Gall Bladder Wall Thickness as a Marker of Portal

ORIGINAL ARTICLE Gall Bladder Wall Thickness as a Marker of in Patients of Alcoholic of 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 from , , , Spontanoeus Bacterial , , 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 . 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 . 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 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 , 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 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

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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 ; 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 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

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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%) with that in history suggestive of Gastrointestinal Group B(81.39%),p value was 0.04, which Bleed, were subjected to Upper suggests significant correlation. The mean GastroIntestinal Endoscopy. The lower of serum albumin levels in group B was end of was assessed for 2.52+_0.455 while mean of group A was presence of varices, for 2.87+_0.485, the p value is 0.01, which congestive gastropathy and peptic ulcer. again confirms a significant correlation The Varices were classified as: between GBWT and serum albumin levels.  Grade I - Small, straight varices Table 2: Correlation of GBWT with  Grade II – Enlarged, tortuous varices that Portal Vein Diameter Portal Group A Group B occupy less than one-third of the lumen vein No. of % of No. of % of diameter  Grade III- Large, coil-shaped varices that Patients Patients Patients Patients (mm) occupy more than one third of the lumen <11.9 8 47.05 4 9.30 Data Analysis 12-15.9 5 29.41 16 37.20 On the basis of ultrasonographic findings, >16 4 23.52 23 53.48 The above table shows the percentage of patients were divided into two groups patients having different portal vein Group A- gall bladder wall thickness <= diameters. The mean of the Portal vein 4mm diameter in group A is 13.11+_2.37 while Group B- gall bladder wall thickness >= mean of that in group B is 14.67+_2.01 4mm ,which shows that the difference is Statistical analysis was done using chi significant, the p value being 0.012. square test and two sample t test on Table 3: Correlation of GBWT with MedCalc. A p value of <0.05 was Ascites and G.I. Bleeding considered as statistically significant. The The following table shows the correlation results were tabulated and represented of GBWT with ascites andupper using Microsoft Office for windows 2010. gastrointestinalbleeding,i.e. history of OBSERVATIONS or malena The 60 patients were divided into two groups, depending on the Gall bladder

Wall thickness, those who had

GBWT<4mm were in Group A, While those with GBWT >= 4mm were in Group

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Gall Bladder Wall Thickness as a Marker of Portal Hypertension

GBWT ASCITES G.I BLEEDING diffuse and less marked thickening , No: of % of No: of % of

Patients Patients Patients Patients contrary to tumor lesions that cause focal GROUP A 9 52.94% 2 11.76% or more exuberant thickening, frequently (<4mm) 12 GROUP greater than 10mm .Increase gall bladder 36 83.72% 9 20.93% B(>=4mm) wall thickness in cirrhotic patients is due It was observed that 9 patients i.e. 52.94% to ascites, decreased peripheral vascular in Group A had ascites as compared to 36 resistance and portal hypertension which patients i.e. 83.71 % in Group B, with shows that GBWT could be p=0.013, which suggests significant multifactorial13 .Liver disease as the cause correlation between GBWT and presence for Gall Bladder wall thickening is of Ascites. While 20.93 % of patients in suggested by the absence of or Group B i.e. 9 patients had evidence of signs of gall bladder in the gastrointestinal bleeding clinically as presence of cirrhotic liver morphology and compared to only 11.76 % i.e. 2 patients in stigmata of portal venous hypertension, Group A, with p=0.412, which is not such as , varices and reversal significant. of hepatopedal flow. In our study it is Table 4: Correlation of GBWT with GI observed that compared to patients with a Bleed and Upper GI Scopy normal gall bladder wall(i.e Group A), GBWT GI BLEED UPPER GI SCOPY patients in Group B had a significantly No: of % of No: of % of

