GASTROENTEROLOGY

1992;102:994-999

Factors Influencing Development of Portal Hypertensive Gastropathy in Patients With Portal Hypertension SHIV K. SARIN, DASIKA V. SREENIVAS, DEEPAK LAHOTI, and ANOOP SARAYA Department of Gastroenterology, G. B. Pant Hospital, New Delhi, India

Portal hypertensive gastropathy (PGP) is an important cause of bleeding in portal hypertension patients. Although hyperdynamic congestion seems to be the underlying mechanism, the factors that influence the development of PGP are not understood. To investigate these, 107 patients [cirrhosis, 35; noncirrhotic portal fibrosis (NCPF), 24; extrahepatic portal vein obstruction (EHPVO), 46; BuddChiari syndrome, 21 were prospectively studied. Eighty-three patients had Child’s A, 17 had Child’s B, and 7 had Child’s C liver disease. Before sclerotherapy, although intravariceal pressure was similar, 4 cirrhosis patients (3.7%) but no NCPF or EHPVO patients had PGP. After sclerotherapy, 21 additional patients (20.3%) developed PGP during a follow-up of 23.2 ~fr3.4 months (range, 1-52). The incidence of PGP was higher in cirrhotic patients (37.1%) than in NCPF (16.7%; P < 0.05)or EHPVO (6.7%; P < 0.01) patients. The probability of developing PGP among all patients at the end of 52 months of followup was 30%, more in cirrhosis than in EHPVO (55% vs. 15%; P < 0.005). Only 2 patients bled from PGP during follow-up. Development of PGP correlated with severity of liver disease, being more common in Child’s C than Child’s A patients (87% vs. 13%; P < 0.001). PGP was seen more often in patients with gastroesophageal varices than in patients with esophageal varices alone (42% vs. 11%; P < 0.01). In conclusion, the results show that development of PGP is significantly influenced by sclerotherapy, severity of liver disease, etiology of portal hypertension, and coexisting gastric varices and is not directly correlated with intravariceal pressure.

N

ext to varices, gastric mucosal lesions are an important cause of upper gastrointestinal bleeding in patients with portal hypertension. These lesions have been variously called erosive gastritis,‘S2 congestive gastropathy,3 mosaic pattern,4 portal hypertensive gastropathy,4 and vascular ectasiaa5 The incidence and profile of portal hypertensive gastropathy (PGP) has been variably reported in different series

of patients. Although Papazian et al. recorded mild to severe forms of gastropathy in all their patients4 and McCormack et al. observed these changes in about half their patients,3 we did not observe these changes as often.6 Hyperdynamic congestion seems to be the underlying mechanism for the development of PGP.7**Papazian et al. have stressed that PGP develops as a result of increased portal pressure per se, irrespective of the etiology of portal hypertension4 However, the number of patients with presinusoidal portal hypertension studied by them was very small. In an earlier study, we observed a significantly greater incidence of PGP in patients with cirrhosis compared with noncirrhotic portal fibrosis (NCPF).’ Thus, other factors do influence the development and severity of PGP.’ While the role of factors such as severity of liver disease, portal pressure, and extent of collateralization has not been well studied, the data on the influence of sclerotherapy in the development of PGP are quite controversia1.3.4 The present study was undertaken to assess the influence of endoscopic sclerotherapy on the development and profile of PGP. In addition, we have attempted to determine the role of other factors such as severity of liver disease, etiology of portal hypertension, presence of gastric varices, and variceal pressure on the occurrence of PGP. Materials and Methods Patients One hundred seven patients with portal hypertension (mean age k SEM, 26.8 + 4.4 years) presenting with variceal bleeding between 1986 and 1989 were carefully evaluated for the presence of PGP, both before and after endoscopic sclerotherapy. The detailed clinical information about the patients is summarized in Table 1. Portal hypertension was caused by cirrhosis of the liver in 35 (alcoholic, 12; nonalcoholic, 23), noncirrhotic portal fibro0 1992 by the American Gastroenterological 0016-5065/92/$3.00

Association

PORTAL HYPERTENSIVE GASTROPATHY 995

March 1992

Table 1. Clinical Features Hypertension

of Patients

With Portal Patients

Parameter

n

Total no. of patients Sex (M/F) Etiology EHPVO NCPF Cirrhosis Alcoholic Nonalcoholic Budd-Chiari syndrome Severity of liver disease Child’s A Child’s B Child’s C Gastric varices Present Absent

107 79/28

%

46 24 35 12 23 2

43 22 33

83 17

78 16 6

36 71

34 66

2

sis (NCPF) in 24, extrahepatic portal vein obstruction (EHPVO) in 46, and the Budd-Chiari syndrome in 2. The etiology of portal hypertension was confirmed according to the criteria described earlier.g The severity of liver disease was assessed by the Child’s criteria.” Every patient had a history of upper gastrointestinal bleeding and was subjected to endoscopic sclerotherapy after proper evaluation and resuscitation. Esophageal varices were graded according to Conn,” and gastric varices were classified as described earlier by us.”

