24 June 1978 SA MEDICAL JOURNAL 1079

delayed by partial release of pressure into the bowelwall. The sign nevertheless indicated the need for immediatesurgery.

REFER£ CES

I. Reyna, R., Sopsr, R. T. and Condon, R. E. (1973): Amer. J. Surg.,125, 667.

2. Wollocb, Y., Dinlsman, M., Weiss, A. et al. (1972): Arcb. Surg.,lOS, 723.

3. Jones, A. W. and Cole, F. M. (1967): Postgrad. med. J., 43, 680.4. Skucas, J., Spatarn, R. and Bruneau, R. J. (1977): Amer. J.

RoeOlgenol., 129, 601.5. Kerting, W. S., McCarver, R. R., Kovarik, J. L. et al. (1961):

Radiology, 76, 733.6. Marsbak, R. H., Blum, S. A. and Eliasopb, J. (1956): J. Amer. med.

Ass., 161, 1626.7. Gbabremalli. G. G., Port, R. B. and Beachley, M. C. (1974): Amer.

J. dig. Dis., 19, 315.8. Davis, L. and Lowman, R. M. (1957): Radiology, 68, 542.9. Dennis, C. (1944): Surgery, IS, 713.

Isolated Gastric Varices - a Separate Entity

Report of Two Cases

S. VAN DER SPUY

SUMMARYGastric varices may develop in the absence of oesophagealvarices and in the absence of portal hypertension. Isolatedgastric varices have only recently emerged as a separateentity. The condition is usually due to underlying pan­

creatic lesions. The diagnosis is made on endoscopy.Bleeding from the varices is best controlled by splenec­tomy, while the pancreatic lesion is dealt with on its ownmerits. Two cases are described to draw attention to thiscondition, and the salient features of this condition are

summarized diagrammatically.

S. Afr. med. J., 53, 1079 (1978).

Gastric varices are usually linked with oesophageal varices,which develop as a result of portal hypertension. Theymay, however, develop in the absence of oesophagealvarices and in the absence of portal hypertension. Iso­lated gastric varices have only recently been recognizedas a separate entity.' The varices result from splenic veinobstruction, which is usually produced by a pancreaticlesion, either chronic pancreatitis or pancreatic carcinoma.Bleeding from this- source is Dest controlled by splenec­tomy, while the pancreatic disorder is dealt with on itsown merits. Two patients seen in the Surgical Clinjcat the Provincial Hospital, Port Elizabeth, are describedto illustrate some of these features.

Department of Surgery, Provincial Hospital, Port ElizabethS. VAN DER SPUY, M.B. CH.B., F.R.C..

Date received: 19 December 1977.

CASE REPORTS

CaseI

A 40-year-old White man with a long history ofabuse of alcohol presented periodically since 1970with attacks of abdominal pain. In April 1974 he de­veloped a mass which was considered to be a pancreaticpseudocyst in the left upper quadrant, but it subsidedover a period of several weeks. Since then he has beenadmjtted to hospital several times with bouts of haema­temesis and melaena for which no cause was revealed bybarium meal examination.

He was extensively investigated during such an admis­sion in March 1975. A barium meal examination showedirregularity of the fundus, and the possibility of fundalvarices was raised for the first time (Fig. 1). At endo­scopy, however, no lesion was found to account for thebleeding. Histological sections of a biopsy specimenshowed essentially normal liver morphology. Hepatic veinwedge pressure was normal (8 mmHg). Splenoportographyshowed that the portal vein was patent, but that the splenicvein was occluded (Fig. 2). There was no evidence ofoesophageal varices, although the veins in the splenichilum were prominent.

In October 1976 the patient developed a severe haema­temesis and melaena. On this occasion the fundus wascarefully scrutinized during endoscopic examination, andlarge varices were noted. The oesophagus, on the otherhand, was free of varices. An operation was carried out inview of the severe, persistent bleeding. The liver ap­peared normal. No prominent portosystemic collaterals

1080 s MEDIESE TYDSKRIF 24 J unie 1978

Fig. 1. A barium meal examination shows irregularityof the fundus of the stomach, suggestive of varices.

Fig. 2. Splenoportogram carried out on case 1 shows apatent portal vein (large arrow) filled via a superiorpolar vein (smaller arrow). 0 oesophageal varices arepresent, but the veins in the splenic hilum are promi­nent.

were in evidence, although the short gastric veins weredistended. The spleen was enlarged and congested, andthe hilum was firmly cemented onto a thickened andfibrotic pancreas. After completion of the splenectomy,the spleen had shrunk to half its original size. Three weeksafter splenectomy there was no endoscopic evidence of

residual varices. Bleeding did not recur during a follow­up period of 1 year.

Comment: In this patient the pancreatic lesion had beensuspected for several years. Its significance in relation tothe gastro-intestinal bleeding, however, was not appre­ciated until the isolated gastric varices were noted. Thepancreatitis did not warrant active measures apart fromabstention from alcohol.

ease 2

A 56-year-old man presented on 18 July 1966 with aI-week history of haematemesis and melaena, precededby abuse of alcohol over a period of 10 years. A bariummeal examination revealed no abnormality. At endo­scopic examination no varices were visible in the oeso­phagus, but large varices were noted in the fundus of thestomach. A small erosion was situated on one of these.On irrigation of the area, brisk bleeding ensued fromthe erosion. Laparotomy was undertaken the same day.The liver was enlarged and appeared cirrhotic, and thespleen was enlarged and the pancreas thickened. Therewas no evidence of dilated portosysternic collaterals. Whenthe fundus of the stomach was opened, large varices, upto 1 cm in diameter, were encountered. These were under­run, and splenectomy and liver biopsy were carried out.

