History

Fact Explanation
Haematemesis Portal hypertension develops as a result of increased vascular resistance due to distorted hepatic architecture in a cirrhotic liver and active intrahepatic vasoconstriction due to a decrease in the endogenous production of nitric oxide and inappropriate production of vasoconstrictors such as endothelin, angiotensin II and leukotrienes .The increase in portal pressure results in the formation of collateral circulation to allow portal blood to be diverted into the systemic circulation at the sites of potential portal systemic anastomoses which gastro-oesophageal veins is a major site.These veins are dilated, tortuous and fragile.Therefore these tend to bleed easily resulting in dark red blood vomitus. [1]
Malena Blood is altered by acid in the stomach and it appear as tarry black colour stools.[1]
Hematochezia When variceal bleeding is rapid and massive this could present as passage of fresh blood per anus, usually with or without stools.[2]
Lethargy ,dyspnoea Anemia due to variceal haemorrhage can present this way.[1]
Risk factors for cirrhosis Past history of blood transfusions (HBV,HCV infection), history of jaundice, other hepatic-related diseases ( autoimmune hepatitis, nonalcoholic steatohepatitis [NASH], diabetes mellitus, and hyperlipidemia) drug usage,alcohol use, high-risk sexual behavior family history of hereditary liver disease (eg, Wilson disease, hemochromatosis), From these we can get an idea about the causative factor for cirrhosis.[1]
Past history of ascites, encephalopathy These are other complications of cirrhosis.[1]
References
  1. SCHUPPAN D, AFDHAL NH. Liver Cirrhosis Lancet [online] 2008 Mar 8, 371(9615):838-851 [viewed 09 July 2014] Available from: doi:10.1016/S0140-6736(08)60383-9
  2. Wilson ID. Hematemesis, Melena, and Hematochezia. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3rd edition. Boston: Butterworths; 1990. Chapter 85. Available from: http://www.ncbi.nlm.nih.gov/books/NBK411/

Examination

Fact Explanation
Pallor Bleeding which leads to anemia can present this way.[1]
Increased pulse rate, hypotension/orthostatic hypotension If bleeding result in hypovolaemia ,pulse rate increases as a compensatory mechanism.When the compensatory mechanisms are insufficient then the blood pressure begins to decline.[1]
Stigmata of liver disease:Gynecomastia, testicular atrophy ,spider angioma,palmar erythema,dupuytren contracture, flapping tremor. If cirrhosis is the cause for portal hypertension.[1]
Splenomegaly Splenomegaly will be seen in portal hypertension.[1]
Jaundice This is seen in cirrhosis and can coexist with oesophageal varices.[1]
Ascites This is a complication of cirrhosis and this could coexist with oesophageal varices.[1]
Liver is not palpable If cirrhosis is the cause for portal hypertension this could be a finding with oesophageal varices.[1]
References
  1. SCHUPPAN D, AFDHAL NH. Liver Cirrhosis Lancet [online] 2008 Mar 8, 371(9615):838-851 [viewed 09 July 2014] Available from: doi:10.1016/S0140-6736(08)60383-9

Differential Diagnoses

Fact Explanation
Peptic ulceration(duodenal /gastric) This can cause fresh red blood with clots occasionally mixed with food with a history of gastritis whereas in oesophageal varices there will be dark venous blood. [1]
Oesophageal ulceration This can cause vomiting of small volumes of bright red blood with a history of GORD but in oesophageal varices there will be dark red blood with a history of cirrhosis in most cases. [1]
Gastric cancer Due to friable blood vessels in the tumor it can cause bleeding.There also will be loss of appetite,early satiety and projectile vomiting if the tumor causes gastric outlet obstruction.[1]
Oesophageal trauma(Mallory-Weiss tear) This can cause small volumes of fresh bright blood preceded by violent or prolonged vomiting and retching whereas in oesophageal varices there will be no such history of prior vomiting.[1]
Vascular malformation( Large or multiple arteriovenous malformations/Gastric antral vascular ectasia /Portal hypertensive gastropathy/Dieulafoy’s lesion) This can cause haematemesis.[1]
Aortoenteric fistula This could cause massive haematemesis with fresh blood and more likely to deteriorate earlier than in bleeding due to oesophageal varices.[1]
References
  1. PALMER K. Management of haematemesis and melaena. Postgraduate Medical Journal [online] 2004 July, 80(945):399-404 [viewed 09 July 2014] Available from: doi:10.1136/pgmj.2003.017558

