Gall Bladder Wall Thickness As a Marker of Portal Hypertension in Patients of Alcoholic Cirrhosis of Liver
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Gall Bladder Wall Thickness as a Marker of Portal Hypertension ORIGINAL ARTICLE Gall Bladder Wall Thickness as a Marker of Portal Hypertension in Patients of Alcoholic Cirrhosis of Liver Jaya Pathak1, Shivangi Gharia2, Zeal Kishor Thakkar3, Kesar Prajapati4, Darshankumar M Raval5 1Associate Professor and Head of Unit, 2,4Resident, 3,5Intern, Department of Medicine, SSG Hospital and Medical College Baroda ABSTRACT BACKGROUND AND OBJECTIVES: One of the major complications of cirrhosis is the occurrence of Portal Hypertension, which can lead to bleeding from Esophageal Varices, Hepatic Encephalopathy, Ascites, Spontanoeus Bacterial Peritonitis, Hepatorenal Syndrome, Hepatopulmonary Syndrome, etc. Early diagnosis and treatment of Portal hypertension is vital to prevent major complications in Cirrhosis of liver. Portal hypertension causes increase in the hydrostatic pressure causing oedema and congestion of Gallbladder also known as Congestive Cholecystopathy. In this study, we have attempted to find the correlation between presence of portal hypertension and increased diffuse Gallbladder Wall Thickness(GBWT). To study the relationship of Portal Hypertension to Diffuse Gallbladder Wall thickness on ultrasonography in patients of Alcoholic Cirrhosis of Liver, without any intrinsic Gallbladder disease. METHODS: In the present study, 60 patients of Alcoholic Cirrhosis of Liver admitted in the medical wards of SSGH, Baroda were studied. Data was collected regarding the history, physical examination, laboratory and radiological investigations, especially Gallbladder wall thickness and Upper GI Endoscopy. RESULTS: Patients were divided into 2 groups as per the Gall Bladder Wall thickness; Group A with GBWT <4mm, which consisted of 17 patients and Group B with GBWT >4mm, which consisted of 43 patients. Comparison of Serum Albumin levels between the two groups showed. CONCLUSION: In patients of Cirrhosis, increased GBWT correlated well with increased Portal Vein diameter, increased incidence of Ascites and presence of Esophageal Varices. Thus, the presence of GBWT on Ultrasonography in patients of cirrhosis without intrinsic gall bladder disease should be considered as an early sign of Portal Hypertension. Keywords: Alcohol, Gall Bladder Wall Thickness, Cirrhosis, Portal Hypertension INTRODUCTION Cirrhosis is a chronic liver disease, compensated stage is more challenging2. characterized by development of fibrosis. Compensated Cirrhosis may progress and The common causes being Alcohol, has two major consequences, Portal Chronic Hepatitis C and B infection. In the hypertension and Hepatic Failure. Portal past, it has been thought that cirrhosis was Hypertension is defined as the elevation of never reversible; however, it has become the hepatic venous pressure gradient apparent that when the underlying insult (HVPG) to > 5mmHg1.Portal that has caused the cirrhosis has been Hypertension is caused by one, increased removed, there can be reversal of fibrosis hepatic resistance to the passage of blood 1. In the early compensated stage of flow through the liver due to regenerative cirrhosis, patients are usually nodules, and second due to increased asymptomatic. Diagnosis of Cirrhosis is splanchnic blood flow secondary to relatively straightforward during the vasodilation1. Progression of fibrosis decompensated stage when the treatment parallels the increase in portal pressure may be problematic, on the contrary, and, frequently, patients with severe diagnosing Cirrhosis while it is still in fibrosis in the pre-cirrhotic stage have a HVPG>5mmHg2. Portal hypertension is *Corresponding Author: associated with the most severe Dr.Zeal Kishor Thakkar, complications of cirrhosis including Intern, Department of Medicine, Ascites and Varicealhemorrhage. Variceal SSG Hospital and Medical College bleedingis an immediate life-threatening Baroda. problem with a 20-30% mortality rate Email: [email protected] associated with each episode of bleeding. The concept of diagnosis of cirrhosis is 52 Int J Res Med. 2017; 6(4); 52-58 e ISSN:2320-2742 p ISSN: 2320-2734 Gall Bladder Wall Thickness as a Marker of Portal Hypertension changing from the documentation of reflect any changes induced by therapy8. histological fibrosis to the identification of Gall bladder wall thickness found on patients truly at risk of developing ultrasonography can be of two types: complications. HVPG is the most robust Diffuse and Focal. Focal is usually due to predictor of clinical decompensation in intrinsic Gall bladder diseases, while patients with compensated cirrhosis and diffuse is associated with many conditions portal hypertension without varices4. It has without intrinsic gall bladder