Diagnosis
of Gangrene
and Perforation Retrograde
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KAZUKO
of the Gallbladder
Cholangiography
BILL1
AND
JOSEPH
are described.
Gangrene
was
identified
in all
three by a shaggy outline of the gallbladder wall with amorphous debris and stones in the lumen. Perforation was identifled in two of the cases by extravasation of contrast material
into
a pericholecystic
the status
abscess.
of the common
duct,
This
information,
was important
as well
large pericholecystic
as
to the surgeon.
Gallbladder perforation, caused by necrosis of all or part of the gallbladder wall, occurs in about 8%-12% of patients with acute cholecystitis [1]. Although high fever, leukocytosis, and tachycardia suggest the diagnosis, the clinical picture may be indistinguishable from uncomplicated acute cholecystitis [1 2]. During preoperative endoscopic retrograde cholangiography, we have encountered abnormalities which suggest gallbladder wall necrosis and which are characteristic of perforation and abscess formation. Endoscopic retrograde cholangiography has been performed 318 times in 272 patients at the Martinez Veterans Administration Hospital since July 1972. Of these examinations, 52 were done to evaluate patients with symptoms of acute cholecystitis, some after the acute phase had subsided. Adequate examinations were obtained in 38. All but one were abnormal, revealing either stones in the gallbladder and/on common duct on blockage of the cystic duct. The three cases described here had a shaggy gallbladder wall with debris in the gallbladder; two also showed leakage of contrast material beyond the gallbladder wall. ,
Case
Case
man
was
complaining
with
38.9#{176}C;pulse,
right
upper
1 10; blood
abdominal pressure,
pain. 80/60.
firm
peaked
at 6.8 mg/dl over
showed
nonvisualization
shaggy
(figs.
lB
with
right
upper
quadrant
3 days after
a 7 day retrograde
gallbladder
period.
admission
Intravenous
of the biliary cholangiography
containing
calculi
and then
fell to
cholangiography
ducts
and gallbladder.
demonstrated
and irregular
a large
debris.
The
cystic duct was short and the common hepatic duct was compressed, presumably by contiguous inflammation (fig. 2). At laparotomy the gallbladder was intensely inflamed and contained dark bile, necrotic debris, and calculi. The infundibulum pressed on the common hepatic duct. The cystic duct
was patent.
of nausea,
Temperature A large
man was admitted
normal Endoscopic
A cholecystostomy
was performed
and a portion
of
the gallbladder wall was biopsied, revealing marked inflammation with local necrosis. The postoperative course was uneventful, and 2 months later cholecystectomy was performed. The infundibulum of the gallbladder was in close proximity to the common hepatic duct. Again the postoperative course was uneventful.
vomiting, and feverishness for 1 day. Similar attacks lasting up to 48 hr had occurred during the previous 2 years, occasionally
associated
debris
2
A 55-year-old
Reports
admitted
irregular
pain and fever for 3 days. Physical examination disclosed a temperature of 39.4#{176}C,and tenderness and guarding in the right upper quadrant. The white blood cell count was 15,600 with 80% polymorphonuclear leukocytes. Serum bilirubin was 1 .1 mg/dl; alkaline phosphatase, 61 U (normal = 35). The fever and abdominal findings resolved in 10 days. Serum bilirubin
1
A 46-year-old
cavity containing
and 1C). At exploratory surgery the gallbladder was perforated and gangrenous. A large subhepatic abscess containing calculi and necrotic debris was drained and a cholecystostomy performed. The common duct was not explored. The postoperative course was stormy, but the patient ultimately recovered and was discharged. He was readmitted 14 months later for interval cholecystectomy. Endoscopic retrograde cholangiography demonstrated a normal extrahepatic biliary tree including a patent cystic duct. The gallbladder showed stricture and deformity at the fundus. An irregular calculus was present in the body of the gallbladder (fig. 1D). Cholecystectomy confirmed these findings. Again the postoperative cou rse was uneventful.
Introduction
Case
P. BELBER2
Intravenous cholangiography failed to visualize the biliary ducts or gallbladder. Endoscopic retrograde cholangiography demonstrated the extrahepatic biliary ducts to be nondilated and free of calculi, but displaced by a large mass. The cystic duct was patent. As the gallbladder filled, stones and debris (fig. 1A) were demonstrated. Subsequently, the contrast medium left the gallbladder through a broad fistulous tract into a
Conventional radiographic procedures are not helpful in the preoperative documentation of gangrenous cholecystltis or gallbladder perforation. Three cases in which preoperative diagnosis was accomplished by endoscoplc retrograde cho-
langiography
by Endoscopic
was mass
was palpated in the right upper abdomen. Laboratory studies revealed hemoglobin 15.6; white blood cell count, 23,900 with 78% polymorphonuclear leukocytes; serum bilirubin, 2.6 mgI dl; SGOT, 51 mU/mi; and alkaline phosphatase, 107 U (normal 35). The patient was placed on ampicillin and improved within a few hours.
Case
3
A 60-year-old man brovascular accident
=
was
hospitalized
resulting
in right
elsewhere
hemiparesis
with
a cere-
and motor
Received I Section
June 20, 1977; accepted after revision September 12, 1977. of Gastrointestinal Radiology, University of California School of Medicine, Davis, and Veterans Administration Hospital, 150 Muir Road, Martinez, California 94553. Address reprint requests to K. Bill at Veterans Hospital. 2 5ection of Gastroenterology. Department of Medicine, University of California, Davis. and Veterans Administration Hospital, Martinez. California 94553.
Am J Roentgenol
© 1978 American
130 :67-70, January 1978 Roentgen Ray Society
67
0361 -803X/78/01
00-0067
$02.00
68
BILL
AND
BELBER
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.
