Br. J. Surg. Vol. 61 (1974) 960-962
Biliary peritonitis without perforation of the
gallbladder in acute cholecystitis
S . J. S . K E N T A N D N. M E N Z I E S - G O W *
SUMMARY
Six patients with biliary peritonitis occurring as a
complication of acute cholecystitis are reported. Five
of the 6 patients had no detectable perforation of the
gallbladder. The literature of this topic is reviewed and
a theory is put forward to account for biliary peritonitis
without perforation of the gallbladder in acute
cholecystitis.
GENERALIZED
biliary peritonitis occurring as a
complication of acute cholecystitis is rare in this
country and when it occurs it is usually associated
with a perforation of the gallbladder. Essenhigh (1968)
reported an incidence of 5.3 per cent of perforation of
the gallbladder in acute cholecystitis, but only 15 of
his 23 patients had generalized biliary peritonitis.
DAbreu (1933) reported an incidence of 2.8 per cent
of biliary peritonitis in 116 patients with acute
cholecystitis. Fifield (1926) found a 2.5 per cent
incidence of perforation in 1066 patients with acute
cholecystitis and 15 of the 28 perforations were
associated with generalized biliary peritonitis.
This paper reports 6 patients with biliary peritonitis
occurring in 33 consecutive patients with acute
cholecystitis admitted to the Kingston and Longrove
Group of Hospitals between 1 October 1971 and
31 March 1972, an incidence of 18.2 per cent. Five of
these patients did not have any demonstrable perforation of the gallbladder at laparotomy. The histories
and findings in these patients are summarized in
Tables Z and ZZ. The first patient is described in detail.
Case report
Case 1 : M. L., a 59-year-old female, presented with a 2-week
history of colicky epigastric pain, nausea and anorexia. On the
day before admission the pain had become more severe and
localized in the right iliac fossa.
On examination the patient had a pulse of 120jminute and a
blood pressure of 90/60. There was no clinical jaundice. The
abdomen showed generalized tenderness with guarding in the
right iliac fossa. The white cell count was 23 OOO/mm3. X-rays
of her chest and abdomen were normal. A diagnosis of perforated acute appendicitis was made.
At laparotomy there was nearly 1 litre of bilestained intraperitoneal fluid with a distended ischaemic gallbladder containing multiple stones. There was no obvious perforation of
the gallbladder, and a cholecystostomy was performed with
removal of the stones. Culture of the intraperitoneal fluid
grew Escherichia coli.
Postoperative recovery was unremarkable. Six months later
she had an elective cholecystectomy with excellent recovery.
Discussion
The incidence of perforated gallbladder and biliary
peritonitis occurring as a complication of acute
960
cholecystitis appears to be higher in the United States
of America than in Great Britain, for Diffenbaugh
et al. (1949) reported an incidence of 25 per cent and
Edwards et al. (1941) recorded an incidence of 11 per
cent. Essenhigh (1968) reported the highest incidence
in the English literature of 5.3 per cent. It is difficult
to find any reason other than chance for the extremely
high incidence (18.2 per cent) reported in this paper,
which only considers a small number of patients with
acute cholecystitis. As the complication is uncommon
in this country, the failure of correct preoperative
diagnosis in most of our patients is not unexpected.
The notable feature in 5 of our patients was the
occurrence of biliary peritonitis without a macroscopic perforation of the gallbladder. This phenomenon
has been previously described in acute cholecystitis
and other conditions such as trauma and choledocholithiasis (Clairmont and Haberer, 1911 ; Buchanan,
1918; Cope, 1925; Pohlman, 1939; McLaughlin, 1942;
Burkitt, 1946; Ellis and Cronin, 1960; Essenhigh,
1968). There have been reports of biliary peritonitis
occurring without biliary pathology of any kind (Cope,
1925; Ellis and Cronin, 1960).
Many theories have been proposed to explain
leakage of bile without perforation of the biliary tract.
Clairmont and Haberer (1911) suggested that bile
passed through the gallbladder wall by filtration.
Schievelbein (1911) suggested leakage from the glands
of Lushka, while Wolff (1912) suggested leakage from
intrahepatic canaliculi. Cope (1925) thought that a
very small perforation, undetectable at laparotomy,
might allow bile t o leak. He suggested that the hole
became sealed off by fibrin and that the perforation
could be caused by infective or traumatic ulceration
of the gallbladder mucosa. However, Ellis and
Cronin (1960) disproved this theory in relation to
acute cholecystitis by carefully examining the excised
gallbladders of 4 patients with biliary peritonitis without perforation of the gallbladder in acute cholecystitis and finding no evidence of perforation.
Langeron et al. (1953) produced evidence to show
that the gallbladder mucosa acts as the barrier to bile
leakage and that bile seeps into the peritoneal cavity
through an area of mucosal necrosis. The evidence is
convincing but the authors make no comment on the
state of the peritoneum overlying the gallbladder.
Both Cope (1925) and Burkitt (1946) believed that the
* Kingston Hospital.
Present address of S. J. S. Kent: St Thomas’s Hospital, London.
Present address of N. Menzies-Cow: The Middlesex Hospital,
London.