Procedure Upper gastrointestinal (UGI) endoscopy was completed using an Olympus GIF-XQ 10 or 20 endoscope (Olympus Optical Company, Tokyo, Japan). The stomach and upper duodenum were carefully looked for, especially by taking the tip of the endoscope close to the mucosa. The fundus of the stomach was specifically screened by retroflexion of the endoscope to detect the presence of PGP and gastric varices. The precise distribution of PGP in the antrum, body, fundus, or whole stomach was carefully recorded. PGP was graded as mild if the presence of discrete cherry red spots with or without mosaic pattern (small elevated erythematous areas outlined by a subtle yellowish network) on the gastric mucosa was observed or severe if the presence of confluent red spots, diffusely distributed in a large portion of the stomach with or without active oozing, was observed. The endoscopist was kept blind to the findings of the previous endoscopy. The presence and grade of PGP were accepted on agreement between the observations of two independent endoscopists on two separate sessions performed at least 1 week apart.

Endoscopic

Scierotherapy

Endoscopic sclerotherapy was performed only for esophageal varices using absolute alcohol as a sclerosant as described previously.13 In brief, intravariceal injections

were given at the lower end of the esophagus using a transof the variceal wall parent Teflon injector. “Blanching” around the injection site was considered desirable. Approximately 15-20 mL of sclerosant was injected during a mean of five sclerotherapy sessions. Some patients included in this study did receive sclerotherapy later for gastric varices. However, data for PGP were collected before gastric variceal sclerotherapy in these patients. Gastric variceal sclerotherapy was not done in any patient if esophageal varices were still present. The end point of sclerotherapy was variceal obliteration. Presence or absence of PGP was carefully looked for before initiating sclerotherapy and at follow-up. During follow-up endoscopies after variceal obliteration, besides a search for PGP, recurrence of esophageal or gastric varices was carefully looked for. Every rebleeding was carefully investigated by performing emergency endoscopy to look for the cause of bleeding. A Sengstaken-Blakemore tube (Porjes S.A., France) was rarely used for the control of variteal bleeding, and only after UGI endoscopy. None of the patients were regularly taking nonsteroidal anti-inflammatory drugs, propranolol, or other portal pressure-reducing agents. A patient was occasionally prescribed antacids or sucralfate. Only 2 patients continued to consume moderate quantities of alcohol during the followup period. Intravariceal

Pressure

Intravariceal pressure was measured before sclerotherapy by using the direct needle puncture technique as described earlier.“’

Statistical

Analysis

Statistical analysis of the differences with respect to different discrete study variables between the groups was tested by applying x2 analysis and Fisher’s Exact Test where appropriate. Statistical significance of the differences in the values of the measurable variables such as intravariceal pressure were tested by Kruskal-Wallis oneway analysis of variance. The number of cases exposed to the risk of development of PGP at different follow-up periods was calculated using the life-table technique. The estimate of cumulative probability of developing PGP beyond a follow-up period of T months was calculated using actuarial survival method of Kaplan and Meier.” The differences in rates of development of PGP between any two groups were tested using the log-rank test.‘”

Results Presclerotherapy Four of the 107 patients (3.7%) had PGP before undergoing sclerotherapy. None of them had presented with bleeding from these mucosal lesions. All 4 patients were cirrhotic, giving an incidence of 11.4% of PGP in cirrhotic patients. There was no significant difference in the incidence of PGP between alcoholic (2 of 1217%) and nonalcoholic (2 of 239%) cirrhotics (Table 2). Two of the patients had Child’s

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GASTROENTEROLOGY Vol. 102, No. 3

SARIN ET AL.

