Acute Renal Failure Following Blunt Civilian Trauma A. J. MATAS, M.D., W. D. PAYNE, M.D., R. L. SIMMONS, M.D., T. J. BUSELMEIER, M.D., C. M. KJELLSTRAND, M.D., F.A.C.P.
Renal failure developed in 20 patients following blunt civilian trauma. Ten recovered normal renal function; 8 currently survive. Survivors and nonsurvivors did not differ in age, time from trauma to anuria, mean blood urea nitrogen or creatinine level prior to the first or to subsequent dialyses. However, there was an increased incidence of sepsis and liver failure in those who died. When outcome was related to site of injury, patients with closed head injury and/or intra-abdominal injury had a worse prognosis than those with thoracic or extremity injury only. Only 2 patients with perforated bowel survived; both had peritoneal dialysis combined with peritoneal lavage with antibiotic solutions. Mortality in patients with posttraumatic renal failure remains high; however, death is usually a result of associated complications rather than a result of the renal failure. Aggressive management of other complications of the trauma, especially sepsis or potential sepsis, is necessary. We recommend peritoneal dialysis combined with peritoneal antibiotic lavage where there is a potential for posttraumatic intraabdominal sepsis associated with renal failure.
PATIENTS surviving the uremic state associated with acute tubular necrosis frequently regain normal renal function and suffer no long term complications. Thus with the advent of hemodialysis, it was hoped that acute renal failure would become an easily manageable problem. Theoretically, if dialysis could maintain the patient throughout the critical uremic period, recovery would be the general rule. These hopes have not been fulfilled. Postoperative and posttraumatic acute renal failure continue to have high morbidity and mor-
tality. 1,2,4,13,2 The role of renal failure and its treatment in this high complication and death rate is unclear. First, the cause of renal failure and its timing in the patient's course are frequently hard to define. Hypotension, hypovolemia, septicemia, drug intoxication and mismanagement of fluid and electrolyte balance have all been implicated as causes of renal failure and any one patient may have more than one of these problems. Second, it is often difficult to determine if the renal failure precedes or is the result of another complication, such as sepsis. Third, when renal failure has Submitted for publication June 21, 1976. Reprint requests: Dr. Carl M. Kjellstrand, Chief, Division of Nephrology, Box 485, University of Minnesota Medical School. Minneapolis, Minnesota 55455.
From the Departments of Medicine and Surgery, University of Minnesota Medical School, Minneapolis, Minnesota
developed, it is unclear how much it affects the patient's subsequent course, i.e., is renal failure important in the complications that develop or are these complications due to the underlying disease? For example, renal failure is thought to be immunosuppressive28 although there is some conflicting evidence.26 Patients with uremia have an increased incidence of septic complications. Thus, when a patient with posttraumatic renal failure develops septic complications, the renal failure is frequently blamed. However, following trauma, patients without renal failure also have a high incidence of septic complications. Similarly, renal failure is also known to impair coagulation18 and again renal failure may be implicated as the etiology of bleeding rather than the trauma or the reparative surgery. We have, therefore, reviewed the course of patients who developed renal failure secondary to non-penetrating trauma in the hope of clarifying the following questions: A) Does the type of trauma or the age and sex of the patient have any prognostic implications? B) Does the dialysis treatment instituted per se have any bearing on the outcome of the patient; i.e., time of initiation of dialysis, type of dialysis (peritoneal or hemodialysis), the frequency of dialysis. C) Does simultaneous failure of other organs have any prognostic implications? D) Are clinical or culture-proven signs of sepsis important prognostically? Methods Twenty patients receiving dialysis at the University of Minnesota between January 1968 and December 1975 for renal failure due to non-penetrating trauma were studied. Cause and timing of renal failure, extent of injury, pathogenesis of renal failure, duration of anuria, long term course and complications were investigated for each patient. We attempted to determine whether outcome is 301
302
MATAS AND OTHERS
related to primary injury, signs of other organ failure (need for respirator > 2 days, bilirubin 5 mg/100 ml), or the technique, timing, or frequency of dialysis. Following diagnosis of renal failure, dialysis was instituted early and was used daily or every other day. The patients treated with hemodialysis were treated with relatively high efficiency dialyzers (Travenol, 145 coils or Gambro Lundia dialyzers). All dialyses were done with regional heparinization according to a previously described method.11 During these, it was attempted not to allow the Lee White clotting time increase over 50%o of normal. Conservative management consisted of anabolic steroids (Durabolin, 100 mg IM twice weekly), the use of antacid phosphate binders (aluminum hydroxide) and oral mycostatin, 100,000 U 4 times daily. Hyperalimentation, pummeling, and frequent pulmonary toilet were used. Almost all patients received broad spectrum antibiotics against documented or assumed infections. Peritoneal dialysis was done either through the use of four quadrant thoracic sump drains placed during surgery or more commonly by puncture between the umbilicus and urinary bladder done percutaneously. Two liter hourly to two hours exchanges containing glucose in a concentration of 1.5, 4.25, or 7% solutions were used. Potassium was added as necessary to control the serum potassium concentration; heparin (500 units/L) was added. If signs of intraperitoneal infections were present, Kanamycin 10 mg/L and Keflin 200-500 mg/L were added. The peritoneal dialysis was continued for 48 to 96 hours depending on the patient's uremia. Results
