported in this study were made on 37 casualties admitted to the Post-traumatic Renal Insufficiency Center, Korea, during the months of April, May, June and July, 1953. Two of these patients were injured in vehicle accidents, 1 was severely burned, and the remaining 34 were wounded by small arms fire or by missiles from exploding mortar shells, hand grenades, or land mines. Resuscitation and initial surgery were carried out at several surgical hospitals. The diagnosis of post-traumatic renal insufficiency was suspected when urinary output was less than 20 ml. per hour provided the systolic blood pressure was above 90 mm. Hg. Plasma potassium determinations carried out on specimens of blood obtained from a few patients at forward surgical hospitals aided in the diagnosis when they were elevated. Patients were transported by air to the Renal Center, a distance of about75 miles. They were admitted directly to the ward where blood pressure, pulse rate, temperature and electrocardiogram were recorded immediately. A catheter was inserted in the bladder if not already present and irrigated to eliminate the possibility of mechanical block. Blood for plasma chemical determinations was drawn and the following analyses were done at once: sodium, potassium, chloride, carbon dioxide capacity, nonprotein nitrogen, calcium and phosphate. The hematocrit and white blood counts were also
73
measured. Thereafter all of the above laboratory procedures were determined daily or more frequently. The analytical methods used have been describedpreviously.10
The clinical management of the patients was the joint responsibility of the medical and surgical staff of the Renal Center. The diagnosis of acute renal insufficiency was made at the center when a patient excreted less than 500 ml. urine per 24 hours in the presence of a stable blood pressure and a reasonable state of hydration. The development of azotemia supported the diagnosis. An autopsy was performed on almost all patients who died. The characteristic kidney lesion4, 7 of post-traumatic renal failure was found in all the autopsied patients grouped under that diagnosis in the present series.
The medical management, which has been discussed elsewhere,9 can be summarized under four headings:
1. Fluid Balance. Total fluid intake per 24 hours usually was restricted to 500 to 800 cc. plus the volume of the obvious fluid output. Whole blood was not counted as fluid intake.
2. Electrolyte Balance. The principal abnormalities noted were increased concentration of plasma potassium, phosphorus and organic acids and decreased concentration of plasma sodium, calcium and bicarbonate. The first group are primarily intracellular substances which accumulate in uremic plasma when cells are devitalized or destroyed. The removal of such cells by thorough débridement diminishes the rate of accumulation of the substances in the plasma. Conversely, a rapid accumulation of these substances in the plasma suggests that devitalized tissue is still present and should be sought for.11 The only electrolyte abnormality which is known to be lethal during oliguria is potassium intoxication, and greatest efforts were directed toward its control.
Replacement of the deficit of sodium caused the potassium concentration to fall. When the salt used was sodium bicarbonate, acidosis was modified at the same time. Replacement of the calcium deficit caused amelioration of the toxic effects of potassium without changing the concentration of potassium in the plasma. Infusions of hypertonic glucose with insulin also lowered potassium concentration and digitalis also antagonized potassium toxicity. If the effectiveness of these measures was exhausted, artificial kidney dialysis was employed.
3. Clinical Uremia. As the plasma NPN concentration rose above approximately 250 mg. per 100 cc., there was a gradual progression of anorexia, nausea, vomiting, hiccups, somnolence and tremulousness. If oliguria had continued untreated, these manifestations would have progressed to death. However, artificial kidney dialysis usually was
74
employed, and the clinical and chemical abnormalities were corrected. When dialysis corrected the chemical abnormalities but not the clinical manifestations, it was found that some other disorder, such as sepsis, and not uremia, was responsible for the symptoms and signs.
4. Supportive Treatment. Maximal caloric intake of carbohydrate and fat (no potassium or protein) is desirable, but nutrition was usually limited to intravenous glucose (100 to 200 gm.) with vitamin supplements. Whole blood transfusions were given freely for anemia.
Twenty-four patients from the present series had post-traumatic renal insufficiency. The diagnosis could not be made in 13 patients admitted to the center, who were, however, treated there. Because the latter patients were seriously wounded, they serve as a control group. Although these patients were not oliguric on the basis of the somewhat arbitrary definition used, they may have sustained renal damage, which may occur in severely wounded battle casualties.3
Results
Table 1 records the distribution of wounds in the two groups of patients. Wounds confined to the extremities formed the largest single category in the oliguric group. This did not obtain in the non-oliguric group. But the combined incidence of patients who sustained extremity wounds, either alone or in combination with injury elsewhere, was not very different in the two groups. All the extremity wounds resulted in muscle damage and presumably the opportunity for ab-
Table 1. Distribution of Wounds in Severely Wounded Patients
|
| Oliguric | Non-oliguric | ||
Number Patients | Per Cent | Number Patients | Per Cent | |
|
Extremity |
11 |
45.8 |
3 |
23.1 |
|
Abdominal |
5 |
20.8 |
3 |
23.1 |
|
Extremity and abdominal |
4 |
16.6 |
4 |
30.7 |
|
Thoraco-abdominal and extremity |
1 |
4.2 |
1 |
7.7 |
|
Thorax and extremity |
1 |
4.2 |
1 |
7.7 |
|
Thorax and spinal cord |
1 |
4.2 |
--- |
--- |
|
Head injury |
1 |
4.2 |
--- |
--- |
|
Burn (60%) |
--- |
--- |
1 |
7.7 |
Total |
|
|
|
|
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sorption of myoglobin into the circulation. For this reason, the relatively high number of patients in the oliguric group whose injuries were confined to the extremities is of interest. However, it is possible that this finding is only a manifestation of the high incidence of extremity wounds in general. Beecher and his associates3 also found extremity wounds to be the most frequent in their combined anuric-oliguric series. Multiple injuries were nearly always present in both oliguric and non-oliguric patients from the present series, which is to be expected in any group of severely wounded battle casualties.
