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Chapter IV

Contents

CHAPTER IV

Diagnosis of Lower Nephron Nephrosis Resulting from Trauma and Shock ("Shock Kidney")

As Derived from Clinicopathologic Correlation

The clinical syndrome of renal insufficiency following traumatic shock had not yet, to our knowledge at the time of this study, been defined in the medical literature. In the interval preceding publication Lucké1 has described, from both clinical and pathologic points of view, a group of similar cases under the term "lower nephron nephrosis." The present study, though now no longer novel, was done independently before his publication and therefore offers unbiased confirmation which seems worthy of record. Since civilian practice brings so few apposite cases under the observation of any single group of investigators, one of our clearest obligations was to attempt definition of this syndrome.

In exploration of a new syndrome the first necessity is establishment of a base of departure; that is, an apparently new combination of symptoms, signs, laboratory observations, or distinctive morphologic lesions. With widening experience, additions to and subtractions from this combination are made until the pattern becomes stabilized, the diagnostic importance of each feature or group of features being assessed by the frequency with which it occurs in the disease in question as compared with its infrequency in other conditions.

Since the case fatality rate of this condition was high, there is little risk of distorting the picture by using the fatal cases to establish the base of departure. In 38 of 60 cases in which necropsy material was available, pigment nephropathy,

    1LUCKÉ, B.: Lower nephron nephrosis. Mil. Surg. 99: 371-396, November 1946.


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the characteristic renal lesion of "shock kidney" which will be described in Chapter IX, was present. In the following discussion the symptomatology in these cases will be presented, comparing the findings as we proceed with the control group of 22 cases in which pigment nephropathy was proved absent at necropsy. To determine whether diagnosis of renal injury can be established beyond reasonable doubt, the fatal cases will be further compared with nonfatal cases in which there was evidence of kidney dysfunction.

Objective Evidence of Renal Insufficiency in Cases of Histologically Proved Nephropathy

Oliguria and Anuria

For purposes of this study, oliguria was defined as a 24-hour output of urine greater than 100 cc. and less than 600 cc.; anuria as an output not exceeding 100 cc. per day. Urine output, known in 35 of the above-mentioned 38 patients with the characteristic renal lesion, had been subnormal for one or more days in all, 15 patients remaining in the oliguric and 20 reaching the anuric level. Oliguria or anuria was present from the onset of shock in all but one case, and in this case the delay was apparent rather than real. The initial shock had been mild, but secondary shock of greater severity occurred after operation and was promptly followed by anuria. The majority of patients showed progression from oliguric to anuric levels, but occasionally anuria was present from the start. In 15 patients with clinical uremia and histologically proved nephropathy, the urine output never declined below the oliguric level. It is worth emphasis that these individuals, often casually referred to as "anuria cases," may never in fact become anuric. Unless 24-hour outputs are carefully measured, significant oliguria may easily be missed.

Nine patients with oliguria (or anuria) failed to show a significant renal lesion at necropsy. This is not surprising, considering the variety of conditions from which these severely wounded men suffered which would tend to lower urine output, such as deficient blood volume, prolonged hypotension, paralytic ileus, infection, and exudation into traumatized areas and into infected serous cavities. In two of the nine oliguria or anuria was intermittent; in both the clinical picture was dominated by severe peritonitis.


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Azotemia

"High azotemia," arbitrarily defined as a nonprotein nitrogen level in the plasma of 65 mg. per 100 cc. or higher, was found in 36 of the 38 proved nephrotic cases; in 1 case no determination was available, and in the remaining 1, death occurred within 35 hours of injury. In this patient the nonprotein level had already climbed to 63 mg. per 100 cc., only 2 points below our arbitrary limit, and there can be no reasonable doubt that this limit would have been passed had he lived a few hours longer. Like oliguria, nitrogen retention was evident from the outset. The retention level climbed steadily, usually from 30 to 40 points a day, the maximal level depending solely on the length of time elapsing before death ensued or, in those who survived, before onset of diuresis. Nitrogen retention, like oliguria, was also observed in the absence of a renal lesion (7 instances) and is explainable on similar grounds.

