History:
  • Symptoms of liver disease
    • Weakness, tiredness, and malaise
    • Anorexia
    • Sudden and massive bleeding with shock on presentation
    • Nausea and vomiting
    • Weight loss - Common with acute and chronic liver disease, mainly due to anorexia and reduced food intake, and regularly accompanies end-stage liver disease, when a loss of muscle mass and adipose tissue often is a striking feature
    • Abdominal discomfort and pain - Usually felt in the right hypochondrium or under the right lower ribs (front, side, or back) and in the epigastrium or the left hypochondrium
    • Jaundice or dark urine
    • Edema and abdominal swelling
    • Pruritus - Usually associated with cholestatic conditions, such as extrahepatic biliary obstruction, primary biliary cirrhosis, sclerosing cholangitis, cholestasis of pregnancy, and benign recurrent cholestasis
    • Spontaneous bleeding and easy bruising
    • Encephalopathic symptoms - Disturbance of the sleep-wake cycle, deterioration in intellectual function, memory loss and, finally, inability to communicate effectively at any level, personality changes, and, possibly, display of inappropriate or bizarre behavior
    • Impotence and sexual dysfunction
    • Muscle cramps - Common in patients with cirrhosis
  • Past medical history
    • Previous jaundice suggests the possibility of a previous acute hepatitis, hepatobiliary disorder, or drug-induced liver disease.
    • Recurrence of jaundice suggests the possibility of reactivation, infection with another virus, or the onset of hepatic decompensation.
    • Patients may have a history of blood transfusion or administration of various blood products.

       

    • A history of schistosomiasis in childhood may be obtained from patients in whom infection is endemic.

       

    • Intravenous drug abuse
  • Family history of hereditary liver disease such as Wilson disease

     

  • Risk factors for upper GI bleeding
    • Bleeding diathesis

       

    • Peptic ulcer disease

       

    • Use of alcohol or nonsteroidal anti-inflammatory drugs (NSAIDs)

       

    • Documented cirrhosis

       

    • Documented episodes of GI tract bleeding

       

    • History of recent vigorous retching or emesis before an attack of hematemesis or melena

Physical:

  • Pallor may suggest active internal bleeding.
  • Low blood pressure, increased pulse rate, and postural drop of blood pressure may suggest blood loss.
  • Parotid enlargement may be related to alcohol abuse and/or malnutrition.
  • Cyanosis of the tongue, lips, and peripheries due to low oxygen saturation may be observed.
  • Patients may experience dyspnea and tachypnea.
  • A hyperdynamic circulation with flow murmur over the pericardium may be present.
  • Jaundice may be present because of impairment of liver function.
  • Look for telangiectasis of the skin, lips, and digits.
  • Gynecomastia results from sex hormone imbalance in liver disease.
  • Fetor hepaticus occurs in portosystemic encephalopathy of any cause (eg, hepatitis, cirrhosis).
  • Palmar erythema and leuconychia may be present in patients with cirrhosis.
  • Ascites, abdominal distention due to accumulation of fluid, may be present. Ascites may be associated with peripheral edema and may involve the abdominal wall and genitalia.
  • Numerous dilated veins radiating out of the umbilicus may be observed. Distended abdominal wall veins may be present, with the direction of venous flow away from the umbilicus.
  • The liver may be small.
  • Splenomegaly occurs in portal hypertension.
  • Testicular atrophy is common in males with cirrhosis, particularly those with alcoholic liver disease or hemachromatosis.
  • Venous hums, continuous noises audible in patients with portal hypertension, may be present as a result of rapid turbulent flow in collateral veins.
  • During the rectal examination, obtain a stool sample for visual inspection. A black, soft, tarry stool on the gloved examining finger suggests upper GI bleeding.

Causes: Diseases interfering with portal blood flow can result in portal hypertension and the formation of esophageal varices. Causes of portal hypertension usually are classified as prehepatic, intrahepatic, and posthepatic.