Investigations - for Diagnosis

Fact Explanation
Upper GI endoscopy To diagnose esophageal varices and to exclude other conditions which present as haemetemesis endoscopy is done. Varices are accepted as the bleeding source, when a venous (nonpulsatile) spurt is seen or when there is fresh bleeding from the esophagogastric junction in the presence of varices or when there is fresh blood in the fundus, when gastric varices are present. In the absence of active bleeding (up to 50% of cases) either a “white nipple sign” or the presence of medium or large varices with no other potential bleeding lesions suggest varices as the source of haemorrhage. Varices are graded as I-IV, using the Paquet grading system. Grade 0:No varices, grade I:Varices, 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. [1][2]
References
  1. BENDTSEN F., KRAG A., MøLLER S.. Treatment of acute variceal bleeding. Digestive and Liver Disease [online] 2008 May, 40(5):328-336 [viewed 09 July 2014] Available from: doi:10.1016/j.dld.2007.12.005
  2. SARANGAPANI A, SHANMUGAM C, KALYANASUNDARAM M, RANGACHARI B, THANGAVELU P, SUBBARAYAN JK. Noninvasive Prediction of Large Esophageal Varices in Chronic Liver Disease Patients Saudi J Gastroenterol [online] 2010, 16(1):38-42 [viewed 11 July 2014] Available from: doi:10.4103/1319-3767.58767

Investigations - Fitness for Management

Fact Explanation
FBC This is not useful in acute setting, but to correct the haemoglobin level in long term this is useful. Also to detect any signs of infection white cell count is observed.[1]
Blood grouping and cross matching In the acute variceal bleeding setting in order to replace the lost blood volume these investigations needed to be done. [1]
Serum electrolytes, serum creatinine Esophageal variceal bleeding can precipitate hepatorenal syndrome.[1]
Prothrombin time and INR In cirrhosis there will be deficiencies in coagulation.To detect these and to correct the deficiencies these investigations are performed.[1]
References
  1. BENDTSEN F., KRAG A., MøLLER S.. Treatment of acute variceal bleeding. Digestive and Liver Disease [online] 2008 May, 40(5):328-336 [viewed 09 July 2014] Available from: doi:10.1016/j.dld.2007.12.005

Investigations - Followup

Fact Explanation
Upper GI endoscopy Size of the varices and the presence of red signs in the varices predict future bleeding tendency.Therefore this investigation help to identify the high risk patients and to decide on whom should we perform banding therapy.Patients can be followed up every 3 months.[1]
References
  1. BROOKS J, WARBURTON R, BEALES IL. Prevention of upper gastrointestinal haemorrhage: current controversies and clinical guidance Ther Adv Chronic Dis [online] 2013 Sep, 4(5):206-222 [viewed 08 July 2014] Available from: doi:10.1177/2040622313492188

Investigations - Screening/Staging

Fact Explanation
Upper GI endoscopy In patients with portal hypertension they should undergo regular endoscopy procedures to detect any development of varices and if detected should be treated accordingly.[1]
References