Histological sections of the liver showed a moderatedegree of fatty degeneration associated with portal cir­rhosis. Sections of the spleen showed evidence of con­gestive splenomegaly as seen in cirrhosis of the liver.

The patient was readmitted 5 months postoperativelywith a small haematemesis. -At endoscopy there was noevidence of residual gastric varices, but a small ulcer waspresent in the antrum. The ulcer responded well to con­servative treatment, and there had been no recurrence ofbleeding when the patient was last seen 1 year aftersplenectomy.

Comment: The diagnosis of isolated gastric varices wasmade without delay in this patient. The underlying pan­creatitis was not suspected until the varices were noted;because the patient was asymptomatic, no active treat­ment was advised. Unfortunately, severe bleeding neces­sitated an emergency operation; confirmatory stUdies(pancreatography and portography) and venous pressuremeasurements were not done.

DISCUSSION

Isolated gastric varices are easily overlooked. Patientstherefore characteristically have a history of recurrentbleeding of unknown origin.' Only if the fundus of thestomach is carefully scrutinized for varices is the diag­nosis likely to be made. Even then, they may be mis­taken for prominent mucosal folds. The tortuosity of thevarices and their bluish colour, however, betray theirtrue nature. Mechanical interference with these varicesis to be avoided; even irrigation of an overlying erosionprecipitated brisk bleeding in case 2. Attempts at biopsyare certainly fraught with danger, as can be expected.

The significance of gastric varices as an isolated find­ing emerged comparatively recently. Rosch' published

24 June 1978 S A MED I C A L· J 0 URN A L 1081

Endoscopy: No varices in

Spleno- portography:

-Splenic v. obstructed

- Portal v. patent"

- Distended .... ,

collaterals "in the hilum

of the spleen

At Operation:

-No striking collaterals

-Liver normal

-Pancreatic lesion is found

-Splenic hilum is frozen-Treatment: Splenectomy

in the fundus

v.

,.... ,

'Gastro-epiploic v.

"Inf. Mesenteric v., ,

'- Sup. Mesenteric: v.

Fig. 3. Diagrammatic representation of the salient findings ill patients with isolated gastric varices.

a study of pancreatic disease by splenoportography in1965. He showed that complete obstruction of the splenicvein may occur, or the splenic vein may be compressedby the pancreatic mass against the vertebral column andlarge vessels. In 1969, Hess' suggested that chronic pan­creatitis and pancreatic carcinoma may result in splenicvein obstruction in 22% of cases. The course of thesplenic vein along the posterosuperior surface of the pan­creas, where it often forms a groove, makes it suscep­tible to mechanical compression and peripancreatic fi­brosis (Fig. 3).

Sutton et al.' reviewed 53 cases of isolated splenic veinthrombosis in the English literature. In almost all thecases isolated gastric varices developed and these maybleed considerably. Johnston and MyersS reported a fur­ther 8 cases, all secondary to disease of the pancreas.Rosch' reported 12 patients with isolated gastric varices,which characteristically presented with recurrent gastro­intestinal bleeding of unknown origin. He stressed theendoscopic diagnosis, i.e. the finding of gastric varicesin the absence of oesophageal varices, and suggested thatthis indicates an underlying pancreatic lesion. Of the 12patients, 10 were found to have chronic pancreatitis, and2 had pancreatic carcinoma. The pancreatic lesion isoften unsuspected and is demonstrated on retrogradepancreatography or at operation. Other confirmatorytests include splenoportography, measurement of portalvenous pressure, and liver biopsy. Splenic vein obstruc­tion is demonstrated on splenoportography with retro­grade flow of blood to the portal vein via the gastricand gastro-epiploic veins. If the left gastric or coronaryveins are patent, oesophageal varices do not develop.The portal vein pressure is normal. Liver biopsy general­ly shows normal hepatic morphology. The salient findings

are summarized in Fig. 3.Treatment is directed at the control of bleeding. This is

best done by splenectomy, which involves ligation of thefeeder vessel, i.e. the splenic artery. It is important tomake the diagnosis pre-operatively. This requires anawareness of the condition, and careful scrutiny of thefundal region of the stomach specifically for varices onendoscopic examination, in all cases in which the causeof bleeding is not apparent or is uncertain. The surgeonis unlikely to make the correct diagnosis at operation thefirst time. There may be few prominent collaterals toattract his attention.

Abuse of alcohol may therefore give rise to two distincttypes of varices; firstly, varices of the oesophagus andstomach due to portal hypertension and cirrhosis of theliver, and secondly, but more rarely, isolated gastric vari­ces due to lienal hypertension and chronic pancreatitis.This raises the inevitable question of whether these con­ditions do not, in fact, coexist on occasion. It would beimportant to recognize this, because the superimpositionof splenic vein obstruction on portal hypertension ap­pears to call for splenectomy as part of the treatmentprogramme. It is suggested, therefore, that in patientsbleeding from varices, special note be taken of thepatency of the splenic vein and its bearing on manage­ment.

REFERENCES

I. Rasch, w. (1974): Endoscopy, 6, 217.

2. Rasch, J. (1965): Radiologe, 5, 274.

3. Hess. W. (1969): Die ChrolJische Pankreut;/;s. AkfuelJe Prohleme ;11der Clrirurgie. Berne: Hans Huber.

4. Sutton, J. P., Yarborough, D. Y. and Richards, T. J. (1970): Arch.Surg., lOO, 623.

5. Johnston, F. R. and Myers, R. T. (1973): Ann. Sur8., 177, 736.