Table 2 records the major complications encountered in the patients under study at the Renal Center. Significant infection was present in 83 per cent of the oliguric patients. These included myositis, peritonitis, septicemia, lung abscess and wound infection. Sixty-three per cent of the non-oliguric patients who survived a sufficient length of time also developed complicating infection. These included myositis, peritonitis (including a patient with overlooked stomach perforation) and a patient with an infected burn.
The most frequent complication found in the oliguric group was myositis, which in this series was found only in the extremities.
Table 2. Significant Complications in Patients at Renal Insufficiency Center
|
| Oliguric 24 Patients | Non-oliguric 13 Patients | ||
Number Patients with Complication | Per Cent | Number Patients with Complication | Per Cent | |
|
Myositis |
15 |
62.5 |
3 |
23.1 |
|
Peritonitis |
2 |
8.3 |
3 |
23.1 |
|
Lung abscess |
1 |
4.2 |
|
|
|
Septicemia |
3 |
12.5 |
|
|
|
Wound infection |
1 |
4.2 |
|
|
|
Burn infection |
|
|
1 |
7.7 |
|
Postoperative shock |
4 |
16.7 |
5 |
38.5 |
|
Uncontrolled hemorrhage |
2 |
8.3 |
1 |
7.7 |
|
Excessive bleeding after secondary dèbridement |
6 |
25 |
1 |
7.7 |
|
Failure arterial repair |
6 |
25 |
|
|
|
Overlooked stomach perforation |
|
|
1 |
7.7 |
|
Evisceration |
1 |
4.2 |
|
|
*More than one complication was found in some patients.
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Necrosis and infection of the muscle appeared to be the result of inadequate initial débridement in most instances. The involved muscles were edematous, discolored, friable and foul-smelling. The lesions were usually localized and often confined to one or more muscle compartments, although systemic manifestations were sometimes severe. However, in several instances muscle involvement was extensive and one case of extensive crepitant myositis of the thigh is included in the series, from which Cl. perfringens was isolated. Temperatures of most of the patients with myositis were between 101 and 104° F., and the pulses were rapid. Leukocytosis with an increase in the per cent of neutrophils was a prominent but not a consistent feature.
The patients did not complain commonly of wound pain, except with manipulation. The apparent absence of pain in some patients may have been because many of them were confused and disoriented. The latter condition appeared to be related to the presence of hypotension, a possible bacterial toxemia and also at times to uremia. The temperatures and pulses were normal in two patients at a time when wound examination revealed extensive muscle necrosis and infection. Bacteriological studies12 from wounds were not always complete but the findings showed a polybacterial flora which included saccharolytic and proteolytic varieties of Clostridia, Streptococci (beta hemolytic, gamma and micro-aerophilic) and a variety of gram-negative bacilli. The available data do not permit a correlation between the clinical appearance of the involved muscle and the microorganisms isolated, except in the patient with crepitant myositis from which Cl. perfringens was isolated.
Clostridial-like myositis was found in amputation stumps to which skin traction had been applied at a forward hospital in four of six patients admitted with such traction. There was no positive evidence that skin traction and possible compression of the distal stump actually promoted the development of muscle necrosis and infection. It is possible that initial débridement was inadequate, but it was probably unwise to apply skin traction to a stump after initial débridement if there was any question as to the viability of the muscle. This would be particularly true if the onset of acute renal failure was suspected because the chemical effects of myositis were more difficult to control when renal failure was present.9
The principles employed in the treatment of muscle necrosis and infection were surgical excision of the involved muscle and the administration of large doses of antibiotics. The latter were usually given empirically as follows: Penicillin was used both intravenously
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and intramuscularly in the crystalline form in doses varying from 300,000 units to 12 million units per day in different patients. In addition, streptomycin or one of the tetracycline compounds was administered; usually 1.0 gm. of the former intramuscularly and 1.5 gm. of the latter was given intravenously or by mouth daily.
Myositis appeared to have been controlled in 9 of the 15 affected oliguric patients. The available data do not permit an accurate evaluation of the effect of the above antibiotics on the myositis in the patients who survived. Six patients died despite aggressive surgery and antibiotic therapy.
The finding of such a high incidence of myositis in the oliguric patients is of interest because of a possible etiological relationship. But acute renal failure was also found in patients with clostridial-like myositis, and conversely, patients were seen with clostridial-like myositis, without oliguria. Unfortunately, the data are insufficient to compare the bacterial flora in the pathological muscle from patients with and without oliguria.
