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Peritoneal Self-Dialysis Following Traumatic Rupture of the Bladder
THE JoURNAL OF UROLOGY
Vol. 91, No. 4 April 1964 Copyright © 1964 by The Williams & Wilkins Co.
Printed in U.S.A.
PERITONEAL SELF-DIALYSIS FOLLOWING TRAUMATIC RUPTURE OF THE BLADDER KWANG WOOK KO, JUDSON RANDOLPH
AND
FRANCIS X. FELLERS
From the Departments of Pediatrics and Surgery, Harvard Medical School and the Departments of Medicine and Surgery, Children's Hospital JVledical Center, Boston, Massachusetts
Perforation of the bladder wall results from blunt trauma or a penetrating injury to the lower abdomen and is usually followed by such a characteristic clinical development that the diagnosis is immediately suspected. Lateral or anterior wounds of the bladder allow extravasation of urine into extraperitoneal tissue planes and local inflammation promptly ensues. Tearing of the dome of the bladder permits free egress of the urine into the peritoneal cavity; bacterial peritonitis promptly occurs in 60 per cent of such cases. 1 - 4 In children, bladder injury may follow minimal trauma. If the diagnosis is not suspected, and the intraperitoneal urine remains sterile, prolonged reabsorption of the urinary constituents through the peritoneal surfaces may result. The opportunity to investigate the metabolic consequences of such an auto-dialysis feed-back system was presented when a 3-year-old girl was admitted to the hospital, 8 days after sustaining minimal trauma. CASE REPORT
G.L., a 3½-year-old white girl, was admitted from another hospital on July 9, 1958 for evaluation of renal disease. Eight days previously, she had fallen from a high chair. Shortly afterwards, she vomited several times and complained of severe abdominal pain and was admitted to a hospital. Physical examination showed a rigid and tenAccepted for publication September 10, 1963. Supported by grants from the New England Kidney Disease Foundation, Inc., and by the National Institutes of Health (H2656). 1 Bacon, S. K.: Rupture of urinary bladder: clinical analysis of 147 cases in the past 10 years. J. Urol., 49: 432-435, 1943. 2 Campbell, M.: Clinical Pediatric Urology. Philadelphia: W. B. Saunders Co., 1951, p. 617. 3 Hershman, H. and Allen, H. L.: Spontaneous rupture of the normal urinary bladder. Surgery, 35: 805--808, 1954. 4 Miller, A. L., Jr., Sharp, L., Anderson, E. V. and Emlet, J. R.: Rupture of the bladder in the newborn. J. Urol., 83: 630-633, 1960.
der abdomen. The initial blood studies showed a hemoglobin of 9 gm./100 ml. and a normal white blood cell count. Urine was amber colored, reaction alkaline, specific gravity 1.012, and showed a 1 plus protein reaction. White cells and many red cells were seen on examination of the sediment. Abdominal tenderness disappeared the following day. Because the child did not pass urine, the bladder was catheterized and only 35 ml. grossly bloody urine was obtained. Intravenous fluids were instituted. By the second hospital day, she became disoriented. The abdomen was distended and few bowel sounds could be heard. Urine showed microscopic hematuria. Penicillin and streptomycin therapy was instituted. Azotemia, acidosis, and hyperkalemia were noted the next day. Catheterization yielded 700 ml. bloody urine, followed by a decrease of the abdominal distension. On the fourth day, generalized convulsions were observed followed by coma and hypotension. Abdominal paracentesis yielded 20 ml. red fluid which clotted. After a transfusion of 250 ml. whole blood, the child improved and the sensorium cleared. Cultures of the urine and paracentesis fluid were sterile. Generalized seizures recurred, and were associated with positive Chvostek and Trousseau signs. The seizures were controlled with intravenous calcium gluconate. By the seventh hospital day, pallor, acidotic breathing, uremic odor, and stupor were present. She was then transferred to the Children's Hospital Medical Center. Physical examination revealed a semi-comatose but well hydrated girl. Temperature was 40.5°C., blood pressure 98/72, pulse 150, and respiration 36/minute. The abdomen was not tender, but it was distended and a fluid wave could be elicited. Blood chemical studies showed sodium 112 meq/L., potassium 5.1 meq/L., chloride 79 meq/L., and CO2 content 12.0 mM./ L. The white blood cell count was normal. Urine analysis showed a clear yellow color,
