Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0008325 (cholecystitis)
 3,686 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Evidence of hepatic dysfunction (clinically, chemically, and morphologically) and biliary-tract abnormalities is common in patients receiving TPN. The entity might present as hepatocellular injury (fatty liver, steatonecrosis), intrahepatic cholestasis, acalculous cholecystitis, or cholelithiasis. Infants manifest primarily intrahepatic cholestasis, whereas adults manifest fatty liver early and intrahepatic cholestasis later in the course of therapy. Both groups are at risk for the development of biliary-tract abnormalities. Although most of these changes in the adult are mild and reversible, a small number of patients have recently been reported to develop progressive liver disease. In infants, however, the changes may be more severe, and lead more frequently to progressive liver disease and death. Although this progression to chronic liver disease is worrisome, it is uncertain whether, in patients on long-term therapy, it is due to the TPN or to other conditions or therapies associated with their clinical condition. The pathogenesis of each of these lesions may be multifactorial, including carbohydrate overfeeding, essential-fatty-acid deficiency, amino-acid deficiencies or imbalances, carnitine deficiency, bile-salt toxicity, lipid emulsions, bile-flow reduction, and gallbladder stasis. Therapies in these patients are aimed at alterations in the preceding etiologies (decreased glucose loads, contraction of the gallbladder). Further work is necessary to delineate the exact mechanisms of this entity, especially with regard to the causal relationships of TPN and this entity and to the development of chronic liver disease.
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PMID:Hepatobiliary abnormalities associated with total parenteral nutrition. 250 58

The potential lethality and predisposing factors of acute acalculous cholecystitis (AAC) are well established; however, preoperative diagnosis remains a challenge. This update of a previous report of 30 cases of AAC at a Level I trauma center describes 14 multiply injured patients who developed AAC and underwent cholecystectomy. All 14 patients had acutely inflamed gallbladders; 6 (42.8%) had areas of necrosis or gangrene. The mortality rate was 7% (1 patient). While the percentage of patients receiving prolonged intensive care (100%), narcotic analgesics (100%), and TPN (93%) correlates with the experience cited previously, the percentage undergoing preoperative diagnostic imaging is unusually high, reflecting a heightened suspicion for AAC. Computed tomographic or sonographic evidence of gallbladder wall thickness greater than or equal to 4 mm, pericholecystic fluid or subserosal edema without ascites, intramural gas, or a sloughed mucosal membrane was considered diagnostic criteria for AAC. We conclude that preoperative computed tomogram or ultrasound imaging leads to earlier recognition of this life-threatening problem.
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PMID:Acute acalculous cholecystitis in critically injured patients. Preoperative diagnostic imaging. 266 24

Patients who receive long-term parenteral nutrition have an increased incidence of both calculous and acalculous cholecystitis. In an attempt to establish guidelines for the clinical management of patients with TPN-induced gallbladder disease, we have reviewed the records of 35 patients who have undergone cholecystectomy for this problem since 1976 at the UCLA Medical Center. The mean age of the 23 adult and 12 children who had cholecystectomy was 29.1 years. Forty percent of these patients required emergency cholecystectomy. The overall operative morbidity was 54 percent, and the hospital mortality was 11 percent. Significant factors contributing to this high rate of complications included a delay in diagnosis, especially in the young children, and increased operative difficulty due to extensive adhesions and intraoperative hemorrhage. Our analysis suggests that patients receiving long-term TPN should have a program of ultrasound surveillance for gallstone formation, elective cholecystectomy when stones first appear, and consideration of cholecystectomy at the time of laparotomy performed for other reasons. Whether TPN-induced gallstones can be prevented through daily stimulated gallbladder emptying awaits the results of future studies.
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PMID:Parenteral nutrition-induced gallbladder disease: a reason for early cholecystectomy. 643 Jan 12

