Results of modified Sugiura operation in variceal bleeding in cirrhotic and noncirrhotic patients

BACKGROUND/AIMS: Esophageal variceal bleeding is a major complication of portal hypertension and the optimal therapeutic modality for each individual patient differs. We reviewed the results of modified Sugiura procedure in patients with variceal bleeding of esophagus. METHODOLOGY: We retrospectively reviewed the charts of 13 patients who were subjected to modified Sugiura procedure (transabdominal esophagogastric devascularization + esophageal stapled transection + splenectomy) for bleeding esophageal varices between 1996 and 2001. Three patients disappeared from routine follow-up and were excluded from the study. Survival, rebleeding and encephalopathy were evaluated. RESULTS: The mean age was 46 (18-56). The etiology of portal hypertension was cirrhosis of liver in six (60%) and portal vein thrombosis in four (40%). One patient had Child-Pugh's Class A, two had Class B and three had Class C cirrhosis. Previous variceal bleeding were confirmed by endoscopy in all patients who had recurrent variceal bleeding despite treatment with beta-blockers (three patients) or endoscopic sclerotherapy +/- band ligation (seven patients). Two were subjected to emergency surgery while the remaining eight were operated on electively. No postoperative mortality was seen. The bleeders were stopped immediately in the emergent cases. During a mean follow-up of 27 (4-53) months, one (10%) patient suffered from encephalopathy and one (10%) from rebleeding at 20th and 28th months after the operation respectively. Three (30%) patients with Child C cirrhosis died due to bleeding (one) and hepatic failure (two) at 4, 25, and 28 months after the surgery. The prognoses of other patients are well at the present time. CONCLUSIONS: In our small number of patients, modified Sugiura procedure was found to be a safe and effective procedure for urgent and long-term control of bleeding varices in patients with portal hypertension due to cirrhosis and noncirrhotic etiology. The outcomes are encouraging in noncirrhotic patients and cirrhotic patients with good liver functions.     

Pigment gallstone composition in cirrhotic and noncirrhotic subjects

The composition of pigment gallstones from patients with and without cirrhosis was compared. Carbonate-containing pigment stones were distinguished from noncarbonate stones by infrared spectroscopy. Calcium was the major cation of each stone group. The major anion in noncarbonate pigment stones was bilirubinate or phosphate, but was carbonate in carbonate stones. The composition of pigment stones from cirrhotic and noncirrhotic patients was similar except that significantly less carbonate was present in carbonate stones, and less pigment (bilirubinate) was present in noncarbonate stones from noncirrhotics. These data suggest that irrespective of the presence of cirrhosis, the formation of noncarbonate pigment stones involves the selective precipitation of calcium bilirubinate and phosphate, whereas carbonate stone formation involves the selective precipitation of calcium carbonate.     

Risk factors for the presence of varices in cirrhotic patients without a history of variceal hemorrhage.

BACKGROUND: Current medical management dictates that all cirrhotic patients without a history of variceal hemorrhage undergo endoscopic screening to detect large varices. However, referral for endoscopic screening of only patients at highest risk for varices may be most cost-effective. The aim of this case-control study was to identify clinical, laboratory, and radiologic findings that predict the presence of varices in patients with cirrhosis. METHODS: Three hundred patients without a history of variceal hemorrhage underwent upper endoscopy as part of an evaluation before liver transplantation. Cases defined as the presence of any varices and cases defined as the presence of large varices were used for examining the risks associated with finding varices on upper endoscopy. Logistic regression was performed to evaluate associations between the presence of varices and patient characteristics. RESULTS: Platelet count and Child-Pugh class were independent risk factors for the presence of any varices and the presence of large varices. For the presence of any varices, a platelet count of 90 x 10(3)/microL or less (odds ratio [OR], 2.4; 95% confidence interval [CI], 1.4-4.0) and advanced Child-Pugh class (OR, 3.0; 95% CI, 1.6-5.6) were independent risk factors. For large varices, a platelet count of 80 x 10(3)/microL or less (OR, 2.3; 95% CI, 1.4-3.9) and advanced Child-Pugh class (OR, 2.8; 95% CI, 1.3-5.8) were independent risk factors associated with varices. CONCLUSIONS: Low platelet count and advanced Child-Pugh class were associated with the presence of any varices and with large varices. These factors allow identification of a subgroup of cirrhotic patients who would benefit most from referral for endoscopic screening for varices.     

