- Email: [email protected]
Faulty Healing of Suprapubic Sinus, Resulting in Fatal Peritonitis1
THE JOURNAL OF UROLOGY
Vol. 60, No. 6, December 1948 Printed in U.S.A.
FAULTY HEALING OF SUPRAPUBIC SINUS, RESULTING IN FATAL PERITONITIS 1 REPORT OF
Two
VIRGIL A. PATE,
CASES IN JR. AND
P ARAPLEmcs
R. CARL BUNTS
From the Urologic and Paraplegic Sections, Veterans Administration Hospital, Richmond, Va.
The purpose of this paper is to report 2 cases of fatal peritonitis in paraplegics, both having been proven at autopsy to be secondary to a break in the continuity of the wall of the urinary bladder and an extraperitoneal extravasation of infected urine from the bladder. The pathological process is thusly described rather than stating that rupture of the bladder occurred because the evidence in both cases points to a faulty closure of an old suprapubic sinus as the primary source of trouble. In each case, following removal of the suprapubic catheter, the sinus had apparently closed spontaneously and, clinically, had remained closed for many months thereafter. However, postmortem examination showed that evidently only the distal portions of these sinuses had been obliterated during the healing process following withdrawal of the suprapubic catheters. It is then postulated that the fibrotic barrier of the unobliterated juxtavesical portion of the suprapubic sinus was overcome by urinary pressure and/ or infection resulting in the extraperitoneal involvement. It may be surmised that this was probably due to: 1) prolonged chronic cystitis with superimposed bouts of acute cystitis, 2) possibly added insult of occasional overdistention of the bladder, and 3) a breakdown in resistance generally and locally. The urine and purulent exudate then dissected between the peritoneum and parietal wall of the abdomen, finally resulting in a peritonitis by direct contiguity. CASE REPORTS
Case 1. V. K., a white man, aged 40, was wounded in action, sustaining shrapnel wounds in the left flank resulting in instant paralysis from the level of D-10. He had an indwelling urethral catheter for 2 weeks following injury, at the end of which time a suprapubic cystostorny was performed. The suprapubic catheter was removed in July 1945 followed by spontaneous healing of the cystostomy sinus. He was then placed on urethral catheter drainage for a period of approximately 3 months, following whlch the urethral catheter was removed and the patient voided about 200 cc at a time (residual unknown). The patient was transferred to Veterans Administration Hospital, Richmond, Virginia, on March 30, 1946. An old, well healed, suprapubic scar measuring 3 by 6 cm. was observed. At this time there was a bladder capacity of 200 cc and residual of 10 cc. Intravenous urography and cystoscopy were essentially negative. 1 Published with permission of the Chief Medical Director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions expl'essed or conclusions drawn by the author.
915
916
VIRGIL A. PATE, JR. AND R. CARL BUNTS
During the next several months treatment was directed chiefly toward clearing up the multiple decubital ulcers, combatting toxemia, and improving his general condition. He had an almost daily (usually evening) low grade fever (99-100 F.). Laboratory reports usually showed moderate to severe anemia and low serum · proteins. Urinalyses were usually negative except for minimal amounts of white blood cells microscopically, and no negative urine cultures were obtained, the chief offenders being Proteus vulgaris and Aerobacter aerogenes. Slight to moderate abdominal distention was present. It was felt that he was suffering from an hepatic cirrhosis secondary to prolonged toxemia. On August 8, 1946 his temperature arose to 103 F., pulse 144 and respiration 24 per minute. The abdomen was more distended and he complained of severe, generalized, abdominal pain. On August 9, 1946, blood nonprotein nitrogen was 28.9 mg. per cent. During the afternoon he became disoriented and later mildly stuporous. The abdomen was markedly distended. No other significant findings could be elicited. On August 10, 1946, he responded poorly, temperature remained subnormal, pulse accelerated and respiration normal. The laboratory reported: red blood cells 4,350,000; hemoglobin 85 per cent (Sahli); white blood cells 13,750, with a differential of 88 per cent neutrophiles and 12 per cent lymphocytes; blood nonprotein nitrogen 55 mg. per cent, creatinine 2.1 mg. per cent; blood sugar 61.5 mg. per cent; icteric index 5.0. Routine urinalysis was negative. On this day (August 10, 1945), 3100 cc of turbid yellow, thin fluid was obtained from an abdominal paracentesis through the right lower quadrant, following which patient had an extremely copious bowel movement. Microscopic examination of the ascitic fluid showed a leukocyte count of 1800 with 82 per cent neutrophiles and 18 per cent lymphocytes. Smear showed many pus cells, no organisms. Culture later revealed Proteus bacillus. Protein in the fluid was 1.4 gm. The same supportive regimen was continued for the next 2 days ( August 11 and 12) and the patient appeared slightly improved, although at times he lapsed into a semicomatose state, had frequent involuntary, large, poorly formed stools, and complained of generalized abdominal pain of the same cramp-like