patients patients patients patients lower serum Albumin levels GROUP 2 11.76% 5 8.3% (2.87+_0.485Vs 2.52+_0.455gm/dl; A(<4mm) GROUP p<0.05).This is in agreement to a study 9 20.93% 38 88.37% B(>=4mm) carried out by T F Wang et al9who The above table shows the correlation of observed that compared to patients with GBWT with clinical evidence of upper GI normal gall bladder wall, patients with gall Bleed and evidence of esophagealvarices bladder wall thickening had significantly on Upper GI scopy. Group B had lower serum albumin levels(3.6+-.6 vs only9patients(20.93%) who had clinical 2.9+-.7gm/dl;p<0.05) . These findings in evidence of Upper GI Bleed, but Upper GI our study of hypoalbuminemia being a scopy revealed presence of varices in 38 significant finding in cirrhotic patients (88.37%) patients as compared to Group A with increased GBWT is not supported by wherein only 2 patients(11.76%) had a few studies by Colli et al14 and clinical evidence of Upper GI Bleed, but Saverymuttu et al15 where there was no presence of varices was seen in 5(8.3%) significant correlation between GBWT and patients. On comparing the Group hypoalbuminemia. Hypoalbuminemia A(8.3%) and B(88.37%) patients for causing oedema can lead to GBWT, but as presence of Esophagealvarices, significant this findings is not supported by quite a correlation(p<0.0001) was found between few studies , it is possible that other factors GBWT and presence of varices on like presence of ascites and portal endoscopy. hypertension may also contribute to the DISCUSSION increased GBWT.16 The normal Portal Increased gallbladder wall thickness could Vein diameter can vary between 7 to 15 be due to different etiologies other than mm while normal portal vein pressure lies gallbladder diseases such as liver diseases, between 5-10 mmHg(14 cm H2O)17.A hypoalbuminemia, ascites, hepatitis, portal vein diameter greater than 13mm is congestive , kidney disease, assumed to be the cutoff point for Portal 10,11 AIDS, malignancy and sepsis . GBWT Hypertension in appropriate clinical is classified as mild (between 4-7mm), settings18. The diameter of Portal Vein is a marked (more than 7mm) and in focal and reflection of the degree of the resistance it diffuse. As a rule, systemic diseases such faces in the liver and the velocity of blood as heart, renal or hepatic failure cause flow within the portal vein.The normal

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Gall Bladder Wall Thickness as a Marker of Portal Hypertension portal vein diameter is 10mm19. Studies gall bladder wall thickening, those with have shown that this value increases with gall bladder wall thickening, i.e. Group B the advancement of liver fibrosis and patients had a higher portal vein diameter subsequently with development of (13.11+_2.37vs 14.67+_2.01;p<0.05) cirrhosis, where the mean Portal vein which is suggestive of increased portal diameter is reported to be around 14mm( venous pressure in Group B. This is 18-20).In our study, it was observed that similar to the observations by T F Wang et compared to the patients with a normal al9 where they studied 77 patients of cirrhosis and found that compared to concluded that finding of Ascites and patients with normal Gall bladder wall, GBWT should be considered a valuable those with increased GBWT had higher sign of transudative ascites and of portal hepatic Venous pressure gradient (13.9+- hypertension whatever its cause.A study 4.5 vs 17.1+-4.1 resp. p<0.01). Another by Brogna et al26showed GBWT to be study by Saverymuttu et al15 where they more in patients of ascites with studied 40 patients of cirrhosis , they cirrhosis(6.7+-2.1mm)as compared to found that GBWT was more in 27 patients ascites due to non cirrhotic cause(2.5+- who had evidence of portal hypertension. 1.6mm) and these findings are supported Ascites is a major of by similar observations made byGeorgiv et cirrhosis,21 occurring in 50% of patients al27and A Mohammdi et al28.In patients over 10 years of follow up22. The with cirrhosis as a result of pathologic development of ascites is an important changes due to Portal hypetension in the landmark in the natural history of cirrhosis liver, there is a stasis of blood in the as it is associated with a 50% mortality viscera and gall bladder , which over two years22,23,24,25 and signifies the leads to congestion and oedema of the need to consider as a GBW, that is more in cirrhotics as therapeutic option.Portal hypertension compared to non cirrhotics28. On increases the hydrostatic pressure within correlating the GBWT with evidence of the hepatic sinusoids and favours upper GI bleed in our study, we did not transudation of fluid into the peritoneal find significant correlation(p cavity. Portal hypertension is critical to the =0.412)between the two. But significant development of ascites, and ascites rarely correlation was found (p<0.001) between develops in patients with a wedged hepatic presence of esophageal varices on upper venous portal gradient of <12 mm Hg. In GI scopy in patients of Group B as against our study we observed that the presence of in patients of Group A. This finding is in Ascites was significantly (p<0.05)more in consistency with the findings in a study by patients of groupB as compared to the Shamsi Ara Begum et al29where they patients of Group A. This was in observed that the mean GBWT was agreement to the positive correlation significantly increased (p<0.05)in Chronic between gall bladder wall thickness and liver disease with Grade 3 and 4 varices presence of ascites (p<0.05) as observed (6.1+-.8mm)as against in Grade 1and 2 by Galipet al13.Similar observations were varices (3.9+-.7mm). Supporting these made by Wang et al9 on studying 77 findings is a study by K R Yousaf et al32 cirrhotic patients,presence of ascites in which concludes that congestive patients with normal GBWT was 8% as cholecystopathy is an important early against 50% in those with increased sonographic sign of evoloving GBWT9. These observations are supported esophagealvarices and portal hypertension by several other studies on comparing in liver cirrhosis30.Esophagealvarices are GBWT in patients of ascites due to the major complication of portal cirrhosis with ascites due to noncirrhotic hypertension. It is detected in about 50% causes.In a study by Colli et al14 , where of cirrhosis patients, and approximately 5– 47 patients of ascites were studied,it was 15% of cirrhosis patients show newly