Ultrastructural changes in cirrhotic and noncirrhotic patients due to hepatectomy

Background/Purpose

Alterations at the ultrastructural level can be identified prior to histological change in the early phase of irreversible cell damage. The aim of this investigation was to compare the ultrastructural changes in cirrhotic and noncirrhotic liver in response to ischemic and reperfusion injury due to hepatectomy.

Methods

Hepatic resections using the same technique were performed in cirrhotic and noncirrhotic patients. Three biopsy specimens (Tru cut) from each patient, in the unresected part of the liver, were studied by transmission electron microscopy: immediately after laparotomy, before releasing of the porta hepatis clamp (ischemic phase), and 30–45?min after reperfusion.

Results

All patients did well after surgery, except for 1 cirrhotic patient who died of liver failure. There were no significant differences in operative time, blood loss, and inflow occlusion times in any of the 15 patients. We found that morphological changes were the same in the 10 non-cirrhotic and 4 cirrhotic patients. Changes during the ischemic phase included nuclear membrane deformity, focal chromatin condensation at the nuclear margin, and swelling of both mitochondria and endoplasmic reticulum. In the reperfusion phase, there were early irreversible changes in the nuclei of some hepatocytes and intramitochondrial particles and increased vacuolization in cytoplasm. Endothelial cells, Kupffer cells, bile canaliculi, and Ito cells were not affected in either the ischemic or the reperfusion phase. However, in the 1 cirrhotic patient who died of liver failure, there were marked swelling and dilated cristae in mitochondria during the ischemic phase and deformity of Ito cells during the reperfusion phase.

Conclusions

In this, the first report of ultrastructural changes due to hepatectomy in cirrhotic patients, we found that the changes were the same as those in non-cirrhotic patients, except for the one cirrhotic patient who had postoperative liver failure.

     

Delayed endoscopy as a risk factor for in-hospital mortality in cirrhotic patients with acute variceal hemorrhage

Background and Aims:  Risk factors for mortality in acute variceal hemorrhage remain incompletely understood. Whether endoscopy timing is associated with risk of mortality has not been investigated. We aimed to investigate risk factors for in-hospital mortality in cirrhotic patients with acute variceal hemorrhage, with emphasis on endoscopy timing.
Methods:  Three hundred and eleven (73% male and 23% female) consecutive cirrhotic patients presenting with acute variceal hemorrhage from July 2004 to July 2007 were investigated. The univariate association of endoscopy timing as the predictor for in-hospital mortality was examined. Independent risk factors for mortality were determined by multivariate logistic regression analysis consisting of clinical, laboratory and endoscopic parameters.
Results:  Twenty-five (8.04%) patients died within admission. By plotting the receiver operating curve of endoscopy timing for mortality, we selected 15 h as the optimal cut-off point to define delayed endoscopy. Multivariate regression analysis revealed that independent risk factors predictive for in-hospital mortality included delayed endoscopy performed 15 h after admission (adjusted odds ratio [aOR] = 3.67; 95% confidence interval [CI], 1.27–10.39), every point increment of model for end-stage liver disease (MELD) score (aOR = 1.16; 95% CI, 1.07–1.25), failure of the first endoscopy (aOR = 4.36; 95% CI, 1.54–12.30) and hematemesis as the chief complaint (compared with melena, aOR = 8.66; 95% CI, 1.06–70.94).
Conclusion:  Delayed endoscopy for more than 15 h, high MELD score, failure of the first endoscopy and hematemesis are independent risk factors for in-hospital mortality in cirrhotic patients with acute variceal hemorrhage.     