The other types of infection recorded in Table 2 do not require much comment. They represented types of infection likely to complicate severe injury. The three cases of septicemia were apparently due in each instance to a single species of microorganism, a hemolytic Staphylococcus, a proteus bacillus, and a paracolon bacillus; only the latter patient died.
The patients with arterial injury and attempted repair who developed oliguria are of interest. The group included three femoral, two posterior tibial, and one brachial artery injury. The systemic effect and pathological sequence following a major arterial injury may be similar in some respects to that encountered in the "crush syndrome."2 It is possible, therefore, that there may have been a direct etiological relationship between the muscle ischemia resulting from arterial injury and subsequent renal failure. But gangrene may occur in an extremity distal to the site of arterial repair without the occurrence of oliguria.13 A review of the records suggests that the poor results obtained following arterial surgery in the six patients under discussion were probably the result of errors in judgment. Primary amputation might have been the wiser choice because of extensive associated injury.
Uncontrolled gastrointestinal tract hemorrhage was a late complication in two patients and may have been due to uremia. Another patient had uncontrolled retroperitoneal bleeding which appeared at autopsy to have originated from lumbar veins or from an overlooked tear in the inferior vena cava. This patient died on the operating
78
table while undergoing a laparotomy in an attempt to control oozing. He had received 25 liters of bank blood.
Excessive bleeding following a secondary débridement of muscle was noted in seven patients. Uremia did not seem to be the cause of the bleeding as the complication was encountered soon after injury when the nonprotein nitrogen was relatively low. All the patients had received low-titer group O blood and there was no clinical evidence that they had sustained a transfusion reaction; moreover, blood specimens drawn during the episodes did not reveal hemolysed plasma. Only one of these patients did not have oliguria but other wounded patients without oliguria (not reported in this paper) were seen at a Mobile Army Surgical Hospital with this complication. The oozing was so profuse that serious blood loss occurred. The only effective method of controlling hemorrhage was either the application of tight compression dressings or extensive cauterization. Hemostats were not very effective except when applied to obvious blood vessels. Otherwise, their use promoted further hemorrhage. Freshly drawn ACD-blood was given to two of these patients but we are not certain of its effect in controlling the oozing. The use of the cautery or of compression in wounds is often not desirable and this was particularly true in the type of wounds under discussion. They were already heavily contaminated with aerobic and anaerobic microorganisms so that any procedure which caused interference with local circulation or promoted tissue necrosis was undesired.
Nine patients in the present series were admitted to the Renal Center in shock or with an unstable blood pressure which could only be maintained at about 100 mm. Hg by the administration of norepinephrine continuously. They had been transported by air from forward hospitals because of oliguria, with the expectation that they could be managed more adequately at the Renal Center. All of them had received initial surgery. Data on their diagnosis and course are presented in Table 3.
Hypotension was associated with infection in four of these patients, and with uncontrolled retroperitoneal bleeding in another. Oliguria persisted in three of the nine hypotensive patients following restoration of the blood pressure by the administration of transfusions and/or norepinephrine. Oliguria did not persist in four others and could not be determined in two patients because of our inability to resuscitate them. The general policy in the Korean theater of operations was to avoid transporting patients with postoperative hypotension. The above patients represented an exception to this rule for the reason given and also because the potential of the Renal Center was being continuously evaluated. These data demonstrate the apparent futility of transporting patients with postoperative hypotension to a renal
79
Table 3. Diagnosis and Result of Patients Admitted to Renal Center With Postoperative Shock
Patient Number | Diagnosis | Result* | Oliguria** |
|
100 |
Overlooked stomach perforation |
Survived |
Absent |
|
107 |
Extensive head injury |
Died (1.5) |
Present |
|
109 |
Multiple abdominal visceral injury |
Died (2) |
Absent |
|
122 |
Multiple extremity wounds |
Died (1) |
|
|
128 |
Uncontrolled retroperitoneal bleeding |
Died (1) |
Present |
|
129 |
Bilateral traumatic amputation thighs |
Died (7) |
Present |
|
130 |
Multiple abdominal and extremity injuries |
Survived |
Absent |
|
131 |
Multiple abdominal visceral injury |
Died (1) |
Absent |
|
139 |
Multiple abdominal and thoracic injury |
Died (2 hrs.) |
|
*Number in parenthesis indicates survival time in days at Renal Center.
**The output of less than 500 ml. urine in 24 hours at the Renal Center in the presence of a stable blood pressure and adequate fluid intake.
failure center, if facilities for resuscitation are available at the forward level. Not only may movement be detrimental to the patient but it is impossible to predict whether or not a hypotensive oliguric patient will develop persistent oliguria.
Comparison of Complications in Patients From Oliguric and Non-oliguric Series
The significance of the differences in incidence of the various complications encountered in the oliguric and non-oliguric patients in this study is somewhat difficult to evaluate. Probably the only important difference was the higher incidence of myositis in the oliguric group. It may be because of this that the incidence of post-débridement bleeding was higher in the oliguric group also.
Fatality Rate and Survival Time
Table 4 records the fatality rate and also the mean survival time of the fatalities in the oliguric and non-oliguric groups. Mortality was high regardless of urinary output although it was somewhat higher in the oliguric series. Thirteen of the oliguric patients excreted less than 100 ml. urine per 24 hours and the fatality rate was 77 per cent. Eleven of the oliguric patients excreted between 100 ml. and 500 ml.
