{"title":"儿童门静脉高压症的临床病理相关性及治疗策略","authors":"Asmita Mahajan, R. Ghildiyal, Prachi S. Karnik","doi":"10.7439/IJBAR.V9I2.4667","DOIUrl":null,"url":null,"abstract":"We studied 51 children with clinical setting of portal hypertension over a period of one and half years. Out of these, 27 (52.94%) were males and 24 (47.05%) were females. All the cases were subjected to biochemical, diagnostic, radiological investigations and liver biopsy. Portal hypertension was diagnosed by demonstrating on USG abdomen/ Doppler, the presence of collaterals of portal vein and esophageal varices on endoscopy. Treatment was initiated depending upon clinical presentation. The most common presenting complaints were hematemesis and malena (35.3%) followed by their combination with abdominal distension (19.6%). 86.3% patients had anemia mostly due to upper GI bleed. 35.3% patients had leucopenia while 47.1% had thrombocytopenia. Only 18 (i.e. 35.3%) had Hypersplenism. Maximum patients who bled more than twice had a mild (41.2%) or severe (29.4%) derangement of prothrombin time. The etiology of portal hypertension turned out to be extra- hepatic portal vein obstruction in 86.3% cases. There were 2 cases each (3.9% each) of Wilson’s disease and Budd-Chiari syndrome. One (2%) was secondary to chronic liver disease due to hepatitis C infection, one was extra- hepatic biliary atresia and one was autoimmune hepatitis. 9.8% cases required drugs in the form of somatostatin drip and all these required a packed cell transfusion as well. 23 patients (45.1%) required only blood transfusion without a somatostatin infusion. Those with severe acute bleeding usually were given somatostatin infusion. The variceal size at presentation was a very important predictor of the morbidity and outcome.","PeriodicalId":13848,"journal":{"name":"International Journal of Biomedical and Advance Research","volume":"38 1","pages":"70-75"},"PeriodicalIF":0.0000,"publicationDate":"2018-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"4","resultStr":"{\"title\":\"Clinicopathological Correlation of Portal Hypertension in Children and Management Strategies\",\"authors\":\"Asmita Mahajan, R. Ghildiyal, Prachi S. Karnik\",\"doi\":\"10.7439/IJBAR.V9I2.4667\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"We studied 51 children with clinical setting of portal hypertension over a period of one and half years. Out of these, 27 (52.94%) were males and 24 (47.05%) were females. All the cases were subjected to biochemical, diagnostic, radiological investigations and liver biopsy. Portal hypertension was diagnosed by demonstrating on USG abdomen/ Doppler, the presence of collaterals of portal vein and esophageal varices on endoscopy. Treatment was initiated depending upon clinical presentation. The most common presenting complaints were hematemesis and malena (35.3%) followed by their combination with abdominal distension (19.6%). 86.3% patients had anemia mostly due to upper GI bleed. 35.3% patients had leucopenia while 47.1% had thrombocytopenia. Only 18 (i.e. 35.3%) had Hypersplenism. Maximum patients who bled more than twice had a mild (41.2%) or severe (29.4%) derangement of prothrombin time. The etiology of portal hypertension turned out to be extra- hepatic portal vein obstruction in 86.3% cases. There were 2 cases each (3.9% each) of Wilson’s disease and Budd-Chiari syndrome. One (2%) was secondary to chronic liver disease due to hepatitis C infection, one was extra- hepatic biliary atresia and one was autoimmune hepatitis. 9.8% cases required drugs in the form of somatostatin drip and all these required a packed cell transfusion as well. 23 patients (45.1%) required only blood transfusion without a somatostatin infusion. Those with severe acute bleeding usually were given somatostatin infusion. The variceal size at presentation was a very important predictor of the morbidity and outcome.\",\"PeriodicalId\":13848,\"journal\":{\"name\":\"International Journal of Biomedical and Advance Research\",\"volume\":\"38 1\",\"pages\":\"70-75\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2018-03-03\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"4\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"International Journal of Biomedical and Advance Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.7439/IJBAR.V9I2.4667\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"International Journal of Biomedical and Advance Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.7439/IJBAR.V9I2.4667","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
Clinicopathological Correlation of Portal Hypertension in Children and Management Strategies
We studied 51 children with clinical setting of portal hypertension over a period of one and half years. Out of these, 27 (52.94%) were males and 24 (47.05%) were females. All the cases were subjected to biochemical, diagnostic, radiological investigations and liver biopsy. Portal hypertension was diagnosed by demonstrating on USG abdomen/ Doppler, the presence of collaterals of portal vein and esophageal varices on endoscopy. Treatment was initiated depending upon clinical presentation. The most common presenting complaints were hematemesis and malena (35.3%) followed by their combination with abdominal distension (19.6%). 86.3% patients had anemia mostly due to upper GI bleed. 35.3% patients had leucopenia while 47.1% had thrombocytopenia. Only 18 (i.e. 35.3%) had Hypersplenism. Maximum patients who bled more than twice had a mild (41.2%) or severe (29.4%) derangement of prothrombin time. The etiology of portal hypertension turned out to be extra- hepatic portal vein obstruction in 86.3% cases. There were 2 cases each (3.9% each) of Wilson’s disease and Budd-Chiari syndrome. One (2%) was secondary to chronic liver disease due to hepatitis C infection, one was extra- hepatic biliary atresia and one was autoimmune hepatitis. 9.8% cases required drugs in the form of somatostatin drip and all these required a packed cell transfusion as well. 23 patients (45.1%) required only blood transfusion without a somatostatin infusion. Those with severe acute bleeding usually were given somatostatin infusion. The variceal size at presentation was a very important predictor of the morbidity and outcome.