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Background and Aim: The aim of this study is to evaluate the epidemiology and impact of bacterial infections at admission in patients with acute decompensation (AD) of cirrhosis., Methods: A cohort with AD of cirrhosis (European Association for the Study of the Liver criteria) admitted at a tertiary center was evaluated between 2013 and 2014 for the presence of bacterial infections at admission. Clinical, demographic, and microbiological data were collected prospectively till death, transplant, or 90 days., Results: Of 179 patients with AD, 102 (56.9%) had bacterial infections at admission. The commonest infections were spontaneous bacterial peritonitis (SBP) (n = 65; 63.7%), spontaneous bacteremia (n = 10; 9.8%), pneumonia (n = 9; 8.8%), urinary tract infection (n = 8; 7.8%), spontaneous bacterial empyema (n = 4; 3.9%), and cellulitis (n = 2; 1.9%). The commonest source was community acquired (n = 85; 83.3%). Serum albumin and sodium levels were lower in infected as compared with non-infected cohort (P = 0.015; for both). Escherichia coli was the commonest organism isolated from SBP (n = 14; 21.5%), urinary tract infection (n = 5; 45.5%), and bacteremia (n = 3; 20%). There was a trend toward higher 28-day mortality in infected cohort as compared with non-infected cohort (48 [52.7%] vs 28 [32%]; P = 0.152). Multidrug-resistant organisms (MDROs) were isolated in 63% of all culture-positive infections. The presence of MDRO was an independent predictor of 28-day mortality., Conclusions: Infections are the leading reason for the occurrence of AD; SBP is the most common infection, and E. coli is the commonest microorganism based on this single-center study of Indian patients with AD of cirrhosis. There is a high prevalence of MDROs among culture-positive infections that independently predict 28-day mortality in AD of cirrhosis., (© 2019 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.)

Background and Aim: Systemic inflammatory response syndrome (SIRS) is an early marker of sepsis and ongoing inflammation and has been reported in large proportion of acute-on-chronic liver failure (ACLF) patients. Whether sepsis is the cause or the result of liver failure is unclear and is vital to know. To address this, the study investigated the course and outcome of ACLF patients without SIRS/sepsis., Methods: Consecutive ACLF patients were monitored for the development of SIRS/sepsis and associated complications and followed till 90 days, liver transplant or death., Results: Of 561 patients, 201 (35.8%) had no SIRS and 360 (64.2%) had SIRS with or without infection. New onset SIRS and sepsis developed in 74.6% and 8% respectively in a median of 7 (range 4-15) days, at a rate of 11% per day. The cumulative incidence of new SIRS was 29%, 92.8%, and 100% by days 4, 7, and 15. Liver failure, that is, bilirubin > 12 mg/dL (odds ratio [OR] = 2.5 [95% confidence interval {CI} = 1.05-6.19], P = 0.04) at days 0 and 4, and renal failure at day 4 (OR = 6.74 [95%CI = 1.50-13.29], P = 0.01), independently predicted new onset SIRS. Absence of SIRS in the first week was associated with reduced incidence of organ failure (20% vs 39.4%, P = 0.003), as was the 28-day (17.6% vs 36%, P = 0.02) and 90-day (27.5% vs 51%,P = 0.002) mortality. The 90-day mortality was 61.6% in the total cohort and that for those having no SIRS and SIRS at presentation were 42.8% and 65%, respectively (P < 0.001)., Conclusion: Liver failure predicts the development of SIRS. New onset SIRS in the first week is an important determinant of early sepsis, organ failure, and survival. Prompt interventions in this 'golden window' before development of sepsis may improve the outcome of ACLF., (© 2017 Journal of Gastroenterology and Hepatology Foundation and John Wiley & Sons Australia, Ltd.)

Hepatic encephalopathy (HE) is a major complication that develops in some form and at some stage in a majority of patients with liver cirrhosis. Overt HE occurs in approximately 30-45% of cirrhotic patients. Minimal HE (MHE), the mildest form of HE, is characterized by subtle motor and cognitive deficits and impairs health-related quality of life. The Indian National Association for Study of the Liver (INASL) set up a Working Party on MHE in 2008 with a mandate to develop consensus guidelines on various aspects of MHE relevant to clinical practice. Questions related to the definition of MHE, its prevalence, diagnosis, clinical characteristics, pathogenesis, natural history and treatment were addressed by the members of the Working Party.

