Study of Upper Gastrointestinal Tract Endoscopic Findings in Portal Hypertension

Introduction: The gut mucosa in portal hypertension is the seat of microcirculatory changes that compromise its integrity and increase its susceptibility to damage. The mucosal changes in portal hypertension may require pharmacological, directed endoscopic or portal decompressive therapy. The objective of the study is to fi nd out various upper gastrointestinal tract endoscopic fi ndings in patients of portal hypertension. Methods: A prospective, cross-sectional, observational study of sixty patients of portal hypertension was conducted from June to October 2009. The esophagus, stomach and upper duodenum was visualized for any changes, especially by taking the tip of the instrument close to the mucosa. Results: Out of total, 60, 47 (78.3%) cases were cirrhotic and 13 (21.7%) cases were non-cirrhotic portal hypertension. The most frequent upper GI endoscopic fi nding was esophageal varices 56 (98.3%) followed by gastropathy 49 (81.6%), gastric hyperemia 19 (31.6%), duodenal hyperemia and erosive gastritis 16 (26.6% in each) and gastric varices 12 (20%). Esophageal varices were equally prevalent among cirrhotic and non cirrhotic portal hypertensive patients, 46 out of 47 (97.9%) and 13 out of 13 (100%) respectively. Gastropathy was more prevalent in cirrhotic patients with 87.2% vs. 75% in NCPF followed by 40% in EHO. However, duodenal ulcers were seen only in EHO 12.5%. Erosive gastritis was more prevalent in EHO (75%) followed by NCPF (60%), however, it was less frequent in cirrhotic portal hypertension (14.8%). Conclusions: The most common upper GI endoscopic fi nding in portal hypertensive patients were found to be esophageal varices followed by gastropathy, peptic ulcer disease (gastric and duodenal hyperemia, chronic gastritis, erosive gastritis, gastric ulcer and duodenal ulcer). _______________________________________________________________________________________


INTRODUCTION
Portal Hypertension is defi ned as a clinical syndrome manifested by hemodynamic changes due to diffi cult blood outfl ow from the portal bed. 1 The common causes of portal hypertension are cirrhosis of liver, non -cirrhotic portal fi brosis and extra hepatic portal vein obstruction due to umbilical sepsis.It may be due to hepatic outfl ow obstruction of varied etiology. 2Although majority of these bleed is due to ruptured gastro esophageal varices some of these bleed may be from ectopic varies at other sites of gastrointestinal tract or from different non variceal lesion like portohypertensive gastroduodenopathy, gastroduodenal ulcer, Mallory Weiss tear, esophago-gastroduodenitis etc.These complementary processes of vasoreactivity and vascular remodeling contribute importantly to increased intra hepatic resistance and represent important targets in the treatment of portal hypertension. 3e topic of varices (esophageal, gastric or ectopic) is well studied, however, the mucosal changes in the context of PH needs further elaboration. 4Therefore need is felt to undertake present study for generating data on various aspects of problems encountered in day to day practice in a referral centre to establish early diagnosis of the etiology, exact site and nature of the bleed and rational management to improve the overall outcome of the disease.

METHODS
A Prospective, cross-sectional observational study of sixty patients of portal hypertension was conducted from Jun, 2008 -Oct, 2009 (15 months) in the Gastroenterology Unit of Department of Medicine, Bir hospital.
Patients with portal hypertension (diagnosed on the basis of history and clinical examination, biochemical analysis, serum ascitic albumin gradient >1.1, ultrasonogram showing splenic index >20 cm, 2 portal vein trunk >15 mm, splenic vein >10 mm, portal systemic collaterals, extra hepatic or portal vein obstruction, cavernous transformation, ascitis) with or without history of upper gastrointestinal bleeding and hepatic encephalopathy and fi t for upper GI endoscopy attending outpatient medical services as well as hospitalized in medical, gastroenterology and hepatobiliary ward were included in the study.Patient with portal hypertension but unfi t for upper GI endoscopy e.g.shock, uncooperative, unconscious, recent MI, arrhythmia, restless etc and age less than 15 years were excluded from the study.
Ethical approval was taken from the concerned authority.Informed written and verbal consent was also taken from the patient.Patients were subjected to endoscopy using video endoscope (Fujinon video endoscope) without any premedication.In all patients, gastroenterologist and trained endoscopist at Bir hospital carried out an upper gastrointestinal endoscopy and required laboratory investigations.
Endoscopy was performed in left lateral position by a forward viewing video endoscope (Fujinon video endoscope).During the examination, esophagus was carefully looked for esophageal varices, any ulcers, esophagitis or any other abnormalities.

