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 Table of Contents  
Year : 2016  |  Volume : 3  |  Issue : 1  |  Page : 41-44

Etiology of ascites in adults living in the Hills of Himachal Pradesh, India: A hospital-based study

1 Department of Medicine, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
2 Department of Gastroenterology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
3 Department of Medicine, Dr. RPGMC, Tanda, Kangra, Himachal Pradesh, India
4 Department of Physiology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India
5 Department of Pathology, Indira Gandhi Medical College, Shimla, Himachal Pradesh, India

Date of Web Publication22-Dec-2015

Correspondence Address:
Sujeet Raina
C-15, Type-V Quarters, Dr. RPGMC Campus, Tanda, Kangra - 176 001, Himachal Pradesh
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/2348-3334.172398

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Aim: Ascites is one of the major complications of liver cirrhosis. In addition, ascites can develop because of peritoneal tuberculosis, malignancy, cardiac, and renal disorders. The purpose of this study was to evaluate epidemiological data on the etiological profile of ascites in adults in a tertiary care hospital in the Northern hilly state of the Western Himalayas. Materials and Methods: A 1-year hospital-based cross section observational study was conducted in the Department of Medicine and Gastroenterology in a tertiary care center of Himachal Pradesh, located in the Northern India. In all 168 patients who were diagnosed as ascites on the basis of history, physical examination, ultrasonography, and of age >18 years were included in the study. Detail history examination and investigation were carried in each case as per protocol. Results: Cirrhosis of liver was the leading cause of ascites in our study (60.7%), tuberculosis was the second most common cause of ascites (13%), malignancy and cardiac disorders were the third (7.7%) most common causes for ascites. Alcohol was the leading cause of cirrhosis in 75 patients (73.5%). Conclusion: The study identified cirrhosis of liver as the leading cause of ascites and alcoholism as the most common cause of cirrhosis. The measures on taking care of preventable risk factors are desired.

Keywords: Ascites, etiology, Himachal Pradesh, Western Himalayas

How to cite this article:
Kumar B, Sharma B, Raina S, Sharma N, Gupta D, Mardi K. Etiology of ascites in adults living in the Hills of Himachal Pradesh, India: A hospital-based study. CHRISMED J Health Res 2016;3:41-4

How to cite this URL:
Kumar B, Sharma B, Raina S, Sharma N, Gupta D, Mardi K. Etiology of ascites in adults living in the Hills of Himachal Pradesh, India: A hospital-based study. CHRISMED J Health Res [serial online] 2016 [cited 2022 May 16];3:41-4. Available from: https://www.cjhr.org/text.asp?2016/3/1/41/172398

  Introduction Top

The word ascites is of Greek origin (askos) and means bag or sac. Ascites describes the condition of pathologic fluid collection within the abdominal cavity.[1],[2],[3],[4],[5] The differential diagnosis of ascites remains a problem in clinical practice. Treatment decisions are directed according to the etiological profile. Diagnostic paracentesis has become increasingly important as the key initial investigation in the assessment of ascites.[2],[3],[4] Cirrhosis is the leading cause of ascites in both developed and developing countries. Tuberculosis is the second most common cause in resource limited nations in comparison to resource rich where peritoneal malignancy follows cirrhosis.[6],[7],[8] Tuberculosis is seen in 30% of the patients with ascites in India.[9] Peritoneal tuberculosis leads to ascites in only 2% cases in the Western world.[1],[2],[3],[4] Epidemiological data on the etiological aspects of ascites are insufficient from this region and has not yet been reported from Himachal Pradesh. Therefore, this study was planned and conducted in a tertiary care hospital providing gastroenterology services in Himachal Pradesh, India located in the Western Himalayas.