characteristics. Temperature ranged between 99 and 101 F., pulse remained 120 per minute, and respiration 20 per minute. However, ascitic fluid appeared to be reformed rapidly and on August 12, 1946 abdominal paracentesis was again carried out with 4800 cc of straw colored fluid obtained. Laboratory report was as follows: "Specific gravity 1.008, smear shows an acute inflammatory exudate; culture, Proteus vulgaris, Aerobacter aerogenes, and streptococcus (non hemolytic).'' On this date a small erosion was noted over the lower angle of previous suprapubic scar, with some serous discharge. On August 13, 1946 he appeared slightly improved. On August 14 his temperature was 101.2 F.; pulse 120 per minute, weak, thready; and respiration was 26 per minute, shallow. The patient complained consistently of abdominal pain when awake, but most of the time seemed disoriented and much weaker. The abdomen was tense and distended. Abdominal paracentesis was again carried out with fluid findings being about the same as
FATAL PERITONITIS IN PARAPLEGICS
917
previously. Laboratory studies on this day were reported as follows: Cephalin flocculation 4+; bromsulphalein, trace; urinalysis was negative except for microscopic study which showed 15 to 20 white blood cells per high power field with many small clumps of pus. Toward evening of this day his condition became moribund. On August 15, 1946 the abdomen was again distended. Sutures which closed the paracentesis wound were removed, the wound being reopened and allowed to drain freely. Temperature remained subnormal, pulse was rapid and thready. There was profuse perspiration. Signs of pulmonary edema were noted. The patient became progressively weaker during the day, and expired at 2 p.m. An adequate urinary output was maintained throughout his illness. The pertinent findings at postmortem examination were as follows: "Midway between the umbilicus and symphysis pubis there is an oval scar measuring 6 by 3 cm., which presents in its lower portion a small ulcer measuring about 1 cm. in diameter and exuding a fairly thick, pinkish gray, foul smelling liquid. "On opening the peritoneal cavity about 3000 cc of cloudy, yellowish fluid having a pungent fecal and ammoniacal odor is found. The peritoneal surfaces are dull and reddish gray with extensive matting together of distended intestinal loops by a greyish white, plastic, fibrinous exudate. There is an extensive necrosis and liquefaction of the abdominal wall from the symphysis pubis to the umbilicus, a thick greenish gray, foul smelling liquid replacing most of the muscle tissue. "The kidneys and ureters are grossly not remarkable. The urinary bladder is small, markedly contracted and contains about 10 cc of dark red, foul smelling, thick, purulent fluid. The mucosa is greyish black and necrotic. The bladder wall is soft, grey, and is obviously invaded by the necrotizing process noted in the mucosa. There is a perforation measuring about 0.5 cm. in diameter on the anterior superior border of the bladder, communicating through the space of Retzius with the previously described sinus and the abscess space that has dissected the anterior abdominal wall to the level of the umbilicus and contains a moderate amount of cloudy, yellow ammoniacal fluid mixed with thick, greyish, purulent material. The abscess space is lined with necrotic muscle and communicates with the lower ulcerated portion of the low midabdominal (suprapubic) scar." On microscopic study of the kidney, the most striking findings were present in the lower nephrons where many hyaline casts and occasional blood cell and blood pigment casts were seen. The tubular epithelium was noted to be swollen, pale, and granular. Many large pigment particles were observed in the tubular epithelial cells. Moderate round cell infiltration was noted in the interstitial tissue. Microscopic sections of the bladder showed focal areas of hemorrhage and diffuse round cell infiltration in the subepithelial layer. The muscularis was thick but otherwise not remarkable. The serosal layer was thickened, very vascular, showed infiltration with polymorphonuclear leukocytes and small round cells and was covered by a small amount of fibrino-purulent exudate. For the sake of brevity, detailed description of the liver, spleen, and other
918
VIRGIL A, PATE, JR. AND R. CARL BUNTS
organs is not included. However, comment by the pathologist is quoted: "It is felt that generalized peritonitis and accompanying ileus was the primary cause of death, but the ascites and severe liver and renal disease are undoubtedly major contributory factors." Final diagnoses included: 1) peritonitis, acute, generalized, and 2) urinary bladder, perforation of, at cystostomy site, with fistula. Case 2. A. G., a white man, aged 27, was wounded in combat June 3, 1945 when struck by shrapnel resulting in a complete transection of the cord at the level of D-9. The patient was placed on urethral catheter drainage for 1 week, at the end of which time a suprapubic cystostomy was performed. He was admitted to Veterans Administration Hospital, Richmond, Va. on April 1, 1946. The patient was for the most part a problem in general care and rehabilitation, treatment including multiple skin grafts, physiotherapy, occupational therapy and general supportive measures. On April 