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.

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.

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.