  • Prehepatic
    • Splenic vein thrombosis
    • Portal vein thrombosis
    • Extrinsic compression of the portal vein
  • Intrahepatic
    • Congenital hepatic fibrosis
    • Hepatic peliosis
    • Idiopathic portal hypertension
    • Sclerosing cholangitis
    • Tuberculosis
    • Schistosomiasis
    • Primary biliary cirrhosis
    • Alcoholic cirrhosis
    • Hepatitis B virus–related and hepatitis C virus–related cirrhosis
    • Wilson disease
    • Hemachromatosis
    • Alpha1-antitripsin deficiency
    • Chronic active hepatitis

       

    • Fulminant hepatitis
  • Posthepatic
    • Budd-Chiari syndrome

       

    • Thrombosis of the inferior vena cava

       

    • Constrictive pericarditis

       

    • Venoocclusive disease of the liver




 


Other Problems to be Considered:

Acute gastric erosions
Portal vein thrombosis
Splenic vein thrombosis
Venoocclusive disease
Alcoholic cirrhosis
Hepatoportal arteriovenous fistula

Gastric varices: These are the source of bleeding in 5-10% of patients with variceal hemorrhage. Higher rates are reported in patients with left-sided portal hypertension due to thrombosis of the splenic vein.

Portal hypertensive gastropathy: This is a common complication of cirrhosis and portal hypertension, but significant bleeding from this source is relatively uncommon.

 

Lab Studies:
 

  • Complete blood count: Results may show anemia, leucopenia, and thrombocytopenia in patients with cirrhosis. Anemia may be secondary to bleeding, nutritional deficiencies, or bone marrow suppression secondary to alcoholism. Many patients with portal hypertension have some degree of hypersplenism. The hematocrit value may be low in patients with upper abdominal bleeding.
  • Type and crossmatch blood and order 6 units of packed red blood cells.
  • Prothrombin time: Because the coagulation factors involved in this test are synthesized by the liver, impairment of the liver function may result in a prolonged prothrombin time.
  • Liver function tests: A mild elevation of the plasma activity of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) may occur in cirrhosis, although activity may be normal.
  • Blood urea, creatinine, and electrolytes: Blood urea and creatinine levels may be elevated in patients with esophageal bleeding. Drug treatment, cirrhosis, ascites, and blood loss may contribute to changes in the serum electrolytes of these patients.
  • Arterial blood gas and pH measurements
  • Hepatic serology helps in the assessment of the cause of cirrhosis.

Imaging Studies:
 

  • Ultrasound of the upper abdomen may be indicated, especially if biliary obstruction or liver cancer is suspected.

Other Tests:
 

  • Rectal examination: Obtain a stool sample for visual inspection. A black, soft, tarry stool on the gloved examining finger suggests upper GI bleeding.

Procedures:
 

  • Endoscopy is required at an early stage to formulate the management plan. If active variceal bleeding or an adherent clot is observed, variceal hemorrhage can be diagnosed confidently. The presence of variceal red color signs (eg, cherry red spots, red whale markings, blue varices) indicates an increased risk of further bleeding.
     
 

Medical Care:

  • Esophageal varices with no history of bleeding
    • Patients with esophageal varices and no prior history of variceal hemorrhage should be treated with nonselective beta-adrenergic blockers (eg, propranolol, nadolol, timolol), provided that the use of beta-blockers is not contraindicated (eg, because of insulin-dependent diabetes mellitus, severe chronic obstructive lung disease, congestive heart failure).

       

    • The dose of nonselective beta-blockers is determined by a 25% decrease in resting heart rate or a decrease in heart rate to 55 beats per minute or the development of adverse effects.

       

    • The use of beta-blockers decreases the risk of initial variceal bleeding by approximately 45%.

       

    • If contraindications to using beta-blockers exist, long-acting nitrates (eg, isosorbide 5-mononitrate) are alternatives.

       

    • Treatment with beta-blockers should be continued indefinitely.

       

    • The role of endoscopic sclerotherapy or variceal ligation for prevention of esophageal variceal hemorrhage is still controversial.