Hypertension

We defined hypertension for purposes of this study as an elevation of the systolic blood pressure to or above 135 mm. Hg and of the diastolic to 90 mm. Hg or higher. By civilian standards these figures must seem low, but it is to be remembered that we were dealing primarily with a homogeneous group of young men between 18 and 30 years of age who had recently suffered severe trauma usually associated with the loss of considerable amounts of blood. By this standard, 20 of 32 patients with the renal lesion whose blood pressures had been recorded were judged to have significant elevations of systolic or diastolic pressure or both. Hypertension rarely appeared within the first 48 hours; it was frequent by 72 hours, and was the rule by 96 hours.

Of the remaining 12 patients with the characteristic renal lesion who failed to show an elevation of blood pressure, 3 died within 2 days of injury and 6 on the third day. In only 3 patients living beyond the 3-day period did hypertension fail to develop. One died on the fourth, 1 on the fifth, and 1 on the seventh day respectively. The last 2 patients also had a severe progressive peritonitis. It seems reasonable to conclude that hypertension is a characteristic if not constant symptom of the syndrome.

The importance of hypertension is increased when viewed from the converse point of view. No patient in this series whose kidneys failed to show pigment


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nephropathy at necropsy had a sustained elevation of blood pressure, although an occasional determination might have been above the arbitrary limit. It must be remembered, however, that no cases of cerebral injury were included in our series. In such cases hypertension secondary to increased intracranial pressure is of course frequent.

Pigment Excretion in the Urine

As part of the routine urine examination of all patients included in this study, the supernatant urine after centrifugation was tested with benzidine for the presence of dissolved heme-containing pigments,2 which, as will be discussed fully in Chapter VIII, were largely hemoglobin and myoglobin.

All patients with morphologic evidence of renal damage excreted benzidine-positive material in the urine. In 11 patients (exclusive of those in whom there was direct trauma to the urinary tract) enough pigment was excreted to make the urine grossly red or brown. In some cases descriptions such as "dark amber" suggest a pigment element, but in the majority amber and yellow were the colors recorded, and only the benzidine test revealed the pigment element. Pigment excretion, furthermore, was in most instances transitory and usually disappeared on the third or fourth day. On the other hand, pigment excretion was observed in 6 patients whose kidneys did not show significant lesions at necropsy.

Other Urinary Findings

Other chapters of this volume contain complete discussions of the chemical abnormalities found in the blood and urine and the results of renal function tests performed during the course of the studies. Repetition would be pointless, especially since these factors have little diagnostic value. However, three urinary abnormalities, determination of which lies within the realm of routine clinical pathology, are worthy of mention since, although of limited diagnostic value, they were constant features of the syndrome.

1. Proteinuria.-All patients with proved renal lesions showed proteinuria. However, since proteinuria was absent in only 14 of the entire series of casualties studied and was present in 51 patients without clinical or anatomic evidence of nephropathy, its diagnostic import is negligible.

    2See Appendix C, section on routine, urinalyses, for technique of performing the test.


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2. Persistent Acidity.-The urine of all patients manifesting nephropathy at necropsy was acid on initial examination. The range of pH was from 5.0 to 6.9 with an average value of 5.8. The urines of the control group ranged from 5.0 to 8.4 with an average of 6.2, overlapping too much to give the figures any diagnostic value. In succeeding specimens the urine from the nephropathic group remained persistently acid with few exceptions, occasionally even despite a therapeutically-induced alkalosis.

3. Fixation of Specific Gravity.-The specific gravities of the initial specimens varied from 1.009 to 1.032, though the majority of specimens fell within the range of 1.020 to 1.026. No significant difference was found in patients with and without nephropathy. Diversity in these initial specimens is not surprising, since it is probable that in many instances part of the urine may have been excreted by the kidney before the patient was wounded. With the passage of time the specific gravity of subsequent specimens declined in the nephropathic group, despite oliguria, and a tendency to fixation between 1.010 and 1.015 became apparent in all the patients with proved renal lesions. Evidence of continued power of urine concentration occasionally helped to distinguish cases of "extrarenal" oliguria and azotemia from the true nephropathies.