.;.
Fig. 1 . -Case 1 . A, Early filling of gangrenous gallbladder and penicholecystic abscess with multiple filling defects produced by debris and stones. Note intact gallbladder wall at neck (arrow). B, Delayed film showing filling of large abscess cavity. C, Lateral view of abscess. D, Study 14 months later showing abnormally shaped gallbladder with stricture and large stone. (Fig. lA reprinted with permission from Belber JP: Endoscopic retrograde cholangiopancreatography (ERCP) and the skinny needle, in Gastrointestinal Disease, 2d ed, edited by Sleisenger MH, Fordtran JS, Philadelphia,
Saunders, 1978) aphasia. tract
Intermittent
infection
and
fever was attributed he was
treated
with
to an ampicillin.
E.
co/i The
urinary patient
was transferred to the Martinez Veterans Administration Hospital 2 weeks later. Physical examination revealed an alert male
with a right hemiplegia and motor aphasia. The abdomen was soft, nontender, and without guarding or palpable masses. Temperature was 39.4#{176}C;white blood cell count, 38,300 with
90% polymorphonuclear
leukocytes;
serum
bilirubin,
1.2
mg/
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GANGRENE
Fig. 2.-Case 2. Gangrenous gallbladder filled with and stones. Note narrowing of common hepatic duct.
AND
PERFORATION
necrotic
debris
dl; SGOT, 92 mU/mI; and alkaline phosphatase, 311 mU/mI (normal 85). The patient was given 1 g Ancef and 1 .7 mg/kg qentamycin every 6 hr. Because of the probability that sepsis was due to -
biliary
tract
disease,
intravenous
cholangiography
was
per-
formed. No portion of the biliary tree was visualized. Endoscopic retrograde cholangiography demonstrated a slightly dilated common bile duct which was free of calculi or other evidence of obstruction. The cystic duct was patent. Contrast material freely entered the gallbladder, demonstrating irregular calculi and inflammatory debris. The outline of the gallbladder was irregular and shaggy (fig. 3). Contrast medium flowed from the gallbladder into a penicholecystic abscess cavity. The pancreatic duct was normal. At laparotomy a perforated gangrenous gallbladder and subhepatic abscess were found. Calculi and necrotic debris were present in the pus. A cholecystectomy was performed and a Ttube was placed in the common duct. The postoperative course was satisfactory. Discussion
Gangrene and perforation of the gallbladder, serious complications of acute cholecystitis, are associated with a higher mortality than uncomplicated cholecystitis. While a great majority of these patients have cholelithiasis, a few cases with acalculous disease have been reported. In the pathogenesis of gangrenous cholecystitis due to cholelithiasis, it is felt that obstruction of the cystic duct, either by edema on stone, is the initial abnormality [1-3]. Increasing distention and inflammation of the gallbladder result. Compression of the blood supply leads to ischemia, necrosis, and perforation. It is noteworthy that although cystic duct obstruction by calculus was initially responsible for the development of gangrene and perforation in our patients, the duct was still patent
OF
69
GALLBLADDER
Fig. 3.-Case 3. Gangrenous gallbladder filled with Multiple sites of perforation are also shown.
debris
and stones.
enough for the gallbladder to fill during endoscopic retrograde cholangiography. In acalculous disease, gangrene may not be related to cystic duct obstruction. Ischemia caused by vascular disease, bacterial invasion, and chemical inflammation have been suggested as the major etiologic factors. Rarely, cystic duct obstruction by neoplasm may be the underlying process. During the early stages of gangrene the outline of the gallbladder wall may appear normal. If necrosis progresses, however, the mucosa becomes edematous and thickened and ultimately sloughs into the lumen. Opacification of the gallbladder reveals a shaggy outline of the wall and irregular filling defects in the lumen representing necrotic debris. Calculi may be present as well. If gangrene progresses to perforation, the contrast matenial may leak beyond the gallbladder wall and outline penicholecystic abscess cavities. Noninvasive methods, including diagnostic ultrasound, CT, or gallium scanning, can indicate the presence of a mass or suggest the possibility of an abscess; however, they do not give the anatomic detail obtainable by good contrast radiographic studies. Oral cholecystography or intravenous cholangiography are not helpful in distinguishing gangrene and perforation from simple acute cholecystitis, primarily because the gallbladder usually does not visualize adequately in such cincumstances [4]. In all three of our patients, the biliary tract was not opacified by intravenous cholangiography. lsch et al. [3] reported nonvisualization by oral or intravenous study in 10 of 12 patients with gallbladder perforation. One of the other patients showed opaque stones and one was normal. Cystic duct obstruction, a common feature of acute cholecystitis with cholelithiasis, is
70
thoughtto
BILL
be the
reason
for
nonfilling
ofthe
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on oral on intravenous studies [5]. However, cases the duct was sufficiently patent during retrograde cholangiography to allow filling bladder by retrograde injection.
gallbladder
in our three endoscopic of the gall-
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WG, BakerJH, and perforation
AND
Cheema MH: ColIecof the gallbladder,
BELBER
!ntAbstrSurg
2. Monfin
114:1-7,
E, Ponka
Arch
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lsch
JH,
1962
JL, Brush
96:567-573, Finneran
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BE: Gangrenous
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1968 JC,
Nahrwold
DL: Perforation 55:451-458, 1971 LO, Olsson 0: Cholecystography gallstone disease. Acta Chir
of
the
J Gastroentero!
4. Edlund Y, Lanner and cholegraphy in Scand 120:366-375, 1961 5. Weens HS, Clements JL Jr: The radiologic diagnosis of acute cholecystitis. Semin Roentgenol 11:245-247, 1976