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Table 4. Fatality Rate and Survival Time at Renal Insufficiency Center
|
| All Patients | Oliguric | Non-oliguric |
|
Admitted |
37 |
24 |
13 |
|
Died |
26 |
18 |
8 |
|
Fatality rate |
70% |
75% |
62% |
|
Average time from injury to death (days) |
7.7 |
8.1±1.32* |
6.5±1.0* |
*Standard error of the mean.
urine per 24 hours; the fatality rate was 73 per cent in that group. The mean survival time from injury to death in fatal cases was not significantly different in the two groups. Two patients in the non-oliguric group who failed to survive postoperative hypotension were excluded from these calculations.
Causes of Death
It is difficult to establish absolute causes of death in a complex disease, and the separation of these causes from the effects of renal disease is somewhat arbitrary. Table 5 lists what were considered to be the principal causes of death in patients from both series. The incidence of death from infection was similar in the two groups although death from myositis was more common in the oliguric group. Renal failure was the immediate cause of death in only one of the oliguric patients.
Table 5. Principal Causes of Death in Patients at Renal Insufficiency Center
|
| Oliguric 24 Patients |
Non-oliguric 13 Patients |
Number of Patients | ||
|
Myositis |
6 |
1 |
|
Peritonitis |
|
2 |
|
Hemorrhage |
2 |
1 |
|
Shock |
|
2 |
|
Septicemia |
1 |
|
|
Head wound |
1 |
|
|
Infected 60% burn |
|
1 |
|
Cerebral embolus |
1 |
|
|
Fat embolus |
1 |
|
|
Multiple injury |
|
1 |
|
Hyperkalemia |
1 |
|
|
Undetermined |
5 |
|
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A relatively rapid rise in plasma potassium developed without symptoms and was first recognized from an electrocardiogram which was taken routinely. The patient died before artificial hemodialysis could be commenced. Death in this patient occurred on the eleventh post-wound day; he had undergone hemodialysis on two previous occasions because of high plasma potassium. The cause of death could not be determined in five other oliguric patients. Deaths in the latter patients did not appear to be due to chemical imbalance, and no lesions were found at autopsy which were considered incompatible with life.
Transportation of Poor-risk Patients to the Renal Center Because of High Plasma Potassium
Operation of the Renal Center on a mobile basis seemed to be impracticable. Therefore, it was necessary to transport patients with acute renal failure to the Center. The plasma potassium level may reach 7 or 8 mEq. per liter within 24 hours of injury in patients with post-traumatic renal insufficiency. Transportation of such patients is usually hazardous because other contraindications to movement are often present also. For example, hypotension, continued bleeding, progressive infection or unstabilized head or chest injury may be present. Nevertheless, because of the fear of early death from potassium intoxication, a number of patients were sent to the Renal Center for possible hemodialysis who would not have been moved otherwise. Upon arrival at the Renal Center aggressive medical and surgical therapy was commenced and hemodialysis carried out if necessary. During the period of this study,16 such patients were admitted to the Renal Center with a plasma potassium above 6.0 mEq. per liter.
Table 6 records data on the subsequent course of these patients. Only 2 of the patients survived although 12 of the others lived 2 days or longer at the Center. None of the deaths were the result of pulmonary edema, hyperkalemia or uremia per se. Hemodialysis was carried out on 11 of these patients, usually more than once; but in only 3 of the patients of whom 2 subsequently died was this done within 24 hours of admission. All of these patients received intensive medical therapy to combat the effect of acute renal failure so that hemodialysis was not considered necessary in every patient. Transportation to the Renal Center was of value to only 2 of these 16 patients if end result alone is considered. Probably all 16 patients would have died if a renal center had not been available to them. However, the data in Table 6 also suggest that the elimination of the renal component as a cause of death may lead to an improved mortality rate if other causes of death can also be controlled.
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Table 6. Clinical Course of Patients Admitted to Renal Center With Plasma Potassium Above 6.0 mEq./L.
Patient No. | Admission K mEq./L. | Dialyzed | Day of First Dialysis after Admission to Renal Center | Final Result | Day of Death after Admission to Renal Center | Apparent Cause of Death |
|
89 |
6.2 |
Yes |
4 |
Died |
21 |
Peritonitis, GI hemorrhage. |
|
91 |
7.1 |
Yes |
6 |
Died |
8 |
Myositis |
|
92 |
7.5 |
Yes |
4 |
Died |
5 |
Multiple lung abscesses |
|
97 |
6.0 |
No |
|
Died |
6 |
Myositis |
|
99 |
7.0 |
No |
|
Died |
4 |
Undetermined, no autopsy |
|
102 |
6.7 |
Yes |
3 |
Recovered |
|
|
|
104 |
8.2 |
Yes |
1 |
Recovered |
|
|
|
107 |
7.8 |
No |
|
Died |
1 |
Massive head injury |
|
108 |
7.3 |
Yes |
4 |
Died |
8 |
Myositis |
|
125 |
6.9 |
Yes |
2 |
Died |
3 |
Undetermined |
|
128 |
8.0 |
Yes |
1 |
Died |
1 |
Uncontrolled retroperitoneal bleeding |
|
129 |
7.0 |
Yes |
2 |
Died |
8 |
Myositis |
|
132 |
6.6 |
No |
|
Died |
3 |
Cerebral edema |
|
133 |
7.0 |
Yes |
3 |
Died |
6 |
Septicemia |
|
135 |
7.5 |
No |
|
Died |
2 |
Undetermined |
|
137 |
7.3 |
Yes |
1 |
Died |
2 |
Undetermined |
Hemodialysis and Survival
Eighteen of the twenty-four oliguric patients presented in this study were dialyzed, usually more than once; six of these dialyzed patients survived. It is believed that the latter would have died if facilities for hemodialysis had not been available to them. But, as discussed above, specific treatment for acute renal failure including hemodialysis will not necessarily save patients with the post-traumatic variety of acute renal failure if there are other surgical complications. The following two case examples are presented to demonstrate that fact in more detail and also to indicate the type of surgical problem encountered.