1, 1946, the suprapubic catheter was removed and the sinus closed spontaneously over the next few days. One month later (May 1946) he was voiding well with a maximal bladder capacity of 705 cc and residual of 5 cc. Cystometric examination showed excellent detrusor function. Except for a short period in the early part of 1947 when there was a rise in the amount of residual urine (corrected by tidal irrigation), he maintained a good vesical function, as demonstrated by an adequate capacity and a low residual. He had fair control by emptying his bladder about every 4 hours and limiting the amount of fluid intake in the evenings. Routine cystoscopic examinations never revealed more than mild chronic cystitis with moderate trabeculation. Frequent and regular laboratory checks revealed consistently normal blood counts, blood chemistry, and serum protein. Urinalyses usually showed negative to a trace of albumin, negative sugar, and, microscopically, from a few to numerous white blood cells. Urine culture persistently showed Aerobacter aerogenes and Pseudomonas aeruginosa. The last intravenous urography on October 1, 1947 was reported as being normal. On the evening of December 27, 1947, about 1 week after returning from leave, he began complaining of generalized abdominal pain of a cramping nature and vomited a moderate amount of thin, watery, greenish fluid. Temperature was 101 F., pulse 122, respiration 22. He was seen at 1 a.m. on December 28 by the ward surgeon who ordered an enema which was given and returned clear. The suspicion of a partial intestinal obstruction was entertained. During the day on December 28 his vomiting persisted at intervals and diarrhea developed. Pain in the abdomen was still complained of; however, little could be found on physical examination. He was seen by the urological service. The residual urine was found to be only 15 cc, but an indwelling urethral catheter was inserted and connected to straight drainage. His temperature dropped during the day to 99 F., although the pulse rate remained accelerated. On December 29 his symptoms persisted in about the same degree and findings were no more conclusive. However, there was noted to be slight abdominal distention and no peristalsis was audible except in the extreme right aspect of the abdomen. The laboratory reported the following: total white blood cells 5,950, with a differential of 77 per cent neutrophils and 23 per cent lymphocytes; he-
FATAL PERITONITIS IN PARAPLEGICS
919
moglobin 14.1 gm.; benzidine on vomitus, positive; urinalysis, microscopic, occasional red blood cells, innumerable white blood cells, many bacteria. He was seen in consultation by the Medical Service and their impression was a severe gastro-enteritis, etiology undetermined. Wangensteen drainage was instituted. The patient received 3000 cc of 5 per cent glucose in normal saline intravenously, sulfaguanidine, and sedation but responded poorly and during the evening became irrational and later stuporous, lapsing into a coma. On December 30 at 12: 15 a.m., Cheyne Stokes respiration ensued. At 6: 15 a.m. there was a period of apnea lasting one and one half minutes followed by a severe tonic convulsion. The laboratory reported blood cytological examination to be suggestive of a severe infection or toxemia. Blood urea nitrogen was 46 mg. per cent; blood sodium chloride 490 mg. per cent, CO2 combining power 47 mg. per cent; fasting blood glucose 106 mg. per cent. A plain film of the abdomen was noncontributory. During the morning his temperature was elevated to 102.2 F.; pulse was 160 per minute and extremely weak and thready; respirations increased to 40 per minute; and blood pressure dropped to 68/38. Urinary output was adequate throughout his illness and was 800 cc on this the last day. In spite of supportive therapy he gradually weakened and expired at 12:00 p.m. The pertinent positive findings at autopsy were as follows: "The lining of the peritoneal cavity is of dull appearance. There is about 200 cc of cloudy, yellowish brown fluid with fibrin present. There is marked injection of the pelvic peritoneum anteriorly and posteriorly. There is extravasation of cloudy, pinkish brmvn fluid retroperitoneally, and between the peritoneum and fascia anteriorly. There is a large, deep purple, extravesical pouch present in the region where one would normally expect bladder. The pouch is paper thin and friable. Extending out from this pouch anteriorly there is a large necrotic sinus which has dissected the fascial layers and filled the space with brownish purulent fluid. Below this pouch is found the bladder which is also of a deep purplish red color and thickened. Further examination reveals a fistulous tract between the extravesical pouch (with its sinuses) and the urinary bladder." Grossly the kidneys were not remarkable except for slight dilatation of the pelves. "On opening the urinary bladder about 5 cc of a pinkish brown, cloudy urine is found. The bladder wall is markedly thickened and injected. The surface is markedly injected and edematous. Trabeculations are prominent. The ureteral orifices are patent. Further examination reveals an opening in the anterosuperior aspect of the bladder, but well lateral to the midline. This opening measures 5 mm. in diameter and communicates with the previously described pouch and its sinuses." On microscopic sections, the kidneys revealed chronic pyelonephritis with a few scattered small areas of focal necrosis. The most significant findings UJpon microscopical examination of the bladder consisted of a marked infiltration of the mucosa and subepithelial layer with lymphocytes and some plasma cells and eosinophils. In the same strata there