343
344
KO, RANDOLPH AND FELLERS
specific gravity 1.008, pH 7 .5, protein 300 mg./ 100 ml., reducing substance 4 plus and microscopic hematuria. The cerebrospinal fluid showed a protein of 64 mg./100 ml. Initial therapy included intravenous hypertonic (3 per cent) saline. Chloramphenicol 250 mg. was given intravenously every 6 hours. By the next morning weight had decreased 1 kg., and the abdomen was concave; surprisingly, the child appeared dehydrated. On 2 occasions during the night, approximately 800 ml. clear urine had been passed through an indwelling catheter. With further fluid therapy, she improved symptomatically, was alert and complained of thirst. A cystogram demonstrated a perforation of the dome of the bladder with free flow into the peritoneal cavity. Surgical repair was immediately undertaken. At operation, a 4 cm.. laceration of the dome of the bladder was repaired. The peritoneal surfaces were less glistening than usual but there was no hyperemia of the serosal surfaces, and no exudate was present. Recovery was uneventful. Followup study revealed a well child with normal urinalysis. RESULTS
The data presented in tables 1-3 have been empirically grouped into 4 periods of the illness. Period 1 represents the 4 days during which continuous deterioration of the patient's clinical TABLE
Period Day
1. Serum data: 0 .5 M 2 surface area
Sodium
Potas-
ium
Chloride
Non-
Carbon Dioxide Content
Protein Nitrogen ing./100 ml.
condition occurred with development of hyponatremia, azotemia, and hyperkalemia. Convulsions were a prominent clinical feature. During period 2, the next 3 days, the child remained critically ill with severe hyponatremia. Period 3 included the first 3 days following transfer from the original hospital and during which time her condition in1proved. In the final period of 3 improvement continued. The assumption that the patient was librating the bladder urine with extracellular fluids through the peritoneal surface was suggested by the electrolyte balance and later was substantiated by radiological and surgical demonstration of a ruptured bladder. Table 4 wm; constructed from the presented data. For the first 2 periods, the daily output of fluid was calculated as having the concentration of the determined serum concentrations. During periods 3 and 4, the actually determined electrolyte concentrations in the urine were used. Period 3 represented about 95 per cent of the urine voided. The last period was incomplete and approximated three-fourths of total output, although the results give the direction of the balance. A large negative sodium balance accrued in period 1. Subsequently, there was sodium retention. Chloride balance suggested a greater loss through period 2 and did not become positive until period 3. The potassium balance, corrected for nitrogen balance by the ratio of 3 mlVI. potassium to J gm. of nitrogen, was calculated for period 1 as follows:
-- -- --- --- ---
1
1
2 3 4
meg/L.
meq/L.
meq/L.
mM./L.
135 132 ll8 115
5.8 6.2 5.7 7.0
104 93 65 79
18 11 15 16
53 70 91 115
---- --- --- --- ---- ----
2
5
6 7
116 117 112
6.5 5.0 5.1
75 83 79
13 12 12
126 ll8 107
-- -- --- --- --- ---- ----
3
8 9 10
121 131 132
3.7 3.4 4.4
86 87 87
28 26 16
84 86 46
-- -- - - - ---- - - - ---- ----
4
11
132
5.6
106
18
37
12 13
139
4.0
93
19
27
Nitrogen Metabolism A) Urinary nitrogen loss .. B) Nitrogen accumulation
Initial NPN. Final NPN .. Increase in NPN. X .65 X body weight (11.0 kg.). C) Ingested nitrogen from intake. D) Net nitrogen metabolism (A+ B - C). Potassium Metabolism A) Tissue metabolism (5.93 X 3). B) Urinary potassium loss.
. .3.43 gm. .550 gm/L 1.250 grn./L. .70 gm./L. 5.00 gm. .2.50 gm. .5.93 gm . .18 mM.
28 mM.
C) Ingested potassium from intake ... 25 mM. D) Net potassium metabolism
(A+ C - B).
+15 mM.