Twenty patients have received dialysis at the University of Minnesota, (January 1968 to December 1975) for acute renal failure following non-penetrating trauma. This represents 20/425 (4.7%) patients dialyzed for acute tubular necrosis, 20/594 (3.4%) patients -receiving dialysis for acute renal failure, and 20/1398 (1.4%) patients dialyzed during this time period. Six of 20 (30%o) patients were seen initially at this hospital; 14/20 were referred after initial management at other hospitals. All patients were in good health prior to their injury. None had previous evidence of renal disease. Table 1 lists causes of trauma and general characteristics for this group of patients. Mean age of the patients was 36 (range 14-74). Eleven were 2 days >5 cemia Dialysis
by
Cause of Death
Survived 19 26
1
Hypotension, hypovolemia 2 Hypotention, hypovolemia, fat embolism 3 39 M MVA Hypotension, hypovolemia 4 21 M MVA Hypotension, hypovolemia 5 22 M Crush Myglobinuria, hemoglobinuria 6 65 M Crush Hypotension 7 54 M Traction Hypovolemia, hemoglobinuria Crush 8 65 M MVA Aortic dissection Recovered Renal Function But Died 9 19 M MVA Hypoxic M M
MVA* MVA
1,5 1,5
+
+
-
+
1,3 1,4
-
-
+t
+
+
_
+
+
1I
4
+:
3
+
_
_
2
+
-
-
_
_
~+
+
Secondary to head injury
(2 yrs.) 10
20
M
MVA
Mannitol toxicity
2
+
-
-
11 Dead 12 13 14
28
M
MVA
Hypotension, transfusion Rx
2
+
+
+
32 41 74
M M F
MVA MVA
Fat embolism
+
_
_
1,4
+
+
+
1,5
+
+
+
1,2,5 1,5 1,5
+
+
+
_
+
+
+
-
-
15 16
17 18
19 53 22
19
72 14
20
23
Hypotension, hypovolemia Sepsis, hypotension, fat emboli, transfusion Rx M MVA Hypovolemia, hypotension M MVA Hypovolemia, hypotension M MVA Hypovolemia, hypotension, fat emboli M Crush Hypovolemia, hypotension F SnowHypovolemia, hypotension, mobile myoglobinuria, hypoxia M Crush Hypovolemia, hypotension MVA
+
Secondary to head injury (3 yrs.) Secondary to head injury Fat embolism
Sepsis, liver failure Sepsis Fat embolism, head injury Sepsis Fat embolism
1,5 1,2,5
+
+
+
+
+
+
Sepsis Head injury
1,4
+
+
+
Sepsis
Motor vehicle accident. 1 = extremity and/or pelvis; 2 = head; 3 intrathoracic; 4== intra-abdominal with perforated bowel; perforated bowel. 4: Respirator needed as part of technique of peritoneal dialysis. *
t
=
All 5 patients with severe closed head injury died result of their injury, although 3 recovered renal function and 2 were discharged to long-term care as a
institutions. Of the 12 patients having renal failure in association with intra-abdominal injury, only 4 survived. Cause of death in 2 was due to associated severe closed head injury, and in one death was due to fat embolism. The remaining 5 patients died of sepsis. Septic deaths occurred not only in patients with perforated bowel
S =
intra-abdominal without
in association with other injuries but also in 2 patients whose only intra-abdominal injury was a ruptured spleen. Only two patients with perforated bowel survived. Both were treated with peritoneal antibiotic lavage. Two more patients, both with head trauma and both treated with peritoneal dialysis, survived renal failure. Both died as a result of their head injury; at the time of death both had normal renal function. Because of our success with this mode of therapy and our feeling
MATAS AND OTHERS
304
TABLE 2. Survivors vs. Nonsurvivors: Patients Developing Renal Failure after Trauma
Survivors
Mean age (yrs.) Trauma to anuria (days) # Dialyses/duration of anuria Mean BUN *prior to 1st dialysis (mg/100 ml) Mean Crt prior to 1st dialysis (mg/100 ml) Mean BUN prior to each dialysis (mg/100 ml) Mean Cr prior to each dialysis (mg/100 ml) Mean K+ prior to each dialysis (mEq/L)
Nonsurvivors
39 2
40 2.7 .6
.52 110
20
124
35
9.1 ± 3.8
9.6 ± 3.8
100 ± 15
113 ± 17
8.2 ± 2.3
9.3 ± 2.6
5 ± 1.0
5.4 ± 1.6
Blood urea nitrogen t Creatinine *
that it should be used in similar patients with intraabdominal sepsis or head injuiry, one case will be described in detail: Case Report A previously healthy 64-year-old man was crushed between two vehicles at work. His injuries appeared superficial and he complained only of relatively mild left flank and abdominal pain; he was able to continue working. However, his pain increased in severity and he sought medical attention 10 hours following his injury. Upon admission to his local hospital, he complained of diffuse abdominal pain. Vital signs were normal. For the next 14 hours his vital signs remained stable; however, he complained of progressively worsening abdominal pain. Twenty-four hours following his injury, his temperature suddenly rose and he became hypotensive and was then transferred to the University of Minne-
Ann. Surg.
*
March 1977
sota Hospitals. Physical examination on admission to the hospital revealed a rectal temperature of 39.8°, pulse of 130/min, and B.P. of 80/50. His abdomen was distended with diffuse tenderness and rigidity and absent bowel sounds. Peritoneal lavage revealed turbid, feculent abdominal fluid with a white blood cell concentration of 16,240/mm3. Blood urea nitrogen was 46 mg/100 ml, creatinine 3.6 mg/100 ml, white blood cell count 9,100-9,800/mm3. He was immediately taken to the Operating Room where severe diffuse fibrinous peritonitis and a blow-out perforation of the small bowel 3 feet proximal to the ileocecal valve were found. The perforation was oversewn, the peritoneum irrigated with 12 liters of normal saline, and catheters were placed for prolonged peritoneal irrigation. Standard, multiperforated adult peritoneal dialysis catheters were placed on each side of the midline above the umbilicus for inflow. French plastic catheters (No. 36) were then introduced through stab wounds in each of the four abdominal quadrants. Postoperatively, the patient had evidence of oliguric renal failure, with hourly urine outputs in the range of 5-10 cc. Intermittent peritoneal irrigation was performed in hourly cycles using 2 L/cycle of standard peritoneal dialysis solution. Glucose percentage and electrolyte concentration were varied according to the fluid and electrolyte status of the patient and according to the dialysate return. Gentamycin (15 mg) was added per liter. The solution was instilled in 20 minutes, allowed to equilibrate for 20-30 minutes and then drained in 10 minutes to complete the cycle. The patient was maintained with assisted ventilation because of respiratory embarassment upon distention of the peritoneum and because of the added circulation imparted to the peritoneal fluid by exaggerated diaphragmatic excursions. This treatment was continued for 5 days, after which there was evidence of increased urinary output and improved renal clearance. Ventilatory support was discontinued and the peritoneal catheters were withdrawn. His subsequent course was complicated by pulmonary sepsis and fungal septicemia which were successfully treated. There was no evidence of residual intra-abdominal sepsis during the remainder of the hospital course.
