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Posthypoxic ascites: A cause of post-traumatic abdominal distention
E M E R G E N C Y CASE REPORT
Posthypoxic Ascites: A Cause of Post-Traumatic Abdominal Distention Bernard J. Urlaub, MD Madison, Wisconsin Joseph A. Moylan, Jr, MD Durham, North Carofina
A p r e v i o u s l y u n r e p o r t e d etiology for post-traumatic a b d o m i n a l distention w a s o b s e r v e d in a 5-year-old girl w h o suffered only h e a d trauma and a p r o l o n g e d period of h y p o x e m i a . When there is a rapid accumulation of peritoneal fluid c o n t a i n i n g a high c o n c e n t r a t i o n of protein but n e g a t i v e for amylase, no e v i d e n c e of b l o o d loss, plus a b n o r m a l serial liver e n z y m e studies and the n e e d for p l a c e m e n t o f large v o l u m e s of fluid, p o s t h y p o x i c ascites should be suspected. Peritoneal aspiration c o n f i r m e d the diagnosis and treatment w a s supportive. B e c a u s e early operative intervention is n e c e s s a r y in pancreatic ascites and treatment is supportive for p o s t h y p o x i c ascites, it is imperative to differentiate them. Urlaub BJ, Moylan JA Jr: Posthypoxic ascites: a cause of post-traumatic abdominal distention. JACEP 5:186-188, March 1976. distention, abdominal; as-
cites, posthypoxic; trauma; lavage, peritoneal. INTRODUCTION A r a p i d i n c r e a s e in a b d o m i n a l g i r t h in the victim of a major accident presents the physician with a difficult diagnostic dilemma. The u s u a l causes for this p o s t - t r a u m a t i c phenomenon are hemoperitoneum from a b d o m i n a l visceral injury, adyn a m i c ileus, p a n c r e a t i c ascites a n d u r i n a r y e x t r a v a s a t i o n . 1 This r e p o r t d e s c r i b e s a n o t h e r e t i o l o g y for t h i s p r o b l e m - - post-hypoxic ascites foll o w i n g p r o l o n g e d h y p o x e m i a in a
From the Department of Surgery, University of Wisconsin Center for Health Sciences, Madison, Wisconsin. Address for reprints: Joseph A. Moylan, Jr, MD, Department of Surgery, Duke University Medical Center, Box 3043, Durham, NC 27710.
Page 186 Volume 5 Number 3
p a t i e n t w i t h a h e a d i n j u r y a n d no abdominal trauma.
Case Report A 5-year-old girl was in the front seat of an automobile involved in a two-car collision. She was not wearing a seat b e a t a n d s t r u c k h e r h e a d on the s t e e r i n g wheel. No other inj u r i e s were observed, Following a prol o n g e d p e r i o d of m a r k e d c y a n o s i s r e s u l t i n g from an obstructed airway, s h e r e c e i v e d m o u t h - t o - m o u t h resp i r a t o r y support from a p a s s i n g regi s t e r e d n u r s e a n d h e r color slowly improved. Upon e x a m i n a t i o n 30 minu t e s l a t e r in a n e a r b y e m e r g e n c y department, after receiving oxygen d u r i n g t r a n s p o r t , she was noted to be l e t h a r g i c w i t h d e p r e s s i o n of all reflexes. H e r p u p i l s were e q u a l l y dilated b i l a t e r a l l y and s l u g g i s h l y reac-
tive. H e r m u s c l e s w e r e flaccid and she was responsive only to deep pain s t i m u l a t i o n . Stool and u r i n a r y incontinence were noted. W h i l e b e i n g t r a n s f e r r e d to University Hospital, she e x h i b i t e d multiple m i n o r focal seizures. I n i t i a l examination at U n i v e r s i t y H o s p i t a l revealed a n a w a k e girl, s p e a k i n g coherently, without any localizing neurologic signs. T h e r e m a i n i n g e x a m i n a t i o n r e v e a l e d no other evidence of injury. There were n o r m a l bowel sounds and a soft, flat, n o n t e n d e r a b d o m e n . A neurological c o n s u l t a n t , ascribed the p a t i e n t ' s prior neurologic defects to a generalized disturbance resulting from a n o x i a . A d m i t t i n g l a b o r a t o r y data included a hematocrit reading of 35%, w h i t e b l o o d cell c o u n t 29,600/cu mm, s e r u m cTeatinine 1.1 mg/100 ml, a n d n o r m a l electrolytes. U r i n a l y s i s was u n r e m a r k a b l e . The r e s u l t s of all r a d i o g r a p h s , including c y s t o g r a m a n d i n t r a v e n o u s pyelogram, were w i t h i n n o r m a l limits. D u r i n g t h e 24-hour period followi n g injury, t h e p a t i e n t ' s a b d o m i n a l girth increased markedly. Bowel sounds r e m a i n e d normal. Hepatomeg a l y was p r e s e n t and m i n i m a l right u p p e r q u a d r a n t t e n d e r n e s s was n o t e d . T o t a l i n t r a v e n o u s f l u i d req u i r e m e n t s to m a i n t a i n a u r i n a r y o u t p u t of 15 cc/hour were twice that predicted for age a n d size. There was no evidence of blood 10ss.