Summary: Diagnosis of Lower Nephron Nephrosis ("Shock Kidney")

Seven phenomena have been described which are characteristic of the renal lesion following traumatic shock. One of these, proteinuria, has no diagnostic value because of its frequency in non-nephropathic cases. Two others, persistent acidity of the urine and fixation of specific gravity at a low level despite oliguria, are of great interest in defining the physiologic abnormality, but proved of limited diagnostic value since therapeutic emergencies frequently prevented verification by suitable test. A tetrad of findings--oliguria, azotemia, pigment excretion, and hypertension--were of practical diagnostic value.

Each of these may be present singly in patients with normal kidneys. So may any pair. The combination of oliguria and azotemia, for instance, was found five times; even the triad of oliguria, azotemia, and pigment excretion was found twice in patients with morphologically normal kidneys. The complete tetrad, however, was never found in this series in patients with normal kidneys. Barring the complication of a head injury, it was concluded that this tetrad might be considered reliable evidence of renal damage.


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Uremic Symptomatology

Subjective symptoms of the type commonly to be expected in uremia were conspicuous primarily by their absence. In the initial stages of the disorder minor symptoms might well have been masked by the greater discomforts of recent trauma, surgery, and anesthesia, or been suppressed by postoperative narcosis. As the days pass, these distractions cease to be of importance, yet again and again statements such as "patient comfortable" and "no complaints" appeared in the records. A brief review of the usual symptoms of renal insufficiency, noting their frequency in this material, is in order.

Headache.-Headache was not mentioned in any case record. Minor complaints might not have been recorded, but even so headache could not have been a conspicuous feature.

Nausea and Vomiting.-Many of our patients had abdominal wounds with subsequent gastric and intestinal surgery complicated by various grades of peritoneal irritation. They were often treated by Wangensteen drainage, making interpretation of gastro-intestinal symptoms difficult. Nausea appeared in three of the crush-syndrome cases and also in three others not complicated by abdominal wounds. In only two of these was it associated with vomiting, once on the seventh and once on the thirteenth day. Persistent hicupping was twice recorded.

Vision-No patient complained of visual difficulties. Eyeground examinations were recorded in nine cases. In six patients the eyes were found to be normal when examined at intervals of from 3 to 10 days, and in three patients were found to be abnormal. Two of the latter patients showed retinal hemorrhages on the fifth and tenth days of disease, respectively, and one showed papilledema on the ninth day.

Consciousness.-Drowsiness was the most frequent cerebral symptom and was noted in 17 instances. Its onset was recorded as early as the second day, as late as the ninth. Very frequently the notation was accompanied by a statement such as "patient drowsy but when aroused answers questions clearly and intelligently." One patient was frankly disoriented, and two were irrational. In 11 patients drowsiness progressed to stupor; in 6 of these the condition was described as coma. This stage seldom antedated death by many hours. Onset of coma was recorded as early as the third and as late as the tenth day. At the time of onset, the nonprotein nitrogen levels ranged from 89 to 305 mg. per 100 cc. of plasma. One patient regained consciousness after a lapse of 2 hours at a time when the


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nonprotein nitrogen level was 339 mg. per 100 cc. of plasma.

Twitchings and Convulsions.-These were very uncommon phenomena. Twitchings were recorded in two patients, convulsions in four; one of these four recovered. Neuromuscular irritability was noted in two other patients in whom Chvostek's sign developed. In both, the symptoms followed vigorous alkali therapy.

Hyperpnea.-Dyspnea or hyperpnea was recorded on 12 occasions, with onset ranging from the fourth to the twelfth day. In six instances it appeared approximately coincidentally with the onset of pulmonary edema and may well have been an effect of the latter. In only a few instances was respiration clearly of the Kussmaul type.