TABLE 3. Outcome by Site of Injury *
Injury Head Injury
Intra-abdominal Injury With or without head injury (a) ruptured spleen
(b) ruptured spleen and perineal destruction (c) ruptured spleen, liver (d) ruptured spleen & bowel (e) diaphragmatic hernia (f) ruptured bladder & bowel (g) ruptured bowel Without head or intra-abdominal injury (a) extremity alone (b) intrathoracic Total * All patients had extremity injuries. t Renal transplant.
No. Patients
Recovering
Currently
Renal Function
Survive
Cause of Death 3 CNS damage
3
3
0
12
3
4
5
1
1
1
0
1 1 1
0
it 0 1 0 0 1
1 0 0 1
1 2 5
20
2
2 2 10
sepsis fat embolism
sepsis 1 sepsis
4
4
3 2
2 sepsis 2 CNS damage
2 8
fat embolism
ACUTE RENAL FAILURE
Vol. 185 . No. 3
Discussion
Post-traumatic renal failure continues to be ciated with
a
asso-
high morbidity and mortality.1'2'4'13'24
However, the patient population is changing.10 Because of improved initial resuscitation techniques, the frequency of acute renal failure associated with lesser trauma has been reduced, whereas an increasing number of patients with more severe trauma are surviving long enough for renal failure to become a major management problem. These patients frequently have many other complications including respiratory insufficiency, sepsis, liver failure, and coagulation abnormalities. Lordon14 and Stone and Knepshield23 have recently reviewed the course of patients with renal failure following military trauma. Rapid resuscitation and evacuation to a definitive treatment center resulted in only a 0.2% incidence of renal failure in Vietnam. Mortality in those developing renal failure remained high (63%) because of associated injuries and sepsis. Patients with lower genitourinary tract, thoracoabdominal, brain, and abdominal injury had a higher mortality than the total patient population. Patients having chest injury without abdominal injury, or having head, face, and extremity injury had a lower mortality. The fatality rate could not be attributed to the management of renal failure, but was related to the extent of associated injuries. Sepsis was the most frequent cause of death. In our series of patients with renal failure following blunt civilian trauma, the outcome was similarly related to site of injury. Patients with severe head injury or intra-abdominal injury did poorly (4/15 survived). Patients without head or intra-abdominal injury had a better prognosis (4/5 survived). In addition, sepsis and respiratory or liver failure were associated with a worse prognosis. Patient age or sex, and duration of anuria were not important. The frequency and timing of dialysis did not seem to contribute to death or survival. Althouh early reports showed that an increased frequency of dialysis is beneficial, we have now almost reached the limit of improvement in this respect as dialysis is employed almost daily. Renal failure in itself did not seem to play a major role in patient death. This is similar to Lordon's conclusion in patients developing renal failure after military trauma,14 to Kjellstrand's findings in patients who develop acute tubular necrosis following renal transplantation,12 and to Casali's findings in patients developing renal failure following cardiovascular operations.11 In our series, one patient never regained kidney function and received a renal transplant 1½ years after
305
trauma. This complication has recently been described by Merino et al. 16 The pathogenesis is unknown. Suspected factors include age, methoxyflurane anesthesia and nephrotoxic antibodies. Our patient was relatively young (26 years old) and did not receive methoxyflurane anesthesia. Fat embolism may have played a role as the renal destructor in our patient. There were three major causes of death in our patient: 1) Fat embolism, 2) Sequelae of severe closed head injury, and 3) Intra-abdominal sepsis. The diagnosis and management of fat embolism has recently been reviewed.27 Although large bone fractures are associated with a higher incidence, it is impossible to predict which patients will develop this complication. Once fat embolism develops, it is unclear how much treatment affects outcome. Similarly, there is little one can do to change the outcome of severe closed head injury once decompressed. However, intra-abdominal sepsis or potential intra-abdominal sepsis can be aggressively managed. Patients with post-traumatic and postoperative renal failure and potential intra-abdominal sepsis comprise a high risk group. These patients should be assumed to have intra-abdominal sepsis until proven otherwise. Our experience, and that reported in the literature, suggests that reexploration be performed if intra-abdominal sepsis is suspected. Delay can be fatal. When perforated bowel and/or purulent peritonitis is found at the time of operation in trauma or at reoperation in the postoperative patients with renal failure, we recommend placing peritoneal catheters. Postoperatively, these catheters can be used for both peritoneal lavage and dialysis. The only two patients in our series who survived renal failure associated with bowel perforation due to blunt trauma were treated in this manner. Peritoneal irrigation with antibiotics at the time of operation has been shown to improve outcome in clinical and experimental peritonitis.3'6'17'19'20-22'25 More recently, continuous peritoneal lavage in the postoperative period has been reported to be beneficial in treatment of patients with severe peritonitis.5,9,15 Lavage acts by: a) washing out digestive enzymes that might have leaked into the peritoneal cavity, b) removing foreign particles, pus, blood, and feces that could nourish bacteria, and c) potentiating the antibiotic effect by allowing the topical application of relatively high doses of these agents.3 When performed in patients with renal failure, peritoneal lavage can also correct fluid and electrolyte balance, remove uremic toxins, and provide calories. Peritoneal dialysis may, therefore, be preferred in two types of post-traumatic patients: In the patient with head injury, peritoneal dialysis has the advantage