Patient No. 110. A 22-year-old Negro male sustained traumatic amputation of both legs following a land mine explosion on 8 June 1953. Tourniquets were applied, and the patient was treated at a battalion aid station 13/4 hours after injury by the administration of 1 liter of dextran, 0.25 grain morphine sulfate, and 0.5 ml. tetanus toxoid. The patient was transferred to a collecting station
83
where he arrived with a blood pressure of 95/60 and a pulse rate of 100. He was subsequently transferred to a clearing station, arriving 4 hours after injury with a blood pressure of 90/?. Fifteen hundred cc. of blood was given, the tourniquets being left in place. Transfer was effected to a Mobile Army Surgical Hospital where the patient was admitted approximately 5 hours after injury. Débridement of a left above-knee stump and right below-knee stump was carried out 71/2 hours after injury. Twenty-five hundred cc. of blood was given during the procedure which was accompanied by a fall in blood pressure to shock levels for a short period of time. The blood pressure stabilized after operation and the urinary output was 1,100 cc. during the following 24 hours. A second débridement of both amputation stumps was done on 10 June (2 days later). Except for an initial drop at the beginning of the procedure, the patient`s blood pressure remained satisfactory throughout the operation. The 24-hour urinary output was 250 cc. on that day.
The patient was transferred to the Renal Center by air on 11 June because of persistent diminished urinary output and a reported plasma potassium of 6.1 mEq./L. He arrived at the Center with a blood pressure of 118/74, a pulse rate of 100 and a temperature of 100° F. He was alert, hiccuping, and complained of nausea. Fluid intake was restricted to about 800 ml. per day, 600,000 units of crystalline penicillin b.i.d., and 0.5 cm. streptomycin b.i.d. were continued, and other general measures for the management of acute renal failure were instituted. The patient vomited at intervals so that for several days the only caloric intake was that received by vein in the form of 25 per cent glucose. Areas of necrotic muscle were found in both amputation stumps on 13 June, requiring re-amputation on both sides. This procedure was tolerated poorly; the blood pressure dropped to 60/20, and 2,500 ml. of blood containing norepinephrine was required. The blood pressure rose to 100 systolic, but again dropped following the return of the patient to his bed; he was given another 1,000 cc. of blood. The shock position was maintained during the night, and the systolic blood pressure remained around 90 mm. Hg. There was considerable bloody drainage from both stumps due to excessive oozing following the re-amputations, which was difficult to control and required tight compression dressings. Subsequently the patient improved but by 16 June he was somewhat stuporous. At that time the nonprotein nitrogen was 255 mg. per 100 cc., and the plasma potassium 8.2 mEq./L. Hemodialysis was carried out but discontinued after21/2hours because blood clots formed in the tubing. The patient was somewhat improved following dialysis; but 2 days later a 6-hour hemodialysis was carried out because of increasing somnolence and a rising NPN and plasma potassium. The response to dialysis was excellent and during the succeeding 4 days urinary output gradually increased. Daily dressings showed progressive granulation of the amputation stumps. On the fifteenth day after injury the 24-hour urinary output was 710 ml., NPN 233 mg. per 100 cc., and plasma potassium 7 mEq./L. The patient was again drowsy so hemodialysis was done once more with a good result. Subsequently, urinary output continued to rise and reached a peak of 6,080 cc. on 2 July. Coincident with the increased urinary output, the patient`s clinical state improved, manifested by increased appetite and alertness. He was subsequently evacuated to Japan for further wound care.
Data regarding fluid balance and laboratory findings are given in Figures 1, 2, and 3. Figure 1 reveals that the patient was febrile throughout his stay at the Renal Center. The hematocrit was subnormal during that time, although a 500 ml. blood transfusion was given almost everyday. Fluid balance was reasonably well managed with diuresis commencing on the fourteenth day.
84
Caloric intake was low for most of the hospital stay. Figures 2 and 3 present the chemical data from the patient and show the effect of artificial hemodialysis on these. The levels of potassium, phosphate and nonprotein nitrogen in the plasma increased during the oliguric phase with return towards normal with hemodialysis. Carbon dioxide capacity fell as oliguria persisted and rose with hemodialysis. The fluctuations in the plasma levels of sodium, chloride and total calcium were not so consistent because of the intermittent therapeutic administration of these agents. It is our opinion that hemodialysis was one of the life-saving procedures used in this patient.