Edema.-Evidence of edema was observed in 25 patients. It appeared as early as the third and as late as the eleventh day, largely depending on the extent of intravenous fluid therapy. Clinical evidence of pulmonary edema was recorded in 12 instances. Either pulmonary or peripheral edema might appear first, and each was observed in the absence of the other. Facial edema was noted only 8 times.

Nonfatal Cases

In examining the clinical records of nonfatal cases in this series to see if diagnosis of renal injury could be established beyond reasonable doubt, we were hampered by incompleteness of observation and record. The findings in 44 patients whose records were fairly complete and who manifested 1 or more of the 4 criteria described above are summarized in the accompanying table.

Three patients presented the complete tetrad of characteristic findings. Two showed the triad of pigment excretion, azotemia, and hypertension, but in both there was uncertainty regarding urine output during the first 48 hours after injury. Two presented the combination of pigment excretion, oliguria, and azotemia, but blood pressure determinations at appropriate time intervals were not recorded. In five others with the same triad, hypertension could be definitely excluded.

Among those with a combination of two principal signs, one patient showed oliguria and hypertension, but nonprotein nitrogen was not determined and the urine was not tested with benzidine. In one case hypertension of notable level (170/120) and azotemia were observed, but urine output was not recorded


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TABLE 51.-PRINCIPAL FINDINGS IN 44 SURVIVING PATIENTS SUSPECTED OF HAVING RENAL INSUFFICIENCY
nor was the urine tested with benzidine during the first 5 days. In Case 130, oliguria and unimpressive azotemia of 69 mg. per 100 cc. were demonstrated, but again the urine was not tested and no postoperative blood pressures were recorded. In another patient, azotemia and pigment excretion were present but no elevation of blood pressure occurred, and the urine excretion for the first 24 hours was 750 cc., which was above our arbitrary limit but nevertheless in the lower range of normality.

Three patients presented the remaining pair of findings: pigment excretion and oliguria. Six patients manifested only transitory oliguria without supporting evidence of nephropathy, and 19 pigment excretion with similar lack of confirmatory findings. In the light of the above findings, let us again evaluate our diagnostic criteria.

As in the fatal group, no patient with other evidence of renal insufficiency failed to show pigment excretion if the urine was tested with benzidine within the first 48 hours after injury. Nineteen patients out of the 44, however, who at no time showed any other evidence of renal damage, excreted benzidine-positive material.


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Oliguria was demonstrated in 15 patients with 1 or more other positive findings. In 3 patients its presence was uncertain and in 6 it was observed in the absence of any other sign. In one questionable case, in which there was pigment excretion and azotemia, oliguria was absent. Oliguria in these patients who survived was, however, sometimes extremely transitory. Among the patients manifesting the complete tetrad, oliguria was of only a day's duration in two cases, and lasted only 2 days in one. The longest duration of oliguria did not exceed 4 days. In none of the cases was output depressed to anuric levels; i.e., below 100 cc. in 24 hours.

Azotemia was observed in 15 of the 44 patients. In no instance was it the sole finding. A plasma nonprotein nitrogen concentration of 88 mg. per 100 cc. accompanied only by pigment excretion occurred in one instance. In 7 patients the maximal level was below 100 mg. per 100 cc., and in 6 the range was between 100 and 150 mg. per 100 cc. of plasma. Two desperately ill patients recovered despite nonprotein nitrogen levels of 247 and 217 mg. per 100 cc. respectively. In 3 patients the azotemia was of such low degree (74, 77, and 69 mg. per 100 cc. respectively) and so transitory (lasting only 1 and 2 days) as to be of doubtful significance. In the other patients it lasted from 3 to 21 days.