MATAS AND OTHERS Ann. Surg. * March 1977 306 of resulting in only slow changes in fluid and electrolyte 13. Kleinknecht, D., Jungers, P., Chanard, J. et al.: Uremic and Non-Uremic Complications in Acute Renal Failure: balance and of osmolarity. This may be less traumatic Evaluation of Early and Frequent Dialysis on Prognosis. to the injured brain than the rapid changes induced Kidney Int., 1:190, 1972. by hemodialysis. Secondly, in the patient with 14. Lordon, R. E., and Burton, J. R.: Post-Traumatic Renal Failure in Military Personnel in Southeast Asia. Am. J. Med., intra-abdominal sepsis, peritoneal dialysis can be com53:137, 1972. bined with antibiotic lavage,thus not only washing out 15. McKenna, J. P., Currie, D. J., MacDonald, J. A. et al.: The Use of Continuous Postoperative Peritoneal Lavage in the contaminated or devitalized tissue but also proManagement of Diffuse Peritonitis. Surg. Gynecol. Obstet., viding high concentrations of antibiotics to the site of 130:254, 1970. infection. 16. Merino, G. E., Buselmeier, T. J., and Kjellstrand, C. M.:
References 1. Alwall, N. and Kjellstrand, C. M.: Acute Renal Failure. A Study of 639 Cases Involving 1,073 Treatments with the Artificial Kidney over the Period 1946- 1961. In Therapeutic and Diagnostic Problems in Severe Renal Failure. Stockholm, Bonniers, 1963; p. 355. 2. Balslov, J. T. and Jorgensen, H. E.: A Survey of 499 Patients with Acute Anuric Renal Insufficiency. Am. J. Med., 34: 753, 1963. 3. Burnett, W. E., Brown, G. R., Jr., Rosemond, G. P., et al.: The Treatment of Peritonitis Using Peritoneal Lavage. Ann. Surg., 145:675, 1957. 4. Casali, R., Simmons, R. L., Najarian, J. S., et al: Acute Renal Insufficiency Complicating Major Cardiovascular Surgery. Ann. Surg., 181:370, 1975. 5. Currie, D. J.: Continuous Peritoneal Lavage. Surg. Gynecol. Obstet., 135:951, 1972. 6. DiVincenti, F. G., and Cohn, I., Jr.: Intraperitoneal Kanamycin in Advanced Peritonitis. A Preliminary Report. Am. J. Surg., 111:147, 1965. 7. Fischer, R. P.: High Mortality of Post-Traumatic Renal Insufficiency in Vietnam: A Review of 96 Cases. Am. Surg. 40:172, 1974. 8. Gjessing, J. and Tomlin, P.: Continuous Peritoneal Lavage. Acta Chir. Scand., 140:124, 1974. 9. Hunt, J. A., Rivlin, M. E., and Clarebout, H. J.: Antibiotic Peritoneal Lavage in Severe Peritonitis: A Preliminary Assessment. S. Afr. Med. J., 49:233, 1975. 10. laina, A., Reisin, E., and Eliahou, H.: Acute Renal Failure in Combat Injuries. J. Trauma, 15:281, 1975. 11. Kjellstrand, C. M. and Buselmeier, T. J.: A Simple Method for Anticoagulation During Pre-and Postoperative Hemodialysis, Avoiding Rebound Phenomenon. Surgery, 72:630, 1972. 12. Kjellstrand, C. M., Casali, R., Simmons, R. L., et al.: Etiology and Prognosis of Acute Post Transplant Renal Failure. Am. J. Med., 61:190-199, 1976.
Postoperative Chronic Renal Failure: A New Syndrome? Ann. Surg., 182:37, 1975. 17. Noon, G. P., Beall, A. C., Jr., Jordan, G. L., Jr., et al.: Clinical Evaluation of Peritoneal Irrigation with Antibiotic Solution. Surgery, 62:73, 1967. 18. Rabiner, S. F. and Drake, R. F.: Platelet Function as an Indicator of Adequate Dialysis. Kidney Int., 7(Suppl. 2): S-144, 1975. 19. Rosemond, G. P., and Goldman, L. I.: Management of Peritonitis Secondary to Perforation of the Alimentary Tract. Surg. Clin. North Am., 42:1481,1962. 20. Rothenberg, S., Silvani, J., Chester, S., et al.: Comparison of the Efficacy of Therapeutic Agents in the Treatment 21. 22. 23. 24. 25. 26. 27.
28.
of Experimentally Induced Diffuse Peritonitis of Intestinal Origin. Ann. Surg., 128:1148, 1948. Schatten, W. E.: Intraperitoneal Antibiotics Administration in the Treatment of Acute Bacterial Peritonitis. Surg. Gynecol. Obstet., 102:339, 1956. Scheinberg, F. B., Glatzer, P., Rutenberg, A. M., and Fine, J.: The Therapeutic Effect of Aureomycin in Experimental Peritonitis in the Dog. Ann. Surg., 134:878, 1951. Schumer, W., Lee, D. K., and Jones, B.: Peritoneal Lavage in Postoperative Therapy of Late Peritoneal Sepsis. Preliminary Report. Surgery, 55:841, 1964. Stone, W. J. and Knepshield, J. H.: Post-Traumatic Acute Renal Insufficiency in Vietnam. Clin. Nephrol., 2:186, 1974. Stott, R. B., Ogg, C. S., Cameron, J. S., and Bewick, M.: Why the Persistently High Mortality in Acute Renal Failure? Lancet, 2:75, 1972. Webel, M. L., Ritts, R. E., Jr., Briggs, W. A., and Light, J. A.: Lymphocyte Blastogenesis in Patients Receiving Hemodialysis. Arch. Intern. Med., 136:682, 1976. Weisz, G. M.: Fat Embolism. Current Problems in Surgery, Ravitch, M. M., Austen, W. G., Scott, H. W., Jr., Fonkalsrud, E. W., and Polk, H. C., Jr. (eds), Chicago, Year Book Medical Publishers, Inc., 1974. Wilson, W. E. C., Kirkpatrick, C. H., and Talmage, D. W.: Suppression of Immunologic Responsiveness in Uremia. Ann. Intern. Med., 62:1, 1965.