920
VIRGIL A. PATE, JR. AND R. CARL BUNTS
were many dilated blood vessels which were filled with red blood cells and which showed marked perivascular lymphocytic infiltration. There were many focal areas of hemorrhage involving the submucosa subepithelial layer. The muscular coats were not remarkable except for marked thickening and small areas of interstitial hemorrhage. Included in the final diagnoses were 1) peritonitis, acute, secondary to perforation of fistulous tract between the urinary bladder and anterior abdominal wall, 2) cystitis, acute, superimposed on chronic, 3) pyelonephritis, chronic bilateral, and 4) scrotum, gangrene, terminal. DISCUSSION
During World War II, suprapubic cystostomy was performed almost routinely on cord injury casualties. This may have been necessary due to the exigencies of the situation. When the Veterans Administration assumed control of this institution with 180 paraplegics in April 1946, the vast majority of cases had undergone suprapubic cystostomy with prolonged drainage, or still had suprapubic tubes in place. One of the primary objectives of our urological service upon assuming control was to close all urinary fistulas wherever possible. It was immediately noted that many of the suprapubic sinuses healed very poorly when allowed to close spontaneously. There was repeated breaking down of the sinus and suprapubic leakage, even when adequate urethral drainage was maintained. Some of the sinuses would appear to be healed for a period of as long as several months and then while the patient was undergoing bladder training in the form of tidal irrigation, or even when voiding well with a low residual, the fistulous tract would break open and drain urine suprapubically. In the ones which did heal spontaneously, the length of time required for healing was greater than for surgical closure. The causes of this failure to close spontaneously in a proper manner are several: 1) Many of the suprapubic cystostomies were improperly performed, the tract bein'g very low at the upper border of the symphysis pubis, 2) most of the cases had undergone prolonged suprapubic drainage and had a very fibrotic, wellestablished fistulous tract, 3) the urine was almost always infected, and 4) the "neurogenic factor", coupled with a diminution in tonicity of the abdominal musculature, may have been involved in the poor healing. At any rate, for the past 18 months, all suprapubic sinuses at this hospital have had primary surgical closure closure rather than being allowed to close spontaneously. In each case, the fistulous tract has been dissected out down to .and including a cuff of bladder, this defect in the bladder being closed in two layers with chromic catgut, and the abdominal wall closed in layers, using in addition a continuous mattress suture of fine stainless steel wire through the anterior rectus sheath. Every case has healed promptly, and apparently completely, following this single surgical procedure. It is ventured that in the future very few paraplegics in civilian life will be submitted to the procedure of suprapubic cystostomy. The cases reported present only one of the rarer, late complications of this form of treatment. How-
FATAL PERITONITIS IN PARAPLEGICS
921
ever, other investigators of this institution will publish in the near future a paper citing the many undesirable sequelae secondary to, or at least coexistent with, suprapubic drainage in paraplegics. It is worth noting that in almost 2 years since the Veterans Administration assumed supervision of the paraplegics at this hospital, there have been 16 deaths on the cord injury service~ Two of these deaths were the cases cited above. With such an incidence, it is worth commenting that in acutely ill paraplegics with an apparent surgical abdomen and who have had a spontaneous closure of a suprapubic sinus, this entity should be excluded. It is generally realized that differential diagnosis of an acute surgical abdomen in a paraplegic is a very difficult matter, but by keeping this condition in mind, it may be possible by urological investigation to establish such a diagnosis in time to be of benefit to the patient. Probably of more importance, is the prophylaxis against such a situation developing by: 1) surgical closure of all long standing suprapubic sinuses in paraplegics; 2) careful physical examination of all spontaneous closures; 3) constant vigilance over those patients still maintained on suprapubic drainage; 4) routine cystoscopic examinations with particular attention to the intravesical site of the old cystostomy sinus; 5) routine cystograms; 6) the usual urological care afforded paraplegics directed toward promoting good vesical function and the avoidance of urosepsis. We are indebted to Dr. Joseph R. Kriz, chief of Department of Pathology, for his helpful suggestions in preparation of the manuscript and for furnishing us with the protocols of the 2 cases reported.
