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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patients with liver cirrhosis undergoing gastrointestinal surgery still suffer from high operative morbid-mortality despite advancements in surgical critical care. The objective of this study is to see if this same relationship applies to patients undergoing esophagectomy for cancer. From 1993 to 2003, sixteen esophageal cancer patients with liver cirrhosis were operated on. They were all male with a mean age of 51.5 years. According to the Child-Pugh classification, 10 patients were Child 'A', 4 patients Child 'B' and Child 'C' in 2 patients. The surgical procedure was through an Ivor-Lewis esophagogastrectomy with intra-thoracic anastomosis. Major morbidity included: 4 respiratory failure, 2 acute renal failure, 3 pneumonia, and one in each of the patients with gastrointestinal bleeding and hepatic failure. The mean follow up among the survivors was 19.1 months. The hospital mortality was 25% (4/16). Using the rate according to Child classification, the mortality rates were: A: 1/10 (10%), B: 2/4 (50%) and C: 2/2 (100%). We conclude that patients with liver cirrhosis in Child-Pugh A could tolerate esophagectomy with an acceptable risk. However, patients with a more advanced state of liver dysfunction are at higher risk for esophagogastrectomy. Careful patient selection and meticulous peri-operative care is warranted in those embarking on surgical resection.
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PMID:Is it safe to perform esophagectomy in esophageal cancer patients combined with liver cirrhosis? 1767 Apr 48

Congenital disorders of glycosylation are a recently recognized group of inherited, multisystem disorders caused by aberrant biosynthesis of glycoproteins. We report the clinical and postmortem findings in a 3-year-old boy with a history of multiple medical issues including developmental delay, epilepsy, chronic protein-losing enteropathy, respiratory failure, nephropathy, coagulopathy, and cardiomyopathy. As part of the workup, isoelectric focusing for congenital disorders of glycosylation showed carbohydrate-deficient transferrin with the mono-oligo/dioligo ratio of 0.700 (normal, 0.075-0.109), indicating an increased level of abnormally glycosylated transferrin. After supportive care, he died secondary to multisystem complications of his disease. General autopsy findings were notable for micronodular liver cirrhosis with iron overload, myocardial ischemia and calcification, and hypertrophied glomeruli. Examination of the brain revealed cerebral and cerebellar atrophy, diffuse astrogliosis, and meningeal fibrosis. This article reveals complete autopsy findings of untyped congenital disorders of glycosylation, congenital disorders of glycosylation-x, with an undefined metabolic basis.
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PMID:Congenital disorder of glycosylation-X: clinicopathologic study of an autopsy case with distinct neuropathologic features. 1795 8

Alpha-1-antitrypsin deficiency (AAT) is one of the three most common lethal genetic diseases in the caucasian population (together with cystic fibrosis and Down syndrome). Its primary manifestation is early-onset panacinar emphysema. Slowly progressive dyspnea is the primary symptom, although some patients initially have symptoms of cough, sputum production, or wheezing. A minority of patients develops hepatic cirrhosis. We present a case of a 40 year-old male, light smoker, with chronic obstructive lung disease with predominance of panacinar emphysema, with AAT deficiency (72 mg/dl; normal values = 200-300 mg/dl) complicated with cor pulmonale and chronic respiratory failure. The main clinical consequence of AAT deficiency is the early onset of panacinar emphysema, typically more severe at the lung bases. Smoking plays an important part in the natural history of the disease, both increasing the severity and decreasing the age at onset of emphysema.
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PMID:A rare case of pulmonary emphysema. 1838 23

Patients with chronic liver disease exhibit various cardiovascular and pulmonary complications. Hepatopulmonary syndrome results in dyspnea due to intrapulmonary arteriovenous shunting and ventilation-perfusion mismatch. Portopulmonary hypertension occurs in patients with portal hypertension. Intrathoracic portosystemic collateral vascular pathways develop in patients with portal hypertension to allow decompression of the portal vein into the systemic circulation. Hepatic hydrothorax may develop in patients with cirrhosis and ascites. Massive necrosis of the liver from any cause may be associated with acute hypoxic respiratory failure, necessitating ventilatory support. Bacterial infection is common in cirrhotic patients because of a compromised host defense system. Hepatocellular carcinoma may produce hematogenous lung metastases, intrathoracic lymph node metastases, direct intracardiac extension, and pulmonary embolism. Interferon therapy for treatment of chronic active hepatitis C may disturb cellular immune activation in some patients and contribute to the onset and progression of sarcoidosis. Awareness of the various thoracic manifestations in chronic liver disease can be helpful for making a differential diagnosis and planning proper management.
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PMID:Thoracic complications of liver cirrhosis: radiologic findings. 1944 18

A 55-year-old male patient with hepatitis B-related liver cirrhosis was found to have advanced hepatocellular carcinoma. His AFP was initially 9828 microg/L and rapidly dropped to 5597 microg/L in ten days after oral sorafenib treatment. However, he developed acute renal failure, hyperkalemia, and hyperuricemia 30 d after receiving the sorafenib treatment. Tumor lysis syndrome was suspected and intensive hemodialysis was performed. Despite intensive hemodialysis and other supportive therapy, he developed multiple organ failure (liver, renal, and respiratory failure) and metabolic acidosis. The patient expired 13 d after admission.
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PMID:Sorafenib induced tumor lysis syndrome in an advanced hepatocellular carcinoma patient. 1976 4