'j
345
PERITONEAL SELF-DIALYSIS FOLLOWING TRAUMATIC BLADDER RUPTURE TABLE
2. Urine data: 0.5 M 2 surface area Calculated* Content
Period
Day
Volume Sodium
Chloride
Potassium
Nitrogen
--meq/L.
ml.
1
1 2 3 4 5 6 7
2
mM.
1000 990 550 1425 1140 1590 970
mM.
mg.
134 124 67 164 132 182
meq/L.
6 6 3.5 10 7 8
99 76 43 110 90 129
-
-
-
615 796 594 1718 1380 1790 926
malt!.
meq/L.
Determined Content
7 8 9 10
3
4
945 1665 430 1140 310 190 220 130 180 150 120 65
11 12 13
(1870 )t (506) (1695)
(428) (527) (218)
108 23 56 130 100 116 23 19 109 16 75 19
102 38 24 148 31 22 5 3 20 2 9 1
9 5 11 4 10 10 36 36 11 31 2 13
8.5 8 5 4.5 3 2 8 5 2 5 1 1
79 15 53 91 85 80 58 58 87 42
75 25 23 102 26 15 3 8 16 6
-
-
-
-
* Mean of serum level used. See text.
t 24-hour recorded TABLE
Period Day
-
3. Fluid intake: 0.5 M 2 surface area
Volume
-- ---
1
-
1 2 3 4
volume. Determined values corrected for total in balances.
Sodium
PotaEsium
Chloride
Dextrose
Nitrogen (Protein/6)
--- -- - - - ---
ml.
mM.
mM.
1000 1350 1250* 2350
0 66 100 147
0 0 12 13
mM.
gm.
50 45 47 87
0 22 43 98
gm.
0 0 0 2.5
----- -- --- --- --- ---
2
3
5 6 7
157 144 174
0 5 11
98 57 98
35 16 40
0 0 1.8
----- -- ------ --- --8 1000 105 0 105 10 9 10
-
1450 1250 1610
2210 1305
115 70
8 33
115 68
101 86
-
----- -- ---- - --- ---
4 5 6
11 12 13
1075 935 1000
38 13 15
36 10 12
* Includes 250 ml. whole blood.
38 17 18
-
-
Similar calculations were made for period 2. Net potassium balance was negative in period 2, and with recovery, balance became positive for potassium.
-
DISCUSSION
Fluid placed in the peritoneal cavity tends to approach the composition and osmolarity of interstitial fluid. Darrow presented the quantitative aspect of this phenomenon in experimental animals. 5 Urine osmolarity is dependent on the state of hydration and thus will vary greatly; the principal substance contributing to this osmotic pressure is urea. In interstitial fluid, sodium and chloride form the primary components of the osmotic pressure. In the patient discussed, concentrated urine which was high in urea and low in sodium and chloride, passed into 5 Schechter, A. J., Cary, M. K., Carpentieri, A. L. and Darrow, D. C.: Changes in composition of fluids injected into the peritoneal cavity. Amer. J. Dis. Child., 46: 1015-1026, 1933.
346
KO, RANDOLPH AND FELLERS TABLE
Period
Fluid Volume ml.
1 Intake Output Balance
4. Balance data Chloride NitroSodium Potasgen sium - - ---- - - - - inM. gm.
313 5950 489 3965 +1995 -176
25 25 +19
163 327 -164
2.50 3.43
------ -------------- -
2 Intake Output Balance
4310 3700 +610
475 319 +56
16
23 -9
253 295 -42
1.80 4.10
------ ------- - - - - - - ---
3 Intake Output Balance
4515 4071 +444
290 262 +28
41 23 (+18)
288 194 +94
2.0
------ ------------- - -
4 Intake Output Balance
3010 66 73 58 (39) (53) (20) 1173 +1837 (+27) (+38) (+20)
Intake included all parenteral and oral fluids. Output neglected stools which were non-diarrheal, and also a small amount of gastric suction in periods 1 and 2. Period 4 output was incomplete. the peritoneal cavity through the laceration. An initial increase in the intraperitoneal fluid volume was necessary to obtain osmolar equality with interstitial fluid. Since the potassium concentration in the urine is greater than in interstitial fluids, potassium moved back into the extracellular fluid. Thus, when the equilibrated solution was excreted, a quantity of fluid, about equivalent to extracellular fluid in electrolyte and nitrogen concentration (and similar to the excretion of glomerular filtrate) would be lost. The result would be loss of sodium, chloride, and water, with partial retention of urea and potassium. In severe renal disease, the same load of nitrogen is excreted py raising the blood nitrogen level. 6 A similar ph~nomenon occurred with this patient when the level of non-protein nitrogen reached a plateau of 105 to 125 mg./100 ml. 6 Gamble, J. L.: Chemical Anatomy, Physiology, and Pathology of Extracellular Fluid, A Lecture Syllabus, 6th ed. Boston: Harvard University Press, 1954.
