Intensive Care Med (1992) 18:245-246
IntensiveCare Medicine 9 Springer-Verlag1992
Case reports
Diagnosis of gallbladder perforation in acute acalculous cholecystitis in critically ill patients Ch. M a d l , G. G r i m m , R, M a l l e k , B. Schneeweil3, W. D r u m l , A . N . L a g g n e r a n d K. L e n z Allgemeines Krankenhaus Wien, University of Vienna, Austria Received: 27 March 1991; accepted: 3 March 1991
Abstract. I n the presence o f ascites u l t r a s o u n d is n o t ap-
Case 3
propriate to distinguish between gallbladder p e r f o r a t i o n a n d acute acalculous cholecystitis. However, the correct a n d early diagnosis of gallbladder p e r f o r a t i o n is import a n t for the t r e a t m e n t a n d prognosis. We report 4 critically ill patients with ascites. All patients h a d evidence of gallbladder p e r f o r a t i o n by u l t r a s o u n d a n d u n d e r w e n t cholecystectomy: 2 p a t i e n t s h a d g a l l b l a d d e r p e r f o r a t i o n , b u t 2 h a d acalculous cholecystitis w i t h o u t perforation. M a r k e d l y elevated s e r u m alkaline p h o s p h a t a s e was the o n l y d i s c r i m i n a t i n g f i n d i n g i n d i c a t i n g gallbladder perforation.
A 18-year-oldgirl presented with septicemia (Staphylococcus aureus), respiratory failure, acute renal failure, hypotension and consumptive coagulopathy with bleeding (6 blood transfusions). While receivingtotal parenteral nutrition she developedright upper quadrant pain and resistance. Alkaline phosphatase was 119 U/I. On sonography, a thickened gallbladder wall (4 ram) and free intra-abdominal fluid around the gallbladder were found. Increased bilirubin content in the ascites (9.9 mg/dl) suggested bilious peritonitis due to gallbladder perforation. Laparatomy with cholecystectomyrevealed bilious ascites, but no gallbladder perforation. Gallbladder inflammation was shown at histological examination.
Case 4
Key words: Acalculous cholecystitis - A l k a l i n e p h o s p h a tase -
Cholecystectomy -
Gallbladder perforation
Case reports Case 1
A 50-year-old woman with bone marrow transplantation was treated with long-term total parenteral nutrition. There was no other risk factor of acute acalculous cholecystitis. 14 days after transplantation the patient complained of right upper quadrant pain and resistance. Alkaline phosphatase was slightly increased (234U/l). On sonography, typical signs of gallbladder perforation were detected. At surgery, only a moderate enlarged gallbladder and clear ascites were found. Aealculous cholecystitis was confirmed histologically.
A 43-year-oldman with a short bowel syndrome after enterectomy for Crohn's disease was admitted to the ICU. He presented with septicemia (E. coli), acute renal failure, hypotension and cerebral disturbance. During total parenteral nutrition for more than 6 weeks, he developed pain and tenderness in the right upper quadrant. Alkaline phosphatase was 1221 U/1. Ultrasound examination showed a thickened gallbladder wall (5 ram), with a partially desquamated mucosal layer, pericholecysticfluid collection around the enlarged gallbladder and free intraabdominal fluid in the lower abdomen. A needle aspiration of pericholecysticfluid collection demonstrated bilious secretion. Immediate cholecystectomy revealed a gangreneous perforated gallbladder.
Case 2 A 19-year-oldwoman was admitted to the ICU 4 weeks after cesarian section for preeclampsia (edema, proteinuria, hypertension) with ARDS and acute renal failure. Mechanical ventilation with PEEP and hemofiltration was performed for 4 weeks. She received opioides, catecholamines, and total parenteral nutrition. She developed septicemia (Pseuclomonas aeruginosa). Clinical examination revealed a painful right upper quadrant palpable mass. Alkaline phosphatase was 2103 U/1. In the presence of ascites, ultrasound was indicative of gallbladder perforation (Fig. 1), which was confirmed by cholecystectomy.