Sepsis is physiologically viewed as a proinflammatory and procoagulant response to invading pathogens. There are three recognized stages in the inflammatory response with progressively increased risk of end-organ failure and death: sepsis, severe sepsis, and septic shock. Patients with cirrhosis are prone to develop sepsis, sepsis-induced organ failure, and death. There is evidence that in cirrhosis, sepsis is accompanied by a markedly imbalanced cytokine response ("cytokine storm"), which converts responses that are normally beneficial for fighting infections into excessive, damaging inflammation. Molecular mechanisms for this excessive proinflammatory response are poorly understood. In patients with cirrhosis and severe sepsis, high production of proinflammatory cytokines seems to play a role in the worsening of liver function and the development of organ/system failures such as shock, renal failure, acute lung injury or acute respiratory distress syndrome, coagulopathy, or hepatic encephalopathy. In addition, these patients may have sepsis-induced hyperglycemia, defective arginine-vasopressin secretion, adrenal insufficiency, or compartmental syndrome. In patients with cirrhosis and spontaneous bacterial peritonitis (SBP), early use of antibiotics and intravenous albumin administration decreases the risk for developing renal failure and improves survival. There are no randomized studies that have been specifically performed in patients with cirrhosis and severe sepsis to evaluate treatments that have been shown to improve outcome in patients without cirrhosis who have severe sepsis or septic shock. These treatments include recombinant human activated C protein and protective-ventilation strategy for respiratory failure. Other treatments should be evaluated in the cirrhotic population with severe sepsis including the early use of antibiotics in "non-SBP" infections, vasopressor therapy, hydrocortisone, renal-replacement therapy and liver support systems, and selective decontamination of the digestive tract or oropharynx.
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PMID:Severe sepsis in cirrhosis. 2037 75

The authors present a study on rates and management of complications of gastric carcinoma surgeries. During a five-year period, a total of 149 patients with gastric carcinomas were operated in the Ist Surgical Clinic (Charles University Faculty Hospital). Radical resections were performed in 121 subjects. In 7 subjects, upper pole resections were performed. 21 subjects underwent paliative therapy or surgical exploration. In the authors' study group, no serious perioperative complications were recorded. The following postoperative complications were observed: fistulas in esophagojejunal anastomosis (8x), duodenal stub fistula (lx), subphrenic abscess (2x), adhesive ileus (1x). In two subjects, esophagojejunal stricture was diagnosed during the late postoperative period. Incisional hernia was diagnosed in two subjects. Two subjects exited- the first one from respiratory failure with ARDS syndrome in esophagojejunal dehiscence, the second subject died of hepatorenal failure in liver cirrhosis. Complications cannot be excluded in any surgical procedure. Should they occur, their timely diagnosis and adequate treatment is required.
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PMID:[Gastric carcinoma--rates and management of surgical treatment complications]. 2051 13

Surgical treatment in hepatocellular carcinoma patients with cardiac involvement is challenging, and its prognosis remains unclear because of its rarity. A 48-year-old male hepatocellular carcinoma patient presented with right atrial involvement through the inferior vena cava and a left atrial mass, which nearly occluded the mitral valve, and extended from a pulmonary metastasis. Emergent surgery was performed due to sudden severe respiratory failure despite profound liver cirrhosis (Child-Pugh class B). Nevertheless, the patients postoperative course was uneventful, and over six months of follow-up, he has shown no remarkable symptoms and has maintained a tolerable liver function.
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PMID:Left atrial metastasis from hepatocellular carcinoma with liver cirrhosis. 2073 26

The patient was a terminally ill 80-year-old man with multiple lung metastases from hepatocellular carcinoma, that had developed following hepatitis-C virus-associated cirrhosis. He was admitted to our hospital with gingival bleeding, and we diagnosed gingival metastasis from hepatocellular carcinoma, based on histological examination. The bleeding could not be controlled, and the patient became dyspneic. After transcatheter arterial embolization, his bleeding was successfully controlled until his death due to respiratory failure. Transcatheter arterial embolization was a safe and effective treatment in our case.
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PMID:A case of hepatocellular carcinoma with bleeding gingival metastasis treated by transcatheter arterial embolization. 2121

Advanced liver disease is associated with hypoxemia and respiratory failure by various mechanisms. Patients with cirrhosis are especially prone to episodes of decompensation requiring intensive care unit admission and management. Such patients may already be in acute liver failure or have decompensated due to a concurrent illness such as spontaneous bacterial peritonitis, sepsis, encephalopathy, varices, or hepatorenal syndrome. Acute respiratory distress syndrome is one of the main reasons for intensive care unit admission and mortality. Overall, critically ill cirrhotic patients frequently progress to multiorgan failure requiring mechanical ventilation. Caring for such patients is therefore understandably complex and extremely challenging. Patients with end-stage liver disease are especially at risk for developing acute respiratory failure and hypoxemia secondary to hepatopulmonary syndrome, portopulmonary hypertension, and hepatic hydrothorax. They should therefore be screened for these conditions because failure to recognize and adequately treat these serious complications of cirrhosis may have devastating consequences. This article is based on a review of the current literature on how to approach and manage acute respiratory failure in advanced liver disease, which is important to intensivists, anesthesiologists, and physicians as a whole.
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PMID:Acute respiratory failure complicating advanced liver disease. 2244 64


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