GI tract is highly vascular.
Major bleeds are threat to survival.
GI bleed may be primary pathology or complication of other disease process.
Upper GI bleeds are larger and more rapid.
Common cause for or complication of ITU admission.
Case summary:
A seventy two year old lady was admitted to intensive care unit following massive haematemesis and malaena. Her background history was as follows-
Hypothyroidism on thyroxin replacement, severe rheumatoid arthritis, idiopathic liver cirrhosis with oesophageal varices for which she had received scerotherapy in the past. She had had admission to intensive care unit for long period in past for decompasated liver failure.
This time she had 4 episodes of large volume haematemesis associated with malaena. She remained haemodynamically stable to start with. She was transferred to HDU to observe her closely. She was started on omeprazole intravenous regimen and terlipressin. Her coagulation remained stable.
While on HDU, she had 4 episodes of haematemesis in quick succession making her haemodynamically unstable and tired. In view of protecting her airway and putting Sengstaken tube for control of variceal bleed decision was taken to electively ventilate her. After endotracheal intubation Sengstaken tube was passed using laryngoscope to guide the insertion. Gastric balloon was inflated with 350 ml air and oesophageal balloon with 75 ml air. This stopped further bleeding from upper GI tract.
Meanwhile, she needed blood transfusions to maintain her haemoglobin around 10g/dl. As the bleeding looked settled, the oesophageal balloon was deflated and sengstaken tube was removed later after deflating stomach balloon.
The medical team carried out OGD scopy while patient was still intubated. There was no evidence of oesophageal bleed, but the gastric fundus showed varices with clot attached to them. No intervention was done as disturbing the clot might have caused more bleeding. The plan was made for repeat scopy later for injection therapy for fundal varices.
The patient was successfully extubated and further care was handed over to gastroenterology team.
Cirrhosis can be caused by a prolonged or intense contact of liver tissue with various substances including excess alcohol, damage by some drugs, poisons such as arsenic, hepatitis, NASH, inherited diseases such as haemochromatosis, and Wilson’s disease. Some times the cause of cirrhosis is not known; the disease is said to be idiopathic.
Portal hypertension is hypertension (high blood pressure) in the portal vein and its branches. It is often defined as a portal pressure gradient (the difference in pressure between the portal vein and the hepatic veins) of 12 mm Hg or greater.
Consequences of portal hypertension are caused by blood being forced down the alternate channels by the increased resistance to flow through the portal system. They include:
· Ascites
- Hepatic encephalopathy
- Increased risk of spontaneous bacterial peritonitis
- Increased risk of hepatorenal syndrome
- Splenomegaly with consequent sequestration therein of red blood cells, white blood cells, and platelets, together leading to mild pancytopenia
- Portacaval anastomoses (Esophageal varices, hemorrhoids, caput medusae), with esophageal varices posing an ongoing risk of life-threatening hemorrhage.
Medical management:
Treatment with a non-selective beta blocker is often commenced once portal hypertension has been diagnosed, and almost always if there has already been bleeding from esophageal varices (either propranolol or nadolol). Addition of a nitrate, such as isosorbide mononitrate, to the beta blocker is more effective than using beta blockers alone and may be the preferred regimen in those people with portal hypertension who have already experienced variceal bleeding. In acute or severe complications of the hypertension, such as bleeding varices, intravenous octreotide (a somatostatin analogue) or intravenous terlipressin (an antidiuretic hormone analogue) is commenced to decrease the portal pressure.
Emergency management of bleeding varices:
Fluid Resuscitation – blood and colloids
Correct coagulopathy
Stop Haemorrhage - tamponade
A Sengstaken-Blakemore tube is generally used only in emergencies where bleeding from presumed varices is impossible to control by administration of medication. It may be difficult to position, particularly in an unwell patient, and may inadvertently be inserted in the trachea, hence endotracheal intubation before the procedure is strongly advised to secure the airway. It is a temporary measure: ulceration and rupture of the esophagus and stomach are recognized complications (1). Also, it can be misplaced into trachea causing massive lung damage (2).
Percutaneous interventions:
Transjugular intrahepatic portosystemic shunting is the creation of a connection between the portal and the venous system. As the pressure over the venous system is lower than over a hypertensive portal system, this would decrease the pressure over the portal system and a decreased risk of complications.
Surgical interventions:
· Distal splenorenal shunt
The most definitive treatment of portal hypertension is a liver transplant.
Our patient was managed on standard therapy and responded well.
References:
1. Bauer JJ, Kreel I, Kark AE. The use of the Sengstaken-Blakemore tube for immediate control of bleeding esophageal varices. Ann Surg 1974;179:273-7.
2. Chien JY, Yu CJ (2005). "Images in clinical medicine. Malposition of a Sengstaken-Blakemore tube". N. Engl. J. Med. 352 (8): e7.
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