Fig. 1. A typical ukrasound finding of suspected gallbladder perforation in the presence of ascites: enlarged gallbladder with sludge - level, thickened wall, pericholecystic fluid col!ection (case 2)
246 Table 1. Laboratory data at time of diagnosis Patient
Diagnosis
AP (U/I)
Bili (mg/dl)
GPT (U/I)
BUN (mg/dl)
Crea (mg/dl)
WBC • 10/1
Temp (~
1 2 3 4
Perforated Perforated Not perforated Not perforated Normal values
1221 2103 119 234 6 0 - 170
10.4 2.9 35.5 2.4 - 1.0
25 21 9 15 - 22
75 44 74 35 9 - 20
3.3 2.5 3.4 0.8 0.7 - 1.3
18.6 26.0 15.7 1.5 4.3 - 9.0
37.0 37.6 37.5 37.0 - 37.0
AP, Alkaline phosphatase; Bili, total bilirubin; GPT, glutamate pyruvate transaminase; BUN, blood urea nitrogen; Crea, creatinine; WBC, white blood cell count; Temp, body temperature
Discussion
Acalculous cholecystitis is a well-known and potentially life-threatening complication in critically ill patients [1, 2]. The complication rate of acute acalculous cholecystitis due to gangrene, empyema or perforation of the gallbladder ranges from 40070 to 100070 [3]. The discrimination between uncomplicated acute cholecystitis and gallbladder perforation is difficult, but a correct and early diagnosis is important for the treatment and prognosis [3, 4]. While acalculous cholecystitis can be successfully treated without open surgery by percutaneous cholecystotomy [1, 5], gallbladder perforation mandatorily needs surgical treatment [6]. We report 4 cases with evidence of gallbladder perforation and ascites on ultrasound. All patients underwent surgery including cholecystectomy. Two patients had gallbladder perforation, but 2 had a histologically proven acalculous cholecystitis. Retrospective analysis of the patients revealed, that alkaline phosphatase was the only finding consistently associated with gallbladder perforation: alkaline phosphatase was markedly increased in the patients with perforation, but normal to slightly increased in the patients with acalculous cholecystitis. In contrast to our 4 patients with acute acalculous gallbladder disease, in patients with gallbladder perforation due to predominately chronic cholecystitis with cholelithiasis elevated alkaline phosphatase was found only in 70070 [6]. Madrazo et al. reported that the diagnosis of gallbladder perforation by sonography may be confused by the presence of ascites, peritonitis or pancreatitis [4]. Accordingly, ultrasound examination was not helpful for the diagnosis in our patients, since all had identical typical signs of gallbladder perforation. Other imaging techniques, such as cholescintigraphy or computertomography, were also not helpful for the diagnosis [7- 9] and, therefore, not performed in our critically ill patients. Clinical signs provide no additional diagnostic informa-
tion: pain and tenderness in the right upper quadrant were present in all patients. Body temperature was not markedly elevated. Other laboratory findings than alkaline phosphatase were not useful for the diagnosis of gallbladder perforation (Table 1). We suggest from our limited series of critically ill patients with ascites, that serum alkaline phosphatase may have a predictive value for discriminating gallbladder perforation from acute acalculous cholecystitis. However, our finding has to be confirmed by further studies. References 1. Long TN, Heimbach DM, Carrico CJ (1978) Acalculous cholecystitis in critically ill patients. Am J Surg 136:31-35 2. Bower R, Mrdeza MA, Block GE (1990) Association of cholecystitis and parenteral nutrition. Nutrition 6:125-130 3. Johnson LB (1987) The importance of early diagnosis of acute acalculous cholecystitis. Surg Gynecol Obstet 164:109-203 4. Madrazo BL, Francis I, Hricak H, Sandler MA, Hudak S, Gitschlag K (1982) Sonographie findings in perforation of the gallbladder. AJR 139:491-496 5. Berger H, Pratschke E, Arbogast H, St~tbler A (1989) Percutaneous cholecystotomy in acute acalculons cholecystitis. Hepatogastroenterology 36:346-348 6. Roslyn J, Busuttil RW (1979) Perforation of the gallbladder: a frequently mismanaged condition. Am J Surg 137:307-312 7. Shuman WP, Rogers JV, Rudd TG, Mack LA, Plumley T, Larson EB (1984) Low sensitivity of sonography and cholescintigraphy in acalculous cholecystitis. A JR 142:531-534 8. Smith R, Rosen JM, Alderson PO (1986) Gallbladder perforation: diagnostic utility of cholescintigraphy in suggested subacute or chronic cases. Radiology 158:63-66 9. Schneider PB (1984) Acalculous cholecystitis: a case with variable cholescintigram. J Nucl Med 25:64-65 Dr. Ch. Madl Department of Medicine IV University of Vienna W~hringer G~irtel f 8 - 2 0 A-1090 Wien