blood on days 4 through 7. At this blood concentration, the observed urinary output would contain a calculated amount of 1.5 gm. of nitrogen daily, an amount which approximated body tissue protein catabolism. Comparing the derived balance data for periods 1 through 3, serum electrolyte values closely followed the theoretical values within limits of such a study. The unexpected development of the hypokalemia shortly after transfer to this hospital was explained by the negative potassium balance. The urinary findings at this time would also be compatible with extracellular fluid. In a patient without previous renal disease, but with systemic acidosis, the presence in the urine of an alkaline reaction, positive reducing reaction, fixed specific gravity and positive protein reaction may be compatible with findings in interstitial fluid. The prolonged course of this child was unusual. Concentrated urine is a strong irritant. Fever and leukocytosis were present and presumably resulted from the irritation. As long as infection did not develop, only the electrolyte changes would be prominent. Survival of this patient would have been unlikely if the constantly changing demands of the electrolyte and fluid requirements had not been met. With the eventual appearance of Aerobacter aerogenes in the urine, both free diffusion and transfer across the peritoneal surface were hindered. The development of peritonitis is predictable in most cases wherein communication exists between the urinary bladder and the peritoneal cavity. Peritoneal infection and serious electrolyte disturbances can be avoided in patients with ruptured bladder by prompt diagnosis and immediate surgical correction. SUMMARY
The consequences of unrecognized rupture of the bladder in a child are described. The convulsions and coma with hyponatremia, hyperkalemia, and azotemia can be explained on the basis of a feed-back, self-dialysis system through the peritoneal surface. The complication of body homeostasis emphasized the need for prompt therapy.
Vol. 91, No. 4 April 1964 Copyright © 1964 by The Williams & Wilkins Co.
Printed in U.S.A.
PERITONEAL SELF-DIALYSIS FOLLOWING TRAUMATIC RUPTURE OF THE BLADDER KWANG WOOK KO, JUDSON RANDOLPH
AND
FRANCIS X. FELLERS
From the Departments of Pediatrics and Surgery, Harvard Medical School and the Departments of Medicine and Surgery, Children's Hospital JVledical Center, Boston, Massachusetts
Perforation of the bladder wall results from blunt trauma or a penetrating injury to the lower abdomen and is usually followed by such a characteristic clinical development that the diagnosis is immediately suspected. Lateral or anterior wounds of the bladder allow extravasation of urine into extraperitoneal tissue planes and local inflammation promptly ensues. Tearing of the dome of the bladder permits free egress of the urine into the peritoneal cavity; bacterial peritonitis promptly occurs in 60 per cent of such cases. 1 - 4 In children, bladder injury may follow minimal trauma. If the diagnosis is not suspected, and the intraperitoneal urine remains sterile, prolonged reabsorption of the urinary constituents through the peritoneal surfaces may result. The opportunity to investigate the metabolic consequences of such an auto-dialysis feed-back system was presented when a 3-year-old girl was admitted to the hospital, 8 days after sustaining minimal trauma. CASE REPORT
G.L., a 3½-year-old white girl, was admitted from another hospital on July 9, 1958 for evaluation of renal disease. Eight days previously, she had fallen from a high chair. Shortly afterwards, she vomited several times and complained of severe abdominal pain and was admitted to a hospital. Physical examination showed a rigid and tenAccepted for publication September 10, 1963. Supported by grants from the New England Kidney Disease Foundation, Inc., and by the National Institutes of Health (H2656). 1 Bacon, S. K.: Rupture of urinary bladder: clinical analysis of 147 cases in the past 10 years. J. Urol., 49: 432-435, 1943. 2 Campbell, M.: Clinical Pediatric Urology. Philadelphia: W. B. Saunders Co., 1951, p. 617. 3 Hershman, H. and Allen, H. L.: Spontaneous rupture of the normal urinary bladder. Surgery, 35: 805--808, 1954. 4 Miller, A. L., Jr., Sharp, L., Anderson, E. V. and Emlet, J. R.: Rupture of the bladder in the newborn. J. Urol., 83: 630-633, 1960.