Vol. 60, No. 6, December 1948 Printed in U.S.A.
FAULTY HEALING OF SUPRAPUBIC SINUS, RESULTING IN FATAL PERITONITIS 1 REPORT OF
Two
VIRGIL A. PATE,
CASES IN JR. AND
P ARAPLEmcs
R. CARL BUNTS
From the Urologic and Paraplegic Sections, Veterans Administration Hospital, Richmond, Va.
The purpose of this paper is to report 2 cases of fatal peritonitis in paraplegics, both having been proven at autopsy to be secondary to a break in the continuity of the wall of the urinary bladder and an extraperitoneal extravasation of infected urine from the bladder. The pathological process is thusly described rather than stating that rupture of the bladder occurred because the evidence in both cases points to a faulty closure of an old suprapubic sinus as the primary source of trouble. In each case, following removal of the suprapubic catheter, the sinus had apparently closed spontaneously and, clinically, had remained closed for many months thereafter. However, postmortem examination showed that evidently only the distal portions of these sinuses had been obliterated during the healing process following withdrawal of the suprapubic catheters. It is then postulated that the fibrotic barrier of the unobliterated juxtavesical portion of the suprapubic sinus was overcome by urinary pressure and/ or infection resulting in the extraperitoneal involvement. It may be surmised that this was probably due to: 1) prolonged chronic cystitis with superimposed bouts of acute cystitis, 2) possibly added insult of occasional overdistention of the bladder, and 3) a breakdown in resistance generally and locally. The urine and purulent exudate then dissected between the peritoneum and parietal wall of the abdomen, finally resulting in a peritonitis by direct contiguity. CASE REPORTS
Case 1. V. K., a white man, aged 40, was wounded in action, sustaining shrapnel wounds in the left flank resulting in instant paralysis from the level of D-10. He had an indwelling urethral catheter for 2 weeks following injury, at the end of which time a suprapubic cystostorny was performed. The suprapubic catheter was removed in July 1945 followed by spontaneous healing of the cystostomy sinus. He was then placed on urethral catheter drainage for a period of approximately 3 months, following whlch the urethral catheter was removed and the patient voided about 200 cc at a time (residual unknown). The patient was transferred to Veterans Administration Hospital, Richmond, Virginia, on March 30, 1946. An old, well healed, suprapubic scar measuring 3 by 6 cm. was observed. At this time there was a bladder capacity of 200 cc and residual of 10 cc. Intravenous urography and cystoscopy were essentially negative. 1 Published with permission of the Chief Medical Director, Department of Medicine and Surgery, Veterans Administration, who assumes no responsibility for the opinions expl'essed or conclusions drawn by the author.
915
916
VIRGIL A. PATE, JR. AND R. CARL BUNTS
During the next several months treatment was directed chiefly toward clearing up the multiple decubital ulcers, combatting toxemia, and improving his general condition. He had an almost daily (usually evening) low grade fever (99-100 F.). Laboratory reports usually showed moderate to severe anemia and low serum · proteins. Urinalyses were usually negative except for minimal amounts of white blood cells microscopically, and no negative urine cultures were obtained, the chief offenders being Proteus vulgaris and Aerobacter aerogenes. Slight to moderate abdominal distention was present. It was felt that he was suffering from an hepatic cirrhosis secondary to prolonged toxemia. On August 8, 1946 his temperature arose to 103 F., pulse 144 and respiration 24 per minute. The abdomen was more distended and he complained of severe, generalized, abdominal pain. On August 9, 1946, blood nonprotein nitrogen was 28.9 mg. per cent. During the afternoon he became disoriented and later mildly stuporous. The abdomen was markedly distended. No other significant findings could be elicited. On August 10, 1946, he responded poorly, temperature remained subnormal, pulse accelerated and respiration normal. The laboratory reported: red blood cells 4,350,000; hemoglobin 85 per cent (Sahli); white blood cells 13,750, with a differential of 88 per cent neutrophiles and 12 per cent lymphocytes; blood nonprotein nitrogen 55 mg. per cent, creatinine 2.1 mg. per cent; blood sugar 61.5 mg. per cent; icteric index 5.0. Routine urinalysis was negative. On this day (August 10, 1945), 3100 cc of turbid yellow, thin fluid was obtained from an abdominal paracentesis through the right lower quadrant, following which patient had an extremely copious bowel movement. Microscopic examination of the ascitic fluid showed a leukocyte count of 1800 with 82 per cent neutrophiles and 18 per cent lymphocytes. Smear showed many pus cells, no organisms. Culture later revealed Proteus bacillus. Protein in the fluid was 1.4 gm. The same supportive regimen was continued for the next 2 days ( August 11 and 12) and the patient appeared slightly improved, although at times he lapsed into a semicomatose state, had frequent involuntary, large, poorly formed stools, and complained of generalized abdominal pain of the same cramp-like characteristics. Temperature ranged between 99 and 