Portal Hypertension
Prognosis and Treatment
Prognosis is critically dependent on liver function. Liver failure is often
the prime cause or a significant associated factor in mortality. The in-hospital
(all inclusive) mortality rates with GI bleeding in Child-Pugh grade A (5 to
10%), B (15 to 25%), and C (50 to 70%) patients allow stratification of patients
to improve assessment of outcome.
Treatment:
All patients with portal hypertension who have GI hemorrhage must be hospitalized.
About 50 to 75% of bleeding episodes in cirrhotic patients are a direct consequence
of portal hypertension: Bleeding is from either ruptured gastroesophageal varices
or diffuse oozing from the gastric mucosa (congestive gastropathy). In congestive
gastropathy, mesenteric venous hypertension leads to congestion of the gastric
mucosa, particularly the fundus, rendering it more susceptible to damage and
bleeding even with minor insults (eg, modest alcohol or aspirin ingestion).
Other causes of GI bleeding (eg, duodenal or gastric ulcer, Mallory-Weiss lacerations)
account for bleeding in the remaining patients.
Standard resuscitation measures include fluid and blood transfusions. Sedatives
should be avoided, in view of possible encephalopathy. In the latter, cleansing
enemas will remove blood products from the bowel, and lactulose will reduce
hepatic encephalopathy. To determine the site of bleeding, endoscopy within
24 h of admission is advisable.
The most difficult, lethal bleeding is caused by variceal rupture. Emergency
measures to stop variceal bleeding include mechanical balloon tamponade, vasoconstrictor
drugs, and particularly endoscopic sclerotherapy, which is considered the first
choice of therapy. Surgery should be avoided, if possible, because of the high
operative mortality rate.
Types of balloon devices for esophageal tamponade are the Minnesota tube with
an esophageal suction port, the Sengstaken-Blakemore tube with both an esophageal
and gastric balloon, and the Linton-Nachlas tube with only a large gastric balloon.
In practice, all are equally effective but potentially dangerous. Only experienced
physicians should use these devices; the complication rate is 10 to 20%, even
in experienced hands. Complications include aspiration pneumonia, esophageal
rupture, and asphyxia.
Vasoactive agents that lower portal pressure are vasopressin (20 u. IV over
10 to 20 min) and a long-acting analog (terlipressin, and somatostatin or one
of its analogs). Prolonged vasopressin infusions at lower dosage (eg, 0.1 to
0.4 u./min given over > 4 h) should be avoided due to side effects of coronary
and mesenteric vasoconstriction that can lead to infarction, renal shutdown
with oliguria, and local tissue necrosis if the IV infusion extravasates. Besides,
long-term use is limited by the development of tachyphylaxis. Concomitant sublingual
nitroglycerin (0.3 mg q 1 h) may help avoid some of the side effects of vasopressin.
European experience with terlipressin suggests that its efficacy and side effects
are comparable to vasopressin. Somatostatin may prove to have fewer side effects
and equivalent efficacy.
The procedure of choice is endoscopic sclerotherapy. Variceal injections of
several types of sclerosing agents effectively control acute bleeding and, later
as elective therapy, eradicate varices once patients have stabilized. Complications
of sclerotherapy include esophageal ulceration and perforation and, rarely,
pulmonary embarrassment or portal vein thrombosis.
Surgery has a limited role. If bleeding is unresponsive or recurrent, the simplest,
safest intervention is esophageal transection with a stapling gun. This controls
bleeding in 90 to 95% of cases. A beneficial effect on survival has yet to be
shown with any form of surgical therapy.
Chronic therapy:
Once the acute bleeding episode is over and the cirrhotic
patient becomes stable , further treatment may be with drugs, sclerotherapy,
or surgery. Propranolol appears to reduce rebleeding risk in a minority of patients,
but responders cannot be easily identified, so routine use cannot yet be recommended.
Other drugs (eg, clonidine, prazosin, ketanserin, and verapamil) are even more
experimental.
Sclerotherapy is currently the procedure of choice, but changes in long-term
prognosis remain unproven. For patients who continue to rebleed despite sclerotherapy,
surgical options include liver transplantation, if indicated, or a shunt procedure
to decompress the portal venous system into the systemic circulation. Various
types of portacaval and mesocaval shunts, as well as the splenorenal shunts
(including the distal splenorenal shunt, the Warren shunt), all divert some
or all of the portal blood away from the liver. These procedures tend to precipitate
hepatic encephalopathy, a disabling condition that has limited the value of
portal decompression. Other side effects include deterioration of liver function
and onset or progression of hepatic iron deposition (hemosiderosis).
table Of Contents
Source: The Merck Manual
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