the first report on laparoscopic cholecystectomy was published in 1985 . nowadays , it is the procedure of choice for removing the gallbladder . the most frequent complications are bile - duct trauma and bleeding . including procedures for acute cholecystitis , the rate of postoperative hemorrhage is below 1% . in particular , patients with liver cirrhosis are at risk . most frequently , the cystic artery , epigastric vessels , and the gallbladder bed were vulnerated . however , few data exist on the incidence of and reasons for bleeding from the gallbladder bed of the liver . therefore , we give an account of 2 patients who experienced a laparoscopic cholecystectomy and died from a seeping hemorrhage . we also disclose risk factors for continuous postoperative bleeding discerned by autopsy and histological examinations . at age 46 , the patient suffered from renal insufficiency requiring dialysis , diabetes type i , hypertension , and cholecystolithiasis . mobilization of the gallbladder from the gallbladder bed of the liver was unproblematic , and an argon laser was used for coagulation . six hours after the operation , the patient 's blood pressure reached 80/50 mm hg , the patient produced cold sweat , and the wound dressing was blood - soaked . the patient was transferred to the intensive care unit , and postoperative circulatory insufficiency was the tentative diagnosis . a man age 65 had undergone aortic valve replacement and suffered from diabetes mellitus type ii and hypertension . the concrements were confirmed by endoscopic retrograde cholangiography . a papillotomy was performed and the bile duct concrements extracted . the gallbladder was inflamed , and adhesions hampered the identification of the cystic duct and cystic artery . hemostasis by electrocoagulation in the gallbladder bed of the liver was also difficult , and styptic stripes were put on the liver surface . in the 16-hour period after the operation , the patient 's blood pressure remained in the normal range , but the pulse rate increased to 120 beats / minute . nineteen hours after the operation , the patient had to be resuscitated , and he died an hour later amid the clinical picture of myocardial infarction and heart failure . paraffin - embedded specimens of liver , spleen , pancreas , kidney , and heart were cut into 4-m to 5-m sections and stained with hematoxylin - eosin ( he ) , masson goldner , elastica van gieson , phosphotungstic acid hematoxylin ( ptah ) , and fat red 7b . at age 46 , the patient suffered from renal insufficiency requiring dialysis , diabetes type i , hypertension , and cholecystolithiasis . mobilization of the gallbladder from the gallbladder bed of the liver was unproblematic , and an argon laser was used for coagulation . six hours after the operation , the patient 's blood pressure reached 80/50 mm hg , the patient produced cold sweat , and the wound dressing was blood - soaked . the patient was transferred to the intensive care unit , and postoperative circulatory insufficiency was the tentative diagnosis . a man age 65 had undergone aortic valve replacement and suffered from diabetes mellitus type ii and hypertension . the gallbladder was inflamed , and adhesions hampered the identification of the cystic duct and cystic artery . hemostasis by electrocoagulation in the gallbladder bed of the liver was also difficult , and styptic stripes were put on the liver surface . in the 16-hour period after the operation , the patient 's blood pressure remained in the normal range , but the pulse rate increased to 120 beats / minute . nineteen hours after the operation , the patient had to be resuscitated , and he died an hour later amid the clinical picture of myocardial infarction and heart failure . paraffin - embedded specimens of liver , spleen , pancreas , kidney , and heart were cut into 4-m to 5-m sections and stained with hematoxylin - eosin ( he ) , masson goldner , elastica van gieson , phosphotungstic acid hematoxylin ( ptah ) , and fat red 7b . the closure of the cystic artery as well as the cystic bile duct was correct . further findings were sparse postmortem lividity , subendocardial bleeding of the left ventricle , cardiac hypertrophy ( 530 grams ) , anemic inner organs , atrophic kidney and pancreas , and medium grade arteriosclerosis . the abdominal cavity contained 1.1 liters of predominantly coagulated blood , especially below the liver . further findings were minor bleeding into the liver tissue adjacent to the gallbladder bed , local necrosis , and fatty liver degeneration ( figure 1 ) . in addition , anemia of the inner organs , chronic pulmonary emphysema , cardiac hypertrophy ( 650 grams ) , unsuspicious artificial aortic valves , medium - grade coronary sclerosis , and zones of scarred myocardium including fresh necrosis in the left ventricle were present . these demonstrated marked vacuolization , decomposition , and intense shrinkage of the liver parenchyma with development of nonnucleated cell necrosis , zones of palisade - like alignment of cell nuclei , siderotic necrosis , blood congestion , and focal tiny bleeding in the adjacent liver tissue ( figure 2 ) . liver ( case 1 ) : vacuolic decomposition of the peripheral liver parenchyma ( center of the figure ) with transition to nonnucleated cell necrosis , which is a sign of thermal injury . the liver had intense siderosis of stellate cells , little siderosis of the parenchyma , and focal necrosis of the parenchyma . vasogenic atrophy and diffuse and nodular diabetic glomerulosclerosis were found in the kidney . the heart had little perivascular and interstitial fibrosis . the gallbladder bed was callous , and the local fatty tissue was infiltrated by granulocytes . some fresh blood , parenchymal necrosis , and some granulocytic reaction were below the liver capsule . focal vacuolization and decomposition was seen in the connective tissue of the liver and the liver parenchyma , in part with palisade - like alignment of the cell nuclei . further findings were focal blood in the vascular walls and blood coated to the liver surface of the gallbladder bed with moderate fibrin - rich zones ( figure 3 ) . zones of old infarction aside fresh ( some hours ) necrosis of muscle fibres were obvious . signs of thermal injury with vacuolic decomposition of the connective tissue of the gallbladder bed of the liver ( right ) and blood imbibed vascular walls ( center ) with increased perfusion . the closure of the cystic artery as well as the cystic bile duct was correct . further findings were sparse postmortem lividity , subendocardial bleeding of the left ventricle , cardiac hypertrophy ( 530 grams ) , anemic inner organs , atrophic kidney and pancreas , and medium grade arteriosclerosis . the abdominal cavity contained 1.1 liters of predominantly coagulated blood , especially below the liver . further findings were minor bleeding into the liver tissue adjacent to the gallbladder bed , local necrosis , and fatty liver degeneration ( figure 1 ) . in addition , anemia of the inner organs , chronic pulmonary emphysema , cardiac hypertrophy ( 650 grams ) , unsuspicious artificial aortic valves , medium - grade coronary sclerosis , and zones of scarred myocardium including fresh necrosis in the left ventricle were present . the closure of the cystic artery as well as the cystic bile duct was correct . further findings were sparse postmortem lividity , subendocardial bleeding of the left ventricle , cardiac hypertrophy ( 530 grams ) , anemic inner organs , atrophic kidney and pancreas , and medium grade arteriosclerosis . the abdominal cavity contained 1.1 liters of predominantly coagulated blood , especially below the liver . further findings were minor bleeding into the liver tissue adjacent to the gallbladder bed , local necrosis , and fatty liver degeneration ( figure 1 ) . in addition , anemia of the inner organs , chronic pulmonary emphysema , cardiac hypertrophy ( 650 grams ) , unsuspicious artificial aortic valves , medium - grade coronary sclerosis , and zones of scarred myocardium including fresh necrosis in the left ventricle were present . these demonstrated marked vacuolization , decomposition , and intense shrinkage of the liver parenchyma with development of nonnucleated cell necrosis , zones of palisade - like alignment of cell nuclei , siderotic necrosis , blood congestion , and focal tiny bleeding in the adjacent liver tissue ( figure 2 ) . liver ( case 1 ) : vacuolic decomposition of the peripheral liver parenchyma ( center of the figure ) with transition to nonnucleated cell necrosis , which is a sign of thermal injury . the liver had intense siderosis of stellate cells , little siderosis of the parenchyma , and focal necrosis of the parenchyma . vasogenic atrophy and diffuse and nodular diabetic glomerulosclerosis were found in the kidney . the heart had little perivascular and interstitial fibrosis . the gallbladder bed was callous , and the local fatty tissue was infiltrated by granulocytes . some fresh blood , parenchymal necrosis , and some granulocytic reaction were below the liver capsule . focal vacuolization and decomposition was seen in the connective tissue of the liver and the liver parenchyma , in part with palisade - like alignment of the cell nuclei . further findings were focal blood in the vascular walls and blood coated to the liver surface of the gallbladder bed with moderate fibrin - rich zones ( figure 3 ) . zones of old infarction aside fresh ( some hours ) necrosis of muscle fibres were obvious . signs of thermal injury with vacuolic decomposition of the connective tissue of the gallbladder bed of the liver ( right ) and blood imbibed vascular walls ( center ) with increased perfusion . these demonstrated marked vacuolization , decomposition , and