Background: There are conflicting data on the prevalence of colorectal adenomas in patients with acromegaly. It has been suggested that the risk of colorectal adenomas may be dependent on the geographic and ethnic origin of the patients., Materials: Sixty consecutive patients with active acromegaly due to somatotropinoma underwent colonoscopy prior to definitive surgery. They included 35 men and 25 women with a mean (+/- SD) age of 37.4 +/- 13.2 years and a lag time between symptomatology and diagnosis of acromegaly of 64.6 +/- 58.0 months. The control group included 160 patients (88 men, 72 women; mean age, 38.2 +/- 14.0 years) with a diagnosis of irritable bowel syndrome who were also subjected to colonoscopy. None of these patients had previous or family history of colonic neoplasm, bleeding or colonic surgery., Results: Colonoscopic examination was complete to the cecum in 52 patients (88%), and to the splenic flexure in the remaining 12%. In the control group, it was complete to the cecum in 144 patients (90%). Four of the acromegalic patients (6.7%) and five in the control group (3.1%; P=0.24) had hyperplastic polyps. No patient in either of the groups had adenomatous polyps or colonic adenocarcinoma. The group of acromegalic patients with and without polyps did not differ significantly in age, duration of disease, growth hormone levels or glycemic status. The number of skin tags, however, was significantly higher (P=0.04) in the polyp group as compared to those without polyps., Conclusion: The present study has failed to demonstrate the high prevalence rate of colonic neoplasia in patients with acromegaly as compared to reports from the Western world., (Copyright 2004 Blackwell Publishing Asia Pty Ltd)

Background and Aims: Neuropathy in association with chronic liver disease, including cirrhosis, is recognized; however, there are differences in the incidence and type of neuropathy reported. The causal relationship of liver disease to neuropathy has been questioned. This study was designed to evaluate the incidence and character of peripheral neuropathy in patients with liver cirrhosis. The effect of alcohol consumption, severity of liver disease and encephalopathy on the incidence and severity of neuropathy were also studied., Methods: Patients having an identifiable cause of peripheral neuropathy, except alcohol, were excluded from the study. Patients with evidence of vitamin B12 deficiency or diabetes were also excluded from the study. In this study, 33 patients with liver cirrhosis were evaluated clinically and electrophysiologically to detect any evidence of peripheral neuropathy. Nerve conduction studies were performed in the upper and lower limbs using surface electrodes. These patients also underwent a detailed clinical examination., Results: Clinical signs of peripheral neuropathy were found in seven (21%) patients. Nerve conduction studies were abnormal in 24 (73%) patients. The pattern of involvement was predominantly of an axonal sensory motor polyneuropathy. Neuropathy was found both in patients with alcohol-related and non-alcohol-related cirrhosis. The presence of encephalopathy did not have a significant bearing on the incidence and severity of neuropathy. The neuropathy was also not significantly related to the severity of liver disease., Conclusions: The present study reveals that a significant number of patients with liver cirrhosis show evidence of peripheral neuropathy, which is present regardless of the etiology of cirrhosis, and is subclinical in a majority of these patients. The cause of neuropathy was probably the liver disease itself, as the incidence and severity of neuropathy in the alcohol-related cirrhosis, although higher, was not significantly different from the neuropathy in patients with non-alcohol-related cirrhosis.