disease, like been clearly demonstrated that the onset of hypoalbuminemia, Right sided heart clinically significant portal hypertension failure, Cirrhosis of Liver, Chronic Kidney (HVPG>10mmHg) marks the progression Disease. Gall Bladder wall thicknening in to a stage at risk of clinical complications. patients with Cirrhosis is mostly due to It is therefore necessary to diagnose raised hydrostatic pressure of vasculature clinical decompensation in otherwise of Gall bladder wall. Gall bladder wall compensated cirrhosis patients, so that thickening is frequently observed and early treatment can be initiated and frequently reported in association with thereby increasing the chances of reversal portal hypertension9,10. Proper diagnosis of fibrosis. In this scenario, non-invasive and management of complications of PHT methods able to mirror the hemodynamic are vital to improving quality of life and threshold play an important role3.Since a reducing mortality in cirrhotic patients. long time ago, simple blood tests were The present study was undertaken with a used in the diagnosis and prognostication view to determine the correlation of of patients with advanced liver diseases. GBWT with presence of The most largely used is a combination of Hypoalbuminemia, Ascites, Portal Vein markers of liver synthetic Diameter, Upper GI Bleed and presence of functions(albumin, bilirubin and EsophagealVarices. prothrombin time) that, together with two MATERIALS AND METHODS clinical variables ( presence and severity Study sample of ascites and encephalopathy), constitute The present study was conducted at Shri the Child Pugh Score5. HVPG is the best Sayaji General Hospital, Vadodara, a surrogate marker in chronic liver disease; tertiary health care institute, from October however the measurement of HVPG has 2015 to November 2016. This was a cross its limitations, such as its sectional study where we enrolled 60 invasiveness6.Upper GI Endoscopy is patients of Alcoholic Cirrhosis of Liver. recommended for screening of Inclusion Criteria EsophagealVarices, so as to start primary Patients diagnosed as having Alcoholic prophylaxis in patients who are at high risk Cirrhosis of Liver, with age more than 18 of Variceal Bleeding. Upper years Gastrointestinal(GI)Endoscopy , as a Exclusion Criteria screening method for diagnosis of Portal Patients with history of Gall Bladder Hypertension is also an invasive and costly diseases or Cholecystitis method. Predicting the presence of Patients with Congestive Cardiac Failure EsophagealVarices by Non Invasive Patients with Chronic Kidney Disease means might increase the compliance and Patients with Serum SGPT would permit to restrict the performance of levels>400U/L endoscopy to those patients with a high 7 Method probability of having varices. The ideal The patients were explained in detail about noninvasive test for diagnosing fibrosis the study, following which an informed and portal hypertension, should be simple consent was taken regarding permission and reproducible, readily available, less for inclusion in the study. Detailed Clinical expensive than a biopsy, and able to history was taken and then patients were predict a full spectrum of fibrosis and subjected to a thorough clinical 53 Int J Res Med. 2017; 6(4); 52-58 e ISSN:2320-2742 p ISSN: 2320-2734 Gall Bladder Wall Thickness as a Marker of Portal Hypertension examination. Blood samples were drawn B. There were 17 patients in Group A, under complete aseptic precautions after while Group B had 43 patients. obtaining informed consent. Blood Comparison amongst both groups was investigations sent included, Complete made with respect to Serum Albumin Hemogram, Liver function tests with levels, Portal Vein diameter, presence of enzymes, Total protein and serum Ascites, history suggesting Upper GI Albumin levels, Prothrombin time bleed,and presence of esophagealvariceson .Additional blood investigations were sent Upper GI endoscopy . depending on the need of the patient’s Table 1: Correlation of GBWT with clinical condition. All the patients Serum Albumin Levels underwent Ultrasonography of Abdomen, Sr. Group A Group B Albumin No. of % of No. of % of for visualisation of hepatic size, liver levels patients patients patients patients echotexture, Portal Vein diameter at porta, (gm/dl) <2.4 3 17.64 20 46.51 Flow in portal vein, Collaterals/Varices 2.5 to 2.9 5 29.41 15 34.88 and Gall Bladder Wall thickness. The >3 9 52.94 8 18.60 patients were subjected to the Ultrasound The above table shows the percentage of in the mornings ,after proper overnight patients having different albumin levels. fasting of atleast 8 hours . The Ultrasound On comparing the percentage of patients of all patients was done by a single having serum albumin levels less than 3 radiologist. All patients, irrespective of a gm/dl in Group A (47.05%)