Patient No. 129. A 23-year-old Negro male who sustained traumatic amputation of both legs and a laceration of the left forearm due to a land mine explosion on 8 July 1953. Tourniquets were applied to the legs and the patient was admitted to a forward surgical hospital 11/2 hours after injury. He was in severe shock and was given 3,000 ml. of blood. Bilateral, guillotine amputations of the thighs and débridement of the forearm wound were commenced 7 hours after injury. A further 3,000 ml. of blood was given during the operative procedure, which lasted 2 hours. The postoperative blood pressure remained at about 110/70 for the first6 hours but then became non-perceptible.
The diagnosis of impending acute renal failure was suspected because no urine could be obtained by catheterization so the patient was transferred by air to
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the Renal Insufficiency Center. He was admitted to the Center approximately 20 hours after injury with a temperature of 103°F., a pulse rate of 150 per minute, and a respiratory rate of 32 per minute. The blood pressure was not perceptible, but the patient`s skin was warm and dry and he was restless and responded slowly to questions. Following the rapid transfusion of 1,000 ml. of blood the pressure returned to 100/80. This then stabilized at about 130/80 approximately 26 hours after injury. The potassium level in the plasma was 7.0 mEq./L. on admission to the Center. Examination of the wounds on the morning after initial surgery revealed a severe myositis involving the entire abductor group of the left thigh stump including the sartorius and vastus medialis muscles. The affected muscles were pulpy, avascular and purple-blue in color. A brownish exudate with a characteristic foul smell was present but crepitation was absent. Other muscle groups in the same thigh appeared uninvolved. The right amputation stump also appeared in satisfactory condition. An extensive débridement was done on the left side, removing the major portion of the medial muscle groups up to the pubic bone. A large metal fragment was found among the necrotic muscle groups in the region of the inguinal ligament, appar-
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ently having traveled up along fascial planes. The blood pressure was unstable during the operative procedure and required continuous supporting blood transfusion. The wound was dressed daily and on each occasion further débridement of progressively involved necrotic muscle was necessary. The first of these procedures was done under anesthesia which precipitated a sustained fall in blood pressure. The subsequent débridements were done without general anesthesia, but the blood pressure fell with each operative procedure even though manipulation was gentle and only dead tissue was excised.
It was obvious early in the patient`s course that a hip disarticulation was required to get above all devitalized infected muscle. However, we were not of the opinion that the patient could tolerate such major surgery. Artificial hemodialysis was performed on two occasions for apparent clinical uremia but the persistence of symptoms after chemical balance was restored was interpreted as evidence that myositis provoked the toxic manifestations. The patient`s blood pressure persisted at hypotensive levels during the final 2 days of life. He remained drowsy and confused and hiccuped constantly. A precordial friction
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rub developed and was thought to be due to mediastinal emphysema. Death occurred on the ninth post-wound day. Examination of the left stump at autopsy revealed residual areas of infected necrotic muscle confined to the posteromedial aspect. Other muscle groups showed areas of discoloration similar to the fish-flesh appearance described in the crush syndrome. The right amputation stump did not appear to be infected. The only other finding of significance was the presence of mediastinal emphysema. The primary cause of death was probably necrotizing myositis with complicating acute renal insufficiency.
Figure 4 shows some of the clinical data from this patient. The course was febrile except for a relatively short period. The pulse and respiratory rates were rapid. The white blood count was persistently elevated and the per cent of neutrophils above normal. The dosages of chemotherapeutic agents were as follows: penicillin, 1 million units every 4 hours intravenously; oxytetracycline, 0.5 gm. intravenously every 6 hours; chloramphenicol, 0.5 gm. orally every 6 hours; and during the last day of illness, erythromycin, 0.4 gm. orally.
Figure 5 records data on daily fluid balance, hematocrit and blood transfusions. The hematocrit fell progressively even though blood transfusions were administered. The patient`s fluid balance was controlled reasonably well.
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Figures 6 and 7 record the chemical data from the patient. The levels of non-protein nitrogen, phosphorus and potassium in the plasma increased as oliguria progressed with return towards normal following hemodialysis. Acidosis was progressive until the seventh post-wound day. The observations on calcium, chloride and sodium were influenced in part by the intermittent administration of these substances and also by hemodialysis.
Comment
The above two patients had sustained similar injuries and both became oliguric. A comparison of the chemical data reveals similar findings with the exception that the abnormal changes progressed more rapidly in patient No. 129. It is believed that this was related to the degree of the pathological changes in the muscle of the left amputation stump. Hemodialysis was first required on the third post-wound day with patient No. 129, whereas it was not needed until the eighth post-wound day with the other patient. But with both patients
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hemodialysis restored the chemical deviations toward normal. Likewise, the other data from each patient which are presented in figures 1, 4, and 5 are quite similar. These observations appear to show that the specific measurable effects of acute renal failure were being controlled in both patients. But patient No. 129 died because of our inability to overcome the progressive necrotizing infection confined to a portion of the left amputation stump.
Discussion
The patients reported in the present study constituted a small selected group of the most severely founded casualties. Many of them were alive only because of extraordinary efforts made by medical personnel at forward levels. Uncontrollable circumstances often prevented the immediate application of all the desired appropriate thera-
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peutic measures. For this reason some of the observations and conclusions reported in this paper are not necessarily applicable to the management of patients with less severe battle injury.