Background and Aims: Gallbladder motor function is impaired in many patients with diabetes, and may be related to cholinergic nerve damage. Cisapride is a prokinetic drug of the gastrointestinal tract and acts by releasing acetylcholine from cholinergic nerve endings. The aim of this study was to determine the effect of cisapride on gallbladder emptying in patients with type 2 diabetes mellitus (DM)., Methods: Gallbladder emptying and tests for autonomic neuropathy (AN) were performed in 27 patients with type 2 DM and in 10 healthy subjects. Gallbladder emptying was studied by using real-time ultrasonography after an overnight fast, and after the subjects received a breakfast that contained 2500 J. Gallbladder emptying was repeated after the treatment with cisapride (10 mg t.i.d.) for 1 week in all subjects., Results: Abnormal gallbladder emptying was present in 14 (51.9%) patients. The residual gallbladder volume (mean +/- SEM) was higher (9.3 +/- 1.0 vs 4.6 +/- 0.6; P = 0.002), and ejection fraction was lower (57.4 +/- 4.0 vs 74.2 +/- 2.4; P = 0.015) in diabetic patients than it was in healthy subjects. Cisapride produced a reduction in fasting and residual volumes (24.6 +/- 2.4 vs 20.0 +/- 1.4; P = 0.034 and 9.3 +/- 1.0 vs 5.9 +/- 1.1; P = 0.00003, respectively), and an improvement in ejection fraction (57.4 +/- 4.0 vs 72.6 +/- 3.8; P = 0.000007). The improvement in gallbladder emptying after cisapride therapy was confined to the patients with AN (n = 13) (57.3 +/- 5.4 vs 80.4 +/- 2.9; P = 0.0017), suggesting denervation supersensitivity with an upregulation of cholinergic receptors. There was no significant change in the ejection fraction in patients without AN (57.5 +/- 6.1 vs 65.4 +/- 6.5; P = NS). Sex, duration of diabetes, peripheral neuropathy, diabetic retinopathy and serum cholesterol level did not influence gallbladder emptying., Conclusion: Impaired gallbladder emptying is common in patients with type 2 DM. Cisapride significantly improves gallbladder emptying in patients with autonomic neuropathy.

Background: Hepatic venous outflow obstruction (Budd-Chiari syndrome) is frequently encountered as a cause of portal hypertension at our centre., Methods and Results: We studied the clinical presentation, therapeutic modalities and outcome of 71 patients with hepatic venous outflow obstruction between 1992 and 1997. Twenty-seven patients presented with acute disease, while 44 had chronic presentation. Abdominal pain, distension, jaundice and upper gastrointestinal bleeding were the commonest presenting symptoms. The majority of patients had distended veins, hepatomegaly, splenomegaly, ascites and ankle oedema. The diagnosis was made on the basis of inferior vena cavography/functional hepatography and pulsed Doppler ultrasonography and/or liver biopsy in 39 patients and pulsed Doppler ultrasonography and/or liver biopsy in 32 patients. Pulsed Doppler ultrasonography accurately detected the site of the block in 31 of 39 patients (79.4%). The obstruction was in the hepatic vein in 20 patients, in the inferior vena cava in 10, and in both in 41 patients. Aetiologically, four had pregnancy-related disease, four tumour-related, three hypercoagulable states, 18 inferior vena cava membranes and 42 were idiopathic. Of 30 patients in whom liver biopsy was carried out, eight had centrizonal congestion and necrosis, 13 had mixed features and nine had established cirrhosis. Seven patients underwent a shunt operation and surgical membranotomy was carried out in one. Three patients (4.2%) died in the hospital., Conclusions: Hepatic venous outflow obstruction is a common problem; patients present with abdominal pain, distension, jaundice, distended veins, ascites and ankle oedema. Chronic presentation is more frequent. Pulsed Doppler ultrasound, venography and liver biopsy are very helpful in diagnosis.

Background: Endoscopic dilatation is the first line of treatment for benign oesophageal strictures. There are limited data available on the use of Celestin dilators., Methods: The efficacy and safety of Celestin dilators was evaluated retrospectively in 61 patients with benign oesophageal strictures. Three hundred and ninety-three dilatations using Celestin dilators were performed over a period of 10 years on an outpatient basis in patients with corrosive, peptic and other causes of benign oesophageal strictures., Results: Initial success was achieved in all patients in the peptic and miscellaneous group and in 91% in the corrosive group of patients. Patients with corrosive strictures required significantly more dilatations for initial success compared with the peptic group (mean 5.82 vs 1.62 P < 0.1). At 6 months follow up after the initial success, 29% of the patients had an excellent response, 56% a good response and 15% a fair response. No patient had a poor response. During the long-term follow up of 10 years, overall dilatation requirement decreased significantly. (72 vs 27 vs 14% of patients requiring dilatation at 1, 5 and 10 years P < 0.05). The dilatation requirement also decreased significantly within the groups (P < 0.05). Patients with corrosive stricture required more frequent dilatations on follow up compared with the other two groups. Complications in the form of oesophageal perforation occurred in only two patients. There was no mortality., Conclusion: Oesophageal dilatation with Celestin dilators is an effective and safe modality for managing patients with benign oesophageal strictures.