Hepatobiliary dysfunctions (TPN-HBD) occur during parenteral nutrition. In older children these are usually reversible whereas in newborns and infants these hepatobiliary abnormalities play a significant role in the morbidity. Cholestasis is a commonly occurring TPN-HBD. It correlates directly with the decreasing gestational age, low birth weight and increasing duration of TPN therapy. The pathogenesis of cholestasis of TPN is multifactorial and predisposed by necrotising enterocolitis, sepsis, cardiac failure, shock, and hypotension. Diagnosis is made with exclusion of other causes of direct hyperbilirubinemia. Most TPN-HBD appear within 4 weeks of starting of TPN but severe complications manifest usually after the 16th week. Histologically there is intralobular cholestasis. In few cases there may be severe portal fibrosis followed by development of micronodular biliary cirrhosis. Enteral starvation, defective bile acid carriers, hypercaloric TPN are the major factors responsible for TPN-HBD, including cholestasis. Biliary complications of TPN-HBD are acalculous, cholecystitis, and cholelithiasis. Bile stasis is a major pathological factor for these. If the calories are provided only by glucose or glucose-containing electrolyte solutions it may lead to cholestasis and other TPN-HBD. Even small oral alimentation (continuous or bolus) during TPN, prevent TPN-HBD. Choleretic agents have been useful in the prevention and management of cholestasis and other parenteral nutrition induced hepatobiliary abnormalities.
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PMID:Hepatobiliary abnormalities and parenteral nutrition. 1102 27

Abnormal LCTs after surgery are common, and consultants are frequently called on to evaluate critically ill patients with abnormal tests. All patients undergoing consideration for elective surgery and a history of either acute or chronic liver disease require careful presurgical evaluation. A thorough history and physical examination, complete blood count, routine electrolytes, LCTs, and a coagulation profile should be ordered. For patients with marginal hepatic reserve, it is important that patient well-being be maximized before any elective operation. The type of surgery to be performed should also be reviewed. All patients with postoperative jaundice should be evaluated for a history of liver disease. The consultant should also review the surgical procedure performed, anesthetic agents administered, other medications used, and whether blood products were given during the perioperative and postoperative periods. The pattern and timing of LCT abnormalities may also give a clue to the underlying disorder. As in the preoperative assessment, a routine complete blood count,electrolyte panel, LCTs, and coagulation profile should be ordered. Unconjugated hyperbilirubinemia can develop as a consequence of blood transfusions, underlying hemolytic disorders, resorbing hematomas, drug effects, or Gilbert's syndrome. A haptoglobin, reticulocyte count, LDH, and Coomb's test should be considered in patients with unconjugated hyperbilirubinemia. Treatment is directed toward the underlying condition. Conjugated hyperbilirubinemia can occur as a result of either intrahepatic or extrahepatic disorders. Markedly abnormal aminotransferases and LDH in conjunction with a normal abdominal ultrasound scan suggest ischemic liver injury, drug-induced hepatitis, or viral infections of the liver. Treatment entails restoration of hepatic perfusion, removal of offending medications, and supportive care or antiviral agents, respectively. Extrahepatic biliary obstruction must be considered in all patients with conjugated hyperbilirubinemia. Abdominal sonography is the best screening test to assess for obstruction. Patients with common bile duct stones usually require ERCP with sphincterotomy and stone removal. Biliary strictures or leaks may require ERCP with balloon dilation of strictures or stent placement for strictures and leaks; percutaneous drainage of bilomas in combination with broad-spectrum antibiotic agents is recommended for patients with bile leaks and large intra-abdominal fluid collections. Surgery may be required for patients with strictures or leaks not amenable to either endoscopic or percutaneous intervention or for patients who have transected bile ducts after laparoscopic cholecystectomy. Medication effects, benign postoperative jaundice, sepsis, TPN, and acalculous cholecystitis are responsible for intrahepatic cholestasis and conjugated hyperbilirubinemia. Treatment includes removal of offending drugs, supportive care, broad-spectrum antibiotic agents with drainage of infected fluid collections, adjustment of TPN, and either cholecystectomy or cholecystostomy, respectively.
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PMID:Postoperative jaundice. 1506 98