Approach to Suspected Variceal Bleeding

Fig. 4.1
Active variceal bleeding at the gastroesophageal junction


Fig. 4.2
Acute variceal hemorrhage with “fibrin plug” identified on a varix (arrow)


Fig. 4.3
Large esophageal varices with red color signs

Several classifications of esophageal varices have been proposed (Tables 4.1 and 4.2), although these classifications are subject to interobserver and intraobserver variations [57]. The simplest and most commonly used classification consists of categorizing the varices as small (≤5 mm) or large (>5 mm) [8]. The presence of red signs, such as red wale marks and cherry red spots, is also described, which increases the risk of variceal hemorrhage. The size of the varices can be overestimated in a partially collapsed lumen, and so assessment of variceal size should be performed with the esophageal lumen distended and the stomach decompressed.

Table 4.1
Classification of esophageal varices per the Japanese Society for portal hypertension


Color (C)


White varices


Blue varices

Length (l)


Long length


Medium length


Short length

Form (F)

Shape and size


Lesions assuming no varicose appearance


Straight small-caliber varices


Moderately enlarged, beady varices


Markedly enlarged, nodular, or tumor-shaped varices

Red color sign (RC)

Red wale markings, cherry red spots, hematocystic spots




Small in number and localized


Intermediate between 1 and 3


Large in number and circumferential

Table 4.2
Paquet’s classification of esophageal varices

Grade 0

No varices

Grade I

Venectasia, disappearing with insufflation

Grade II

Larger, clearly visible, usually straight varices, not disappearing with insufflation

Grade III

More prominent varices, locally coil-shaped and partly occupying the lumen

Grade IV

Tortuous, sometimes grape-like varices occupying the esophageal lumen

The classification by Sarin is the most widely used classification system for gastric varices since it is simple to use and guides therapy. Gastric varices are classified on the basis of their location in the stomach and relationship with esophageal varices (Fig. 4.4).


Fig. 4.4
Sarin classification of gastric varices . (a) Type 1 gastroesophageal varices (GOV 1) are typically a continuation of esophageal varices into the lesser curvature of the stomach. (b) Type 2 gastroesophageal varices (GOV 2) are esophagogastric varices extending into the fundus. (c) Type 1 isolated gastric varices (IGV 1) are gastric fundal varices without the presence of esophageal varices. (d) Type 2 isolated gastric varices (IGV 2) are varices at ectopic sites in the stomach outside the cardiofundal region

Preprocedural Management

The initial management of variceal bleed is aimed at controlling the present episode as well as preventing further rebleeding, a phenomenon common in the first week and associated with increased mortality.


It is the cornerstone to the success of endotherapy and survival. Initial resuscitative measures include protection of airway, breathing, and circulation. Resuscitation efforts should be initiated at the same time as initial assessment in the emergency department and continued during the patient’s hospitalization. Most patients with suspected variceal bleeding should be admitted to a monitored intensive care setting. At least one large-bore (16 or 18 G) catheter should be placed intravenously (IV), and two IV lines should be placed when the patient has ongoing bleeding. Arterial blood gas analysis should be performed, with continuous pulse oximetry monitoring. Preprocedural endotracheal intubation for airway protection is required in the presence of active hematemesis, grade III and IV hepatic encephalopathy, anticipated difficulties with airway (e.g., short, thick neck) or sedation (e.g., active alcohol abuser), and other factors that predispose to aspiration [8]. Otherwise, the need for airway protection should continuously be assessed during endoscopy, with prompt temporary termination of the procedure if the risk for aspiration is deemed high (e.g., large-volume blood and clots retained in the stomach).

Gastrointestinal hemorrhage is poorly tolerated in cirrhotics compared to non-cirrhotics, and these patients are prone to renal failure. Colloids are preferred for volume resuscitation. The aims of volume replacement are to maintain a systolic blood pressure around 90–100 mmHg, a heart rate <100 beats per minute, a central venous pressure (CVP) of 1–5 mmHg, and minimum urine output of 40 mL/h. Blood transfusion in variceal hemorrhage should be initiated early, but a restrictive transfusion strategy is recommended. Overtransfusion leads to a rebound increase in portal pressure and increases the risk of rebleeding. Transfusion of packed red blood cells (PRBCs) should be done with the goal of maintaining the hematocrit level between 25 and 30 % and the hemoglobin level around 7–8 g/dL [9], although transfusion policy should be individualized and consider additional factors, such as age, comorbidities, hemodynamic instability, and ongoing bleeding. There are insufficient data to make specific management recommendations regarding coagulopathy and thrombocytopenia, and utilization of INR is not a reliable gauge of the coagulation status in cirrhotic patients. In practice, however, transfusion of platelets and plasma products to maintain a platelet count >40,000 and INR <2.5, respectively, in the peri-endoscopic period are reasonable thresholds. The use of recombinant activated factor VII (rFVIIa) in cirrhotic patients with acute variceal bleeding is not recommended. The promising role of thromboelastogram (TEG) in the peri-transplant period can be extrapolated for TEG-guided correction of coagulopathy.

Administration of Vasoactive Agents

The administration of a vasoactive drug to control variceal bleeding in cirrhotics was first used in clinical practice in 1962. Vasopressin was the agent used. Presently, various agents are available, and the selection of a particular vasoactive drug depends upon availability, local resources, and cost. In a patient with suspected variceal bleeding, the administration of a vasoactive agent is initiated at the time of admission and can be discontinued should subsequent endoscopy reveal a nonvariceal cause for the acute episode of hemorrhage.