IntensiveCare Medicine 9 Springer-Verlag1992
Case reports
Diagnosis of gallbladder perforation in acute acalculous cholecystitis in critically ill patients Ch. M a d l , G. G r i m m , R, M a l l e k , B. Schneeweil3, W. D r u m l , A . N . L a g g n e r a n d K. L e n z Allgemeines Krankenhaus Wien, University of Vienna, Austria Received: 27 March 1991; accepted: 3 March 1991
Abstract. I n the presence o f ascites u l t r a s o u n d is n o t ap-
Case 3
propriate to distinguish between gallbladder p e r f o r a t i o n a n d acute acalculous cholecystitis. However, the correct a n d early diagnosis of gallbladder p e r f o r a t i o n is import a n t for the t r e a t m e n t a n d prognosis. We report 4 critically ill patients with ascites. All patients h a d evidence of gallbladder p e r f o r a t i o n by u l t r a s o u n d a n d u n d e r w e n t cholecystectomy: 2 p a t i e n t s h a d g a l l b l a d d e r p e r f o r a t i o n , b u t 2 h a d acalculous cholecystitis w i t h o u t perforation. M a r k e d l y elevated s e r u m alkaline p h o s p h a t a s e was the o n l y d i s c r i m i n a t i n g f i n d i n g i n d i c a t i n g gallbladder perforation.
A 18-year-oldgirl presented with septicemia (Staphylococcus aureus), respiratory failure, acute renal failure, hypotension and consumptive coagulopathy with bleeding (6 blood transfusions). While receivingtotal parenteral nutrition she developedright upper quadrant pain and resistance. Alkaline phosphatase was 119 U/I. On sonography, a thickened gallbladder wall (4 ram) and free intra-abdominal fluid around the gallbladder were found. Increased bilirubin content in the ascites (9.9 mg/dl) suggested bilious peritonitis due to gallbladder perforation. Laparatomy with cholecystectomyrevealed bilious ascites, but no gallbladder perforation. Gallbladder inflammation was shown at histological examination.
Case 4
Key words: Acalculous cholecystitis - A l k a l i n e p h o s p h a tase -
Cholecystectomy -
Gallbladder perforation
Case reports Case 1
A 50-year-old woman with bone marrow transplantation was treated with long-term total parenteral nutrition. There was no other risk factor of acute acalculous cholecystitis. 14 days after transplantation the patient complained of right upper quadrant pain and resistance. Alkaline phosphatase was slightly increased (234U/l). On sonography, typical signs of gallbladder perforation were detected. At surgery, only a moderate enlarged gallbladder and clear ascites were found. Aealculous cholecystitis was confirmed histologically.
A 43-year-oldman with a short bowel syndrome after enterectomy for Crohn's disease was admitted to the ICU. He presented with septicemia (E. coli), acute renal failure, hypotension and cerebral disturbance. During total parenteral nutrition for more than 6 weeks, he developed pain and tenderness in the right upper quadrant. Alkaline phosphatase was 1221 U/1. Ultrasound examination showed a thickened gallbladder wall (5 ram), with a partially desquamated mucosal layer, pericholecysticfluid collection around the enlarged gallbladder and free intraabdominal fluid in the lower abdomen. A needle aspiration of pericholecysticfluid collection demonstrated bilious secretion. Immediate cholecystectomy revealed a gangreneous perforated gallbladder.
Case 2 A 19-year-oldwoman was admitted to the ICU 4 weeks after cesarian section for preeclampsia (edema, proteinuria, hypertension) with ARDS and acute renal failure. Mechanical ventilation with PEEP and hemofiltration was performed for 4 weeks. She received opioides, catecholamines, and total parenteral nutrition. She developed septicemia (Pseuclomonas aeruginosa). Clinical examination revealed a painful right upper quadrant palpable mass. Alkaline phosphatase was 2103 U/1. In the presence of ascites, ultrasound was indicative of gallbladder perforation (Fig. 1), which was confirmed by cholecystectomy.