Seven patients showed definite hypertension which ranged from 128/90 in Case 54 to 180/115 in Case 138. Blood pressure was not recorded for two patients who presented the triad of pigment excretion, oliguria, and azotemia, but did not become elevated in five other patients presenting the same combination. The remaining two patients in this group had, respectively, azotemia of more than 17 days' duration with a maximum nonprotein nitrogen level of 247 mg. per 100 cc., and azotemia of over 7 days'duration with a nonprotein nitrogen level of 140 mg. per 100 cubic centimeters. Hypertension was never observed without other evidence of renal insufficiency. Once hypertension developed it was very persistent, even after the nonprotein nitrogen had dropped to normal levels. The shortest duration of hypertension observed was 12 days, and in one patient it was still present at 22 days.

In summary, pigment excretion appeared to be a constant phenomenon in the shock kidney but was seen also in many patients who never showed evidence of renal failure. Oliguria likewise was frequently seen in the absence of renal failure. In positive cases it might be extremely transitory and the volume not greatly depressed. Azotemia was a constant and, except in the presence of severe complications or in the moribund state, a reliable sign of renal failure. Eleva-


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tion of blood pressure in the absence of a head injury was inconstant. When present it constituted the most important confirmatory criterion.

On these grounds it is reasonable to conclude that all seven surviving patients manifesting hypertension did, in fact, have "shock kidney." In six of these azotemia was proved, and in the seventh the nonprotein nitrogen level was not recorded. Eight other patients showed azotemia supported by one or more other criteria of renal injury. In three patients azotemia was so slight and transitory as to be of doubtful significance. In the remainder it was of sufficient severity or was bolstered by enough other confirmatory evidence to justify the diagnosis of renal injury.

We conclude, then, that a minimum of 11 and a possible maximum of 14 of our patients developed and survived "shock kidney." In comparison with 38 fatal cases of histologically proved shock kidney, this indicates a case fatality rate of approximately 75 percent.

SUMMARY AND CONCLUSIONS

The clinical records of 60 patients on whom necropsy was performed were analyzed from the standpoint of factors relating to renal function, and the findings in the group of 38 with histologically demonstrated pigment nephropathy were compared with those of the 22 in whom this lesion was not present. It became apparent that the clinical syndrome of renal insufficiency which follows shock is remarkable chiefly for the scarcity and mildness of its symptoms. Little that the patient complained of served to call attention to the condition. Drowsiness slowly deepening into stupor was the most common symptom, but it might be absent almost until death. The only common sign was edema, either pulmonary or peripheral.

Laboratory and blood pressure findings provided more useful criteria. Seven findings were present with great constancy in the nephropathic cases that appeared only sporadically or never in the control group. These were in ascending order of diagnostic importance: proteinuria, persistent acidity of the urine, excretion of benzidine-positive material, oliguria, azotemia, fixation of specific gravity of the urine at a low level, and hypertension. It was found that the diagnosis of nephropathy could only be made by the systematic recording of four factors in every patient who was resuscitated from shock: (1) the total urinary output, (2) the presence of benzidine-positive material in the urine, (3) the nonprotein


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nitrogen level in the blood plasma, and (4) the systolic blood pressure. The symptom complex of oliguria, pigment excretion, azotemia, and hypertension established the diagnosis. It is probable that in some cases oliguria was too transient to be recognizable, and certain that in some cases hypertension did not develop. If the patient survived beyond 4 days, fixation of specific gravity and constant acidity of the urine afforded important confirmatory evidence.

These diagnostic criteria of nephropathy were then applied in a review of the records of the nonfatal cases in the series. It was concluded that a minimum of 11 and a possible maximum of 14 had had a pigment nephropathy. Using the former figure, the case fatality rate is approximately 75 percent.

CASES OF SPECIAL INTEREST IN THIS CHAPTER

Nonfatal

13 44 72 109 133

27 54 81 112 138

29 60 87 125 150

37 71 104 130

Fatal

8 26 52 85 108 122

12 31 55 86 116 123

22 41 65 88 117 129

24 47 66 95 118 131

25 49 74 97 120 136

80 98 A-30

Crush Syndrome Fatalities

69 70 78 93 132

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