       

    • Combined sclerotherapy and treatment with nonselective beta-blockers offer no advantages over the use of beta-blockers alone for prevention of esophageal varices hemorrhage.
  • Bleeding esophageal varices
    • Assess the rate and volume of bleeding. Check blood pressure and pulse with the patient in the supine position and with the patient in a sitting position.

       

    • Gain venous access and obtain blood for immediate hematocrit. Obtain a type and crossmatch. Measure the platelet count and prothrombin time. Send blood for renal and liver function tests and measure serum electrolytes.

       

    • Provide emergency treatment as outlined below.
  • Emergency treatment
     

       

    • Promptly resuscitate and restore circulating blood volume of patients with suspected cirrhosis and variceal hemorrhage

       

    • Establish intravenous access for blood transfusion. While the blood is being crossmatched, start rapid infusion of 5% dextrose and colloid solution until blood pressure is restored and urine output is adequate.

       

    • Establish airway protection in patients with massive upper GI tract bleeding, especially if the patient is not fully conscious.

       

    • If indicated, correct clotting factor deficiencies with fresh frozen plasma, fresh blood, and vitamin K-1.

       

    • Insert a nasogastric tube to assess the severity of bleeding and to lavage gastric contents before endoscopy.

       

    • Consider pharmacologic therapy (octreotide or somatostatin) and endoscopy as soon as the patient has been resuscitated. The aim is to establish the cause and to control the bleeding.

       

    • Endoscopic therapy probably has replaced balloon tamponade as the initial therapy for variceal bleeding. Balloon tamponade now rarely is necessary, and, when it is used, it must be performed by experienced personnel because it is potentially dangerous.
  • Endoscopic therapy
     

       

    • Sclerotherapy

         

      • Sclerotherapy is successful in controlling acute esophageal variceal bleeding in 80-90% of patients. Control should be obtained with 1-2 sessions. Patients continuing to bleed after 2 sessions should be considered for alternative methods to control their bleeding.

         

      • In the United States, sodium tetradecyl sulfate or sodium morrhuate generally has been used as a sclerosant, while polidocanol or ethanolamine has been more popular in Europe. Variations in the technique or the sclerosant used have not been shown to influence the outcome.

         

      • Serious complications related to sclerotherapy have been reported in 15-20% of patients, with an associated mortality rate of 2%.

         

      • Complications of sclerotherapy may include mucosal ulceration, bleeding, esophageal perforation, mediastinitis, and pulmonary complications. Long-term complications, such as esophageal stricture formation, also may occur.

       

    • Endoscopic variceal ligation (banding)

         

      • Endoscopic variceal ligation is based on the widely used technique of rubber-band ligation of hemorrhoids. The esophageal mucosa and the submucosa containing varices are ensnared, causing subsequent strangulation, sloughing, and eventual fibrosis, resulting in obliteration of the varices.

         

      • Endoscopic ligation requires placement of an opaque cylinder over the end of the endoscope. This decreases the endoscopic field of view and may allow pooling of blood. Thus, in patients with active bleeding, visualization may be impaired more with ligation than with sclerotherapy.

         

      • Recent trials have demonstrated that ligation and sclerotherapy achieved similar rates of initial hemostasis in patients whose varices were actively bleeding at the time of treatment.

         

      • Local complications are less common with ligation compared to sclerotherapy. For example, esophageal strictures were found to be less common with ligation compared to sclerotherapy. Systemic complications, such as pulmonary infections and bacterial peritonitis, were not significantly different in the 2 groups. However, a trend was observed toward a decrease in these 2 complications in patients treated with ligation.