Table 2. The Incidence of PGP in Different Groups Group

n

EHPVO NCPF

Cirrhosis Child’s grade A B C Etiology Alcoholic Nonalcoholic Budd-Chiari syndrome “No significant difference

between

No. of presclerotherapy PGP patients (%) -

No. of postsclerotherapy PGP patients (%)

Time of appearance (mo; mean + SEM)

4 (8.7%) 4 (16.7%) 13 (37.4%)

46 24 35

4 (11.4%)

11 17 7

2 (18%) 2 (29%)

3 (27%) 6 (35%) 4 (57%)

12 23 2

2 (17%) 2 (9%) -

5 (42%) 8 (35%) -

15.3 f 7.5 13.0 + 7.2 6.2 f 2.8

the three groups.

A and the other 2 had Child’s C liver disease. None of the patients with NCPF or EHPVO had PGP. Postsclerotherapy Twenty-one additional patients (20.3%) developed PGP during or on follow-up after obliteration of varices. The mean duration of follow-up was 23.2 f 3.4 months (range, l-52. months). The incidence was much higher in patients with cirrhosis (37.1%) than in those with NCPF (16.7%; P < 0.05) or EHPVO (8.7%; P < 0.01). The etiology of cirrhosis did not influence the incidence of PGP. After sclerotherapy, PGP was seen in 42% of alcoholic cirrhotics and 35% of nonalcoholic cirrhotics; the difference was not significant (Table 2). In the two Child’s C liver disease patients having PGP before sclerotherapy, the PGP persisted until the end of the follow-up period. In the other 2 patients with Child’s A cirrhosis, PGP disappeared 5 and 24 months after sclerotherapy and was not seen again until the end of follow-up. The PGP was mild in 14 patients and severe in 11. The severity of the lesions did not change appreciably after sclerotherapy. The mean time for the appearance of PGP was 8.5 + 2.5 months, the earliest appearance being after only two sessions of sclerotherapy and the last to appear being 52 months after sclerotherapy. It was not significantly different between patients with cirrhosis (6.2 k 2.8 months), NCPF (13.0 + 7.2 months), and EHPVO (15.3 f 7.5 months) (Table 2). The mean number of sclerotherapy sessions required for variceal obliteration were compared among patients who developed PGP (7.1 + 3.4) and those who did not (4.6 + 2.1); the difference was significant (P < 0.01). The probability or the cumulative rate of development of PGP among all cases at the end of 52 months of follow-up was observed to be 30.3%. The incidence of PGP among patients with cirrhosis, NCPF, and EHPVO was 54.7%, 21.8%, and 14.9%, respectively. The difference in rates between cirrhosis and

NCPF was significant only at the 10% level. The difference was highly significant between cirrhosis and EHPVO (P < 0.005) but not between NCPF and EHPVO patients. Liver Disease Status The severity of liver disease influenced the appearance of PGP. Two of the 83 patients (2.4%) with Child’s A liver disease had PGP before sclerotherapy compared with 2 of the 7 (29%) with Child’s C disease; the difference was significant (P < 0.05). After sclerotherapy, 6 of the 7 patients (87%) with Child’s C, 6 of the 17 (35%) with Child’s B, and 11 (EHPVO, 4; NCPF, 4; cirrhosis, 3) of the 83 (13%) with Child’s A disease had PGP; the differences between Child’s C and A were significant (P < 0.001). Relation With Gastric Varices Thirty-six of the 107 patients (34%) had gastric varices in addition to esophageal varices before sclerotherapy. The incidence of gastric varices in EHPVO (38%), NCPF (33%), and cirrhosis (28%) was comparable. PGP developed more often in patients who had coexisting gastric varices before undergoing sclerotherapy than in patients who had only esophageal varices (42% vs. 11%; P < 0.01). Recurrence in the form of gastric varices after esophageal variceal obliteration was seen in 4 patients; 1 each with NCPF and EHPVO and the other 2 with cirrhosis. PGP was noticed in 2 of them with the appearance of gastric varices. Relation With Intravariceal

Pressure

Intravariceal pressure was measured in 37 patients before sclerotherapy. There was no significant difference in the variceal pressure in patients with cirrhosis (19.4 f 7.9 mm Hg), EHPVO (21.0 f 8.1 mm Hg), and NCPF (23.4 + 2.6 mm Hg) (Figure 1). Intravariceal pressure in 8 patients who developed PGP

PORTAL

0

CIRRHOSIS

NCPF

EHPVO

Figure 1. Intravariceal pressure in patients with cirrhosis, NCPF, and EPVO. There was no significant difference in the variceal pressure between the three groups. Values in circles are number of patients.