  Materials and Methods Top

This cross section observational study was conducted in a tertiary care center of Himachal Pradesh, located in the Northern India over a period of 1 year. All indoor patients who were diagnosed as ascites on the basis of history, physical examination, ultrasonography, and of age >18 years were included in the study after getting the informed consent. Patients who had a diagnostic paracentesis within 3 weeks (cause was already established), secondary cause of peritonitis and unwilling to participate in the study were excluded. The patients included in the study were evaluated by detailed history. Questionnaire regarding risk factors was included in history which included: Alcohol history including amount and duration of alcohol intake, blood transfusion, surgery, needle prick, tattoo, and high risk behavior. Detailed examination was performed in every case and clinical presentation was recorded. Ascitic fluid paracentesis was done under all aseptic conditions. Ascitic fluid was analyzed for biochemistry, cytology, gram staining, acid fast bacillus staining, malignant cells, culture, and sensitivity. Serum-ascites albumin gradient (SAAG) and adenosine deaminase (ADA) was estimated in all patients. For culture, 10 ml of ascitic fluid was inoculated in two blood culture bottles at the bedside and was sent immediately to the microbiology laboratory. Specific etiology oriented investigations were carried out. Tubercular ascites was diagnosed on the basis of low SAAG (<1.1), high protein (>2.5), ADA more than 40 IU/L, lymphocytic predominance on cytology, and response to antitubercular therapy. Serological markers such as antinuclear antibodies, an antibody against liver-kidney-microsomes, antismooth muscle antibodies, immunoglobulin A, tissue transglutaminase antibody were done on the basis of clinical profile and if indicated. Serum ceruloplasmin, urinary copper levels and slit lamp examination for Kayser–Flesher ring was done if indicated. All obese patients in whom other etiology of cirrhosis was ruled out were placed under nonalcoholic steatohepatitis as a possible cause for cirrhosis. Ultrasound abdomen was done in all patients followed by computed tomography if the ultrasound was inconclusive or there was evidence of hepatocellular carcinoma. Upper gastrointestinal endoscopy was performed in all patients with cirrhosis unless contraindication was present. Severity of disease was done according to Child-Turcotte-Pugh (CTP) score in cirrhosis patients. The study was approved by Institutional Ethics Committee. The data, thus collected, was analyzed on Microsoft Excel sheet 2010 and percentages were calculated.

  Results Top

One hundred and sixty-eight patients with ascites were included in the study. The age group of study population ranged from 20 years to 87 years and the mean age was 51.5 years. One hundred and eight (64.2%) were males and 60 (35.7%) were females. The male to female ratio was 1.75:1. A total of 117 (69.6%) patients were in the age group of 41–70 years. The causes of ascites observed with their frequency are as shown in [Table 1]. Alcohol was the leading cause of cirrhosis in 75 patients (73.5%), hepatitis B was the cause in 14 patients (13.72%), and hepatitis C was the cause of cirrhosis in one patient (0.98%). Alcohol and hepatitis B was the cause in one patient (0.98%), and hepatitis C and alcohol was the cause in two patients (1.96%). Three patients (2.94%) had autoimmune cirrhosis and six patients had cryptogenic cirrhosis (5.88%). Of 102 patients of cirrhosis, high SAAG (>1.1 g/dl) was observed in 99 (97.0%) patients and 3 (2.9%) patients had low SAAG (<1.1 g/dl). Three patients had a high SAAG with high protein (ascitic albumin >2.5 g/dl) and all had ADA >40. Of 102 patients of cirrhotic ascites, 73 patients (71.56%) had lymphocyte as predominant cell and 29 patients (28.43%) had neutrophils as predominant cells. Of 102 patients of cirrhotic ascites, a total of 32 (31.3%) patients had peritoneal fluid infection. Among these 32 patients, 13 patients (40.6%) had culture positive SBP, 16 patients (50.00%) had culture negative neutrocytic ascites, and three patients (9.37%) had monomicrobial nonneutrocytic bacterascites. Among the culture, positive 12 patients had  Escherichia More Details coli on the culture of ascitic fluid, three patients had Enterococcus and one patient had Klebsiella Pneumoniae. In addition, 3 (2.9%) patients of cirrhosis had evidence of mixed ascites in the form of tubercular peritonitis. Among total patients of cirrhosis (102), four patients (3.92%) were in CTP Class A, 56 patients (54.90%) were in CTP Class B, and 42 patients (41.17%) were in CTP Class C. Ascitic fluid cytology for malignant cells was positive in 13 (7.73%) patients. Among them, seven patients (53.84%) had ovarian carcinoma, four patients (30.76%) had gastrointestinal tract malignancy, one patient (7.69%) each had carcinoma pancreas and non-Hodgkin's lymphoma. There was one patient of non-Hodgkin's lymphoma, who was diagnosed on ascitic fluid cytology. He had ascites, abdominal lymphadenopathy, hepatosplenomegaly, and mass in right iliac fossa. He did not have any external lymphadenopathy. Among 22 patients of tubercular ascites, 2 (9.09%) patients had acid-fast bacteria (AFB) positive on Zeil–Neilson's staining. The mean age of patients with tuberculosis was 45.5 years. Among the 13 patients with cardiac ascites, three had dilated cardiomyopathy, eight had cor pulmonale, and one each had hypertensive heart disease and pericarditis. Among the 10 patients with renal cause of ascites, six had chronic renal failure and four had nephrotic syndrome.
Table 1: Etiology of ascites

