Management of Variceal Bleeding

A 50 year-old man with a history of alcoholism attended to the emergency department having been found at home comatose.

He had a reduced Glasgow coma score on admission and was vomiting blood. He was not protecting his airway and was tachypnoeic, tachycardic and had a reduced systolic blood pressure. His oxygen saturations were low and there were coarse crackles on his chest. Old notes showed that on previous endoscopy oesophageal and gastric varices were found. He was cachectic with hepatosplenomegaly but no signs of ascites.. He was rumoured to be abstinent from alcohol and had been previously well up to one day ago when he was last seen. There was some report that he had been behaving oddly over the last 5 days though.


Supplemental oxygen was provided and the decision to intubate was made. An initial attempt to insert a Sengstaken-blakemore tube was abandoned until the patient was intubated using a rapid sequence intubation technique. The gastric balloon was inflated and put under tension. Blood tests showed a reduced haemoglobin level but no clotting abnormality. Transfusion of packed red cells was made.

Medical therapy included beginning a course of prophylactic antibiotics. Terlipressin was started at 2mg intravenously four times daily. He was also started on high dose proton pump inhibitors, lactulose and thiamine supplements.

The gastric balloon was left inflated for 10 hours and as there was no haemodynamic sign of further bleeding was then deflated. Oesophagogastrocopy the next morning on the intensive care unit showed only grade 1 varices with no recent stigmata of bleeding and some mild gastric erosions.

He continued to be haemodynamically stable and sedation was weaned. He did not wake up as expected on sedation hold and his ammonia level was found to be raised. Over the course of the next 2 days he improved and was extubated successfully and discharged to the ward.

Describe the management of variceal bleeding.

James Day
Portal hypertension is a complication of cirrhosis and is the causative factor behind gastroesophageal varices and subsequent bleeding. Variceal haemorrhage is associated with clinical stigmata of chronic liver disease. At diagnosis of liver disease 40% of those with compensated cirrhosis and 60% of those with ascites have varices. A small number 4.4/100,000 present with variceal haemorrhage as their presenting feature.

The mortality rate from acute variceal bleed has been reducing over the last 20 years from 42 to 14% (1). This is likely to be due to improved treatments available e.g. endoscopic variceal ligation and vasoactive drugs. Immediate mortality from uncontrolled bleeding is 5-8%.

Treatment however is not geared towards individual patients and their disease severity. Standard treatment involves the use of splanchnic vasoconstrictive medications such as terlipressin or somatostatin or analogues e.g. octreotide started from time of admission for 2-5 days. This is combined with endoscopic therapy, preferably endocscopic variceal ligation at time of diagnostic endoscopy within 12 hrs of admission together with short term prophylactic antibiotics either a cephalosporin or quinolone.

Endoscopic therapy should involve band therapy rather than sclerotherapy. There is a better outcome with regards to all cause mortality, re-bleeding and death due to bleeding (2). This has been shown in a meta-analysis of various randomised controlled trials (RCT) and is advised by the SIGN guidelines. The only issue is that banding ligation is technically harder than injection therapy and ultimately haemostatic control must be achieved.

The optimal therapy used does depend on the anatomical location of the varices. They can either be oesophageal, oesophageal-gastric or gastric. Two RCTs have shown that cyanoacrylate injection has better outcomes than banding for oesophageal-gastric and gastric varices (3, 4) and another retrospective study showed that cyanoacrylate injection was more cost effective than transjugular intrahepatic portosystemic stent shunt TIPSS (5).

Placement of a TIPSS is considered a salvage procedure for the 10-20% in whom standard therapy fails or used as rescue therapy in the secondary prophylaxis phase of treatment. It is very effective in stopping bleeding with a haemostasis rate of 93% and rebleeding rate of 12%. Mortality at 6 weeks remains high at 35% for patients where TIPSS is used as a rescue therapy.

However two RCTs have shown that early placement (within 24-48hrs of admission) is associated with improved outcomes in high risk patients (i.e. patients with a hepatic venous pressure gradient (HPVG) >20mmHg (6) or with Child Pugh class C diseases with a score of 10-13 (7)). They showed that there was a reduced risk of re-bleeding with a 97% chance of remaining re-bleed free vs 50% for the medical group. The rate of survival was also improved with 6 week survivability of 97% vs 67%. Interestingly the patients treated with TIPSS

showed a 1 year survival of 87% which is very high given the severe status of their liver disease.

The SIGN guidelines 2009 are the most up to date in the U.K. and advise the use of TIPSS only as a salvage technique in uncontrolled variceal haemorrhage.

Lessons learnt

The current guideline advice is to treat all patients with varcieal bleeding alike. It seems that the evidence is no starting to show that risk stratification may be important in determining the best treatment for the individual. On risk-benefit balance it seems that early use of TIPSS in high risk (Child class disease B and C) patients may be beneficial. This obviously will place increased demands on a service that is currently not easily accessible and available. Further studies need to be seen to confirm what is shown in these recent studies.


  1. CarbonellN,PauwelsA,Serfatyl,FourdanO,LevyVG,PouponR.Improved survival after variceal bleeding in patients with cirrhosis over the past two decades. Hepatology 2004; 40: 652-659.
  2. Laine L, Cook D. Endoscopic ligation compared with sclerotherapy for treatment of esophageal variceal bleeding. A meta-analysis. Ann Intern Med 1995;123(4):280-7.
  3. Lo GH, Lai KH, Cheng JS, Chen MH, Chiang HT. A prospective,randomized trial of butyl cyanoacrylate injection versus band ligation in the management of bleeding gastric varices. Hepatology2001;33(5):1060-4.
  4. Tan PC, Hou MC, Lin HC, Liu TT, Lee FY, Chang FY, et al. A randomized trial of endoscopic treatment of acute gastric variceal hemorrhage: N-butyl-2 cyanoacrylate injection versus band ligation. Hepatology 2006;43(4):690-7.
  5. Mahadeva S, Bellamy MC, Kessel D, Davies MH, Millson CE. Cost- effectiveness of N-butyl-2-cyanoacrylate (histoacryl) glue injections versus transjugular intrahepatic portosystemic shunt in the management of acute gastric variceal bleeding. Am J Gastroenterol 2003;98(12):2688-93.
  6. Monescillo A, Martínez-Lagares F, Ruiz-del-Arbol L, et al. Influence of portal hypertension and its early decompression by TIPS placement on the outcome of variceal bleeding. Hepatology 2004;40:793-801.
  7. Garcia-Pagán JC, Caca K, Bureau C, et al. An early decision for PTFE-TIPS improves survival in high risk cirrhotic patients admitted with an acute variceal bleeding: a multicenter RCT. Hepatology 2008;48:Suppl:373A-374A. abstract.

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