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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Confrontation of the clinical, radiologic and morphologic data in a lot of 274 patients operated for non-lithiasic cholecystopathies during the 1966-1972 period, led to the following conclusions: - the painful choleic syndrome whose duration and frequency increase progressively, refractory to the conservative treatment, is a basic criterion in establishing the surgical treatment; - any change in the radiologic image of the gallbladder, especially those evoking a partial or totally inefficient contractile effort are of diagnostic value, suggesting the necessity of the operation, when confirmed by a similar clinical context; - the morphologic substrate consists in inflammatory lesions (infiltrations, atrophy of the mucosa, sclerosis), or degenerative lesions (cholecystoses) due to the reaction of the gallbladder walls to the irritative-chemical action of the bile hyperconcentrated by intermittent stasis caused by an incomplete cystic obstacle; - both types of lesions may determine with time obstruction of the cystic duct (acute cholecystitis), changes in the choledochoduodenal confluence (odditis), co-affection of the pancreas and liver (cholecystopancreatitis, chronic reactive hepatitis); - the late results lend support to the surgical treatment in such circumstances.
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PMID:[Radioclinical and morphological comparisons in non-lithiasic gallbladder diseases]. 12 8

Liver biopsy was done at the time of operation in 125 consecutive upper abdominal procedures to assess the incidence of unsuspected or undiagnosed hepatic abnormalities. Specifically excluded were hepatic lesions unexpectedly identified at laparotomy. Sixty-seven percent of the liver biopsy specimens were abnormal, the most frequent findings being fatty metamorphosis, cholestasis, triaditis, fibrosis, inflammatory infiltrate, cholangitis, cirrhosis, and hepatitis. The most frequent operation performed was cholecystectomy. In 63 patients with chronic cholecystitis, there was a 51% incidence of abnormal liver histology, while in nine patients with acute cholecystitis, the incidence was 78%. In 83% of all other operations, abnormal liver biopsy specimens were identified. Bile leakage, hemorrhage, and infection did not occur in this series, despite inclusion of patients with severe biliary obstruction, abnormal clotting factors, and intra-abdominal sepsis. New techniques of histochemical enzyme analysis and electron microscopy are expected to enhance the clinical correlation of occult hepatic lesions. We conclude that liver biopsy in a safe, informative adjunct to all upper abdominal procedures.
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PMID:'Routine' liver biopsy in upper abdominal surgery. 88 45

The authors studied the data concerning 101 patients who had undergone erroneous laparotomy for suspected acute surgical disease; these accounted for 0.4% of all the patients who were operated on for emergency indications in the same period. Eleven patients died. The operation was undertaken for an erroneous diagnosis of acute appendicitis (32 patients), acute cholecystitis (18), perforating gastric ulcer (15), peritonitis of unknown etiology (14), acute intestinal obstruction (5), strangulated hernia (3), destructive pancreatitis (3), tumor of the large intestine complicated by obstruction (3), abdominal abscess (2), thrombosis of the mesenteric vessels (1), ovarian apoplexy (1), closed abdominal trauma with injury to the viscera (4 patients). Diseases simulating the clinical picture of "acute abdomen" but not requiring an emergency operation were as follows: female reproductive (20 patients), pancreatic (11), renal diseases (11), hepatitis, cirrhosis of the liver (10), cardiovascular (9), pulmonary diseases (5), mesoadenitis (5), Crohn's disease (3), chronic colitis (3), carcinomatosis of the peritoneum (3), herpes zoster (3), and other diseases and injuries (20 patients). The main causes of the diagnostic and tactical errors were objective difficulties in the differential diagnosis due to similar symptomatology, as well as errors in the examination of the patient and haste in making a decision to make an operation.
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PMID:[Erroneous laparotomy in emergency surgery]. 177 33

Cholecystagogue cholescintigraphy can be employed as a means of (1) confirming the surgeon's and/or gastroenterologist's clinical impression of symptomatic chronic acalculous biliary disease, (2) better understanding the pathophysiology of gallbladder disease, (3) preparing patients for hepatobiliary scintigraphy who have fasted for longer than 24-48 hours and who are suspected of acute cholecystitis, and (4) reducing the time required to confirm the clinical impression of acute cholecystitis. Morphine-augmented cholescintigraphy is also used to decrease the time required to determine cystic duct patency. Phenobarbital-augmented cholescintigraphy is used as a means of increasing the accuracy of hepatobiliary scintigraphy in differentiating neonatal hepatitis from biliary atresia. Nonpharmacological interventions and augmentations have been employed to maintain the high degree of accuracy of cholescintigraphy in confirming the clinical impression of acute cholecystitis. The efficacy of these modalities in detecting acute and chronic disorders of the hepatobiliary tree as well as how and why they are performed comprise the contents of this article.
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PMID:Augmented cholescintigraphy: its role in detecting acute and chronic disorders of the hepatobiliary tree. 186 48

Ultrasound examinations of 563 patients with right upper quadrant pain and a clinical suspicion of acute cholecystitis were reviewed. In 31 patients, a tender, dilated gall-bladder with a thick (more than 4 mm) partly hypoechoic wall without any detectable calculi was found on the emergency examination. This was interpreted as due to acute acalculous cholecystitis. None of the patients was critically ill. Twenty-one of the patients had follow-up studies with either oral cholecystography, cholangiography, or ultrasound. Fourteen of the 21 had gall-bladder calculi while seven did not. These seven patients presumably represent the true frequency (1.2%) of acute acalculous cholecystitis in this clinical setting. In five other patients with an initial diagnosis of acute acalculous cholecystitis the gall-bladder wall thickening probably was secondary to concomitant pancreatitis, appendicitis, hepatitis or peptic ulcer disease. A meticulous and careful search for gall-bladder calculi should be performed in the presence of a dilated, tender thick-walled gall-bladder.
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PMID:The clinical importance of a thick-walled, tender gall-bladder without stones on ultrasonography. 187 51