March 1976 J ~ P
p a r a c e n t e s i s yielded s t r a w colored fluid t h a t contained p r o t e i n and was positive for s u g a r b u t n e g a t i v e for asylase a n d blood. A s i m u l t a n e o u s ~arinalysis was n e g a t i v e for protein, sugar a n d b l o o d . B e c a u s e of h e r hepatomegaly, a . 9 9 m / T c sulfur colloid and 131 rose bengal liver-spleen scan w e r e o b t a i n e d . The scan confirmed t h e c l i n i c a l o b s e r v a t i o n of hepatomegaly and d e m o n s t r a t e d uniform h e p a t i c m e t a b o l i c f u n c t i o n without a n y evidence of localized injury. L a b o r a t o r y t e s t s r e v e a l e d a slightly i n c r e a s e d s e r u m a m y l a s e , 200 somogyi units; a n a l k a l i n e phosphatase of 12.1 IU/liter; and s e r u m glutamic o x a l o a c e t i c t r a n s a m i n a s e (sGOT) of 128 IU/liter, a n d a lactic dehydrogenase (LDH) of 273 IU/liter. The ascites resolved s p o n t a n e o u s l y over a 72-hour period a n d the LDH and SGOT r e t u r n e d to n o r m a l levels. The a l k a l i n e p h o s p h a t a s e r e m a i n e d elevated to levels consistent with the bone g r o w t h p a t t e r n for t h i s a g e group. The h o s p i t a l course was otherwise u n r e m a r k a b l e . T h e focal s e i z u r e s were controlled on p h e n o b a r b i t a l . An electroencephalogram showed a mild generalized d i s t u r b a n c e of c e r e b r a l fanction a n d t h e p a t i e n t r e m a i n e d asymptomatic a f t e r d i s c h a r g e . No f~lrther s e q u e l l a e were observed during a one y e a r follow-up.
~DISCUSSION Hemoperitoneum is one Of the most common p o s t - t r a u m a t i c etiologies of abdominal distention. 1 Injuries t o the spleen or liver m a y r e s u l t in significant p e r i t o n e a l b l e e d i n g . H y p o t e n si0n, a f a l l i n g h e m a t o c r i t and abdominal t e n d e r n e s s along with distention ~re t h e e a r l y s i g n s o f h e m o p e r : Lt0neum p e r m i t t i n g a p r e s u m p t i v e tiagnosis of i n t r a - a b d o m i n a l bleed,~g. The diagnosis can be confirmed ~ith a paracentesis. In r e c e n t series, ~lsen a n d Douglas 2 reported t h a t a red b l o o d cell c o u n t g r e a t e r t h a n [00,000 cells/cu m m in the a s p i r a t e d ~uid is indicative of a major abdomilal injury r e q u i r i n g operative inter~ention. Adynamic ileus is a n o t h e r common '.~Use of r a p i d increase in a b d o m i n a l ~irth f o l l o w i n g an a c c i d e n t . M a n y leural, h o r m o n a l a n d metabolic facors i n f l u e n c e t h e d e v e l o p m e n t of
• [ ] March • P 1976
a d y n a m i c ileus. 3 It is very common following spinal injuries, retroperitoneal hematoma and other t r a u m a . Absen't bowel sounds, t h e lack of t e n d e r n e s s in the presence of abdominal distention and the uniform d i s t r i b u t i o n of gas t h r o u g h o u t the g a s t r o i n t e s t i n a l t r a c t on abdominal radiographs are signs of a d y n a m i c ileus. The absence of fluid on p e r i t o n e a l t a p a n d ret.urn of a clear i r r i g a t i o n fluid is confirmatory.
