1. Haematemesis and melaena were the principal symptoms
in 60 per cent of the cases of portal hypertension treated in
the Professorial Surgical Unit of the Royal Infirmary,
Edinburgh. The source of the bleeding was the lower end of
the oesophagus and the cardia and fundus of the stomach, where
the subepithelial and subglandular plexuses form part of one
important anastomotic link between the portal and the systemic
venous circulations when there is obstruction to the normal
flow of portal blood through the liver. Because it is
separated only by epithelium from the lumen of the oesophagus,
the subepithelial plexus has been classified as a dangerous
or vulnerable type of collateral circulation, whereas the
anastomoses which occur in the falciform ligament and retro - peritoneally lie deep in the tissues and are entirely
beneficial.
2. The presence of such oesophageal varices is regarded
as the major indication for surgical intervention, but
statistical analysis does not show that the survival rate
after operation is significantly better than after medical
treatment alone. Possible reasons for this paradox have
been discussed, and particular stress has been laid upon the
selection of patients for operation and the selection of the
time for operation in individual cases.
3. The other indications for operation in portal hypertension are a depression of the numbers of circulating
granulocytes or platelets sufficiently severe to be causing
symptoms or interfering with recovery from intercurrent
illness, and splenomegaly which is already painful or is so large as to be a potential source of danger to the patient.
There is some evidence to suggest that once the pattern of
the collateral circulation is determined in the individual
case, it does not change. Hence, if such symptoms occur in
a patient in whom there is no history of haematemesis and no demonstrable oesophageal varices, splenectomy may be performed
as the operation of deliberate choice. That splenectomy alone
is not the elective operation in patients who have been
bleeding before operation or who have demonstrable varices in
the oesophagus is indicated by the high percentage of such
cases in which haematemesis recurs.
4. Experience with limited oesophago-gastrectomy in the
treatment of portal hypertension is still small, and the
time which has elapsed since surgery is too short to permit
other than tentative opinions about its usefulness. It may
have a more adverse effect upon the functional efficiency of
the cirrhotic liver than portal -systemic anastomosis,
especially when it is followed by difficulty in swallowing
or regurgitation of food. At present it appears to be
indicated in children, in young people and in any patient who
has had recurrence of bleeding after other forms of surgical
!intervention.
5. In cases with hepatic cirrhosis, operation is always
followed by deterioration in hepatic function, the degree
and duration of the changes in the biochemical tests depending
principally
upon the pre- operative condition of the liver.
If this period of functional depression is successfully
weathered, tests done at intervals of a year or more after
operation indicate that the functional efficiency of the liver
at that time is not significantly different from its preoperative state, irrespective of the type of operation
performed. It is because of the immediate impact of surgery
upon the decompensated liver that there is so high a mortality
after operation in cases with ascites, for ascites is typicallyi
a sign of hepatic failure. Such cases should be treated by
medical measures and should be submitted to portal -systemic
venous anastomosis only when no further benefit can be
expected from medical treatment alone and when there is the
additional risk of haemorrhage from oesophageal varices.
6. The propriety of any form of surgery in portal hypertension associated with hepatic cirrhosis has been discussed.
The two outstanding causes of death in these cases are gastrooesophageal haemorrhage and hepatic failure. Haemorrhage is
the principal cause of death in nearly 50 per cent of cases
not submitted to surgery. Frequently the amount of blood
lost is small compared, for example, with the loss from a bleeding peptic ulcer, but the effect of even temporary
hypotension and hypoxia on the already damaged liver may be
an extensive and fatal parenchymal necrosis. The prognosis
in cirrhosis is evidently worse where the possibility of
haemorrhage from oesophageal varices exists, and this is the
feature which it is the prime aim of surgery to relieve.
7. Further improvement in the results of treatment of
Portal Hypertension depends less upon the elaboration of
surgical techniques than upon better assessment of the
functional efficiency of the liver and the development of
quicker and more effective methods of preparing for operation
the patient in whom severe hepatic dysfunction exists along
with clinical evidence of portal hypertension.