101 F., pulse remained 120 per minute, and respiration 20 per minute. However, ascitic fluid appeared to be reformed rapidly and on August 12, 1946 abdominal paracentesis was again carried out with 4800 cc of straw colored fluid obtained. Laboratory report was as follows: "Specific gravity 1.008, smear shows an acute inflammatory exudate; culture, Proteus vulgaris, Aerobacter aerogenes, and streptococcus (non hemolytic).'' On this date a small erosion was noted over the lower angle of previous suprapubic scar, with some serous discharge. On August 13, 1946 he appeared slightly improved. On August 14 his temperature was 101.2 F.; pulse 120 per minute, weak, thready; and respiration was 26 per minute, shallow. The patient complained consistently of abdominal pain when awake, but most of the time seemed disoriented and much weaker. The abdomen was tense and distended. Abdominal paracentesis was again carried out with fluid findings being about the same as
FATAL PERITONITIS IN PARAPLEGICS
917
previously. Laboratory studies on this day were reported as follows: Cephalin flocculation 4+; bromsulphalein, trace; urinalysis was negative except for microscopic study which showed 15 to 20 white blood cells per high power field with many small clumps of pus. Toward evening of this day his condition became moribund. On August 15, 1946 the abdomen was again distended. Sutures which closed the paracentesis wound were removed, the wound being reopened and allowed to drain freely. Temperature remained subnormal, pulse was rapid and thready. There was profuse perspiration. Signs of pulmonary edema were noted. The patient became progressively weaker during the day, and expired at 2 p.m. An adequate urinary output was maintained throughout his illness. The pertinent findings at postmortem examination were as follows: "Midway between the umbilicus and symphysis pubis there is an oval scar measuring 6 by 3 cm., which presents in its lower portion a small ulcer measuring about 1 cm. in diameter and exuding a fairly thick, pinkish gray, foul smelling liquid. "On opening the peritoneal cavity about 3000 cc of cloudy, yellowish fluid having a pungent fecal and ammoniacal odor is found. The peritoneal surfaces are dull and reddish gray with extensive matting together of distended intestinal loops by a greyish white, plastic, fibrinous exudate. There is an extensive necrosis and liquefaction of the abdominal wall from the symphysis pubis to the umbilicus, a thick greenish gray, foul smelling liquid replacing most of the muscle tissue. "The kidneys and ureters are grossly not remarkable. The urinary bladder is small, markedly contracted and contains about 10 cc of dark red, foul smelling, thick, purulent fluid. The mucosa is greyish black and necrotic. The bladder wall is soft, grey, and is obviously invaded by the necrotizing process noted in the mucosa. There is a perforation measuring about 0.5 cm. in diameter on the anterior superior border of the bladder, communicating through the space of Retzius with the previously described sinus and the abscess space that has dissected the anterior abdominal wall to the level of the umbilicus and contains a moderate amount of cloudy, yellow ammoniacal fluid mixed with thick, greyish, purulent material. The abscess space is lined with necrotic muscle and communicates with the lower ulcerated portion of the low midabdominal (suprapubic) scar." On microscopic study of the kidney, the most striking findings were present in the lower nephrons where many hyaline casts and occasional blood cell and blood pigment casts were seen. The tubular epithelium was noted to be swollen, pale, and granular. Many large pigment particles were observed in the tubular epithelial cells. Moderate round cell infiltration was noted in the interstitial tissue. Microscopic sections of the bladder showed focal areas of hemorrhage and diffuse round cell infiltration in the subepithelial layer. The muscularis was thick but otherwise not remarkable. The serosal layer was thickened, very vascular, showed infiltration with polymorphonuclear leukocytes and small round cells and was covered by a small amount of fibrino-purulent exudate. For the sake of brevity, detailed description of the liver, spleen, and other
918
VIRGIL A, PATE, JR. AND R. CARL BUNTS
organs is not included. However, comment by the pathologist is quoted: "It is felt that generalized peritonitis and accompanying ileus was the primary cause of death, but the ascites and severe liver and renal disease are undoubtedly major contributory factors." Final diagnoses included: 1) peritonitis, acute, generalized, and 2) urinary bladder, perforation of, at cystostomy site, with fistula. Case 2. A. G., a white man, aged 27, was wounded in combat June 3, 1945 when struck by shrapnel resulting in a complete transection of the cord at the level of D-9. The patient was placed on urethral catheter drainage for 1 week, at the end of which time a suprapubic cystostomy was performed. He was admitted to Veterans Administration Hospital, Richmond, Va. on April 1, 1946. The patient was for the most part a problem in general care and rehabilitation, treatment including multiple skin grafts, physiotherapy, occupational therapy and general supportive measures. On April 1, 1946, the suprapubic catheter