Surgical Care:

Surgical care and therapeutic radiologic procedures for variceal hemorrhage

Approximately 5-10% of patients with esophageal variceal hemorrhage have conditions that cannot be controlled by endoscopic and/or pharmacologic treatment. Balloon tamponade (eg, Minnesota tube, Sengstaken-Blakemore tube, Linton-Nachlas tube) may be used as a temporary option in their management. Definitive salvage options may include the following:

  • Surgical interventions include the following:
    • Portosystemic shunt
    • Devascularization (transabdominal devascularization of the lower 5 cm of the esophagus and the upper two thirds of the stomach, with staple gun transection of the lower esophagus) rarely is performed but may have a role in patients with portal and splenic vein thrombosis who are not suitable candidates for shunt procedures and who continue to have variceal bleeding despite endoscopic and pharmacologic treatment.
    • Orthotopic liver transplantation is the treatment of choice in patients with advanced liver disease.
  • Therapeutic radiologic procedures include the following:
    • Percutaneous transhepatic embolization of gastroesophageal varices (PTE) involves catheterization of the gastric collaterals that supply blood to varices via the transhepatic route. A variety of agents had been used, with varying degrees of success in controlling acute bleeding. Generally, this procedure is less effective than endoscopic sclerotherapy for treatment of variceal hemorrhage and is much less effective compared to medical and surgical options. Thus, it should be reserved for situations in which acute variceal bleeding is not controlled by pharmaceutical treatment, endoscopic sclerotherapy, or endoscopic variceal ligation and in which contraindications for surgical management are present.
    • Transjugular intrahepatic portosystemic shunts (TIPS) are an effective salvage procedure for stopping acute variceal hemorrhage after failure of medical and endoscopic treatment. However, this procedure is associated with a number of complications; 20% of patients develop encephalopathy, and 50% may occlude their shunt in 1 year. Thus, it should be considered as a bridge to subsequent liver transplantation.

Consultations: Consider early consultation with a gastroenterologist and a surgeon, particularly for patients with active bleeding from esophageal varices.

Diet: In patients with hemodynamically significant upper GI tract bleeding, a nasogastric tube should be in place for 24 hours to assist in identifying any rebleeding. Gastric lavage may be performed frequently through the nasogastric tube, and the volume and appearance of material aspirated from the stomach should be recorded. Do not allow any food by mouth.

 

     
 

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. They 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 or octreotide is now the preferred therapy prior to endoscopy.
 

Drug Category: Vasoconstrictors -- Reduce portal blood flow and, therefore, the flow of blood in the gastroesophageal collaterals because of their vasoconstrictor effects on the splanchnic vascular system.

Drug Name
 
Vasopressin (Pitressin) -- Has vasopressor and antidiuretic hormone (ADH) activity. Increases water resorption at distal renal tubular epithelium (ADH effect) and promotes smooth muscle contraction throughout the vascular bed of the renal tubular epithelium (vasopressor effects). However, vasoconstriction also is 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.
Adult Dose 0.2-0.4 U/min IV; after bleeding stops, continue at same dose for 12 h and taper off over 24-48 h
Pediatric Dose Initial: 0.002-0.005 U/kg/min, titrate dose prn; not to exceed 0.01 U/kg/min; after bleeding stops, continue at same dose for 12 h and taper off over 24-48 h
Contraindications Documented hypersensitivity; coronary artery disease; severe arrhythmias; MI; respiratory failure; stroke
Interactions Lithium, epinephrine, demeclocycline, heparin, and alcohol may decrease effects; chlorpropamide, urea, fludrocortisone, clofibrate, and carbamazepine may potentiate effects
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in cardiovascular disease, seizure disorders, nitrogen retention, asthma, or migraine; excessive doses may result in hyponatremia; complications (eg, MI, arrhythmia, mesenteric ischemia, heart failure, pulmonary edema, stroke, vertigo, fever, headache) may occur during infusion; adverse reactions include tremor, wheezing, bronchoconstriction, abdominal cramps, nausea, and vomiting; hyponatremia due to antidiuresis may occur; should be administered as an infusion in a peripheral vein and not by central venous line because it can cause severe coronary artery vasospasm; combined use with nitroglycerin allows enhancement of reduction of portal blood pressure and a decrease in the systemic adverse effects of vasopressin therapy (decrease in mortality is not significant); nitroglycerin usually is administered SL/IV/TD
Drug Name
 
Terlipressin (Glypressin) -- Synthetic analog 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 biological activity compared to vasopressin.
Adult Dose 2 mg q4-6h IV for up to 48 h
Pediatric Dose Not established
Contraindications Documented hypersensitivity; coronary artery disease
Interactions Drugs known to potentiate the effects include chlorpropamide, clofibrate, and carbamazepine
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Compared to vasopressin, adverse effects are less severe

Drug Category: Antisecretory agents -- Used as adjunct to nonoperative management of secreting cutaneous fistulas of the stomach, duodenum, small intestine (jejunum and ileum), or pancreas.