d e r a n g e m e n t of a l l c e l l u l a r functions. H e p a t i c tissue is well known to be h i g h l y s u s c e p t i b l e to hypoxic states. H y p o x e m i a also results in inc r e a s e d blood flow to the g a s t r o i n testinal organs, particularly the liver. 6 The c o m b i n a t i o n of high flow state and cellular damageT, s may produce exudative processes with f o r m a t i o n of ascitic fluid w i t h a high p r o t e i n c o n c e n t r a t i o n , as was seen in this case.
U r i n a r y e x t r a v a s a t i o n from a rupt u r e d b l a d d e r or l a c e r a t e d u r e t e r is a n i n f r e q u e n t c a u s e of a b d o m i n a l distention. 4 As sterile u r i n e is not irritating, abdominal findings are often lacking. The diagnosis is usually m a d e by p e r f o r m i n g r e t r o g r a d e cystogram and intravenous pyelog r a m after gross or microscopic hem a t u r i a a r e discovered on u r i n a l y s i s .
In our case, a n e g a t i v e a m y l a s e det e r m i n a t i o n in the p e r i t o n e a l fluid distinguished posthypoxic ascites from p a n c r e a t i c ascites. There was a m i n i m a l t r a n s i e n t e l e v a t i o n in t h e s e r u m a m y l a s e in t h i s child but not in t h e h i g h a n d p e r s i s t e n t r a n g e s u s u a l l y found in d i r e c t i n j u r y to a previously u n d i s e a s e d pancreas.
P o s t - t r a u m a t i c p a n c r e a t i c ascites is a n o t h e r r a r e cause of a b d o m i n a l distention. 3 The p h e n o m e n o n is most often associated with pre-existent chronic p a n c r e a t i t i s a n d p a n c r e a t i c pseudocyst. Only four cases of postt r a u m a t i c p a n c r e a t i c ascites in pat i e n t s w i t h o u t prior p a n c r e a t i c dise a s e h a v e b e e n d o c u m e n t e d in t h e l i t e r a t u r e . 4 The etiology of this process is t h o u g h t to be l e a k a g e from a d i s r u p t e d p a n c r e a t i c duct or pseudocyst. T h e s e r u m a m y l a s e m a y be n o r m a l or only s l i g h t l y e l e v a t e d i n p a t i e n t s w i t h long t e r m chronic pancreatitis b u t is m a r k e d l y e l e v a t e d in p a t i e n t s free of previous p a n c r e a t i c disease. The diagnosis of:post-traumatic p a n c r e a t i c a s c i t e s is c o n f i r m e d b y a n a l y s i s of t h e a s c i t i c f l u i d . T h e a m y l a s e c o n c e n t r a t i o n o f the ascitic f l u i d is m a r k e d l y e l e v a t e d in a l l cases of p a n c r e a t i c ascites, including those patients with chronic pancreatitis. M e a s u r e m e n t of the p r o t e i n content of t h e p e r i t o n e a l fluid helps in the differential diagnosis of t r a n s udative hepatic diseases, such as cir-' rhosis, and p a n c r e a t i c ascites. In t h e former, t h e p r o t e i n c o n t e n t r a n g e s from 0.5 gm/100ml to 1.5 gm/100ml while in t h e l a t t e r t h e r a n g e is 2.9 gm/100ml to.5.7 gm/100ml. Our case r e p o r t i l l u s t r a t e s a n o t h e r etiology for e a r l y a b d o m i n a l distention in t r a u m a p a t i e n t s . S u e m i t s u 5 has demonstrated that prolonged periods of h y p o x i a can cause major
• It is i m p o r t a n t to d i s t i n g u i s h posthypoxic ascites from p a n c r e a t i c ascites as t h e t r e a t m e n t s are different. In p a n c r e a t i c ascites early operative i n t e r v e n t i o n is i n d i c a t e d as the etiol• ogy is p r e s u m e d to be a c o n t i n u e d p a n c r e a t i c fluid leak. The t r e a t m e n t of posthypoxic ascites is conservative a n d supportive. I n t r a v a s c u l a r fluid loss m a y be large and such loss m u s t be c a r e f u l l y m o n i t o r e d . In our patient, t h e r e was e a r l y , u n e x p l a i n e d oliguria. F l u i d r e q u i r e m e n t exceeded the expected needs. These findings w e r e b a s e d on t h i r d s p a c e f l u i d shifts, poor p e r i p h e r a l perfusion and t r a n s i e n t hypovolemia. Repeated e v a l u a t i o n of liver function tests will help delineate the m a g n i t u d e and d u r a t i o n of c e l l u l a r d a m a g e . W i t h more extensive liver damage, severe metabolic and hematologic d e r a n g e m e n t s could develop a n d f u r t h e r l a b o r a t o r y evaluation m a y be indicated, ie, s e r u m proteins, p r o t h r o m b i n time, fibrinogen and o t h e r clotting studies. The SGOT and LDH were m a r k e d l y elevated in t h i s case b u t did r e v e r t to n o r m a l d u r i n g t h e p a t i e n t ' s convalescence.