der abdomen. The initial blood studies showed a hemoglobin of 9 gm./100 ml. and a normal white blood cell count. Urine was amber colored, reaction alkaline, specific gravity 1.012, and showed a 1 plus protein reaction. White cells and many red cells were seen on examination of the sediment. Abdominal tenderness disappeared the following day. Because the child did not pass urine, the bladder was catheterized and only 35 ml. grossly bloody urine was obtained. Intravenous fluids were instituted. By the second hospital day, she became disoriented. The abdomen was distended and few bowel sounds could be heard. Urine showed microscopic hematuria. Penicillin and streptomycin therapy was instituted. Azotemia, acidosis, and hyperkalemia were noted the next day. Catheterization yielded 700 ml. bloody urine, followed by a decrease of the abdominal distension. On the fourth day, generalized convulsions were observed followed by coma and hypotension. Abdominal paracentesis yielded 20 ml. red fluid which clotted. After a transfusion of 250 ml. whole blood, the child improved and the sensorium cleared. Cultures of the urine and paracentesis fluid were sterile. Generalized seizures recurred, and were associated with positive Chvostek and Trousseau signs. The seizures were controlled with intravenous calcium gluconate. By the seventh hospital day, pallor, acidotic breathing, uremic odor, and stupor were present. She was then transferred to the Children's Hospital Medical Center. Physical examination revealed a semi-comatose but well hydrated girl. Temperature was 40.5°C., blood pressure 98/72, pulse 150, and respiration 36/minute. The abdomen was not tender, but it was distended and a fluid wave could be elicited. Blood chemical studies showed sodium 112 meq/L., potassium 5.1 meq/L., chloride 79 meq/L., and CO2 content 12.0 mM./ L. The white blood cell count was normal. Urine analysis showed a clear yellow color,
343
344
KO, RANDOLPH AND FELLERS
specific gravity 1.008, pH 7 .5, protein 300 mg./ 100 ml., reducing substance 4 plus and microscopic hematuria. The cerebrospinal fluid showed a protein of 64 mg./100 ml. Initial therapy included intravenous hypertonic (3 per cent) saline. Chloramphenicol 250 mg. was given intravenously every 6 hours. By the next morning weight had decreased 1 kg., and the abdomen was concave; surprisingly, the child appeared dehydrated. On 2 occasions during the night, approximately 800 ml. clear urine had been passed through an indwelling catheter. With further fluid therapy, she improved symptomatically, was alert and complained of thirst. A cystogram demonstrated a perforation of the dome of the bladder with free flow into the peritoneal cavity. Surgical repair was immediately undertaken. At operation, a 4 cm.. laceration of the dome of the bladder was repaired. The peritoneal surfaces were less glistening than usual but there was no hyperemia of the serosal surfaces, and no exudate was present. Recovery was uneventful. Followup study revealed a well child with normal urinalysis. RESULTS
The data presented in tables 1-3 have been empirically grouped into 4 periods of the illness. Period 1 represents the 4 days during which continuous deterioration of the patient's clinical TABLE
Period Day
1. Serum data: 0 .5 M 2 surface area
Sodium
Potas-
ium
Chloride
Non-
Carbon Dioxide Content
Protein Nitrogen ing./100 ml.
condition occurred with development of hyponatremia, azotemia, and hyperkalemia. Convulsions were a prominent clinical feature. During period 2, the next 3 days, the child remained critically ill with severe hyponatremia. Period 3 included the first 3 days following transfer from the original hospital and during which time her condition in1proved. In the final period of 3 improvement continued. The assumption that the patient was librating the bladder urine with extracellular fluids through the peritoneal surface was suggested by the electrolyte balance and later was substantiated by radiological and surgical demonstration of a ruptured bladder. Table 4 wm; constructed from the presented data. For the first 2 periods, the daily output of fluid was calculated as having the concentration of the determined serum concentrations. During periods 3 and 4, the actually determined electrolyte concentrations in the urine were used. Period 3 represented about 95 per cent of the urine voided. The last period was incomplete and approximated three-fourths of total output, although the results give the direction of the balance. A large negative sodium balance accrued in period 1. Subsequently, there was sodium retention. Chloride balance suggested a greater loss through period 2 and did not become positive until period 3. The potassium balance, corrected for nitrogen balance by the ratio of 3 mlVI. potassium to J gm. of nitrogen, was calculated for period 1 as follows:
-- -- --- --- ---
1
1
2 3 4
meg/L.