Drug Name
 
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.
Adult Dose 250 mcg bolus, followed by a 250-500 mcg/h continuous infusion; maintain for 2-5 d if successful
Pediatric Dose Not established
Contraindications Documented hypersensitivity
Interactions Epinephrine, demeclocycline, and thyroid hormone supplementation may decrease effects
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions May exacerbate or cause gall bladder disease; alters balance in counter-regulatory hormones and may cause hypothyroidism and cardiac conduction defects; modest effect on systemic circulation—mild reduction of cardiac output and bradycardia; may adversely affect renal function in patients with cirrhosis
Drug Name
 
Octreotide (Sandostatin) -- Synthetic octapeptide. Compared to somatostatin, has similar pharmacological actions with greater potency and longer duration of action.
Adult Dose 25-50 mcg/h IV continuous infusion; may be followed by initial IV boluses of 50 mcg; treat for up to 5 d
Pediatric Dose 1-10 mcg/kg IV q12h; dilute in 50-100 mL NS or D5W
Contraindications Documented hypersensitivity
Interactions May reduce effects of cyclosporine; patients on insulin, oral hypoglycemics, beta-blockers, and calcium channel blockers may need dose adjustments
Pregnancy B - Usually safe but benefits must outweigh the risks.
Precautions Tachyphylaxis may develop on repeated IV bolus injections; adverse effects primarily related to altered GI motility and include nausea, abdominal pain, diarrhea, and increased incidence of gallstones and biliary sludge; because of alteration in counter-regulatory hormones (insulin, glucagon, and GH), hypoglycemia or hyperglycemia may be observed; bradycardia, cardiac conduction abnormalities, and arrhythmias have been reported; due to inhibition of TSH secretion, hypothyroidism also may occur; caution in renal impairment; cholelithiasis may occur

Drug Category: Beta-adrenergic blockers -- May block effect of vasodilators, decrease platelet adhesiveness and aggregation, and increase release of oxygen to tissues.

Drug Name
 
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.
Adult Dose 40 mg PO bid initially, titrate to achieve heart rate reduction of 25%
Pediatric Dose 0.5-1 mg/kg/d divided q6-8h, titrate q3-5d; usual dose 2-4 mg/kg/d (higher doses may be needed); not to exceed 16 mg/kg/d or 60 mg/d
Contraindications Documented hypersensitivity; uncompensated congestive heart failure; bradycardia; cardiogenic shock; AV conduction abnormalities
Interactions Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase with propranolol
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely

Drug Category: Vasodilators -- Reduce the intrahepatic vascular resistance without decreasing peripheral or portal-collateral resistance.

Drug Name
 
Nitroglycerin (Nitro-Bid, Nitrostat, Deponit) -- Causes relaxation of vascular smooth muscle by stimulating intracellular cyclic guanosine monophosphate production. Result is a decrease in blood pressure.
Adult Dose 2.5-9 mg PO q8-12h; 2.5-15 mg/24h TD patch
Pediatric Dose Not established
Contraindications Documented hypersensitivity; severe anemia; shock; postural hypotension; head trauma; closed-angle glaucoma; cerebral hemorrhage
Interactions Aspirin may increase nitrate serum concentrations; marked symptomatic orthostatic hypotension may occur with coadministration of calcium channel blockers (dose adjustment of either agent may be necessary); beta-blockers may enhance hypotensive effects
Pregnancy C - Safety for use during pregnancy has not been established.
Precautions Caution in coronary artery disease and low systolic blood pressure; tolerance may develop after chronic use; patients with cirrhosis are less likely to develop full tolerance compared to patients with coronary artery disease