Vasopressin and Its Analogs

Vasopressin is the most powerful splanchnic vasoconstrictor, decreasing blood flow to all splanchnic organs, with resultant decrease in portal venous inflow and thus the portal pressure. Because of its short half-life, vasopressin is given as a continuous infusion of 0.2–0.4 U/min IV, which can be increased to a maximum of 0.8 U/min. Bosch et al. demonstrated a decrease in HVPG of 23 % and decrease in intravariceal pressure of 14 % [10]. Due to its vasoconstrictive action in various vascular beds, the use of vasopressin is hampered by multiple side effects, including cardiac events (e.g., myocardial ischemia, arrhythmia), hypertension, bowel ischemia, limb gangrene, and cerebrovascular accidents. These adverse effects can lead to drug withdrawal in up to 25 % of patients [11]. To decrease the risk of complications, vasopressin should be used at the lowest effective dose for no more than 24 h and should always be combined with a vasodilator, such as nitroglycerin, to decrease its systemic hemodynamic effects. Because of the frequency and potential for serious side effects, as well as the availability of safer drug alternatives, the use of vasopressin has practically been abandoned.

Terlipressin is a synthetic analog of vasopressin with a longer biological half-life and significantly less side effects. It has an immediate vasoconstricting action, followed by a delayed effect due to slow transformation of terlipressin into vasopressin by the enzymatic cleavage of triglycyl residues. A single bolus of 2 mg of terlipressin decreased HVPG by 21 % and azygous blood flow by 25 %, which lasted for up to 4 h [12]. The overall efficacy of terlipressin in controlling variceal bleeding is 75–80 % at 48 h [13] and 67 % at 5 days [14]. Terlipressin has been shown to significantly improve control of bleeding and survival when compared to placebo [13, 15] and is the only vasoactive drug that has been shown to improve survival. However, terlipressin can provoke ischemic complications and severe dysrhythmia. Therefore, it should be used with caution or avoided altogether in select patients with a history of ischemic heart or cerebrovascular disease, limb or gut vasculopathy, or heart rhythm disorders.

Terlipressin is given as a 2 mg bolus IV every 4 h during the first 2 days. The dose is halved after bleeding is controlled and can be maintained for up to 5 days. Terlipressin is not available in the USA, but is commonly used in other countries in the setting of acute variceal bleeding. The administration of terlipressin at low dose in a continuous infusion has been tested in cirrhotic patients and septic shock with promising results [16, 17], but its use in acute variceal bleeding remains indeterminate and cannot be recommended as of yet.

Somatostatin and Its Analogs

Somatostatin and its analogs are potent vasoconstrictors by decreasing release of vasodilators (mainly glucagon) and by a direct splanchnic vasoconstrictive effect. Their main advantage over vasopressin is that they are relatively safe and can be used continuously for 5 days or even longer. Randomized trials and meta-analyses [18, 19] have demonstrated that somatostatin significantly improves control of bleeding when compared to placebo, but not survival [20]. On the other hand, its beneficial effect on the control of bleeding and early rebleeding is similar to that of terlipressin and with a better safety profile. Despite its favorable side-effect profile, intravenous infusion of somatostatin has been shown to predispose to renal vasoconstriction with subsequent reduction in glomerular filtration rate, free water clearance, and sodium excretion in patients with cirrhosis with ascites. Major side effects are rare and minor side effects include nausea, vomiting, and hyperglycemia, which occur in nearly one-third of patients. Because of its short half-life, somatostatin is given as a bolus injection of 250 μg followed by a continuous infusion of 250 μg/h IV [21]. Octreotide is a synthetic analog of natural somatostatin with a similar mechanism of action but a longer half-life. However, this does not result in longer hemodynamic effects [22, 23], probably due to the development of tachyphylaxis or rapid desensitization [24]. Octreotide is administered as a 50 μg bolus followed by a continuous infusion of 50 μg/h for 3–5 days.

Antibiotic Prophylaxis

Bacterial infection is a well-known serious complication of cirrhosis. Up to 20 % of cirrhotic patients who are hospitalized due to GI bleeding present with bacterial infections, and an additional 50 % will develop an infection while in hospital [25]. This risk is especially high in those patients with poor liver function (i.e., Child’s class B and C) [26]. Among infections, spontaneous bacterial peritonitis (SBP) is most common, followed by urinary tract infections, pneumonia, and multisite infections. In cirrhotic patients presenting with acute GI bleeding and ascites, a diagnostic tap of the ascites is required. Enteric flora is responsible for the majority of infections, and E. coli is the pathogen most commonly responsible. The infections probably impair coagulation and, hence, contribute to failure to control initial bleeding or early rebleeding. Antibiotic prophylaxis in cirrhotic patients with upper GI bleeding favorably impacts the rates of acute bacterial infections, rebleeding, and mortality. If oral intake is feasible, the recommended antibiotic is norfloxacin 400 mg twice daily for 7 days. Norfloxacin is a poorly absorbed quinolone that selectively inhibits gram-negative bacteria in the gut, which is the source of infection. An intravenous fluoroquinolone can be given if oral administration is not an option.

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May 30, 2017 | Posted by in GASTROENTEROLOGY | Comments Off on Approach to Suspected Variceal Bleeding
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