(17.7 k 8.7 mm Hg) was compared with 29 patients who did not develop PGP (20.8 ~fr7.6 mm Hg) after sclerotherapy; the difference was not significant (Figure 2).

Bleeding From PGP Emergency endoscopy was performed in all patients presenting with UGI bleeding. A total of 29 episodes of UGI bleeding were recorded in 17 patients. The bleeding was from varices in 15 patients. Only in 2 patients was the bleeding found to be a result of PGP.

HYPERTENSIVE

GASTROPATHY

997

ent study provides a unique opportunity to investigate this issue because it includes a large number of patients with different etiologies of portal hypertension. The study material includes patients with prehepatic (EHPVO), intrahepatic presinusoidal and perisinusoidal (NCPF), and intrahepatic sinusoidal and postsinusoidal (cirrhosis) portal hypertension. The influence of factors such as endoscopic sclerotherapy, severity of liver disease, and presence of gastric varices has also been studied in these different groups of portal hypertensive patients. During the last decade, endoscopic sclerotherapy has emerged as the first line of management for acute variceal bleeding as well as for prevention of variceal rebleeding.13 In addition to variceal recurrence and complications related to the technique, PGP has been alleged to develop following sclerotherapy.3s4 However, none of the studies have provided conclusive data. In the study by McCormack et al., PGP developed in 6 patients after sclerotherapy, whereas in another 5 patients it disappeared after sclerotherapy.3 The observations of the present study, conducted prospectively in 107 patients, clearly show that sclerotherapy induces development of PGP. Only 4 patients (3.7%) had PGP before receiving 21 additional patients (20.3%) develsclerotherapy; oped PGP after sclerotherapy. Endoscopic sclerotherapy induced PGP irrespective of the etiology of portal hypertension. A several-

Location PGP was located in the fundus and upper body of the stomach in 21 of the 25 patients (84%). In 2 patients, it was limited only to the body. In 1 case gastropathy involved the fundus and the body, whereas in another the whole stomach was affected. Discussion The results of the present prospective study clearly show that PGP is relatively uncommon in our population of portal hypertensive patients. At the time of initial presentation, PGP was found in only 4 patients (3.7%). We observed a similar low incidence of 2.6% of PGP in a previous studys6 Similar reports of gastric mucosal lesions being an uncommon cause of bleeding in patients with portal hypertension have been reported by other workers from India.‘7J8 The incidence of PGP in the West, on the other hand, is reported to be considerably high.4*7 Why is there such variability in the incidence of PGP? The pres-

PGP(+)

POP(-)

Figure 2. Intravariceal pressure in patients with and without PGP. There was no significant (NS) difference between the two groups.

998 SARINET AL.

fold increase in the incidence occurred in patients with EHPVO, NCPF, and cirrhosis. What could be the mechanism by which sclerotherapy induces PGP? Because of occlusion of the varices by sclerotherapy, the sizable collateral flow at the cardia must be accommodated. This could occur by redistribution of the blood flow in the gastric microcirculation,lg increased flow via the periesophageal venous network, or redirection of the esophageal venous flow from mucosa to submucosa. Although the exact mechanism is not clear, it is possible that a state of acute congestion develops in the gastric microcirculation because of obstruction to venous outflow after sclerotherapy. This is not merely a passive congestion; it is a hyperdynamic congestion because portal hypertension per se is a hyperdynamic circulatory state.’ Studies on the measurement of gastric mucosal blood flow have been inconclusive, mainly for technical reasons; some workers have found an increase20~21 and others have observed a decrease in gastric blood flow in portal hypertension.“,” It would be more relevant to development of PGP to assess the extent of arteriovenous shunting and the distribution of blood flow between the luminal and serosal surfaces of the mucosa before and after sclerotherapy. Newer methods to quantitate mucosal blood flow such as reflectance spectrophotometry’g and laser Doppler studies may be of help. Is portal pressure the sole determinant for the development of PGP, as suggested by some investigators?3,4 In fact, Eleftheriadis et al. believe that PGP and ectopic varices have a common origin.23 This seems unlikely because not every patient with portal hypertension or variceal obliteration develops PGP. Another objection to portal pressure as the only factor in the development of PGP is based on our observations on intravariceal pressure, which closely reflects portal venous pressure.14 Whereas the variceal pressure was not different among patients with cirrhosis, NCPF, and EHPVO, PGP was seen only in cirrhotics before sclerotherapy. Moreover, the variceal pressure was not different between patients with and without PGP (Figure 2). Therefore, besides pressure, other related factors such as development of portosystemic shunts, ectopic varices, and individual variability in the gastric microcirculation may determine the chances of development of PGP in a given patient. Pre-existing gastric varices greatly influence the development of PGP. In the present study, 36 patients had gastric varices before undergoing sclerotherapy. Forty-two percent of these patients developed PGP compared with only 11% of patients who had no gastric varices before sclerotherapy, clearly indicating that the chances of development of PGP are quite high (nearly four times higher) if a patient