Biliary peritonitis in acute cholecystitis
Table I : PRESENTATION AND PREOPERATIVE DIAGNOSIS
1
Age
(yr)
59
Sex
F
Duration
of illness
2 wk
2
84
M
36 hr
3
94
F
5d
4
78
F
I wk
5
61
F
2d
Generalized peritonism, maximal in
left iliac fossa
Generalized peritonism, jaundice,
mass in right hypochondrium
Generalized peritonism
63
M
3d
Generalized Deritonism
Case
6
*A
Physical signs
Generalized peritonism, maximal
in right iliac fossa
Generalized peritonism
WBC
23 000/mm3
1 5 000/mm3
35 000/mm3
3 OOO/mms
34 000/mm3
14 OOO/mmY
4 000imm3
Preoperative diagnosis
Perforated acute appendicitis
Peritonitis. ? Cause
Perforated diverticulitis
Cholecystitis with biliary
peritonitis
Acute cholecystitis with
biliary peritonitis*
Peritonitis. ? Cause
previous oral cholecystogram had shown gallstones.
Table 11: OPERATIVE FINDINGS, PROCEDURE AND OUTCOME
Case
Findings
Perforation
1
Biliary peritonitis. Distended ischaemic
gallbladder containing gallstones
Biliary peritonitis. Ischaemic gallbladder containing gallstones
Biliary peritonitis. Gallbladder distended and inflamed containing gallstones. Common bile duct dilated
and full of stones
Biliary peritonitis. Distended ischaemic
gallbladder containing gallstones
Biliary peritonitis. Distended ischaemic
gallbladder containing gallstones
Biliary peritonitis. Inflamed gallbladder
containing gallstones
No perforation
2
3
4
5
6
Procedure
Cholecystostomy with
removal of stones
Cholecystostomy with
removal of stones
Cholecystectomy.
Choledocholithotomy
Course
Recovery. Cholecystectomy
6 months later
Died while recovering from
myocardial ischaemia
Septicaemia. Died after
4 days
No perforation
Cholecystostomy with
removal of stones
Cholecystectomy
Died after 4 weeks of
bronchopneumonia
Recovery
Perforation of
1.3 cm in gall-
Cholecystostomy with
removal of stones
Recovery
No perforation
No perforation
No perforation
visceral peritoneum overlying the biliary tract would
act as a barrier to bile, and indeed the importance
given by the majority of present-day surgeons to the
peritoneum in intestinal anastomoses is partly based
on the supposition that the peritoneum is ‘waterproof’.
It is clearly impossible to confirm or refute these
various theories in a retrospective study, but if bile
leaks from the gallbladder either there must be a
perforation or the niucosa and peritoneum must have
become permeable to bile. On the basis of our cases,
we wish to suggest that the ischaemia of these two
layers that occurs in some cases of acute cholecystitis
causes them to become permeable to bile and leads to
bile peritonitis. If the ischaemia causes necrosis of
both the gallbladder mucosa and the overlying
peritoneum, then frank perforation results.
In acute cholecystitis there is an outpouring of
inflammatory exudate from the gallbladder mucosa
into the lumen. If the cystic duct is obstructed the
gallbladder will become distended with inflammatory
exudate. Acute overdistension of any hollow organ
causes impairment of the circulation in its wall. For
example, ischaemic necrosis due to distension by
inflammatory exudate leads to perforation in acute
appendicitis.
In our 5 patients without a demonstrable gallbladder perforation the gallbladder was either
distended, frankly ischaemic or both distended and
ischaemic (Table ZZ). The average age of these patients
was 73 years (range 59-94), a finding which suggests
that ischaemia of the gallbiadder due to distension
72
might have been augmented by either arteriosclerosis
or low cardiac output.
We therefore suggest that the following sequence
of events may lead to leakage of bile into the peritoneal cavity in acute cholecystitis without perforation
of the gallbladder: Cystic duct occluded by stone+
Acute obstructive cholecystitis+Distension of gallbladder by inflammatory exudate4schaemia of gallbladder wall-tGallbladder wall becomes permeable to
bile.
The relief of distension after leakage of bile into the
peritoneal cavity results in an improvement in the
gallbladder circulation and unless the ischaemia has
caused necrosis of both the peritoneum and mucosa,
frank perforation will not occur. It may be argued
that it is difficult to reconcile very large quantities of
bilestained fluid in the peritoneal cavity with leakage
from a gallbladder with an occluded cystic duct. It is
probable that the leaking bile is diluted and increased
in volume by the inflammatory exudate that it
provokes from the peritoneum. Alternatively, if the
occlusion of the cystic duct were only partial or intermittent, fresh bile could periodically enter the gallbladder from the common bile duct.
This theory is open to a possible criticism. There was
no objective evidence that the fluid found in the
peritoneal cavity of the patients described in this paper
contained bile from the gallbladder and it is unfortunate that no samples of intraperitoneal fluid were
taken for analysis. In the 4 patients personally treated
by the present authors the fluid found in the peritoneal
961
S. J. S. Kent and N. Menzies-Gow
cavity was of the same appearance as bile obtained
from the gallbladder when a cholecystostomy was
performed and it is reasonable to suppose that bile
had leaked from the gallbladder. Also in 4 of the 5
patients with no perforation of the gallbladder, there
was no evidence of stones in the common bile duct so
that in these patients it is unlikely that bile had leaked
from an obstructed common bile duct rather than the
gallbladder.
Acknowledgements
We would like to thank Mr L. R. Leask and Mr
W. J. D. Bradfield for allowing us to report their
patients, and Mr B. T. Jackson for his help in the
preparation of this paper.
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