intense shrinkage of the liver parenchyma with development of nonnucleated cell necrosis , zones of palisade - like alignment of cell nuclei , siderotic necrosis , blood congestion , and focal tiny bleeding in the adjacent liver tissue ( figure 2 ) . liver ( case 1 ) : vacuolic decomposition of the peripheral liver parenchyma ( center of the figure ) with transition to nonnucleated cell necrosis , which is a sign of thermal injury . the liver had intense siderosis of stellate cells , little siderosis of the parenchyma , and focal necrosis of the parenchyma . vasogenic atrophy and diffuse and nodular diabetic glomerulosclerosis were found in the kidney . the heart had little perivascular and interstitial fibrosis . these demonstrated marked vacuolization , decomposition , and intense shrinkage of the liver parenchyma with development of nonnucleated cell necrosis , zones of palisade - like alignment of cell nuclei , siderotic necrosis , blood congestion , and focal tiny bleeding in the adjacent liver tissue ( figure 2 ) . liver ( case 1 ) : vacuolic decomposition of the peripheral liver parenchyma ( center of the figure ) with transition to nonnucleated cell necrosis , which is a sign of thermal injury . the liver had intense siderosis of stellate cells , little siderosis of the parenchyma , and focal necrosis of the parenchyma . vasogenic atrophy and diffuse and nodular diabetic glomerulosclerosis were found in the kidney . the heart had little perivascular and interstitial fibrosis . the gallbladder bed was callous , and the local fatty tissue was infiltrated by granulocytes . some fresh blood , parenchymal necrosis , and some granulocytic reaction were below the liver capsule . focal vacuolization and decomposition was seen in the connective tissue of the liver and the liver parenchyma , in part with palisade - like alignment of the cell nuclei . further findings were focal blood in the vascular walls and blood coated to the liver surface of the gallbladder bed with moderate fibrin - rich zones ( figure 3 ) . zones of old infarction aside fresh ( some hours ) necrosis of muscle fibres were obvious . signs of thermal injury with vacuolic decomposition of the connective tissue of the gallbladder bed of the liver ( right ) and blood imbibed vascular walls ( center ) with increased perfusion . blood with fibrin coats the liver surface ( bottom right ) . the gallbladder bed was callous , and the local fatty tissue was infiltrated by granulocytes . some fresh blood , parenchymal necrosis , and some granulocytic reaction were below the liver capsule . focal vacuolization and decomposition was seen in the connective tissue of the liver and the liver parenchyma , in part with palisade - like alignment of the cell nuclei . further findings were focal blood in the vascular walls and blood coated to the liver surface of the gallbladder bed with moderate fibrin - rich zones ( figure 3 ) . zones of old infarction aside fresh ( some hours ) necrosis of muscle fibres were obvious . signs of thermal injury with vacuolic decomposition of the connective tissue of the gallbladder bed of the liver ( right ) and blood imbibed vascular walls ( center ) with increased perfusion . blood with fibrin coats the liver surface ( bottom right ) . in both cases , the prosecution ordered preliminary proceedings to investigate the reasons for blood oozing . the cases were evaluated on the basis of the external hospital 's charts and the autopsy conducted by the institute of legal medicine , university of hamburg . according to these data , the death of the first patient was caused by bleeding into the abdominal cavity and hemorrhagic shock . the blood in the abdominal cavity of the second patient was not enough to cause circulatory shock . however , the blood loss caused an extracardiac workload and increased the consumption of energy and oxygen . therefore , bleeding was a factor that caused death . the clinical courses and the autopsies in both cases revealed blood oozing from the gallbladder bed . anastomotic branches of the cystic artery to the left or right hepatic artery were reported in 12% . however , none of those vascular anastomoses were found in either case . cystic arteries that lead from the right hepatic artery , run through the most cranial part of calot 's triangle , ascend between the gallbladder and the liver , and encircle the gallbladder with 5 to 7 branches have been identified in 2% of patients . if the trunk of such arteries has not been ligated or identified , the surgeon has to deal with several small branches that have to be closed individually . this involves the risk of missing one or several small branches , which can result in persistent blood oozing . however , the autopsies of the 2 cases presented reveal correct closures of the cystic arteries . liver cirrhosis , consumptive coagulopathy , sepsis , and infection can cause