REFERENCES 1. Shires GT: Care of the Trauma Patient, New York, McGraw-Hill, 1966, p 354-411. 2. Olsen WR, Douglas HH: Abdominal paracentesis and peritoneal lavage in blunt abdominal trauma. J T r a u m a 11:824-829, 1971. 3. Landman MD, Longmire WP Jr: Neural and hormonal influences of Volume 5 Number 3 Page 187
peritonitis in paralytic ileus. A m Surg 33:756-762, 1967. 4. Smith DR: General Urology, ed 8. Los Altos, California, Lange Medical Publications, 1975. 5. C h a n g CH, Chen KM: Post-traumatic pancreatic ascites. A m J Surg 122:129131, 1971. 6. Cameron JL, Anderson RP, Zuidema
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GD: P a n c r e a t i c ascites. Surg Gynecol Obstet 125:328-332, 1967.
vein under hypoxia and pulmonary era. bolism. Jap Circ J 33:391-397, 1969.
7. S u e m i t s u I, I k e d a K, H o s h i y a S: Metabolic effects of hypoxia a n d hypercapnia on the liver related with hepatic circulation. Jap Circ J 28:119-122, 1964.
9. S h e a r L: Ascites: p a t h o g e n e s i s and t r e a t m e n t . Postgrad Med 53:165-170, 1973.
8. Matsuno H: Hepatic circulation study: I. Relation of hepatic artery a n d portal
10. Losowsky MS, Scott BB: Ascites a/~d oedema in liver disease~ Br Med J 3:336. 338, 1973.
March i976 J ~ P
Posthypoxic Ascites: A Cause of Post-Traumatic Abdominal Distention Bernard J. Urlaub, MD Madison, Wisconsin Joseph A. Moylan, Jr, MD Durham, North Carofina
A p r e v i o u s l y u n r e p o r t e d etiology for post-traumatic a b d o m i n a l distention w a s o b s e r v e d in a 5-year-old girl w h o suffered only h e a d trauma and a p r o l o n g e d period of h y p o x e m i a . When there is a rapid accumulation of peritoneal fluid c o n t a i n i n g a high c o n c e n t r a t i o n of protein but n e g a t i v e for amylase, no e v i d e n c e of b l o o d loss, plus a b n o r m a l serial liver e n z y m e studies and the n e e d for p l a c e m e n t o f large v o l u m e s of fluid, p o s t h y p o x i c ascites should be suspected. Peritoneal aspiration c o n f i r m e d the diagnosis and treatment w a s supportive. B e c a u s e early operative intervention is n e c e s s a r y in pancreatic ascites and treatment is supportive for p o s t h y p o x i c ascites, it is imperative to differentiate them. Urlaub BJ, Moylan JA Jr: Posthypoxic ascites: a cause of post-traumatic abdominal distention. JACEP 5:186-188, March 1976. distention, abdominal; as-
cites, posthypoxic; trauma; lavage, peritoneal. INTRODUCTION A r a p i d i n c r e a s e in a b d o m i n a l g i r t h in the victim of a major accident presents the physician with a difficult diagnostic dilemma. The u s u a l causes for this p o s t - t r a u m a t i c phenomenon are hemoperitoneum from a b d o m i n a l visceral injury, adyn a m i c ileus, p a n c r e a t i c ascites a n d u r i n a r y e x t r a v a s a t i o n . 1 This r e p o r t d e s c r i b e s a n o t h e r e t i o l o g y for t h i s p r o b l e m - - post-hypoxic ascites foll o w i n g p r o l o n g e d h y p o x e m i a in a
From the Department of Surgery, University of Wisconsin Center for Health Sciences, Madison, Wisconsin. Address for reprints: Joseph A. Moylan, Jr, MD, Department of Surgery, Duke University Medical Center, Box 3043, Durham, NC 27710.