Fig. 1. A typical ukrasound finding of suspected gallbladder perforation in the presence of ascites: enlarged gallbladder with sludge - level, thickened wall, pericholecystic fluid col!ection (case 2)
246 Table 1. Laboratory data at time of diagnosis Patient
Diagnosis
AP (U/I)
Bili (mg/dl)
GPT (U/I)
BUN (mg/dl)
Crea (mg/dl)
WBC • 10/1
Temp (~
1 2 3 4
Perforated Perforated Not perforated Not perforated Normal values
1221 2103 119 234 6 0 - 170
10.4 2.9 35.5 2.4 - 1.0
25 21 9 15 - 22
75 44 74 35 9 - 20
3.3 2.5 3.4 0.8 0.7 - 1.3
18.6 26.0 15.7 1.5 4.3 - 9.0
37.0 37.6 37.5 37.0 - 37.0
AP, Alkaline phosphatase; Bili, total bilirubin; GPT, glutamate pyruvate transaminase; BUN, blood urea nitrogen; Crea, creatinine; WBC, white blood cell count; Temp, body temperature
Discussion
Acalculous cholecystitis is a well-known and potentially life-threatening complication in critically ill patients [1, 2]. The complication rate of acute acalculous cholecystitis due to gangrene, empyema or perforation of the gallbladder ranges from 40070 to 100070 [3]. The discrimination between uncomplicated acute cholecystitis and gallbladder perforation is difficult, but a correct and early diagnosis is important for the treatment and prognosis [3, 4]. While acalculous cholecystitis can be successfully treated without open surgery by percutaneous cholecystotomy [1, 5], gallbladder perforation mandatorily needs surgical treatment [6]. We report 4 cases with evidence of gallbladder perforation and ascites on ultrasound. All patients underwent surgery including cholecystectomy. Two patients had gallbladder perforation, but 2 had a histologically proven acalculous cholecystitis. Retrospective analysis of the patients revealed, that alkaline phosphatase was the only finding consistently associated with gallbladder perforation: alkaline phosphatase was markedly increased in the patients with perforation, but normal to slightly increased in the patients with acalculous cholecystitis. In contrast to our 4 patients with acute acalculous gallbladder disease, in patients with gallbladder perforation due to predominately chronic cholecystitis with cholelithiasis elevated alkaline phosphatase was found only in 70070 [6]. Madrazo et al. reported that the diagnosis of gallbladder perforation by sonography may be confused by the presence of ascites, peritonitis or pancreatitis [4]. Accordingly, ultrasound examination was not helpful for the diagnosis in our patients, since all had identical typical signs of gallbladder perforation. Other imaging techniques, such as cholescintigraphy or computertomography, were also not helpful for the diagnosis [7- 9] and, therefore, not performed in our critically ill patients. Clinical signs provide no additional diagnostic informa-
tion: pain and tenderness in the right upper quadrant were present in all patients. Body temperature was not markedly elevated. Other laboratory findings than alkaline phosphatase were not useful for the diagnosis of gallbladder perforation (Table 1). We suggest from our limited series of critically ill patients with ascites, that serum alkaline phosphatase may have a predictive value for discriminating gallbladder perforation from acute acalculous cholecystitis. However, our finding has to be confirmed by further studies. References 1. Long TN, Heimbach DM, Carrico CJ (1978) Acalculous cholecystitis in critically ill patients. Am J Surg 136:31-35 2. Bower R, Mrdeza MA, Block GE (1990) Association of cholecystitis and parenteral nutrition. Nutrition 6:125-130 3. Johnson LB (1987) The importance of early diagnosis of acute acalculous cholecystitis. Surg Gynecol Obstet 164:109-203 4. Madrazo BL, Francis I, Hricak H, Sandler MA, Hudak S, Gitschlag K (1982) Sonographie findings in perforation of the gallbladder. AJR 139:491-496 5. Berger H, Pratschke E, Arbogast H, St~tbler A (1989) Percutaneous cholecystotomy in acute acalculons cholecystitis. Hepatogastroenterology 36:346-348 6. Roslyn J, Busuttil RW (1979) Perforation of the gallbladder: a frequently mismanaged condition. Am J Surg 137:307-312 7. Shuman WP, Rogers JV, Rudd TG, Mack LA, Plumley T, Larson EB (1984) Low sensitivity of sonography and cholescintigraphy in acalculous cholecystitis. A JR 142:531-534 8. Smith R, Rosen JM, Alderson PO (1986) Gallbladder perforation: diagnostic utility of cholescintigraphy in suggested subacute or chronic cases. Radiology 158:63-66 9. Schneider PB (1984) Acalculous cholecystitis: a case with variable cholescintigram. J Nucl Med 25:64-65 Dr. Ch. Madl Department of Medicine IV University of Vienna W~hringer G~irtel f 8 - 2 0 A-1090 Wien