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  Discussion Top

Etiology of ascites can be suspected from history and examination, but ascitic fluid analysis is an important investigation to diagnose the cause. In the United States, cirrhosis of liver is the most common cause of ascites (85%), followed by nonhepatic causes such as cardiac failure (3%) and peritoneal malignancy (2%). Approximately 5% of patients with ascites have two or more causes of ascites formation, that is, “mixed” ascites. Usually, these patients have cirrhosis plus one other cause, e.g., peritoneal carcinomatosis or peritoneal tuberculosis.[10] The majority of patients who present with ascites have underlying cirrhosis, with the remainder being due to malignancy, heart failure, tuberculosis, pancreatitis, and other rare causes.[1],[2],[3],[4]

In India, cirrhosis of liver is the most common cause of ascites (55%) followed by tuberculosis (30%).[9]

Males constituted predominant number of our patients due to the sociocultural reasons of liquor consumption. According to the alcohol  Atlas More Details of India, the prevalence of alcohol use among men in Himachal Pradesh is between 25% and 49%.[11] Liquor consumption is perceived as a part of the social and religious life of the tribal population of Himachal Pradesh.[12] In our study, we found that ascites due to cirrhosis of liver constituted the largest group and 73.5% of them were alcohol related. The results are comparable to other studies.[13],[14] Our study is comparable to the published data though the total percentage of patients with cirrhosis and ascites is less in our study as compared to the Western literature. This is because tuberculosis is more prevalent in developing countries which contribute a good amount of patients with ascites.

Among patients with cirrhotic ascites 31.3% patients were found to have SBP. The frequency of SBP among hospitalized patients with advanced cirrhosis varies from 10% to 30%.[15] E. coli was the most common organism isolated on culture and is consistent with the literature.[16] In our study, tuberculosis is the second most common cause of ascites which is comparable to other developing countries and was observed in 13% of patients. Zeil–Neilson's staining yielded AFB positivity in 9% patients. Peritoneal tuberculosis accounts for 0.5–1% of all tuberculosis related hospital admissions with an overall mortality rate of 7%.[17] In India 10% patients with abdominal tuberculosis present with ascites.[17] The yield of organisms on smear and culture is low. Staining for acid fast bacilli is positive in <3 per cent of cases.[18] Tuberculous infection of the peritoneum is rare in developed countries but not infrequent in countries with a high prevalence of TB.[19],[20] It is commonly seen in individuals <40 years of age. The patients with tubercular ascites had a mean age of 45.5 years which is lower than the cumulative mean age of 51.5 years. Tuberculous peritonitis often exhibits female predominance. Individuals with HIV infection, cirrhosis, diabetes, malignancy, and those receiving continuous ambulatory peritoneal dialysis are at high risk for tuberculous peritonitis. Mixed ascites was observed in 2.9% patients. All patients had features of underlying cirrhosis and peritoneal tuberculosis. Peritoneal tuberculosis in the presence of hepatic cirrhosis is a not only a diagnostic problem but a therapeutic challenge also. In a patient of compensated cirrhosis suspect tubercular ascites if patient decompensates or if ascites increases or is resistant ascites despite adequate diuretic treatment and sodium restriction. Symptoms of tubercular activity in the form of anorexia, fever, weight loss are helpful. Tubercular ascites in the setting of cirrhosis reveals a high SAAG, high protein ascites with a lymphocytic predominant high cell count fluid.[21] Peritoneal fluid ADA has a sensitivity of 100% and specificity of 97% for making a diagnosis of tubercular ascites. The optimal cut-off value defined is 39 IU/L.[22] Treatment of tuberculosis in patients with underlying cirrhosis is a challenge because of the compromised liver functions and high risk of hepatotoxicity.[23] Malignant ascites was observed in 7.7% of cases in this study. Malignant ascites accounts for approximately 10% of all cases of ascites.[24] Ovarian carcinoma is the most common cause of malignant ascites in our region and the second most common cause is gastrointestinal malignancy. Malignant ascites is a sign of peritoneal carcinomatosis, the presence of malignant cells in the peritoneal cavity. Tumors causing carcinomatosis are more commonly secondary peritoneal surface malignancies which include: Ovarian, colorectal, pancreatic, and uterine; extra-abdominal tumors originating from lymphoma, lung, and breast; and a small number of unknown primary tumors.[25] Two patients were diagnosed as having scrub typhus. Scrub typhus is endemic in large parts of India including Himachal Pradesh and can cause multi-organ failure and death.[26] Ascites as a complication has been reported in pediatric patients.[27]

The advantages of this study are that the causes of ascites in this region were known which help us in directing treatment decisions and predicting the outcome. Knowledge of the causes also allows discussing the preventive measures. Focus on primary prevention by abstaining from alcohol consumption and preventive hepatitis B vaccination is the measures recommended. We conclude that in our region cirrhosis is the most common cause of ascites and alcoholism is the most common cause of cirrhosis.