meq/L.
meq/L.
mM./L.
135 132 ll8 115
5.8 6.2 5.7 7.0
104 93 65 79
18 11 15 16
53 70 91 115
---- --- --- --- ---- ----
2
5
6 7
116 117 112
6.5 5.0 5.1
75 83 79
13 12 12
126 ll8 107
-- -- --- --- --- ---- ----
3
8 9 10
121 131 132
3.7 3.4 4.4
86 87 87
28 26 16
84 86 46
-- -- - - - ---- - - - ---- ----
4
11
132
5.6
106
18
37
12 13
139
4.0
93
19
27
Nitrogen Metabolism A) Urinary nitrogen loss .. B) Nitrogen accumulation
Initial NPN. Final NPN .. Increase in NPN. X .65 X body weight (11.0 kg.). C) Ingested nitrogen from intake. D) Net nitrogen metabolism (A+ B - C). Potassium Metabolism A) Tissue metabolism (5.93 X 3). B) Urinary potassium loss.
. .3.43 gm. .550 gm/L 1.250 grn./L. .70 gm./L. 5.00 gm. .2.50 gm. .5.93 gm . .18 mM.
28 mM.
C) Ingested potassium from intake ... 25 mM. D) Net potassium metabolism
(A+ C - B).
+15 mM.
'j
345
PERITONEAL SELF-DIALYSIS FOLLOWING TRAUMATIC BLADDER RUPTURE TABLE
2. Urine data: 0.5 M 2 surface area Calculated* Content
Period
Day
Volume Sodium
Chloride
Potassium
Nitrogen
--meq/L.
ml.
1
1 2 3 4 5 6 7
2
mM.
1000 990 550 1425 1140 1590 970
mM.
mg.
134 124 67 164 132 182
meq/L.
6 6 3.5 10 7 8
99 76 43 110 90 129
-
-
-
615 796 594 1718 1380 1790 926
malt!.
meq/L.
Determined Content
7 8 9 10
3
4
945 1665 430 1140 310 190 220 130 180 150 120 65
11 12 13
(1870 )t (506) (1695)
(428) (527) (218)
108 23 56 130 100 116 23 19 109 16 75 19
102 38 24 148 31 22 5 3 20 2 9 1
9 5 11 4 10 10 36 36 11 31 2 13
8.5 8 5 4.5 3 2 8 5 2 5 1 1
79 15 53 91 85 80 58 58 87 42
75 25 23 102 26 15 3 8 16 6
-
-
-
-
* Mean of serum level used. See text.
t 24-hour recorded TABLE
Period Day
-
3. Fluid intake: 0.5 M 2 surface area
Volume
-- ---
1
-
1 2 3 4
volume. Determined values corrected for total in balances.
Sodium
PotaEsium
Chloride
Dextrose
Nitrogen (Protein/6)
--- -- - - - ---
ml.
mM.
mM.
1000 1350 1250* 2350
0 66 100 147
0 0 12 13
mM.
gm.
50 45 47 87
0 22 43 98
gm.
0 0 0 2.5
----- -- --- --- --- ---
2
3
5 6 7
157 144 174
0 5 11
98 57 98
35 16 40
0 0 1.8
----- -- ------ --- --8 1000 105 0 105 10 9 10
-
1450 1250 1610
2210 1305
115 70
8 33
115 68
101 86
-
----- -- ---- - --- ---
4 5 6
11 12 13
1075 935 1000
38 13 15
36 10 12
* Includes 250 ml. whole blood.
38 17 18
-
-
Similar calculations were made for period 2. Net potassium balance was negative in period 2, and with recovery, balance became positive for potassium.