If the onset of oliguria is a direct reflection of the magnitude or degree of tissue damage, it may be impossible to obtain valid control patients in studying the clinical course of post-traumatic renal insufficiency. The control subjects used in this study were severely injured and had been sent to the Renal Center because acute renal failure was suspected. Some of them had elevated nonprotein nitrogen plasma levels, but the degree of change manifested by the chemical data was much greater in the oliguric group.
The data from this study do not reveal any new factors of possible etiological significance in acute renal failure. Severe shock had been
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present in 23 of the oliguric patients and was probably present in the other patient also. An inadequate history prevents a positive statement about the presence or absence of shock in the latter patient. All but three of the non-oliguric patients also had histories of severe shock and again the histories were inadequate where shock was not recorded. Therefore, the presence of severe shock following battle injury is not necessarily followed by persistent oliguria after resuscitation. This confirms the observations of the Second Auxiliary Surgical Group in World War II.5 They reported a 7.1 per cent incidence of oliguria (including anuria) in 140 patients admitted to forward hospitals with a systolic blood pressure under 41 mm. Hg. The incidence was 2.5 per cent in patients admitted with a systolic pressure between 41 and 70 mm. Hg.
Wounds confined to the extremities were more common in oliguric patients from the present study; because extremity wounds were not present in all of the oliguric patients, their significance as an etiological factor is hard to evaluate. Specific analyses for myoglobin were not performed. For the same reason the possible etiological significance of the high incidence of clostridial-like myositis is in doubt. A transfusion reaction in shocked patients was thought to be etiologically significant in two of the oliguric patients. Three others sustained direct injury to one kidney and these, too, may have been coincidental rather than truly significant in the etiology of the renal syndrome. It is possible that renal damage was the result of the cumulative effects of several insults which individually were insufficient to produce the lesion.
The high incidence of surgical complications in both the oliguric and non-oliguric patients was not surprising considering the circumstances. Of particular interest was the high incidence of infection found in both the oliguric and non-oliguric patients reported in this study. This was thought to be the primary cause of death in approximately 45 per cent of the fatalities. The effect of severe injury and of acute renal failure on resistance to infection in battle casualties has been the subject of a separate study by one of us (H. H. B.); these results have been reported in detail in another communication.10 No evidence has been found that such patients were more prone to infection because of a deficiency in the natural or acquired antibacterial defense mechanisms. It was difficult to obtain reliable data in Korea on the incidence of serious infection in patients with severe battle injury who were not admitted to the Renal Center. And, as discussed above, the problem of securing valid control subjects with comparable injury but no renal disease may be insurmountable. However, the
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incidence of infection was of the same order in the two small groups reported in this paper.
Complicating infection renders the control of the specific effects of acute renal failure much more difficult even if artificial hemodialysis is used.9 Therefore, it is of the utmost importance to recognize infection early and to institute vigorous treatment without further delay. We found it important to examine all wounds at once in patients newly admitted to the Center, regardless of the accompanying history. Immediate secondary débridement was necessary in 14 of the 37 patients from the present study. Subsequently the wounds should be examined at least once a day to be certain that devitalized tissue or progressive infection are not present. Secondary débridements should be done as soon as the need is recognized and should be thorough and radical if oliguria is present. Likewise, it may be wiser to amputate an extremity without delay if there is any doubt about its viability rather than temporize in the interest of conserving a limb. Patients with post-traumatic renal insufficiency present such a poor prognosis that an error in judgment on the conservative side in wound management may precipitate a fatality. Nor may there be sufficient time to correct such an error because of the rapid deterioration of the clinical state. However, it was not always possible to undertake the desired radical surgery in some patients because of their extremely poor tolerance of any manipulation. In other patients, in whom excessive bleeding had followed secondary débridement, the subsequent débridements were sometimes curtailed because of the fear of serious hemorrhage. The above recommendations do not necessarily apply to other less severely wounded non-oliguric patients where the therapy of acute renal failure is not a factor. In the latter type of casualty the policy of minimal disturbance of wounds during the period between initial débridement and secondary closure was usually satisfactory.
The data presented on the transportation of patients with high plasma potassium levels to the Renal Center for possible hemodialysis are not encouraging. Only two patients survived and only one of these required dialysis within 24 hours of admission; but none of the deaths were due to hyperkalemia.
The arrival of patients at the Renal Center with high plasma potassium levels who were also in shock and whose wounds required débridement because of myositis presented a particularly difficult problem. Resuscitation was first attempted and then a decision had to be made on whether to dialyze the patient`s blood or débride the wounds. If the latter was done first, there was the risk of sudden death on the operating table, possibly due to a further increase in the level
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of potassium in association with anesthesia, hypotension, or wound manipulation. Furthermore, the heparinization required during the subsequent hemodialysis might promote bleeding from the freshly débrided wounds. If hemodialysis was done first, then myositis might progress during the 6 to 8 hours required for hemodialysis. When such a decision was required in patients reported in this study, hemodialysis was done first; but because most of the patients died eventually, there is little evidence that the decision was the correct one.