diffuse seeping hemorrhage associated with operative procedures , but those findings were not true for these patients . hemodialysis might be associated with the genesis of siderosis , and this was confirmed in the parenchyma of the liver and spleen of the first patient . in turn , siderosis can cause liver cell necrosis , which was histologically evident . a series of postmortem experiments quantified the heat damage of the liver caused by cautery and laser coagulation . the other was transmission of heat resulting in swelling of parenchyma , damaged cell nuclei , and peliosis - like changes in the liver sinus with loss of the endothelium . in both cases , the inflammatory reaction of acute and subacute cholecystitis can involve the connective tissue next to the gall - bladder bed and cause marked vascularization . those inflammatory alterations as well as fibrosis following chronic or recurrent cholecystitis increase perioperative morbidity . hence , they might be a relative contraindication for laparoscopic procedures and might increase the rate of conversion to conventional cholecystectomy . in the second case , fibrin glue was recommended to stop diffuse blood oozing from the gallbladder bed . in both cases reported herein , the histological examination of the gallbladder bed of the liver revealed alterations increasing the vulnerability of the liver . in the first case , this was true for the siderosis , which was most probably also the reason for the necrosis of the liver parenchyma . in the second case , it was true for the fatty degeneration of the liver . each of the mentioned factors ( fatty liver degeneration , siderosis , alteration caused by chronic and recurrent cholecystitis , thermal injury to the liver parenchyma ) was involved in initiating and perpetuating blood oozing . in the first case , hemorrhage was the sole cause of death . in the second case on the other hand , bleeding and existing heart disease led to death . according to the circumstances of death and autopsy findings , the fatal bleeding derived from the gallbladder bed . the bleeding must have derived from small vessels not detectable by gross or microscopic inspection . the medical experts came to the conclusion that both surgical procedures were lege artis , but the postoperative monitoring was criticized as fragmentary . the experts did not come to the conclusion that the death could have been prevented with forensic certainty even if the required postoperative standards had been adhered to . the charges in both cases were dropped . in our point of view , it is not possible to make any recommendations concerning the frequency and the risk factors . these were the only cases in the last 10 years , and we therefore can not offer any reliable recommendations . an exact preoperative clinical and laboratory examination is essential to decide the correct surgical procedure ( laparoscopic versus conventional surgery ) . thorough surgical dissection in anatomical layers , the use of thermocoagulation , sutures , and clips can control bleeding . local procoagulant drugs ( eg , fibrin glue ) are not routinely used but might be an option . postoperative ultrasound examinations can detect fluid collections in the abdominal cavity , and a test for hemoglobin can detect its decline . therefore , both measures can indicate hemorrhage and can be used as a rationale for an adequate action . in case of lethal postoperative hemorrhage , fatty liver degeneration , siderosis , chronic as well as recurrent cholecystitis , and thermal injury are able to initiate and perpetuate lethal blood oozing .
background and objectives : blood oozing after cholecystectomy is a rare but potentially life - threatening complication . 
 recently , 2 patients died from this cause . 
 the deaths resulted in criminal proceedings and medical experts were called in . 
 the objective of this report is to describe their findings and to elucidate preoperatively unknown risk factors of bleeding.methods:medical records , autopsy , and histological examination of the liver , heart , pancreas , spleen , and kidney pertaining to 2 recent cases of laparoscopic cholecystectomy were examined . 
 current literature on this topic was reviewed.results:preoperative risks included renal insufficiency , diabetes mellitus , and cardiopathy . 
 the histological examination , in particular of the gallbladder bed of the liver , disclosed siderosis , inflammation , and fatty degeneration . 
 these factors supported and perpetuated blood oozing . 
 postoperative ultrasonography and a hemogram might have detected and prevented death.conclusion:inflammatory alterations , siderosis , and fatty degeneration of the liver are risk factors of postoperative hemorrhage . 
 autopsy and histological examination can detect those factors . 
 adequate postsurgical observation is mandatory , especially for patients at risk .