Portal Hypertension and Variceal Hemorrhage

doi:10.1016/j.mcna.2009.03.008

Medical Clinics of North America

Volume 93, Issue 4, July 2009, Pages 837-853

https://doi.org/10.1016/j.mcna.2009.03.008 Get rights and content

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Portal hemodynamics and pathogenesis of varices

Varices are portosystemic collaterals formed after preexisting vascular channels have been dilated by portal hypertension. The major sites of collaterals are around the rectum, umbilicus (“caput medusa”), retroperitoneum, and distal esophagus/proximal stomach. Portal hypertension is a clinical syndrome defined by a portal venous pressure gradient exceeding 5 mm Hg. It can arise from any condition interfering with the blood flow at any level within the portal system and can be classified as

Natural history of varices and predictors of hemorrhage

Varices do not form at an HVPG less than 12 mm Hg.5, 6 Although a threshold portal pressure of 12 mm Hg is required for the development of varices, once varices develop, the risk of rupture is largely determined by the variceal-wall tension (T), which, according to Frank's modification of Laplace's law (T = P × R/W) is a function of the transmural pressure (P), the radius (R) of the vessel, and the thickness of the vessel wall (W).⁷ P is directly related to the HVPG; therefore a reduction in

Diagnosis

A screening esophagogastroduodenoscopy (EGD) for the diagnosis of esophageal and gastric varices is recommended when the diagnosis of cirrhosis is made.¹⁶ The NIEC has classified esophageal varices as F1, F2, and F3 (corresponding to small, medium, and large [> 5 mm]) with or without red signs (red wale marks, cherry-red spots or hematocystic spots). The frequency of surveillance endoscopies with no or small varices depends on their natural history. In patients with compensated cirrhosis who

Preprimary prophylaxis

It is well established that varices do not develop until the HVPG exceeds 12 mm Hg. In animal models, the use of nonselective β-blockers has been shown to decrease the risk for the development of varices.²⁴ A large multicenter, placebo-controlled, double-blinded trial failed to show benefit of nonselective β-blockers (timolol) in the prevention of varices.¹² Thus, β-blockers are currently not recommended for preprimary prophylaxis.

Primary prophylaxis

Therapy for primary prophylaxis against variceal bleeding has evolved considerably over the past decade.

General Measures

The initial resuscitative measures offer the earliest opportunity to influence the outcome of an episode of acute variceal bleeding (Fig. 1 for a management algorithm). Many of the physiologic responses to hemorrhage may be impaired in patients with portal hypertension. A patient with suspected bleeding varices should be managed in an intensive care unit with appropriate expertise available in the medical and nursing staff. Initial resuscitation should follow the classic airway, breathing,

Secondary prophylaxis

The natural history following the onset of variceal hemorrhage may be divided into 2 phases:² an acute phase, which lasts approximately 6 weeks, and the long-term course. The former is characterized by a high probability of recurrent hemorrhage after a short period of hemostasis. The risk for such early rebleeding is greatest in the first 48 hours after admission. The median rebleeding rate in untreated individuals is around 60% within 1 to 2 years of the index hemorrhage, with a mortality of

Summary

Gastroesophageal variceal hemorrhage is a common and devastating complication of portal hypertension and is a leading cause of death in patients with cirrhosis. Many advances in the management of portal hypertension have occurred in the last 10 years. Although the role of EVL in primary prophylaxis is not established, effective therapy in the form of nonselective β-blockers is well accepted. The treatment of acute variceal bleeding is aimed at volume resuscitation, correction of coagulopathy,