DISCUSSION
The common Upper Gastro Intestinal endoscopic fi ndings as esophageal varices in our study was supported by a study done by Moazzam et al study, 6 where they also found esophageal varices as the most common upper GastroIntestinal endoscopic fi ndings in portal hypertension (44%).In our study non variceal Upper GastroIntestinal fi ndings as gastopathy, gastric and duodenal hyperemia, erosive gastritis were also one of the manifestations of chronic liver disease and is the commonest cause of upper GI bleeding.The causes of portal hypertension may be extra hepatic, intra hepatic, and post hepatic.Ruptured gastro esophageal varices are the commonest cause of bleeding. 7Other non variceal causes of bleeding include peptic ulcer disease, gastrodudenitis, Mallory weiss tear, hemostatic defects. 8Recently, portal hypertensive vasculopathy involving gastropathy, duodenal hyperemia has been recognized as an additional non variceal cause of GI bleeding in portal hypertension. 9rtal hypertension in the developed countries who bleed are 40% due to non variceal causes where alcoholic cirrhosis and alcoholism predominate the aetiology of portal hypertension.As aetiological factors, demographic profi les differs in Nepal, above incidence of bleeding appears unlikely to be the cause of GI bleeding in developing countries.However occasional case reports are available on peptic ulcer disease as the cause of bleeding in portal hypertension in India. 10 the present study, most common cause of portal hypertension was cirrhosis accounting 47 out of 60 (78.3%) followed by non-cirrhotic portal fi brosis eight out of 60 (13.3%) and Extra hepatic obstruction fi ve out of 60 (8.3%).Among non cirrhotic causes noncirrhotic portal fi brosis was frequent eight (61.6%)than extra hepatic obstruction fi ve (38.4%).This is in conformity with earlier reports from India, 28 15 the esophageal varices was the most frequent upper GI endoscopic fi ndings 81% followed by gastropathy 28%, gastric varices 16, duodenal ulcer 14%, esophagitis 9% and gastric ulcer 7%.This study support the fi ndings observed in our study as esophageal varices is the most common upper GI endoscopic fi ndings followed by gastropathy.But the gastric varices was not found as a cause of upper GI bleeding in patients in our study.In another study, congestive gastropathy was the second most common abnormality (28%) after esophageal varices (81%) then gastric varices 16%, esophagitis 9%, gastric ulcer 7% and duodenal ulcer 14%. 13The prevalence of endoscopic features in one study, they observed red signs in 40% of the patients with esophageal varices Vs 76%, 13 a mosaic pattern in 82% (Vs 94% in the Papazain et al), 14 congestive gastropathy in 98% Vs 53% of Mc Cormack et al, 45 and gastric varices in 12% Vs 16% in the Palmer's study. 16 our study prevalence of esophageal varices were equally prevalent among cirrhotic and non-cirrhotic portal hypertensive patients, 46 out of 47 (97.9%) and 13 out of 13 (100%) respectively.Among non-cirrhotic patients, esophageal varices were present equally in EPO and NCPF (100% in each).Gastropathy was more prevalent in cirrhotic patients with 87.2% (41 out of 47) vs. 75% (six out of eight) in NCPF followed by 40% (two out of fi ve) in EPO.Gastric varices, chronic gastritis, gastroduodenitis and gastric ulcers were found only in cirrhotic portal hypertensive patients.However, duodenal ulcers were seen only in EPO 12.5% (one out of eight).Erosive gastritis was more prevalent in EPO, six out of eight (75%) followed by three out of fi ve (60%) in NCPF, however, it was less frequent in cirrhotic portal hypertension seven out of 47 (14.8%).
In other studies, [17][18][19][20] the prevalence of esophageal varices ranged widely between 60-95% in cirrhotic patients.The prevalence of esophageal varices ranged between 24% and 69% in cirrhotics with a mean of 59%.In another studies, 21,22 esophageal varices was present in 68% patients of NCPF by barium swallow study and another reported esophageal varices in 96% cases of NCPF.