Renal failure developed in 20 patients following blunt civilian trauma. Ten recovered normal renal function; 8 currently survive. Survivors and nonsurvivors did not differ in age, time from trauma to anuria, mean blood urea nitrogen or creatinine level prior to the first or to subsequent dialyses. However, there was an increased incidence of sepsis and liver failure in those who died. When outcome was related to site of injury, patients with closed head injury and/or intra-abdominal injury had a worse prognosis than those with thoracic or extremity injury only. Only 2 patients with perforated bowel survived; both had peritoneal dialysis combined with peritoneal lavage with antibiotic solutions. Mortality in patients with posttraumatic renal failure remains high; however, death is usually a result of associated complications rather than a result of the renal failure. Aggressive management of other complications of the trauma, especially sepsis or potential sepsis, is necessary. We recommend peritoneal dialysis combined with peritoneal antibiotic lavage where there is a potential for posttraumatic intraabdominal sepsis associated with renal failure.
PATIENTS surviving the uremic state associated with acute tubular necrosis frequently regain normal renal function and suffer no long term complications. Thus with the advent of hemodialysis, it was hoped that acute renal failure would become an easily manageable problem. Theoretically, if dialysis could maintain the patient throughout the critical uremic period, recovery would be the general rule. These hopes have not been fulfilled. Postoperative and posttraumatic acute renal failure continue to have high morbidity and mor-
tality. 1,2,4,13,2 The role of renal failure and its treatment in this high complication and death rate is unclear. First, the cause of renal failure and its timing in the patient's course are frequently hard to define. Hypotension, hypovolemia, septicemia, drug intoxication and mismanagement of fluid and electrolyte balance have all been implicated as causes of renal failure and any one patient may have more than one of these problems. Second, it is often difficult to determine if the renal failure precedes or is the result of another complication, such as sepsis. Third, when renal failure has Submitted for publication June 21, 1976. Reprint requests: Dr. Carl M. Kjellstrand, Chief, Division of Nephrology, Box 485, University of Minnesota Medical School. Minneapolis, Minnesota 55455.
From the Departments of Medicine and Surgery, University of Minnesota Medical School, Minneapolis, Minnesota
developed, it is unclear how much it affects the patient's subsequent course, i.e., is renal failure important in the complications that develop or are these complications due to the underlying disease? For example, renal failure is thought to be immunosuppressive28 although there is some conflicting evidence.26 Patients with uremia have an increased incidence of septic complications. Thus, when a patient with posttraumatic renal failure develops septic complications, the renal failure is frequently blamed. However, following trauma, patients without renal failure also have a high incidence of septic complications. Similarly, renal failure is also known to impair coagulation18 and again renal failure may be implicated as the etiology of bleeding rather than the trauma or the reparative surgery. We have, therefore, reviewed the course of patients who developed renal failure secondary to non-penetrating trauma in the hope of clarifying the following questions: A) Does the type of trauma or the age and sex of the patient have any prognostic implications? B) Does the dialysis treatment instituted per se have any bearing on the outcome of the patient; i.e., time of initiation of dialysis, type of dialysis (peritoneal or hemodialysis), the frequency of dialysis. C) Does simultaneous failure of other organs have any prognostic implications? D) Are clinical or culture-proven signs of sepsis important prognostically? Methods Twenty patients receiving dialysis at the University of Minnesota between January 1968 and December 1975 for renal failure due to non-penetrating trauma were studied. Cause and timing of renal failure, extent of injury, pathogenesis of renal failure, duration of anuria, long term course and complications were investigated for each patient. We attempted to determine whether outcome is 301
302
MATAS AND OTHERS
related to primary injury, signs of other organ failure (need for respirator > 2 days, bilirubin 5 mg/100 ml), or the technique, timing, or frequency of dialysis. Following diagnosis of renal failure, dialysis was instituted early and was used daily or every other day. The patients treated with hemodialysis were treated with relatively high efficiency dialyzers (Travenol, 145 coils or Gambro Lundia dialyzers). All dialyses were done with regional heparinization according to a previously described method.11 During these, it was attempted not to allow the Lee White clotting time increase over 50%o of normal. Conservative management consisted of anabolic steroids (Durabolin, 100 mg IM twice weekly), the use of antacid phosphate binders (aluminum hydroxide) and oral mycostatin, 100,000 U 4 times daily. Hyperalimentation, pummeling, and frequent pulmonary toilet were used. Almost all patients received broad spectrum antibiotics against documented or assumed infections. Peritoneal dialysis was done either through the use of four quadrant thoracic sump drains placed during surgery or more commonly by puncture between the umbilicus and urinary bladder done percutaneously. Two liter hourly to two hours exchanges containing glucose in a concentration of 1.5, 4.25, or 7% solutions were used. Potassium was added as necessary to control the serum potassium concentration; heparin (500 units/L) was added. If signs of intraperitoneal infections were present, Kanamycin 10 mg/L and Keflin 200-500 mg/L were added. The peritoneal dialysis was continued for 48 to 96 hours depending on the patient's uremia. Results
Twenty patients have received dialysis at the University of Minnesota, (January 1968 to December 1975) for acute renal failure following non-penetrating trauma. This represents 20/425 (4.7%) patients dialyzed for acute tubular necrosis, 20/594 (3.4%) patients -receiving dialysis for acute renal failure, and 20/1398 (1.4%) patients dialyzed during this time period. Six of 20 (30%o) patients were seen initially at this hospital; 14/20 were referred after initial management at other hospitals. All patients were in good health prior to their injury. None had previous evidence of renal disease. Table 1 lists causes of trauma and general characteristics for this group of patients. Mean age of the patients was 36 (range 14-74). Eleven were 2 days >5 cemia Dialysis