  FOLLOW-UP Section 8 of 10   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography
 

Further Inpatient Care:
 

  • Because of the frequency and severity of recurrent variceal bleeding, effective preventive treatment is mandatory in patients surviving an episode of acute variceal bleeding. This may include one of the following options:
    • Elective portocaval shunt
    • Distal splenorenal shunt
    • Devascularization procedures
    • Sclerotherapy
    • Endoscopic variceal banding ligation
    • TIPS

Further Outpatient Care:
 

  • The administration of propranolol and other nonselective beta-blockers in patients with cirrhosis reduces the portal pressure by reducing the portal collateral flow. This results from splanchnic vasoconstriction promoted by the blockade of vasodilating beta2-adrenoceptors in the splanchnic circulation and by decreasing heart rate and cardiac output due to blockade of cardiac beta1-adrenoceptors.
  • Beta-blocker therapy is indicated in patients with esophageal varices and in patients treated for variceal hemorrhage with sclerotherapy or banding. Patients selected for beta-blocker therapy should have no contraindications to beta-blockers.

In/Out Patient Meds:
 

  • Adjust the dose of beta-blockers.
  • If therapy with beta-blockers is not successful, addition of a second drug (eg, nitroglycerin, a long-acting nitrate) should be considered in an attempt to further decrease HVPG.

Transfer:
 

  • Patients with acute esophageal bleeding require urgent treatment in a hospital setting.

Complications:
 

  • Severe and persistent upper GI hemorrhage (ie, requiring >5-U transfusion)
  • High morbidity and mortality (30-40% of the group with severe persistent GI hemorrhage) - Factors such as underlying liver disease and associated abnormalities of the renal, cardiovascular, and immune systems contribute to the high morbidity and mortality.
  • Complications associated with GI bleeding - Vascular collapse; the sequelae of hypotension, cardiomyopathy, arrhythmias, aspiration pneumonia, sepsis, spontaneous bacterial peritonitis, overtransfusion, and rebound rebleeding of varices; and encephalopathy
  • Complications related to blood transfusion
  • Complications related to therapeutic procedures used in management of bleeding esophageal varices
    • Balloon tamponade - Aspiration pneumonia, esophageal perforation, superficial lesions of the gastric mucosa, pressure necrosis to the nasal passages, mouth, or lips
    • Sclerotherapy - Perforation of the esophagus (2-6%), esophageal ulceration and bleeding (2-13%), pleural effusion (16-48%), fever (30%), chest pain (40%), and esophageal stricture (7%)
    • Variceal banding - Rebleeding during the course of banding
    • Surgical procedures - For example, distal splenorenal shunt surgery is associated with an increased incidence of hepatic encephalopathy.
    • Liver transplantation - Rejection, infection, sepsis, and complications related to immunosuppressive drugs used postoperatively.

       

    • Complications related to pharmacotherapy

Prognosis:
 

  • Patients with HVPG of 20 mm Hg measured 48 hours after esophageal varices bleeding have a higher 1-year mortality rate.
  • Other factors that can affect prognosis of patients with esophageal varices include the following:
    • Rebleeding
    • Child classification, especially the presence of ascites
    • Active alcohol intake in patients with chronic alcohol-related liver diseases
    • Occurrence of complications (eg, bacteremia and/or endotoxemia, spontaneous bacterial peritonitis, portosystemic encephalopathy, hepatorenal syndrome)
  • Several factors are known to influence the prognosis of esophageal bleeding. These include the following:
    • The natural course of the disease causing portal hypertension
    • The severity of portal hypertension

       

    • The location and number of the bleeding varices

       

    • The functional status of the liver and the severity of liver disease (early rebleeding, within 5 d of admission, occurred in 21% of patients classified as Pugh grade A, 40% of patients classified as grade B, and 63% of patients classified as grade C)

       

    • Presence of associated systemic disorders

       