Tuberculous peritonitis: a study comparing cirrhotic and noncirrhotic patients

Tuberculous peritonitis is a rare disease, which often goes unrecognized because of the subtle clinical clues and its insidous onset. We retrospectively analyzed the records of 37 cases of tuberculous peritonitis diagnosed over a 15-year period, and compared the clinical and diagnostic features of cirrhotic and noncirrhotic patients. In cirrhotic patients, tuberculous peritonitis can simulate ascites from liver disease or spontaneous bacterial peritonitis. The diagnosis is difficult in these patients because the ascitic fluid may not be of the exudative type as a result of the low albumin level in serum, and lymphocytes do not predominate in all cases. Adenosine deaminase (ADA) activity in ascitic fluid was elevated (higher than 40 U/L) in all 11 patients (four patients with hepatic cirrhosis). The time required to achieve a correct diagnosis was significantly longer in cirrhotic than in noncirrhotic patients. The overall mortality was 13%, with deaths occurring exclusively among cirrhotic patients. We emphasize that tuberculous peritonitis in cirrhotic patients can present an atypical picture. A considerable element of suspicion is necessary.     

Propranolol in the prevention of recurrent variceal hemorrhage in cirrhotic patients. A controlled trial

A double-blind controlled study of long-acting propranolol in the secondary prevention of variceal hemorrhage was conducted in 81 cirrhotic patients. After the index hemorrhage, all patients were treated with injection sclerotherapy on one occasion to secure hemostasis and then randomized within 72 h to propranolol or placebo therapy which was continued for 2 yr. Study endpoints were severe recurrence of variceal hemorrhage or death. Forty-two patients did not fulfill the entry criteria for the study. Thirty-eight patients received propranolol of whom 18 (47%) had further hemorrhage, 14 died, eight had side-effects (2 withdrawals), and 3 did not complete follow-up. Forty-three patients received placebo of whom 33 (77%) had further hemorrhage, 19 died, 5 had side-effects (2 withdrawals), and 5 failed to complete follow-up. The median time from onset of hemorrhage to starting drug therapy was 6 days for both groups. Life table analysis showed an equivalent incidence of further hemorrhage in both groups over the first 60 days, following which the propranolol group did consistently better than the placebo group. There was a significantly lower incidence of rebleeding in modified Child's C patients receiving propranolol (39%) than those on placebo (90%). No statistically significant effect on mortality was seen. In this study, propranolol reduced the incidence of late recurrence of variceal hemorrhage in patients with cirrhosis.     

Thrombelastographic changes and early rebleeding in cirrhotic patients with variceal bleeding

BACKGROUND: Routine coagulation tests do not necessarily reflect haemostasis in vivo in cirrhotic patients, particularly those who have bleeding varices. Thrombelastography (TEG) can provide a global assessment of haemostatic function from initial clot formation to clot dissolution. AIM: To evaluate TEG changes in cirrhotic patients with variceal bleeding and their association with early rebleeding. PATIENTS/METHODS: Twenty cirrhotic patients with active variceal bleeding had serial TEG and routine coagulation tests daily for seven days. The TEG variables before the day of rebleeding (n = 6) were compared with those of patients without rebleeding (n = 14). RESULTS: Baseline characteristics of the rebleeding and non-rebleeding groups were comparable apart from a higher incidence of uncontrolled infection on the day of rebleeding in the rebleeding group (p = 0.007). The patients in the rebleeding group were more hypocoagulable before the day of rebleeding as shown by longer r (42 v 24 mm, p < 0.001) and k (48 v 13 mm, p < 0.001) and smaller a (12 v 38 degrees, p < 0.001) compared with the mean of daily results of the non-rebleeding group. Routine coagulation tests, however, showed no significant differences between the two groups. CONCLUSION: The results of serial TEG measurements suggest that hypocoagulability may be associated with early rebleeding in cirrhotic patients.     