was removed and the sinus closed spontaneously over the next few days. One month later (May 1946) he was voiding well with a maximal bladder capacity of 705 cc and residual of 5 cc. Cystometric examination showed excellent detrusor function. Except for a short period in the early part of 1947 when there was a rise in the amount of residual urine (corrected by tidal irrigation), he maintained a good vesical function, as demonstrated by an adequate capacity and a low residual. He had fair control by emptying his bladder about every 4 hours and limiting the amount of fluid intake in the evenings. Routine cystoscopic examinations never revealed more than mild chronic cystitis with moderate trabeculation. Frequent and regular laboratory checks revealed consistently normal blood counts, blood chemistry, and serum protein. Urinalyses usually showed negative to a trace of albumin, negative sugar, and, microscopically, from a few to numerous white blood cells. Urine culture persistently showed Aerobacter aerogenes and Pseudomonas aeruginosa. The last intravenous urography on October 1, 1947 was reported as being normal. On the evening of December 27, 1947, about 1 week after returning from leave, he began complaining of generalized abdominal pain of a cramping nature and vomited a moderate amount of thin, watery, greenish fluid. Temperature was 101 F., pulse 122, respiration 22. He was seen at 1 a.m. on December 28 by the ward surgeon who ordered an enema which was given and returned clear. The suspicion of a partial intestinal obstruction was entertained. During the day on December 28 his vomiting persisted at intervals and diarrhea developed. Pain in the abdomen was still complained of; however, little could be found on physical examination. He was seen by the urological service. The residual urine was found to be only 15 cc, but an indwelling urethral catheter was inserted and connected to straight drainage. His temperature dropped during the day to 99 F., although the pulse rate remained accelerated. On December 29 his symptoms persisted in about the same degree and findings were no more conclusive. However, there was noted to be slight abdominal distention and no peristalsis was audible except in the extreme right aspect of the abdomen. The laboratory reported the following: total white blood cells 5,950, with a differential of 77 per cent neutrophils and 23 per cent lymphocytes; he-
FATAL PERITONITIS IN PARAPLEGICS
919
moglobin 14.1 gm.; benzidine on vomitus, positive; urinalysis, microscopic, occasional red blood cells, innumerable white blood cells, many bacteria. He was seen in consultation by the Medical Service and their impression was a severe gastro-enteritis, etiology undetermined. Wangensteen drainage was instituted. The patient received 3000 cc of 5 per cent glucose in normal saline intravenously, sulfaguanidine, and sedation but responded poorly and during the evening became irrational and later stuporous, lapsing into a coma. On December 30 at 12: 15 a.m., Cheyne Stokes respiration ensued. At 6: 15 a.m. there was a period of apnea lasting one and one half minutes followed by a severe tonic convulsion. The laboratory reported blood cytological examination to be suggestive of a severe infection or toxemia. Blood urea nitrogen was 46 mg. per cent; blood sodium chloride 490 mg. per cent, CO2 combining power 47 mg. per cent; fasting blood glucose 106 mg. per cent. A plain film of the abdomen was noncontributory. During the morning his temperature was elevated to 102.2 F.; pulse was 160 per minute and extremely weak and thready; respirations increased to 40 per minute; and blood pressure dropped to 68/38. Urinary output was adequate throughout his illness and was 800 cc on this the last day. In spite of supportive therapy he gradually weakened and expired at 12:00 p.m. The pertinent positive findings at autopsy were as follows: "The lining of the peritoneal cavity is of dull appearance. There is about 200 cc of cloudy, yellowish brown fluid with fibrin present. There is marked injection of the pelvic peritoneum anteriorly and posteriorly. There is extravasation of cloudy, pinkish brmvn fluid retroperitoneally, and between the peritoneum and fascia anteriorly. There is a large, deep purple, extravesical pouch present in the region where one would normally expect bladder. The pouch is paper thin and friable. Extending out from this pouch anteriorly there is a large necrotic sinus which has dissected the fascial layers and filled the space with brownish purulent fluid. Below this pouch is found the bladder which is also of a deep purplish red color and thickened. Further examination reveals a fistulous tract between the extravesical pouch (with its sinuses) and the urinary bladder." Grossly the kidneys were not remarkable except for slight dilatation of the pelves. "On opening the urinary bladder about 5 cc of a pinkish brown, cloudy urine is found. The bladder wall is markedly thickened and injected. The surface is markedly injected and edematous. Trabeculations are prominent. The ureteral orifices are patent. Further examination reveals an opening in the anterosuperior aspect of the bladder, but well lateral to the midline. This opening measures 5 mm. in diameter and communicates with the previously described pouch and its sinuses." On microscopic sections, the kidneys revealed chronic pyelonephritis with a few scattered small areas of focal necrosis. The most significant findings UJpon microscopical examination of the bladder consisted of a marked infiltration of the mucosa and subepithelial layer with lymphocytes and some plasma cells and eosinophils. In the same strata there