Page 186 Volume 5 Number 3
p a t i e n t w i t h a h e a d i n j u r y a n d no abdominal trauma.
Case Report A 5-year-old girl was in the front seat of an automobile involved in a two-car collision. She was not wearing a seat b e a t a n d s t r u c k h e r h e a d on the s t e e r i n g wheel. No other inj u r i e s were observed, Following a prol o n g e d p e r i o d of m a r k e d c y a n o s i s r e s u l t i n g from an obstructed airway, s h e r e c e i v e d m o u t h - t o - m o u t h resp i r a t o r y support from a p a s s i n g regi s t e r e d n u r s e a n d h e r color slowly improved. Upon e x a m i n a t i o n 30 minu t e s l a t e r in a n e a r b y e m e r g e n c y department, after receiving oxygen d u r i n g t r a n s p o r t , she was noted to be l e t h a r g i c w i t h d e p r e s s i o n of all reflexes. H e r p u p i l s were e q u a l l y dilated b i l a t e r a l l y and s l u g g i s h l y reac-
tive. H e r m u s c l e s w e r e flaccid and she was responsive only to deep pain s t i m u l a t i o n . Stool and u r i n a r y incontinence were noted. W h i l e b e i n g t r a n s f e r r e d to University Hospital, she e x h i b i t e d multiple m i n o r focal seizures. I n i t i a l examination at U n i v e r s i t y H o s p i t a l revealed a n a w a k e girl, s p e a k i n g coherently, without any localizing neurologic signs. T h e r e m a i n i n g e x a m i n a t i o n r e v e a l e d no other evidence of injury. There were n o r m a l bowel sounds and a soft, flat, n o n t e n d e r a b d o m e n . A neurological c o n s u l t a n t , ascribed the p a t i e n t ' s prior neurologic defects to a generalized disturbance resulting from a n o x i a . A d m i t t i n g l a b o r a t o r y data included a hematocrit reading of 35%, w h i t e b l o o d cell c o u n t 29,600/cu mm, s e r u m cTeatinine 1.1 mg/100 ml, a n d n o r m a l electrolytes. U r i n a l y s i s was u n r e m a r k a b l e . The r e s u l t s of all r a d i o g r a p h s , including c y s t o g r a m a n d i n t r a v e n o u s pyelogram, were w i t h i n n o r m a l limits. D u r i n g t h e 24-hour period followi n g injury, t h e p a t i e n t ' s a b d o m i n a l girth increased markedly. Bowel sounds r e m a i n e d normal. Hepatomeg a l y was p r e s e n t and m i n i m a l right u p p e r q u a d r a n t t e n d e r n e s s was n o t e d . T o t a l i n t r a v e n o u s f l u i d req u i r e m e n t s to m a i n t a i n a u r i n a r y o u t p u t of 15 cc/hour were twice that predicted for age a n d size. There was no evidence of blood 10ss.