Shunt surgery is considered to be the treatment of choice in patients with non-cirrhotic portal hypertension. There is little data on the effect of side-to-side lieno-renal (SSLR) shunt on oesophageal variceal size, splenic size and splenic pulp pressure (SPP) in patents with non-cirrhotic portal hypertension. We evaluated pre- and postoperatively endoscopic grading of varices, splenic size and SPP for predicting shunt patency in 86 patients with non-cirrhotic portal hypertension: 56 with extrahepatic portal venous obstruction (EHPVO) and 30 with non-cirrhotic portal fibrosis (NCPF). The EHPVO patients with patent shunts (n = 47) showed significant reduction in SPP (pre-operative 43.56 +/- 7.9 vs postoperative 29.96 +/- 0.5 vs 0.92 +/- 0.8). Patients with blocked shunt (n = 9) did not show significant reduction in SPP and varices grades. However, there was reduction in spleen size (8.6 +/- 3.0 vs 6.3 +/- 4.3). In the NCPF group, 28 had patent shunts and showed significant reduction in SPP (46.3 +/- 13.5 vs 33.8 +/- 7.6 cm of saline), splenic size (9.1 +/- 3.3 vs 6.8 +/- 4.6 cm below costal margin) and varices grades (2.8 +/- 0.7 vs 1.05 +/- 0.96). As only two patients with NCPF had blocked shunts, no statistical comparison between patients with patent and patients with blocked shunts could be done. In conclusion, following SSLR, there is a significant reduction in SPP and varices grades in patients with patent shunts. Endoscopic grading of varices can be used to predict shunt patency. However, spleen size is not a good criteria for predicting shunt patency.

Evoked responses have not been studied in patients with acute severe hepatitis (ASH) with or without hepatic encephalopathy. This prospective study was undertaken to find out diagnostic as well as prognostic value of visual evoked responses (VER), and brain stem auditory evoked responses (BAER) in patients with ASH with or without encephalopathy. Visual evoked responses and BAER were studied in 20 patients (14 males and six females) with ASH. The patients were diagnosed as having severe hepatitis if acute hepatitis was associated with raised serum bilirubin and serum transaminases, and if they had a prothrombin time index of < 50%. After a detailed neuropsychiatric examination of each patient, the study sample was divided into two groups of 10 patients: ASH without encephalopathy (ASH-WOE), and ASH with encephalopathy (fulminant hepatic failure, FHF). The median P100 latencies of FHF patients were significantly increased compared with controls and patients in the ASH-WOE group. Abnormal P100 latencies, exceeding 95th percentile values of the controls, were present in one patient in the ASH-WOE group and six patients in the FHF group. The median interpeak latencies I-III, III-V and I-V were significantly prolonged in the FHF group. Interpeak latencies III-V were also increased significantly in patients in the ASH-WOE group. While abnormal BAER were seen frequently in both groups, VER abnormalities were largely confined to patients in the FHF group. In the FHF group, six out of 10 patients survived and exhibited clinical improvement in the status of hepatic encephalopathy. Evoked responses were repeated after 2-3 weeks of recovery in these patients and VER abnormalities showed a tendency to normalize, thereby suggesting a prognostic implication. The incidence of abnormal VER in hepatic encephalopathy complicating ASH far exceeded that of abnormal BAER. Markedly prolonged P100 latencies in FHF patients indicate poor prognosis.