-
DISCUSSION
Fluid placed in the peritoneal cavity tends to approach the composition and osmolarity of interstitial fluid. Darrow presented the quantitative aspect of this phenomenon in experimental animals. 5 Urine osmolarity is dependent on the state of hydration and thus will vary greatly; the principal substance contributing to this osmotic pressure is urea. In interstitial fluid, sodium and chloride form the primary components of the osmotic pressure. In the patient discussed, concentrated urine which was high in urea and low in sodium and chloride, passed into 5 Schechter, A. J., Cary, M. K., Carpentieri, A. L. and Darrow, D. C.: Changes in composition of fluids injected into the peritoneal cavity. Amer. J. Dis. Child., 46: 1015-1026, 1933.
346
KO, RANDOLPH AND FELLERS TABLE
Period
Fluid Volume ml.
1 Intake Output Balance
4. Balance data Chloride NitroSodium Potasgen sium - - ---- - - - - inM. gm.
313 5950 489 3965 +1995 -176
25 25 +19
163 327 -164
2.50 3.43
------ -------------- -
2 Intake Output Balance
4310 3700 +610
475 319 +56
16
23 -9
253 295 -42
1.80 4.10
------ ------- - - - - - - ---
3 Intake Output Balance
4515 4071 +444
290 262 +28
41 23 (+18)
288 194 +94
2.0
------ ------------- - -
4 Intake Output Balance
3010 66 73 58 (39) (53) (20) 1173 +1837 (+27) (+38) (+20)
Intake included all parenteral and oral fluids. Output neglected stools which were non-diarrheal, and also a small amount of gastric suction in periods 1 and 2. Period 4 output was incomplete. the peritoneal cavity through the laceration. An initial increase in the intraperitoneal fluid volume was necessary to obtain osmolar equality with interstitial fluid. Since the potassium concentration in the urine is greater than in interstitial fluids, potassium moved back into the extracellular fluid. Thus, when the equilibrated solution was excreted, a quantity of fluid, about equivalent to extracellular fluid in electrolyte and nitrogen concentration (and similar to the excretion of glomerular filtrate) would be lost. The result would be loss of sodium, chloride, and water, with partial retention of urea and potassium. In severe renal disease, the same load of nitrogen is excreted py raising the blood nitrogen level. 6 A similar ph~nomenon occurred with this patient when the level of non-protein nitrogen reached a plateau of 105 to 125 mg./100 ml. 6 Gamble, J. L.: Chemical Anatomy, Physiology, and Pathology of Extracellular Fluid, A Lecture Syllabus, 6th ed. Boston: Harvard University Press, 1954.
blood on days 4 through 7. At this blood concentration, the observed urinary output would contain a calculated amount of 1.5 gm. of nitrogen daily, an amount which approximated body tissue protein catabolism. Comparing the derived balance data for periods 1 through 3, serum electrolyte values closely followed the theoretical values within limits of such a study. The unexpected development of the hypokalemia shortly after transfer to this hospital was explained by the negative potassium balance. The urinary findings at this time would also be compatible with extracellular fluid. In a patient without previous renal disease, but with systemic acidosis, the presence in the urine of an alkaline reaction, positive reducing reaction, fixed specific gravity and positive protein reaction may be compatible with findings in interstitial fluid. The prolonged course of this child was unusual. Concentrated urine is a strong irritant. Fever and leukocytosis were present and presumably resulted from the irritation. As long as infection did not develop, only the electrolyte changes would be prominent. Survival of this patient would have been unlikely if the constantly changing demands of the electrolyte and fluid requirements had not been met. With the eventual appearance of Aerobacter aerogenes in the urine, both free diffusion and transfer across the peritoneal surface were hindered. The development of peritonitis is predictable in most cases wherein communication exists between the urinary bladder and the peritoneal cavity. Peritoneal infection and serious electrolyte disturbances can be avoided in patients with ruptured bladder by prompt diagnosis and immediate surgical correction. SUMMARY
The consequences of unrecognized rupture of the bladder in a child are described. The convulsions and coma with hyponatremia, hyperkalemia, and azotemia can be explained on the basis of a feed-back, self-dialysis system through the peritoneal surface. The complication of body homeostasis emphasized the need for prompt therapy.