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Gall Bladder Wall Thickness as a Marker of Portal Hypertension formed varices or worsening of varices Portal hypertension. Philadelphia: WB each year. As a result any increase in Saunders Co; 1964, 50 portal venous pressure will lead to 6. Bosch J, Abraldes JG, Berzigotti A, development of esophagealvarices Garcia-Pagan JC. The clinical use of ,bleeding from which is the most important HVPG measurement in Chronic liver complication of liver cirrhosis and a major disease. Nat Rev cause of death. Therefore, identifying the GastroenterolHepatol 2009; 6:573-582 non invasive markers to predict 7. De Frachis R. Non invasive (and esophagealvariceal bleeding during the minimally invasive) diagnosis of follow up may be an important tool for a esophagealvarices. J hepatol 2008; better management of cirrhotic patients31. 49:520-7 CONCLUSION 8. Bonekamp S, Kamel I, Solga S, Clark In the patients of Cirrhosis of liver, here J- Can imaging modalities diagnose we had enrolled patients of Alcoholic and stage hepaticfibrosis and cirrhosis Cirrhosis, the presence of accurately?. J Hepatol 2009; 50:17-35 Hypoalbuminemia, increased Portal vein 9. 9.Wang TF,et al .Gall –bladder wall diameter, presence of Ascites and presence thickening in patients with liver of esophagealvarices, which are cirrhosis. J Gastroenterol Hepatol parameters suggesting portal hypertension, .1997 Jun;12(6):445-9 were significantly more in those cirrhotic 10. Dayananda L, Moorthy S, Prabhu NK, patients who had increased diffuse Gall et al. Diagnostic value of gall bladder Bladder wall thickness. Hence, the wall thickness in patients with ascites. presence of Diffuse GBWT on Indian J Gastroenterol. 2006;25:44– Ultrasonography in patients without 45. intrinsic gall bladder disease should be 11. Loreno M, Travali S, Bucceri AM, et considered as a sign of Portal al. Ultrasonographic study of Hypertension. gallbladder wall thickness and REFERENCES emptying in cirrhotic patients without 1. Longo DL, Fauci AS, Kasper DL, gallstones. Gastroenterol Res Pract. Hauser SL, Jameson J, Loscalzo J. 2009;2009:683040–683040. eds. Harrison’s Principles of Internal 12. Van Breda Vriesman AC, Engelbrecht Medicine 19the. New York, NY: MR, SmithuisRH ,et al. Diffuse Gall McGraw-Hill;2015 Bladder Wall Thickness: Differential 2. Kumar M , Kumar A, HissarSetal. Diagnosis. AJR Am J Hepatic Vein Pressure Gradient as a Roentgenol.2007; 188:495-501 predictor of cirrhosis in Chronic Liver 13. Esroz G, Ozutemiz O, Akarca U et al. Disease because of Hepatitis B Virus. GBWT as a sign of esophagealvarices Liver Int 2008;28: 690-8 in Chronic Liver Disease. J 3. BogdanProcopet, Annalisa Berzigotti- Gastroentrology 1999; 10:44-46 Diagnosis of cirrhosis and portal 14. Colli A, Cocciolo M, Buccino G, et al. hypertension: Imaging ,non Thickening of the gallbladder wall in invasivemarkersof fibrosis and liver ascites. J Clin Ultrasound. biopsy. Report, 1991;19:357–9. [PubMed] Vol5, Issue2,1 May 2017, Pg 79-89 15. Saverymuttu SH, Grammatopoulos A, 4. Ripoll C, Groszman R, Garcia-Tsao Meanock CI, Maxwell JD, Joseph G- HVPG predicts clinical AEA. Gallbladder wall thickening decompensation in patients with (congestive cholecystopathy) in compensated cirrhosis. chronic liver disease: a sign of portal Gastroenterology 2007; 133:481-8 hypertension. British Journal of 5. Child C, Turcotte J. Surgery and Radiology. 1990;63(756):922–925. Portal Hypertension. The Liver and

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