by
Cause of Death
Survived 19 26
1
Hypotension, hypovolemia 2 Hypotention, hypovolemia, fat embolism 3 39 M MVA Hypotension, hypovolemia 4 21 M MVA Hypotension, hypovolemia 5 22 M Crush Myglobinuria, hemoglobinuria 6 65 M Crush Hypotension 7 54 M Traction Hypovolemia, hemoglobinuria Crush 8 65 M MVA Aortic dissection Recovered Renal Function But Died 9 19 M MVA Hypoxic M M
MVA* MVA
1,5 1,5
+
+
-
+
1,3 1,4
-
-
+t
+
+
_
+
+
1I
4
+:
3
+
_
_
2
+
-
-
_
_
~+
+
Secondary to head injury
(2 yrs.) 10
20
M
MVA
Mannitol toxicity
2
+
-
-
11 Dead 12 13 14
28
M
MVA
Hypotension, transfusion Rx
2
+
+
+
32 41 74
M M F
MVA MVA
Fat embolism
+
_
_
1,4
+
+
+
1,5
+
+
+
1,2,5 1,5 1,5
+
+
+
_
+
+
+
-
-
15 16
17 18
19 53 22
19
72 14
20
23
Hypotension, hypovolemia Sepsis, hypotension, fat emboli, transfusion Rx M MVA Hypovolemia, hypotension M MVA Hypovolemia, hypotension M MVA Hypovolemia, hypotension, fat emboli M Crush Hypovolemia, hypotension F SnowHypovolemia, hypotension, mobile myoglobinuria, hypoxia M Crush Hypovolemia, hypotension MVA
+
Secondary to head injury (3 yrs.) Secondary to head injury Fat embolism
Sepsis, liver failure Sepsis Fat embolism, head injury Sepsis Fat embolism
1,5 1,2,5
+
+
+
+
+
+
Sepsis Head injury
1,4
+
+
+
Sepsis
Motor vehicle accident. 1 = extremity and/or pelvis; 2 = head; 3 intrathoracic; 4== intra-abdominal with perforated bowel; perforated bowel. 4: Respirator needed as part of technique of peritoneal dialysis. *
t
=
All 5 patients with severe closed head injury died result of their injury, although 3 recovered renal function and 2 were discharged to long-term care as a
institutions. Of the 12 patients having renal failure in association with intra-abdominal injury, only 4 survived. Cause of death in 2 was due to associated severe closed head injury, and in one death was due to fat embolism. The remaining 5 patients died of sepsis. Septic deaths occurred not only in patients with perforated bowel
S =
intra-abdominal without
in association with other injuries but also in 2 patients whose only intra-abdominal injury was a ruptured spleen. Only two patients with perforated bowel survived. Both were treated with peritoneal antibiotic lavage. Two more patients, both with head trauma and both treated with peritoneal dialysis, survived renal failure. Both died as a result of their head injury; at the time of death both had normal renal function. Because of our success with this mode of therapy and our feeling
MATAS AND OTHERS
304
TABLE 2. Survivors vs. Nonsurvivors: Patients Developing Renal Failure after Trauma
Survivors
Mean age (yrs.) Trauma to anuria (days) # Dialyses/duration of anuria Mean BUN *prior to 1st dialysis (mg/100 ml) Mean Crt prior to 1st dialysis (mg/100 ml) Mean BUN prior to each dialysis (mg/100 ml) Mean Cr prior to each dialysis (mg/100 ml) Mean K+ prior to each dialysis (mEq/L)
Nonsurvivors
39 2
40 2.7 .6
.52 110
20
124
35
9.1 ± 3.8
9.6 ± 3.8
100 ± 15
113 ± 17
8.2 ± 2.3
9.3 ± 2.6
5 ± 1.0
5.4 ± 1.6
Blood urea nitrogen t Creatinine *
that it should be used in similar patients with intraabdominal sepsis or head injuiry, one case will be described in detail: Case Report A previously healthy 64-year-old man was crushed between two vehicles at work. His injuries appeared superficial and he complained only of relatively mild left flank and abdominal pain; he was able to continue working. However, his pain increased in severity and he sought medical attention 10 hours following his injury. Upon admission to his local hospital, he complained of diffuse abdominal pain. Vital signs were normal. For the next 14 hours his vital signs remained stable; however, he complained of progressively worsening abdominal pain. Twenty-four hours following his injury, his temperature suddenly rose and he became hypotensive and was then transferred to the University of Minne-
Ann. Surg.
*
March 1977
sota Hospitals. Physical examination on admission to the hospital revealed a rectal temperature of 39.8°, pulse of 130/min, and B.P. of 80/50. His abdomen was distended with diffuse tenderness and rigidity and absent bowel sounds. Peritoneal lavage revealed turbid, feculent abdominal fluid with a white blood cell concentration of 16,240/mm3. Blood urea nitrogen was 46 mg/100 ml, creatinine 3.6 mg/100 ml, white blood cell count 9,100-9,800/mm3. He was immediately taken to the Operating Room where severe diffuse fibrinous peritonitis and a blow-out perforation of the small bowel 3 feet proximal to the ileocecal valve were found. The perforation was oversewn, the peritoneum irrigated with 12 liters of normal saline, and catheters were placed for prolonged peritoneal irrigation. Standard, multiperforated adult peritoneal dialysis catheters were placed on each side of the midline above the umbilicus for inflow. French plastic catheters (No. 36) were then introduced through stab wounds in each of the four abdominal quadrants. Postoperatively, the patient had evidence of oliguric renal failure, with hourly urine outputs in the range of 5-10 cc. Intermittent peritoneal irrigation was performed in hourly cycles using 2 L/cycle of standard peritoneal dialysis solution. Glucose percentage and electrolyte concentration were varied according to the fluid and electrolyte status of the patient and according to the dialysate return. Gentamycin (15 mg) was added per liter. The solution was instilled in 20 minutes, allowed to equilibrate for 20-30 minutes and then drained in 10 minutes to complete the cycle. The patient was maintained with assisted ventilation because of respiratory embarassment upon distention of the peritoneum and because of the added circulation imparted to the peritoneal fluid by exaggerated diaphragmatic excursions. This treatment was continued for 5 days, after which there was evidence of increased urinary output and improved renal clearance. Ventilatory support was discontinued and the peritoneal catheters were withdrawn. His subsequent course was complicated by pulmonary sepsis and fungal septicemia which were successfully treated. There was no evidence of residual intra-abdominal sepsis during the remainder of the hospital course.