Role of prophylactic antibiotics in cirrhotic patients with variceal bleeding

Bacterial infections are common in cirrhotic patients with acute variceal bleeding,occurring in 20%within48 h.Outcomes including early rebleeding and failure to control bleeding are strongly associated with bacterial infection.However,mortality from variceal bleeding is largely determined by the severity of liver disease.Besides a higher Child-Pugh score,patients with hepatocellular carcinoma are particularly susceptible to infections.Despite several hypotheses that include increased use of instruments,greater risk of aspiration pneumonia and higher bacterial translocation,it remains debatable whether variceal bleeding results in infection or vice versa but studies suggest that antibiotic prophylaxis prior to endoscopy and up to 8 h is useful in reducing bacteremia and spontaneous bacterial peritonitis.Aerobic gram negative bacilli of enteric origin are most commonly isolated from cultures,but more recently,gram positives and quinolone-resistant organisms are increasingly seen,even though their clinical significance is unclear.Fluoroquinolones(including ciprofloxacin and norfloxacin)used for short term(7 d)have the most robust evidence and are recommended in most expert guidelines.Short term intravenous cephalosporin(especially ceftriaxone),given in a hospital setting with prevalent quinolone-resistant organisms,has been shown in studies to be beneficial,particularly in high risk patients with advanced cirrhosis.     

Plasma catecholamines in patients with presinusoidal portal hypertension: comparison with cirrhotic patients and nonportal hypertensive subjects

During a hemodynamic study, plasma catecholamine concentrations were measured in the pulmonary artery and in the hepatic vein in 18 presinusoidal portal hypertensive patients. Results were compared with those in 15 nonportal hypertensive subjects and in 24 cirrhotic patients in good condition (grade A, according to Pugh's classification). Plasma norepinephrine concentrations in the pulmonary artery or in the hepatic vein were not significantly different between nonportal hypertensive subjects (mean +/- S.E.M.: 271 +/- 36 and 83 +/- 11 pg/ml, respectively) and presinusoidal portal hypertensive patients (273 +/- 33 and 84 +/- 11 pg/ml, respectively). These concentrations were, however, elevated in cirrhotic patients (408 +/- 47 and 256 +/- 45 pg/ml, p less than 0.05 in comparison with the two other groups). These differences suggest that increased sympathetic nervous activity in cirrhosis is associated with the presence of liver disease or increase in sinusoidal pressure. Differences in plasma epinephrine concentrations were not significant among the three groups of patients. However, the existence of a significant correlation between pulmonary artery plasma epinephrine concentration and cardiac index (r2 = 0.46, p less than 0.01) in patients with presinusoidal portal hypertension suggests that the adrenal medulla could play a role in the pathophysiology of the hyperkinetic syndrome of these patients.     

The prevalence and spectrum of colonic lesions in patients with cirrhotic and noncirrhotic portal hypertension

Portal hypertension diffusely affects the gastrointestinal tract. The frequency and profile of distinct colonic mucosal lesions (portal colopathy) and rectal varices (RV; veins >4 cm above the anal verge) is not well studied. Fifty consecutive patients with portal hypertension (25 with cirrhosis, 10 with noncirrhotic portal fibrosis [NCpf], and 15 with extrahepatic portal vein obstruction [EHPVO]) were assessed clinically and by upper and lower gastrointestinal (GI) endoscopy. Colorectal lesions were seen in 35 (70%) patients, significantly more often in bleeders than in nonbleeders. Rectal varices were detected in 22 (44%) patients; larger and more often seen in EHPVO (80%) than in cirrhosis (28%) and NCPF (30%) (P < .01) patients. Portal colopathy was seen in 26 (52%) patients, with nearly similar frequency in cirrhotics, NCPF, and EHPVO patients. Previous sclerotherapy or presence of gastric varices had little influence on the development of these lesions. An association (P < .01) was, however, seen between the presence of colopathy and portal gastropathy. Overt bleeding was seen in 8% and 4% of patients with RV and colopathy, respectively. In conclusion, our results demonstrate that colorectal lesions are present in about two thirds of patients with portal hypertension. Patients with portal hypertension and lower GI bleeding should be colonoscoped. Patients with extrahepatic portal vein obstruction may in turn benefit from baseline sigmoidoscopic examination to define the presence and size of rectal varices.     