Sonographic identification of thickening of the gallbladder wall that consists of multiple striations (alternate hypoechoic and hyperechoic layers) has been considered strong evidence of the presence of acute cholecystitis. We studied 27 patients in whom sonograms showed striated thickening of the gallbladder wall to determine the diagnostic significance of this finding. Striations were classified as focal or diffuse. Sonograms were correlated with pathologic findings in 16 patients and with clinical diagnoses and laboratory findings in 11. Patients were categorized as having cholecystitis with or without gangrene or edema of the gallbladder wall unrelated to gallbladder disease. Striated thickening of the gallbladder wall was due to cholecystitis in 10 patients, and all 10 had gangrenous changes at surgery or at pathologic examination. Striations were focal in eight of these patients and diffuse in two. Striated thickening of the gallbladder wall was due to edema of the wall unrelated to gallbladder disease in 17 patients. Causes included congestive heart failure (n = 4), renal failure (n = 5), liver disease (hepatic failure [n = 1], hepatitis [n = 6]), ascites (n = 2), hypoalbuminemia (n = 3), pancreatitis (n = 1), blockage of the lymphatic/venous drainage of the gallbladder (n = 2), and prominent Rokitansky-Aschoff sinuses (n = 1). More than one abnormality was present in five patients. Striations were focal in 11 of these patients and diffuse in six. The sonographic finding of striated gallbladder wall thickening is no more specific for cholecystitis than the observation of gallbladder wall thickening by itself, and it may occur in a variety of diseases. However, in the clinical setting of acute cholecystitis, the presence of striations suggests gangrenous changes in the gallbladder. The extent of the striations (focal or diffuse) is not useful in predicting the cause of the striated gallbladder wall thickening.
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PMID:Sonography of the gallbladder: significance of striated (layered) thickening of the gallbladder wall. 201 56

We report a retrospective series of 20 cases of peri-hepatitis diagnosed using the laparoscope. They were all young women who were nulliparous or primiparous. In eight cases, the dominant clinical picture was of acute cholecystitis. In the other cases, asymptomatic peri-hepatitis was discovered when the laparoscope had been used to try to diagnose acute salpingitis. Chlamydia trachomatis is the principal aetiological agent (in 18 cases) and it has overtaken the gonococcus which was the common one in early publications but here was responsible for only one case. Treatment with tetracyclines or quinolones always brings about a cure. Whenever a young woman complains of pain in the right hypochondrium, one has to think of this infection as well as diagnosing and treating the associated salpingitis early.
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PMID:[Chlamydia trachomatis perihepatitis (Fitz Hugh-Curtis syndrome). Apropos of 20 cases]. 214 4

Ultrasonography has a primary role in the imaging of biliary disease. Most cases are straightforward, but the authors emphasize unusual manifestations, uncommon diseases, and artifacts that may present diagnostic challenges. Issues in differential diagnosis are discussed for the following findings: internal gallbladder echoes (calculi vs tumefactive sludge, air, hematobilia, parasitic infestation, cholecystosis, neoplasia, and artifacts), gallbladder wall thickening (acute cholecystitis vs acalculous cholecystitis, artifacts, ascites, hypoalbuminemia, hepatitis, and sclerosing cholangitis), pericholecystic fluid (cholecystitis vs ascites, perforated ulcer, and trauma), bile duct dilatation (biliary obstruction vs sclerosing cholangitis, biliary air, anomalous portal system, biliary atresia, Caroli disease, and cholangiocarcinoma), perinatal and neonatal biliary disease, and sclerosing cholangitis.
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PMID:Pitfalls and differential diagnosis in biliary sonography. 218 99

Alterations of the gallbladder wall is a well known sonographic sign of acute cholecystitis. But thickening of the gallbladder wall is also found in patients without intrinsic gallbladder disease. We present our experience on this regard in patients with cirrhosis, acute viral hepatitis, infectious mononucleosis, halothane hepatitis, fulminant hepatic failure, malaria due to plasmodium falciparum, heart failure, severe malnutrition due to gastric obstruction, septicemia, pyogenic hepatic abscess, amoebic hepatic abscess and in a 14 years old patient with fracture of the skull-acute anemia-shock. Most of these diseases affected the liver directly or indirectly. Knowledge of these alterations of the gallbladder wall in these circumstances are important in order to avoid a the erroneous diagnosis of acute cholecystitis.
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PMID:[Ultrasonographic changes in the gallbladder wall in non-gallbladder diseases]. 253 57

An investigation of specific course of the disease in 911 patients operated upon for acute cholecystitis with bilirubinemia has shown that mechanical jaundice resulting from choledocholithiasis takes place in a third of the patients. Obstruction of the bile duct was confirmed in 27.1% of the patients during cholangiography. Prevalence of a number of factors was noted indicating of a toxic lesion of the liver (destructive forms of acute cholecystitis in 81.0% of the patients, higher level of bilirubinemia in long terms of the disease, the presence of coexistent pancreatitis in 30.5%, cholangitis--in 39.3%). An investigation of 207 bioptates of the liver in acute cholecystitis has revealed fatty degeneration of hepatocytes in 56.5%, pericholangitis--in 43.0%, cholestasis--in 21.3% of the cases. The cause of jaundice in acute cholecystitis mainly is an alteration of the hepatic cells due to pyo-resorptive intoxication manifested as cholestasis and hepatitis.
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PMID:[Pathogenesis of jaundice in acute cholecystitis]. 259 23


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