TABLE 3. Outcome by Site of Injury *
Injury Head Injury
Intra-abdominal Injury With or without head injury (a) ruptured spleen
(b) ruptured spleen and perineal destruction (c) ruptured spleen, liver (d) ruptured spleen & bowel (e) diaphragmatic hernia (f) ruptured bladder & bowel (g) ruptured bowel Without head or intra-abdominal injury (a) extremity alone (b) intrathoracic Total * All patients had extremity injuries. t Renal transplant.
No. Patients
Recovering
Currently
Renal Function
Survive
Cause of Death 3 CNS damage
3
3
0
12
3
4
5
1
1
1
0
1 1 1
0
it 0 1 0 0 1
1 0 0 1
1 2 5
20
2
2 2 10
sepsis fat embolism
sepsis 1 sepsis
4
4
3 2
2 sepsis 2 CNS damage
2 8
fat embolism
ACUTE RENAL FAILURE
Vol. 185 . No. 3
Discussion
Post-traumatic renal failure continues to be ciated with
a
asso-
high morbidity and mortality.1'2'4'13'24
However, the patient population is changing.10 Because of improved initial resuscitation techniques, the frequency of acute renal failure associated with lesser trauma has been reduced, whereas an increasing number of patients with more severe trauma are surviving long enough for renal failure to become a major management problem. These patients frequently have many other complications including respiratory insufficiency, sepsis, liver failure, and coagulation abnormalities. Lordon14 and Stone and Knepshield23 have recently reviewed the course of patients with renal failure following military trauma. Rapid resuscitation and evacuation to a definitive treatment center resulted in only a 0.2% incidence of renal failure in Vietnam. Mortality in those developing renal failure remained high (63%) because of associated injuries and sepsis. Patients with lower genitourinary tract, thoracoabdominal, brain, and abdominal injury had a higher mortality than the total patient population. Patients having chest injury without abdominal injury, or having head, face, and extremity injury had a lower mortality. The fatality rate could not be attributed to the management of renal failure, but was related to the extent of associated injuries. Sepsis was the most frequent cause of death. In our series of patients with renal failure following blunt civilian trauma, the outcome was similarly related to site of injury. Patients with severe head injury or intra-abdominal injury did poorly (4/15 survived). Patients without head or intra-abdominal injury had a better prognosis (4/5 survived). In addition, sepsis and respiratory or liver failure were associated with a worse prognosis. Patient age or sex, and duration of anuria were not important. The frequency and timing of dialysis did not seem to contribute to death or survival. Althouh early reports showed that an increased frequency of dialysis is beneficial, we have now almost reached the limit of improvement in this respect as dialysis is employed almost daily. Renal failure in itself did not seem to play a major role in patient death. This is similar to Lordon's conclusion in patients developing renal failure after military trauma,14 to Kjellstrand's findings in patients who develop acute tubular necrosis following renal transplantation,12 and to Casali's findings in patients developing renal failure following cardiovascular operations.11 In our series, one patient never regained kidney function and received a renal transplant 1½ years after
305
trauma. This complication has recently been described by Merino et al. 16 The pathogenesis is unknown. Suspected factors include age, methoxyflurane anesthesia and nephrotoxic antibodies. Our patient was relatively young (26 years old) and did not receive methoxyflurane anesthesia. Fat embolism may have played a role as the renal destructor in our patient. There were three major causes of death in our patient: 1) Fat embolism, 2) Sequelae of severe closed head injury, and 3) Intra-abdominal sepsis. The diagnosis and management of fat embolism has recently been reviewed.27 Although large bone fractures are associated with a higher incidence, it is impossible to predict which patients will develop this complication. Once fat embolism develops, it is unclear how much treatment affects outcome. Similarly, there is little one can do to change the outcome of severe closed head injury once decompressed. However, intra-abdominal sepsis or potential intra-abdominal sepsis can be aggressively managed. Patients with post-traumatic and postoperative renal failure and potential intra-abdominal sepsis comprise a high risk group. These patients should be assumed to have intra-abdominal sepsis until proven otherwise. Our experience, and that reported in the literature, suggests that reexploration be performed if intra-abdominal sepsis is suspected. Delay can be fatal. When perforated bowel and/or purulent peritonitis is found at the time of operation in trauma or at reoperation in the postoperative patients with renal failure, we recommend placing peritoneal catheters. Postoperatively, these catheters can be used for both peritoneal lavage and dialysis. The only two patients in our series who survived renal failure associated with bowel perforation due to blunt trauma were treated in this manner. Peritoneal irrigation with antibiotics at the time of operation has been shown to improve outcome in clinical and experimental peritonitis.3'6'17'19'20-22'25 More recently, continuous peritoneal lavage in the postoperative period has been reported to be beneficial in treatment of patients with severe peritonitis.5,9,15 Lavage acts by: a) washing out digestive enzymes that might have leaked into the peritoneal cavity, b) removing foreign particles, pus, blood, and feces that could nourish bacteria, and c) potentiating the antibiotic effect by allowing the topical application of relatively high doses of these agents.3 When performed in patients with renal failure, peritoneal lavage can also correct fluid and electrolyte balance, remove uremic toxins, and provide calories. Peritoneal dialysis may, therefore, be preferred in two types of post-traumatic patients: In the patient with head injury, peritoneal dialysis has the advantage