March 1976 J ~ P
p a r a c e n t e s i s yielded s t r a w colored fluid t h a t contained p r o t e i n and was positive for s u g a r b u t n e g a t i v e for asylase a n d blood. A s i m u l t a n e o u s ~arinalysis was n e g a t i v e for protein, sugar a n d b l o o d . B e c a u s e of h e r hepatomegaly, a . 9 9 m / T c sulfur colloid and 131 rose bengal liver-spleen scan w e r e o b t a i n e d . The scan confirmed t h e c l i n i c a l o b s e r v a t i o n of hepatomegaly and d e m o n s t r a t e d uniform h e p a t i c m e t a b o l i c f u n c t i o n without a n y evidence of localized injury. L a b o r a t o r y t e s t s r e v e a l e d a slightly i n c r e a s e d s e r u m a m y l a s e , 200 somogyi units; a n a l k a l i n e phosphatase of 12.1 IU/liter; and s e r u m glutamic o x a l o a c e t i c t r a n s a m i n a s e (sGOT) of 128 IU/liter, a n d a lactic dehydrogenase (LDH) of 273 IU/liter. The ascites resolved s p o n t a n e o u s l y over a 72-hour period a n d the LDH and SGOT r e t u r n e d to n o r m a l levels. The a l k a l i n e p h o s p h a t a s e r e m a i n e d elevated to levels consistent with the bone g r o w t h p a t t e r n for t h i s a g e group. The h o s p i t a l course was otherwise u n r e m a r k a b l e . T h e focal s e i z u r e s were controlled on p h e n o b a r b i t a l . An electroencephalogram showed a mild generalized d i s t u r b a n c e of c e r e b r a l fanction a n d t h e p a t i e n t r e m a i n e d asymptomatic a f t e r d i s c h a r g e . No f~lrther s e q u e l l a e were observed during a one y e a r follow-up.
~DISCUSSION Hemoperitoneum is one Of the most common p o s t - t r a u m a t i c etiologies of abdominal distention. 1 Injuries t o the spleen or liver m a y r e s u l t in significant p e r i t o n e a l b l e e d i n g . H y p o t e n si0n, a f a l l i n g h e m a t o c r i t and abdominal t e n d e r n e s s along with distention ~re t h e e a r l y s i g n s o f h e m o p e r : Lt0neum p e r m i t t i n g a p r e s u m p t i v e tiagnosis of i n t r a - a b d o m i n a l bleed,~g. The diagnosis can be confirmed ~ith a paracentesis. In r e c e n t series, ~lsen a n d Douglas 2 reported t h a t a red b l o o d cell c o u n t g r e a t e r t h a n [00,000 cells/cu m m in the a s p i r a t e d ~uid is indicative of a major abdomilal injury r e q u i r i n g operative inter~ention. Adynamic ileus is a n o t h e r common '.~Use of r a p i d increase in a b d o m i n a l ~irth f o l l o w i n g an a c c i d e n t . M a n y leural, h o r m o n a l a n d metabolic facors i n f l u e n c e t h e d e v e l o p m e n t of
• [ ] March • P 1976
a d y n a m i c ileus. 3 It is very common following spinal injuries, retroperitoneal hematoma and other t r a u m a . Absen't bowel sounds, t h e lack of t e n d e r n e s s in the presence of abdominal distention and the uniform d i s t r i b u t i o n of gas t h r o u g h o u t the g a s t r o i n t e s t i n a l t r a c t on abdominal radiographs are signs of a d y n a m i c ileus. The absence of fluid on p e r i t o n e a l t a p a n d ret.urn of a clear i r r i g a t i o n fluid is confirmatory.
d e r a n g e m e n t of a l l c e l l u l a r functions. H e p a t i c tissue is well known to be h i g h l y s u s c e p t i b l e to hypoxic states. H y p o x e m i a also results in inc r e a s e d blood flow to the g a s t r o i n testinal organs, particularly the liver. 6 The c o m b i n a t i o n of high flow state and cellular damageT, s may produce exudative processes with f o r m a t i o n of ascitic fluid w i t h a high p r o t e i n c o n c e n t r a t i o n , as was seen in this case.
U r i n a r y e x t r a v a s a t i o n from a rupt u r e d b l a d d e r or l a c e r a t e d u r e t e r is a n i n f r e q u e n t c a u s e of a b d o m i n a l distention. 4 As sterile u r i n e is not irritating, abdominal findings are often lacking. The diagnosis is usually m a d e by p e r f o r m i n g r e t r o g r a d e cystogram and intravenous pyelog r a m after gross or microscopic hem a t u r i a a r e discovered on u r i n a l y s i s .
In our case, a n e g a t i v e a m y l a s e det e r m i n a t i o n in the p e r i t o n e a l fluid distinguished posthypoxic ascites from p a n c r e a t i c ascites. There was a m i n i m a l t r a n s i e n t e l e v a t i o n in t h e s e r u m a m y l a s e in t h i s child but not in t h e h i g h a n d p e r s i s t e n t r a n g e s u s u a l l y found in d i r e c t i n j u r y to a previously u n d i s e a s e d pancreas.