GASTROENTEROLOGYVol. 102.No.3

presents with gastroesophageal varices. The increased association of PGP with gastric varices could again be explained by redistribution of gastric blood flow after obliteration of esophageal varices. Gastric varices are known to communicate with esophageal varices through a network of submucosal veins.“*” The sclerosant injected intravariceally into the esophageal varices is likely to flow down and occlude the gastric varices and in turn enhance the chances of development of PGP. On the other hand, because the blood flow at the cardia is bidirectionaLz4 occasionally the pre-existing gastropathy may disappear after sclerotherapy because the flow from the esophagus to the gastric mucosa gets obliterated. This was seen in 2 of our patients. An important observation in our study was that the development of PGP was greatly influenced by the severity of the liver disease. Patients with Child’s C liver disease had PGP significantly more often, both before and after sclerotherapy, compared with patients with Child’s A or B liver disease. An increased incidence of PGP in patients with Child’s C liver disease could possibly be related to humoral substances,21’22 neuronal influences, or some unidentified factors.’ Does the etiology of portal hypertension influence the incidence of PGP? Seventy of the 107 patients in the present study (65%) had noncirrhotic portal hypertension: 24 had NCPF and 46 had EHPVO. Although 11% of the cirrhotics had PGP before sclerotherapy, none of the NCPF or EHPVO patients had PGP. This confirms our earlier observations.6 Even after sclerotherapy, the incidence of PGP remained low and could be explained by near-normal liver functions in patients with EHPVO and NCPF. PGP was predominantly located in the fundus of the stomach. This could also be explained on the basis of the venous drainage and microcirculation of the stomach.25 Bleeding from PGP was not a common feature in our patients. Of all the UGI bleeding episodes observed in these patients, PGP was responsible for bleeding in only 2 patients, maybe because the PGP is not as severe in our patients as in the Western patients. In conclusion, our results clearly show that development of PGP is strongly influenced by variceal obliteration achieved by endoscopic sclerotherapy, severity of liver disease, and coexisting gastric varices. Although increased portal pressure is a prerequisite, an interplay between several factors, as discussed above, determines the development of PGP in a patient with portal hypertension. More studies are needed to enable one to predict which patients will develop PGP and which will bleed from it.

PORTAL HYPERTENSIVE GASTROPATHY

March 1992

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1487. 22. Manabe T, Suzuki T, Honjo I. Changes of gastric blood flow in

experimentally induced cirrhosis of the liver. Surg Gynecol Obstet 1978;147:753-757. 23. Eleftheriadis E, Otzampass K, Tzartinoglou E, Alvanou A, Aletras H. Congestive gastropathy and antral varices: is there an association? Endoscopy 1989;21:208-211. 24. McCormack TT, Smith PM, Rose JD, Johnson AG. Perforating veins and blood flow in esophageal varices. Lancet 1983;2:1442-1444. 25. Kitano S, Terblanche

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-Received December 3, 1990. Accepted August 5, 1991. Address requests for reprints to: S. K. Sarin, M.D., D.M., Department of Gastroenterology, G. B. Pant Hospital, New Delhi 110 002, India. Part of this work was presented at the 41st annual meeting of the American Association for Study of the Liver, at Chicago, 1990 and was abstracted in Hepatology 1990;12:853. The authors thank the Indian Council of Medical Research for partial financial assistance to carry out this study. They are also grateful to Dr. K. R. Sundram, Additional Professor, Biostatistics, A.I.I.M.S., and Dr. N. S. Murthi Assistant Director, Biostatistics, C.R.C., New Delhi. for their help in statistical analysis.

Factors influencing development of portal hypertensive gastropathy in patients with portal hypertension.

Portal hypertensive gastropathy (PGP) is an important cause of bleeding in portal hypertension patients. Although hyperdynamic congestion seems to be ...
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