Læknablaðið - 15.10.1986, Qupperneq 39

LÆKNABLAÐIÐ
265
hættu og hafa sjúkdóminn ávallt i huga ef þeir
hafa einkenni frá kviðarholi, brengluð lifrarpróf
eða hita.
í ljósi þess hversu algeng alvarleg slys eru hér á
landi miðað við nágrannalöndin, má búast við
vaxandi fjölda þessara tilfella á næstu árum ef sú
þróun heldur áfram, sem átt hefur sér siað hins
síðari ár.
SUMMARY
Acute acalculous cholecystitis. Six case histories.
This article reviews acute acalculous cholecystitis (AAC)
which has been an increasing entity the last decades.
This is a hazardous disease which usually developes in
critically ill patients, suffering from massive trauma,
burns, major operations etc. The best diagnostic
procedures are believed to be ultrasonography and
cholescintigraphy and the only effective treatment is
surgical (cholecystectomy and cholecystostomy).
Six cases, which were diagnosed at the Reykjavik City
Hospital during a six year period (1980-1986) are
presented here.
The first case was a 70 years old male who developed
AAC 30 days after beginning cytostatic therapy for
histiocytic lymphoma. At operation he was found to
have perforation of the gallbladder and was septic. No
gallstones were found. He never made full recovery and
died a month later.
The second case was a 44 years old male who developed
AAC 23 days after an operation of a stab wound of the
abdomen. The diagnosis was confirmed at operation
and he made a good recovery after cholecystostomy
(and cholecystectomy 6 weeks later). No gallstones were
found.
The third case was a 72 years old male who developed
AAC after an operation for ileus and made good
recovery after cholecystectomy.
The fourth case was a 25 years old male who was
admitted in shock, suffering from a massive shotgun
wound of the abdomen. The patient’s conditions
stabilized after multiple blood transfusions and surgical
repair of the wound, but a few days Iater he developed
acute renal failure which was treated by hemodialysis.
He was also treated by hyperalimentation. A month
later he developed signs of acute cholecystitis and
diagnosis of AAC was confirmed at operation. He made
good recovery after cholecystectomy.
The fifth case was a 43 years old male admitted 10 days
after a coronary bypass operation. At the beginning of
the operation he had an attack of ventricular fibrillation
and was suspected afterwards of having developed a
myocardial infarction during or after the operation. The
following days he had low grade fever and was suspected
to have Dressler’s syndrome. His condition did not get
any better and 20 days after the operation he had
developed signs of cholecystitis. The diagnosis of AAC
was conftrmed at operation and the patient recovered.
The sixth case was a 64 years old male admitted after
being run down by a car. He was found to have a
fracture of the pelvis and fractures of both knees. He
was confused but his conditions was otherwise stable.
No abnormalities were found in the abdomen or in the
thorax. His mental conditions got worse and he
developed acute renal failure. In the third week he
became septic and developed signs of acute abdomen.
The diagnosis of AAC was confirmed at operation. The
patient recovered.
The causes of this disease are unknown but it is believed
that the fundamental change is vascular damage in the
gallbladder wall through a factor XII dependent
pathway. Why the gallbladder is affected is unknown,
but this vascular damage in conjunction with
dehydration, fasting and narcotic analgesics could be
detrimental to the gallbladder. Narcotic analgesics cause
spasms of the sphinter of Oddi and prolonged fasting
and dehydration cause thickening of the gallbladder
contents, both delaying emtying of the gallbladder.
Today no preventible factors are known. It is therefore
necessary to follow critically ill patients closely and
always have this disease in mind if fever or signs from
the abdomen arise.