Management - Specific Treatments

Fact Explanation
Acute management (in esophageal variceal haemorrhage) Initial procedures are to secure and protect the airway, especially in order to prevent pulmonary aspiration, an increased risk phenomena, which is further exacerbated by endoscopic procedures. Therefore intubation should be considered at an early stage, especially in encephalopathic patients or in case of uncontrolled severe bleeding.Patients should be monitored with pulse oximetry with a possibility to supply oxygen and presence of facilities for suction of airway. Establish a large caliber IV access and give crystalloid fluid up to 1L if tachycardic or hypotensive.Only use O negative blood if the patient is critical otherwise wait for cross matched blood. Catheterise the patient and maintain a fluid balance chart while monitoring the pulse rate,BP, and urinary output. Clinical trials have shown that an 80 mg bolus of omeprazole followed by a 72 hour infusion of 8 mg/hour significantly reduces the risk of re-bleeding and need for emergency surgery and start blood transfusion if large amount of haematemesis had occurred.Vasopressins and also Intravenous octreotide infusions will lower portal blood pressure and during the patient's initial hospitalization can prevent rebleeding . Vasodilators (isosorbide mononitrate) reduce intrahepatic vascular resistance without decreasing the peripheral or portal-collateral resistance. In liver disease consider FFP to correct clotting deficiencies. Rockall risk score is used for the risk assessment after acute gastrointestinal haemorrhage. [3][5]
Primary prevention of bleeding The mainstay of treatment is currently nonselective beta blockers.The aim of this treatment is to reduce portal pressure, with a target portal pressure gradient of less than 12 mmHg.Nonselective beta blockers (usually propranolol or nadolol) are preferred as the beta-1 inhibition reduces cardiac output and hence blood flow into the mesenteric system, whilst beta-2 blockade induces splenic vasoconstriction further resulting in decreased portal flow and pressure. Alternative therapy is to perform endoscopic banding variceal ligation (EVBL)which induces thrombosis in the esophageal varices. [1]
Secondary Prevention of bleeding. It has been reported that the combination of oral isorbide mononitrate and nadalol provides a survival advantage compared with repeat banding in secondary prevention, despite being significantly less effective at preventing rebleeding.The current recommendations are for combination therapy (endosopic and pharmacological) to be started as soon as possible after initial bleeding episode. Endoscopic sclerotherapy is no longer recommended as it has been shown that EVBL is superior in regards to rebleeding rates, mortality and the development of strictures. Percutaneous creation of a transjugular intrahepatic portosystemic shunt (TIPS) through a jugular route connects the hepatic and portal veins in the liver. This reduces portal pressure by diverting portal blood flow from the liver, thus reducing variceal bleeding but it increases the risk of encephalopathy. In cases of massive or uncontrolled bleeding, balloon tamponade provides a “bridge” to definitive treatment with TIPS or portosystemic surgical shunt.The most frequently used balloon is the 4-lumen modified Sengstaken–Blakemore tube, which employs a gastric and an esophageal balloon. [1] [2]
Treatment and prevention of complications to bleeding Bacterial infections are frequent in cirrhosis, and up to 20% of patients with cirrhosis and gastrointestinal bleeding have a bacterial infection at initial hospitalisation and further 50% may later during the hospitalisation develop infection. Most frequent causes of bacterial infections are urinary tract infections, spontaneous bacterial peritonitis.Presence of bacterial infections seem to be closely related to prognosis in bleeding cirrhotic patients, moreover bacterial infections are also associated with a higher risk of variceal rebleeding. All cirrhotics with upper gastrointestinal bleeding should receive prophylactic treatment with antibiotics either Quinolones or intravenous cephalosporins for 5–7 days.Aminoglycosides should be avoided due to risk of renal toxicity. Keep the urine output maintained over 40 ml/per hour. The intravascular volume should be maintained and nephrotoxic drugs should be avoided, especially aminoglycosides and NSAID.Renal failure may develop due to variceal bleeding and hypovolaemic shock in which case dialysis should be considered. [3]
Surgical Management Active bleeding which cannot be controlled by endoscopic therapy either because torrential haemorrhage obscures the bleeding point or when active bleeding continues despite successful application of endoscopic therapy surgery is considered.esophageal transection is also an option. Liver transplantation is considered in advanced liver disease.[4]
References
  1. BROOKS J, WARBURTON R, BEALES IL. Prevention of upper gastrointestinal haemorrhage: current controversies and clinical guidance Ther Adv Chronic Dis [online] 2013 Sep, 4(5):206-222 [viewed 08 July 2014] Available from: doi:10.1177/2040622313492188
  2. DIB N, OBERTI F, CALèS P. Current management of the complications of portal hypertension: variceal bleeding and ascites CMAJ [online] 2006 May 9, 174(10):1433-1443 [viewed 08 July 2014] Available from: doi:10.1503/cmaj.051700
  3. BENDTSEN F., KRAG A., MøLLER S.. Treatment of acute variceal bleeding. Digestive and Liver Disease [online] 2008 May, 40(5):328-336 [viewed 09 July 2014] Available from: doi:10.1016/j.dld.2007.12.005
  4. PALMER K. Management of haematemesis and melaena. Postgraduate Medical Journal [online] 2004 July, 80(945):399-404 [viewed 09 July 2014] Available from: doi:10.1136/pgmj.2003.017558
  5. ROCKALL T A, LOGAN R F, DEVLIN H B, NORTHFIELD T C. Risk assessment after acute upper gastrointestinal haemorrhage.. Gut [online] 1996 March, 38(3):316-321 [viewed 11 July 2014] Available from: doi:10.1136/gut.38.3.316