Esophageal Varices Medication
- Author: Samy A Azer, MD, PhD, MPH; Chief Editor: Julian Katz, MD more...
Medication Summary
Two major categories of drugs (vasoconstrictors and vasodilators) are used to treat acute bleeding related to portal hypertension.
The main advantages to using vasoactive agents include the ability to treat variceal bleeding in the emergency department, lowering of the portal pressure, and offering the endoscopist a clearer view of varices because of less active bleeding. Vasoactive agents represent an ideal treatment for sources of portal hypertensive bleeding other than esophageal varices (eg, gastric varices >2 cm below the gastroesophageal junction or portal hypertensive gastropathy).
In the treatment of acute variceal bleeding, somatostatin, terlipressin, or octreotide is now the preferred therapy before performing endoscopy. Intravenous infusions of octreotide will lower portal blood pressure and can prevent rebleeding during the patient's initial hospitalization.
Vasoconstrictors
Class Summary
Vasoconstrictors reduce portal blood flow and/or increase resistance to variceal blood flow inside the varices. Therefore, these drugs reduce blood flow in the gastroesophageal collaterals because of their vasoactive effects on the splanchnic vascular system.
Vasopressin (Pitressin)
Has vasopressor and antidiuretic hormone (ADH) activity. Increases water resorption at the distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). However, vasoconstriction is also increased in splanchnic, portal, coronary, cerebral, peripheral, pulmonary, and intrahepatic vessels. Decreases portal pressure in portal hypertension.
Notable adverse effect is coronary artery constriction that may dispose patients with coronary artery disease to cardiac ischemia. This can be prevented with concurrent use of nitrates. Rarely used.
Terlipressin (Glypressin)
Synthetic analogue of vasopressin. Only pharmacologic agent shown to reduce mortality from variceal bleeding.
Widely used in Europe. In the United States, has orphan drug status to treat bleeding esophageal varices.
Has longer biologic activity compared with vasopressin.
Significantly reduces portal and variceal pressure and azygos flow. Beneficial when combined with sclerotherapy. Also has advantage of preserving renal function (particularly important in patients with cirrhosis).
Antisecretory Agents
Class Summary
Antisecretory agents are used as adjuncts to nonoperative management of secreting cutaneous fistulas of the stomach, duodenum, small intestine (jejunum and ileum), or pancreas.
Somatostatin (Zecnil)
Naturally occurring tetradecapeptide isolated from the hypothalamus and pancreatic and enteric epithelial cells. Diminishes blood flow to portal system due to vasoconstriction, thus decreasing variceal bleeding. Has similar effects as vasopressin but does not cause coronary vasoconstriction. Rapidly cleared from the circulation, with an initial half-life of 1-3 min.
Octreotide (Sandostatin)
Synthetic octapeptide. Compared with somatostatin, has similar pharmacologic actions with greater potency and longer duration of action.
Beta-adrenergic Blockers
Class Summary
Beta-adrenergic blockers may block the effect of vasodilators, decrease platelet adhesiveness and aggregation, and increase the release of oxygen to tissues.
Propranolol (Inderal)
Competitive nonselective beta-adrenergic receptor antagonist without intrinsic sympathomimetic activity. Competes with adrenergic neurotransmitters (eg, catecholamines) for binding at sympathetic receptor sites. Similar to atenolol and metoprolol, propranolol blocks sympathetic stimulation mediated by beta1-adrenergic receptors in the heart and vascular smooth muscles.
Vasodilators
Class Summary
Vasodilators reduce the intrahepatic vascular resistance without decreasing peripheral or portal-collateral resistance.
Nitroglycerin PO (Nitro-Bid, Nitrostat, Deponit)
Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in blood pressure.
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