920
VIRGIL A. PATE, JR. AND R. CARL BUNTS
were many dilated blood vessels which were filled with red blood cells and which showed marked perivascular lymphocytic infiltration. There were many focal areas of hemorrhage involving the submucosa subepithelial layer. The muscular coats were not remarkable except for marked thickening and small areas of interstitial hemorrhage. Included in the final diagnoses were 1) peritonitis, acute, secondary to perforation of fistulous tract between the urinary bladder and anterior abdominal wall, 2) cystitis, acute, superimposed on chronic, 3) pyelonephritis, chronic bilateral, and 4) scrotum, gangrene, terminal. DISCUSSION
During World War II, suprapubic cystostomy was performed almost routinely on cord injury casualties. This may have been necessary due to the exigencies of the situation. When the Veterans Administration assumed control of this institution with 180 paraplegics in April 1946, the vast majority of cases had undergone suprapubic cystostomy with prolonged drainage, or still had suprapubic tubes in place. One of the primary objectives of our urological service upon assuming control was to close all urinary fistulas wherever possible. It was immediately noted that many of the suprapubic sinuses healed very poorly when allowed to close spontaneously. There was repeated breaking down of the sinus and suprapubic leakage, even when adequate urethral drainage was maintained. Some of the sinuses would appear to be healed for a period of as long as several months and then while the patient was undergoing bladder training in the form of tidal irrigation, or even when voiding well with a low residual, the fistulous tract would break open and drain urine suprapubically. In the ones which did heal spontaneously, the length of time required for healing was greater than for surgical closure. The causes of this failure to close spontaneously in a proper manner are several: 1) Many of the suprapubic cystostomies were improperly performed, the tract bein'g very low at the upper border of the symphysis pubis, 2) most of the cases had undergone prolonged suprapubic drainage and had a very fibrotic, wellestablished fistulous tract, 3) the urine was almost always infected, and 4) the "neurogenic factor", coupled with a diminution in tonicity of the abdominal musculature, may have been involved in the poor healing. At any rate, for the past 18 months, all suprapubic sinuses at this hospital have had primary surgical closure closure rather than being allowed to close spontaneously. In each case, the fistulous tract has been dissected out down to .and including a cuff of bladder, this defect in the bladder being closed in two layers with chromic catgut, and the abdominal wall closed in layers, using in addition a continuous mattress suture of fine stainless steel wire through the anterior rectus sheath. Every case has healed promptly, and apparently completely, following this single surgical procedure. It is ventured that in the future very few paraplegics in civilian life will be submitted to the procedure of suprapubic cystostomy. The cases reported present only one of the rarer, late complications of this form of treatment. How-
FATAL PERITONITIS IN PARAPLEGICS
921
ever, other investigators of this institution will publish in the near future a paper citing the many undesirable sequelae secondary to, or at least coexistent with, suprapubic drainage in paraplegics. It is worth noting that in almost 2 years since the Veterans Administration assumed supervision of the paraplegics at this hospital, there have been 16 deaths on the cord injury service~ Two of these deaths were the cases cited above. With such an incidence, it is worth commenting that in acutely ill paraplegics with an apparent surgical abdomen and who have had a spontaneous closure of a suprapubic sinus, this entity should be excluded. It is generally realized that differential diagnosis of an acute surgical abdomen in a paraplegic is a very difficult matter, but by keeping this condition in mind, it may be possible by urological investigation to establish such a diagnosis in time to be of benefit to the patient. Probably of more importance, is the prophylaxis against such a situation developing by: 1) surgical closure of all long standing suprapubic sinuses in paraplegics; 2) careful physical examination of all spontaneous closures; 3) constant vigilance over those patients still maintained on suprapubic drainage; 4) routine cystoscopic examinations with particular attention to the intravesical site of the old cystostomy sinus; 5) routine cystograms; 6) the usual urological care afforded paraplegics directed toward promoting good vesical function and the avoidance of urosepsis. We are indebted to Dr. Joseph R. Kriz, chief of Department of Pathology, for his helpful suggestions in preparation of the manuscript and for furnishing us with the protocols of the 2 cases reported.