    • Continued alcohol abuse
    • Response to emergency treatment

Patient Education:
 

  • All patients with esophageal varices should take beta-blockers to reduce the risk of bleeding unless beta-blockers are contraindicated by coexisting medical conditions. Patients also should be educated about the adverse effects of beta-blockers and the possible risks of their abrupt discontinuation.
  • Educate patients about the benefits and disadvantages of available treatment options.
  MISCELLANEOUS Section 9 of 10   Click here to go to the previous section in this topic Click here to go to the top of this page Click here to go to the next section in this topic
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography
 

Medical/Legal Pitfalls:
 

  • Vasopressin should not be administered via a central line, especially in elderly patients.
  • Initiating therapy to prevent recurrent bleeding as soon as the acute bleeding episode is controlled adequately is critical.
  • Liver transplantation should be considered for patients with end-stage liver disease. The selection of candidates is dictated by the patient's clinical status, etiology of cirrhosis, abstinence from alcohol, and availability of a donor organ.

Special Concerns:
 

  • Patients with massive acute bleeding from esophageal varices who refuse blood transfusions because of their religious beliefs may constitute a challenge to the treating team.
  BIBLIOGRAPHY Section 10 of 10   Click here to go to the previous section in this topic Click here to go to the top of this page
Author Information Introduction Clinical Differentials Workup Treatment Medication Follow-up Miscellaneous Bibliography
 

  • Bornman PC, Krige JE, Terblanche J: Management of oesophageal varices. Lancet 1994 Apr 30; 343(8905): 1079-84[Medline].
  • Garcia-Tsao G: Portal hypertension. Curr Opin Gastroenterol 2000; 16: 282-289.
  • Garcia-Tsao G: Angiotensin II receptor antagonists in the pharmacological therapy of portal hypertension: a caution. Gastroenterology 1999 Sep; 117(3): 740-2[Medline].
  • Gotzsche PC, Gjorup I, Bonnen H, et al: Somatostatin v placebo in bleeding oesophageal varices: randomised trial and meta-analysis. BMJ 1995 Jun 10; 310(6993): 1495-8[Medline].
  • Gupta TK, Toruner M, Chung MK, Groszmann RJ: Endothelial dysfunction and decreased production of nitric oxide in the intrahepatic microcirculation of cirrhotic rats. Hepatology 1998 Oct; 28(4): 926-31[Medline].
  • Hanisch E, Doertenbach J, Usadel KH: Somatostatin in acute bleeding oesophageal varices. Pharmacology and rationale for use. Drugs 1992; 44 Suppl 2: 24-35; discussion 70-2[Medline].
  • Patch D, Armonis A, Sabin C, et al: Single portal pressure measurement predicts survival in cirrhotic patients with recent bleeding. Gut 1999 Feb; 44(2): 264-9[Medline].
  • Poo JL, Jimenez W, Maria Munoz R, et al: Chronic blockade of endothelin receptors in cirrhotic rats: hepatic and hemodynamic effects. Gastroenterology 1999 Jan; 116(1): 161-7[Medline].
  • Shulkes A, Wilson JS: Somatostatin in gastroenterology. BMJ 1994 May 28; 308(6941): 1381-2[Medline].
  • Williams SG, Westaby D: Management of variceal haemorrhage. BMJ 1994 May 7; 308(6938): 1213-7[Medline].

 

 

NOTE:
Medicine is a constantly changing science and not all therapies are clearly established. New research changes drug and treatment therapies daily. The authors, editors, and publisher of this journal have used their best efforts to provide information that is up-to-date and accurate and is generally accepted within medical standards at the time of publication. However, as medical science is constantly changing and human error is always possible, the authors, editors, and publisher or any other party involved with the publication of this article do not warrant the information in this article is accurate or complete, nor are they responsible for omissions or errors in the article or for the results of using this information. The reader should confirm the information in this article from other sources prior to use. In particular, all drug doses, indications, and contraindications should be confirmed in the package insert. FULL DISCLAIMER

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