Diabetes mellitus is associated with gastroesophageal variceal bleeding in cirrhotic patients

Diabetes mellitus (DM) has been reported to increase the risk of complications of liver cirrhosis of any etiology and subsequent survival. However, the impact of DM on the development of gastroesophageal variceal bleeding (GEVB) remains unclear. We aimed to elucidate whether DM is an independent risk factor for GEVB among cirrhotic patients. A total of 146 consecutive patients with liver cirrhosis (Child-Pugh Class A, n = 75; Class B, n = 40; and Class C, n = 31) were prospectively enrolled. Data on clinical and biochemical characteristics and history of ascites, GEVB, hepatic encephalopathy, and spontaneous bacterial peritonitis were retrospectively reviewed. Of these 146 patients, 37 (25%) had DM. Patients with DM had significantly higher ratio of Child-Pugh Class B/C (p = 0.043), renal insufficiency (p = 0.002), and history of GEVB (p = 0.006) compared with non-DM patients. GEVB was associated with Child-Pugh Class B/C (p = 0.001), ascites (p = 0.002), hepatic encephalopathy (p = 0.023), and low platelet counts (p < 0.001). Based on stepwise multiple logistic regression analysis, Child-Pugh class B/C [odds ratio (OR) = 4.90, p = 0.003] and DM (OR = 2.99, p = 0.022) were identified as independent predictors of GEVB. In the subgroup analysis, DM significantly correlated with GEVB in patients with Child-Pugh Class A (p = 0.042), but not in patients with Child-Pugh Class B/C (p = 0.128). DM is independently associated with GEVB in cirrhotic patients, especially in those with Child-Pugh Class A.     

食管曲张静脉压力是预测肝硬化曲张静脉破裂出血的主要危险因素

目的:前瞻性研究影响肝硬化食管曲张静脉破裂出血的主要危险因素.方法:随访未发生过食管曲张静脉出血的57例肝硬化患者1年.采用内镜下无创性食管曲张静脉气囊测压仪检测曲张静脉压,研究终点为出现食管曲张静脉出血.研究食管曲张静脉内镜下表现、食管曲张静脉压力、肝功能分级、肝硬化病因及腹水指标与食管曲张静脉破裂出血的关系.结果:1年内34例(59.6%)患者发生首次食管曲张静脉破裂出血.单因素分析显示,食管曲张静脉压力(P=0.001)、曲张静脉直径(P=0.006)、内镜下红色征(P=0.012)与出血风险有关.进一步的多因素Logistic回归分析显示,食管曲张静脉压力是预测首次出血最主要的危险因子(OR=2.817,P=0.003),其受试者工作曲线(ROC)下面积为0.98.预测出血的食管曲张静脉压力截值为25.3 mm Hg(1 mm Hg=0.133 kPa),其敏感性与特异性均为91%.结论:食管曲张静脉压力是预测食管曲张静脉破裂出血的主要危险因素.     

Beta blocker prophylaxis for patients with variceal hemorrhage

GOALS: To characterize beta blocker therapy for the primary and secondary prevention of variceal hemorrhage. BACKGROUND: Variceal hemorrhage is one of the more frequent and severe complications of portal hypertension due to liver disease. Beta blocker therapy has been demonstrated to decrease risk of first bleed in patients with evidence of varices and recurrent bleeding and mortality in patients with history of prior variceal hemorrhage. STUDY: A total of 106 patients with liver disease hospitalized with suspected variceal hemorrhage were retrospectively reviewed. RESULTS: Half of patients had known varices, 44 (41.5%) of whom had experienced prior variceal hemorrhage. Only 21 (20%) were receiving beta blocker therapy at admission and 41 (48%) at discharge. The majority were not receiving therapy for primary prophylaxis (94%). Specific characteristics associated with beta blocker use could not be identified, although more patients with history of greater than two variceal hemorrhages were receiving beta blocker at admission (73% vs. 41%, P = 0.04) CONCLUSIONS: This study suggests that liver disease patients with varices are often not receiving beta blocker therapy to reduce risk of first or subsequent variceal hemorrhage. Opportunity exists to optimize use of this proven prophylactic treatment and bridge an apparent gap in standard of care.