There appears to be little advantage in transporting other oliguric patients in whom the immediate danger from hyperkalemia is not great to a renal center if any of the well-established contraindications for moving patients are present. The anti-potassium fluids and electrolyte therapy advocated by Meroney and Herndon may be life-saving in such a situation.9
The fatality rate and survival time of the small series of oliguric patients reported in this study were somewhat different from those reported by Beecher and his associates.3 The fatality rate for anuric patients was 14 per cent better and for oliguric patients 26 per cent worse than those reported in the World War II study. The latter difference is hard to understand and may be due to the smallness of the present series. But a significant finding in the present study is that the primary cause of death was thought to be the result of renal failure per se in only one patient. In the World War II study, uremia was the primary cause of death in 67 per cent of the fatalities. From this it seems apparent that careful medical management supplemented by artificial hemodialysis may control the abnormalities resulting from acute renal failure. Because such abnormalities may be lethal, their control is essential. It is equally clear that such management is only one facet in the therapy of patients with post-traumatic renal insufficiency. Other derangements, either apparent or unknown, which are responsible for the high fatality rate associated with this syndrome must also be sought for and treated.
Summary
1. The surgical care of 24 patients with post-traumatic renal failure (lower nephron nephrosis) and of 13 seriously wounded but non-oliguric casualties has been discussed. The effects of acute renal failure were controlled by careful medical management and also by artificial hemodialysis.
2. Significant infection was the most frequent complication encountered in both groups; the incidence was 83 per cent in the oliguric patients and 63 per cent in the non-oliguric patients.
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3. Myositis, usually of a localized type and probably secondary to traumatic devascularization of muscle, was the most frequent complication found in the oliguric group. This could not be adequately controlled in 6 of 15affected patients.
4. Other serious complications occurring in both groups of patients were postoperative shock and excessive wound bleeding after secondary débridement.
5. The fatality rate was high in both groups and the mean survival time of fatal cases from each group was not significantly different.
6. Renal failure was the immediate cause of death in only one of the oliguric patients. The principal causes of death in all of the fatal cases have been listed. Complicating infection was responsible for approximately 45 per cent of fatalities in each group.
7. Artificial hemodialysis was considered to be a life-saving procedure in one-third of the patients from the present series so treated. The data appear to show that the renal component can be eliminated as a cause of death in patients with post-traumatic renal insufficiency. If the fatality rate is to be further improved, then other causes of death must also be eliminated.
8. Severe trauma and shock were the only etiological factors consistently present in patients developing oliguria. Reaction to blood transfusion was not a prominent factor in the etiology of lower nephron nephrosis inpatients from the present series.
9. If serious progressive surgical complications are present, a patient with lower nephron nephrosis probably should not be transported to a specific renal treatment center for possible artificial hemodialysis.
10. Complications of injury, especially infection, must be recognized early and treated aggressively to facilitate the control of the effects of renal failure.
References
1. Minami, S.: Über Nierenveränderungen Nach Verschüttung. Virchows Arch. F. Path. Anat. 245: 247-267, 1923.
2. Bywaters, E. G. L.: Ischemic Muscle Necrosis, Crushing Injury, Traumatic Edema, Crush Syndrome, Traumatic Anuria, Compression Syndrome; Type of Injury Seen in Air Raid Casualties following Burial beneath Debris. J. A. M. A. 124: 1103-1109 (April 15), 1944.
3. The Physiologic Effects of Wounds: The Board for the Study of the Severely Wounded. Office of The Surgeon General, Department of the Army, Washington, D. C.
4. Lucké, B.: Lower Nephron Nephrosis (renal lesions of the crush syndrome, of burns, transfusions, and other conditions affecting lower segment of nephrons). Mil. Surgeon 99: 371-396 (Nov.), 1946.
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5. Report of Second Auxiliary Surgical Group, World War II. Library of The Surgeon General, Washington, D. C.
6. Corcoran, A. C., and Page, I. H.: Crush Syndrome: Post-traumatic Anuria. Observations on Genesis and Treatment. J. A. M. A. 134: 436-441 (May 31), 1947.
7. Moon, V. H.: Acute Tubular Nephrosis, a Complication of Shock. Ann. Int. Med. 39: 51-60 (July), 1953.
8. Oliver, J., MacDowell, M., and Tracy, A.: The Pathogenesis of Acute Renal Failure Associated with Traumatic and Toxic Injury. Renal Ischemia, Nephrotoxic Damage and the Ischemuric Episode. J. Clin. Invest. 30: 1305-1438 (December), 1951.
9. Meroney, W. H., and Herndon, R. F.: The Management of Acute Renal Insufficiency. J. A. M. A. 155: 877-883 (July 3), 1954.
10. Balch, H. H., Jr.: The Effect of Severe Battle Injury and of Post-traumatic Renal Failure on Resistance to Infection. To be published.
11. Meroney, W. H.: The P: NPN Ratio in Plasma as an Index of Devitalization of Muscle during Oliguria. Surg., Gynec. & Obst. In press.
12. Lindberg, R. B.: Personal communication.
13. Hughes, C. W.: Personal communication.
14. Moore, F. D., and Ball, M. R.: The Metabolic Response to Surgery, p. 5 Charles C. Thomas, Publisher, 1952.