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Conflicts of interest

There are no conflicts of interest.

  References Top

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Moore KP, Aithal GP. Guidelines on the management of ascites in cirrhosis. Gut 2006;55 Suppl 6:vi1-12.  Back to cited text no. 3
Kuiper JJ, van Buuren HR, de Man RA. Ascites in cirrhosis: A review of management and complications. Neth J Med 2007;65:283-8.  Back to cited text no. 4
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Runyon BA, Montano AA, Akriviadis EA, Antillon MR, Irving MA, McHutchison JG. The serum-ascites albumin gradient is superior to the exudate-transudate concept in the differential diagnosis of ascites. Ann Intern Med 1992;117:215-20.  Back to cited text no. 10
Alcohol Atlas of India. Available from: http://www.indianalcoholpolicy.org/alcohol_atlas.html. [Last accessed on 2014 Dec 07].  Back to cited text no. 11
Bali R, Gupta R, Chand M, Chauhan JK. Alcoholism – A social evil among the tribals of Kinnaur district of Himachal Pradesh. J Farm Sci 2011;1:137-44.  Back to cited text no. 12
Maskey R, Karki P, Ahmed SV, Manandhar DN. Clinical profile of patients with cirrhosis of liver in a tertiary care hospital, Dharan, Nepal. Nepal Med Coll J 2011;13:115-8.  Back to cited text no. 13
Bindu CB, Nayak UB, Souza SD. A study of etiological factors in ascities – A cross sectional study. Int J Recent Trends Sci Technol 2014;12:494-6.  Back to cited text no. 14
Rimola A, García-Tsao G, Navasa M, Piddock LJ, Planas R, Bernard B, et al. Diagnosis, treatment and prophylaxis of spontaneous bacterial peritonitis: A consensus document. International Ascites Club. J Hepatol 2000;32:142-53.  Back to cited text no. 15
Akriviadis EA, Runyon BA. Utility of an algorithm in differentiating spontaneous from secondary bacterial peritonitis. Gastroenterology 1990;98:127-33.  Back to cited text no. 16
Dineeen P, Homan WP, Grafe WR. Tuberculous peritonitis: 43 years' expereince in diagnosis and treatment. Ann Surg 1976;184:717-22.  Back to cited text no. 17
Mugula DD. Abdominal tuberculosis in Chingola-Zambia: Pattern of presentation. East Cent Afr J Surg 2006;11:41-6.  Back to cited text no. 18
Sharma MP, Bhatia V. Abdominal tuberculosis. Indian J Med Res 2004;120:305-15.  Back to cited text no. 19
Uzunkoy A, Harma M, Harma M. Diagnosis of abdominal tuberculosis: Experience from 11 cases and review of the literature. World J Gastroenterol 2004;10:3647-9.  Back to cited text no. 20
Kim NJ, Choo EJ, Kwak YG, Lee SO, Choi SH, Woo JH, et al. Tuberculous peritonitis in cirrhotic patients: Comparison of spontaneous bacterial peritonitis caused by Escherichia coli with tuberculous peritonitis. Scand J Infect Dis 2009;41:852-6.  Back to cited text no. 21
Riquelme A, Calvo M, Salech F, Valderrama S, Pattillo A, Arellano M, et al. Value of adenosine deaminase (ADA) in ascitic fluid for the diagnosis of tuberculous peritonitis: A meta-analysis. J Clin Gastroenterol 2006;40:705-10.  Back to cited text no. 22
Kumar N, Kedarisetty CK, Kumar S, Khillan V, Sarin SK. Antitubercular therapy in patients with cirrhosis: Challenges and options. World J Gastroenterol 2014;20:5760-72.  Back to cited text no. 23
Runyon BA. Care of patients with ascites. N Engl J Med 1994;330:337-42.  Back to cited text no. 24
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Sharma A, Mahajan S, Gupta ML, Kanga A, Sharma V. Investigation of an outbreak of scrub typhus in the himalayan region of India. Jpn J Infect Dis 2005;58:208-10.  Back to cited text no. 26
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