Primary sclerosing cholangitis (PSC) is considered to be rare in India. The aim of the present study was to investigate the incidence, clinical profile and outcome of PSC seen in a tertiary care centre. Over a period of 10 years (July, 1984-June, 1994) 18 patients of PSC were diagnosed at cholangiography (14 patients by endoscopic retrograde cholangiopancreatography, two patients by percutaneous transhepatic cholangiography and two patients by both methods). The presence of secondary causes, such as choledocholithiasis, biliary tract surgery, congenital biliary tract anomalies, cholangiocarcinoma and pancreatic diseases, were excluded. These patients were evaluated retrospectively with respect to their clinical presentation, radiological findings, presence of associated idiopathic ulcerative colitis (IUC), treatment instituted and outcome. The mean (+/- s.d.) age at diagnosis of PSC was 39.0 (+/- 16.1) years with a male:female ratio of 1.57:1. Nine (50%) patients had associated IUC. The diagnosis of the IUC preceded that of PSC in all but one case. Fifteen (83.3%) patients had cholestatic jaundice at presentation, while three (16.7%) patients had asymptomatic rise of alkaline phosphatase. Three (16.7%) patients had recurrent cholangitis and five (27.8%) patients developed portal hypertension during the course of the disease. At cholangiography, intrahepatic radicles were involved in all and extrahepatic radicles in 12 (66.6%) cases. Patients were managed with steroids (n = 7), colchicine (n = 3), ursodeoxycholic acid (UDCA; n = 2) and methotrexate (n = 1), along with symptomatic measures. Mean duration of follow up available in 11 (61%) patients was 20.1 months (range: 1 month-8 years). Four (36.4%) patients died. Steroids and colchicine did not have any effect while the one patient on UDCA and one on methotrexate showed improvement. In conclusion, in India PSC does not seem to be a rare entity. Its clinical profile and outcome are somewhat similar to those seen in Western countries.

Hepatic venous outflow tract obstruction, Budd-Chiari syndrome (BCS), leads to portal hypertension and to the development of collaterals that bypass the obstruction. Described here is a BCS patient with an unusually large transdiaphragmatic collateral between the left hepatic and left innominate veins, which decompressed the oesophageal varices. This has not been reported earlier in the literature.

Percutaneous liver biopsy with Menghini or Trucut needle as an outpatient procedure was performed on 159 patients over a 3.5-year period. No major complications were observed. Liver biopsy is recommended as an outpatient procedure, which would reduce the patient load on limited hospital beds and economize on the hospital resources.

Thirty-eight children, aged 1-15 years, with portal hypertension and recent variceal bleeding, were treated with repeated endoscopic sclerotherapy. Thirty-six of them had extrahepatic portal venous obstruction. Obliteration of varices was achieved in 35 (92%) patients requiring an average of 5.3 sessions per patient. Major complications occurred in seven patients, three of whom had oesophageal perforations and four had oesophageal stricture. Sclerotherapy significantly reduced the rate of rebleeding after the start of sclerotherapy and more so after variceal obliteration.

Patients with chronic hepatic encephalopathy have been shown to have low serum zinc levels. Moreover, in a controlled study, significant improvement was seen in these patients on oral zinc supplementation. Information on zinc status in fulminant hepatic failure is insufficient. Serum and urinary zinc abnormalities were studied in 22 patients with fulminant hepatic failure (FHF) and they were compared with age- and sex-matched controls. The mean serum zinc values were significantly less in patients with FHF (72.7 +/- 3.7 micrograms/100 mL versus 107.9 +/- 6.2 micrograms/mL) while the urinary zinc values were significantly higher compared with controls (603.5 +/- 9.3 micrograms/24 h versus 334.4 +/- 10 micrograms/24 h). The serum zinc levels significantly and progressively decreased, while urinary zinc significantly increased after admission in patients with FHF. The serum zinc values in the group that survived were significantly higher than those in the group of patients who died. Correspondingly, urinary zinc was lower in survivors than in the group that expired. This study indicates that serum and urinary zinc levels could be used as a prognostic indicator in FHF. A therapeutic trial with zinc supplementation is justified in this group of patients.

Large natural/spontaneous shunts on splenoportovenography were demonstrated in 10 of 93 patients with non-cirrhotic portal fibrosis. There was significantly less bleeding in patients with spontaneous shunt than in those having no shunt. Large oesophageal varices (grade III-IV) were seen more frequently in patients without spontaneous shunt.