MATAS AND OTHERS Ann. Surg. * March 1977 306 of resulting in only slow changes in fluid and electrolyte 13. Kleinknecht, D., Jungers, P., Chanard, J. et al.: Uremic and Non-Uremic Complications in Acute Renal Failure: balance and of osmolarity. This may be less traumatic Evaluation of Early and Frequent Dialysis on Prognosis. to the injured brain than the rapid changes induced Kidney Int., 1:190, 1972. by hemodialysis. Secondly, in the patient with 14. Lordon, R. E., and Burton, J. R.: Post-Traumatic Renal Failure in Military Personnel in Southeast Asia. Am. J. Med., intra-abdominal sepsis, peritoneal dialysis can be com53:137, 1972. bined with antibiotic lavage,thus not only washing out 15. McKenna, J. P., Currie, D. J., MacDonald, J. A. et al.: The Use of Continuous Postoperative Peritoneal Lavage in the contaminated or devitalized tissue but also proManagement of Diffuse Peritonitis. Surg. Gynecol. Obstet., viding high concentrations of antibiotics to the site of 130:254, 1970. infection. 16. Merino, G. E., Buselmeier, T. J., and Kjellstrand, C. M.:
References 1. Alwall, N. and Kjellstrand, C. M.: Acute Renal Failure. A Study of 639 Cases Involving 1,073 Treatments with the Artificial Kidney over the Period 1946- 1961. In Therapeutic and Diagnostic Problems in Severe Renal Failure. Stockholm, Bonniers, 1963; p. 355. 2. Balslov, J. T. and Jorgensen, H. E.: A Survey of 499 Patients with Acute Anuric Renal Insufficiency. Am. J. Med., 34: 753, 1963. 3. Burnett, W. E., Brown, G. R., Jr., Rosemond, G. P., et al.: The Treatment of Peritonitis Using Peritoneal Lavage. Ann. Surg., 145:675, 1957. 4. Casali, R., Simmons, R. L., Najarian, J. S., et al: Acute Renal Insufficiency Complicating Major Cardiovascular Surgery. Ann. Surg., 181:370, 1975. 5. Currie, D. J.: Continuous Peritoneal Lavage. Surg. Gynecol. Obstet., 135:951, 1972. 6. DiVincenti, F. G., and Cohn, I., Jr.: Intraperitoneal Kanamycin in Advanced Peritonitis. A Preliminary Report. Am. J. Surg., 111:147, 1965. 7. Fischer, R. P.: High Mortality of Post-Traumatic Renal Insufficiency in Vietnam: A Review of 96 Cases. Am. Surg. 40:172, 1974. 8. Gjessing, J. and Tomlin, P.: Continuous Peritoneal Lavage. Acta Chir. Scand., 140:124, 1974. 9. Hunt, J. A., Rivlin, M. E., and Clarebout, H. J.: Antibiotic Peritoneal Lavage in Severe Peritonitis: A Preliminary Assessment. S. Afr. Med. J., 49:233, 1975. 10. laina, A., Reisin, E., and Eliahou, H.: Acute Renal Failure in Combat Injuries. J. Trauma, 15:281, 1975. 11. Kjellstrand, C. M. and Buselmeier, T. J.: A Simple Method for Anticoagulation During Pre-and Postoperative Hemodialysis, Avoiding Rebound Phenomenon. Surgery, 72:630, 1972. 12. Kjellstrand, C. M., Casali, R., Simmons, R. L., et al.: Etiology and Prognosis of Acute Post Transplant Renal Failure. Am. J. Med., 61:190-199, 1976.
Postoperative Chronic Renal Failure: A New Syndrome? Ann. Surg., 182:37, 1975. 17. Noon, G. P., Beall, A. C., Jr., Jordan, G. L., Jr., et al.: Clinical Evaluation of Peritoneal Irrigation with Antibiotic Solution. Surgery, 62:73, 1967. 18. Rabiner, S. F. and Drake, R. F.: Platelet Function as an Indicator of Adequate Dialysis. Kidney Int., 7(Suppl. 2): S-144, 1975. 19. Rosemond, G. P., and Goldman, L. I.: Management of Peritonitis Secondary to Perforation of the Alimentary Tract. Surg. Clin. North Am., 42:1481,1962. 20. Rothenberg, S., Silvani, J., Chester, S., et al.: Comparison of the Efficacy of Therapeutic Agents in the Treatment 21. 22. 23. 24. 25. 26. 27.
28.
of Experimentally Induced Diffuse Peritonitis of Intestinal Origin. Ann. Surg., 128:1148, 1948. Schatten, W. E.: Intraperitoneal Antibiotics Administration in the Treatment of Acute Bacterial Peritonitis. Surg. Gynecol. Obstet., 102:339, 1956. Scheinberg, F. B., Glatzer, P., Rutenberg, A. M., and Fine, J.: The Therapeutic Effect of Aureomycin in Experimental Peritonitis in the Dog. Ann. Surg., 134:878, 1951. Schumer, W., Lee, D. K., and Jones, B.: Peritoneal Lavage in Postoperative Therapy of Late Peritoneal Sepsis. Preliminary Report. Surgery, 55:841, 1964. Stone, W. J. and Knepshield, J. H.: Post-Traumatic Acute Renal Insufficiency in Vietnam. Clin. Nephrol., 2:186, 1974. Stott, R. B., Ogg, C. S., Cameron, J. S., and Bewick, M.: Why the Persistently High Mortality in Acute Renal Failure? Lancet, 2:75, 1972. Webel, M. L., Ritts, R. E., Jr., Briggs, W. A., and Light, J. A.: Lymphocyte Blastogenesis in Patients Receiving Hemodialysis. Arch. Intern. Med., 136:682, 1976. Weisz, G. M.: Fat Embolism. Current Problems in Surgery, Ravitch, M. M., Austen, W. G., Scott, H. W., Jr., Fonkalsrud, E. W., and Polk, H. C., Jr. (eds), Chicago, Year Book Medical Publishers, Inc., 1974. Wilson, W. E. C., Kirkpatrick, C. H., and Talmage, D. W.: Suppression of Immunologic Responsiveness in Uremia. Ann. Intern. Med., 62:1, 1965.