P o s t - t r a u m a t i c p a n c r e a t i c ascites is a n o t h e r r a r e cause of a b d o m i n a l distention. 3 The p h e n o m e n o n is most often associated with pre-existent chronic p a n c r e a t i t i s a n d p a n c r e a t i c pseudocyst. Only four cases of postt r a u m a t i c p a n c r e a t i c ascites in pat i e n t s w i t h o u t prior p a n c r e a t i c dise a s e h a v e b e e n d o c u m e n t e d in t h e l i t e r a t u r e . 4 The etiology of this process is t h o u g h t to be l e a k a g e from a d i s r u p t e d p a n c r e a t i c duct or pseudocyst. T h e s e r u m a m y l a s e m a y be n o r m a l or only s l i g h t l y e l e v a t e d i n p a t i e n t s w i t h long t e r m chronic pancreatitis b u t is m a r k e d l y e l e v a t e d in p a t i e n t s free of previous p a n c r e a t i c disease. The diagnosis of:post-traumatic p a n c r e a t i c a s c i t e s is c o n f i r m e d b y a n a l y s i s of t h e a s c i t i c f l u i d . T h e a m y l a s e c o n c e n t r a t i o n o f the ascitic f l u i d is m a r k e d l y e l e v a t e d in a l l cases of p a n c r e a t i c ascites, including those patients with chronic pancreatitis. M e a s u r e m e n t of the p r o t e i n content of t h e p e r i t o n e a l fluid helps in the differential diagnosis of t r a n s udative hepatic diseases, such as cir-' rhosis, and p a n c r e a t i c ascites. In t h e former, t h e p r o t e i n c o n t e n t r a n g e s from 0.5 gm/100ml to 1.5 gm/100ml while in t h e l a t t e r t h e r a n g e is 2.9 gm/100ml to.5.7 gm/100ml. Our case r e p o r t i l l u s t r a t e s a n o t h e r etiology for e a r l y a b d o m i n a l distention in t r a u m a p a t i e n t s . S u e m i t s u 5 has demonstrated that prolonged periods of h y p o x i a can cause major
• It is i m p o r t a n t to d i s t i n g u i s h posthypoxic ascites from p a n c r e a t i c ascites as t h e t r e a t m e n t s are different. In p a n c r e a t i c ascites early operative i n t e r v e n t i o n is i n d i c a t e d as the etiol• ogy is p r e s u m e d to be a c o n t i n u e d p a n c r e a t i c fluid leak. The t r e a t m e n t of posthypoxic ascites is conservative a n d supportive. I n t r a v a s c u l a r fluid loss m a y be large and such loss m u s t be c a r e f u l l y m o n i t o r e d . In our patient, t h e r e was e a r l y , u n e x p l a i n e d oliguria. F l u i d r e q u i r e m e n t exceeded the expected needs. These findings w e r e b a s e d on t h i r d s p a c e f l u i d shifts, poor p e r i p h e r a l perfusion and t r a n s i e n t hypovolemia. Repeated e v a l u a t i o n of liver function tests will help delineate the m a g n i t u d e and d u r a t i o n of c e l l u l a r d a m a g e . W i t h more extensive liver damage, severe metabolic and hematologic d e r a n g e m e n t s could develop a n d f u r t h e r l a b o r a t o r y evaluation m a y be indicated, ie, s e r u m proteins, p r o t h r o m b i n time, fibrinogen and o t h e r clotting studies. The SGOT and LDH were m a r k e d l y elevated in t h i s case b u t did r e v e r t to n o r m a l d u r i n g t h e p a t i e n t ' s convalescence.
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peritonitis in paralytic ileus. A m Surg 33:756-762, 1967. 4. Smith DR: General Urology, ed 8. Los Altos, California, Lange Medical Publications, 1975. 5. C h a n g CH, Chen KM: Post-traumatic pancreatic ascites. A m J Surg 122:129131, 1971. 6. Cameron JL, Anderson RP, Zuidema
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7. S u e m i t s u I, I k e d a K, H o s h i y a S: Metabolic effects of hypoxia a n d hypercapnia on the liver related with hepatic circulation. Jap Circ J 28:119-122, 1964.
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