In present study among esophageal varices, Grade II varices were the most common fi ndings accounting 43.5% followed by grade IV (28.26%) and III (21.74%) among cirrhotic portal hypertensive patients.In NCPF and EPO, grade II varices were also frequent accounting 37.5% and 60% respectively followed by III and IV both accounting equal in frequency 25% in NCPF and 20% in EPO.In a study done by Ehab et al, 71 among fi fty cirrhotic patients esophageal varices were found in 45 out of 50(90%).Among them endoscopic fi ndings showed 14 patients with grade I (28%), 13 patients with grade II (26%), 16 patients with grade III (32%) and one patient with grade IV (2%).This study supported the fi ndings observed in present study where variceal grading in cirrhotic portal hypertensive patients as grade II and III were frequent fi ndings.
The prevalence of gastric varices in patients with portal hypertension was diffi cult to establish correctly but it ranged from 16-60%. 24,25Gastric varices may be present in association with esophageal varices or independently.Isolated gastric varices may be seen in the absence of esophageal varices which was rare with a reported incidence of 8-12%. 22,24In our study, the incidence of gastric varices was 20% in cirrhotic portal hypertension but not found in patients of NCPF and EPO.Similar results were reported in some other studies where prevalence of gastric varices reported was 19% 22 , 31%, 26 and16%, 16 Sarin et al. 22 noted gastric varices in 53% in cirrhosis, 20.25% in NCPF and 20.6% in EPO and 6.16% in hepatic outfl ow obstruction.This difference may be due to the difference in the stage of severity of disease at the time of study and sample size.
In the present study, incidence of erosive gastritis was 26.6%, chronic gastritis was 13.3%, gastric ulcer was 6.7%, gastodudenitis was 5% and duodenal ulcer was 1.7% in case of portal hypertension.In the cirrhotic patients, erosive gastritis was found in14.8%,chronic gastritis in 17%, gastric ulcer in 8.5% and gastrodudenitis in 6.5%.In EPO, erosive gastritis was found in 60% and in NCPF erosive gastritis was found in 75% and duodenal ulcer was found in 1.5%.[29][30] The prevalence of portohypertensive gastropathy was 81.6% in present study.This fi nding was in concordance with the fi ndings of previous studies where PHG ranged from 51-94%. 14,15,31,32In contrast, very high incidence of PHG has been reported mainly from the west.The incidence of PHG was slightly higher in cirrhotics (87.2%) than in NCPF (75%) and EPO (40%).Similar fi ndings have been reported by other indian investigators. 22The difference in incidence of PHG in cirrhosis and non-cirrhotics may be because of involvement of humoral factors, 33 and more severe forms of liver disease in cases of cirrhosis. 9verity of liver disease was adjusted by child pugh's.More than 80% of NCPF and EPO were of grade A and among cirrhotics, one third of the patients were of Grade A (31.9 %), 40.4% were of Grade B and 27.7% of Grade C. No cases of grade C was found in EPO and NCPF.Our study showed that decompensated liver diseases were found mostly among cirrhotic patients with portal hypertension.

CONCLUSIONS
The major upper GI changes in cases of portal hypertension were esophageal varices, gastropathy and peptic ulcer disease (gastric and duodenal hyperaemia, gastritis, ulcers and erosions).Esophageal varices were equally prevalent among cirrhotic and non-cirrhotic portal hypertensive patients.The frequent variceal grading were grade II/III in those patients.Gastropathy is more prevalent in cirrhotic patients followed by NCPF and EPO.Gastric varices, chronic gastritis, gastroduodenitis and gastric ulcers were found only in cirrhotic portal hypertensive patients.