Esophageal Varices

Know how bad the liver is - endoscopy grades varix size and red spots; Child-Pugh and MELD scores estimate how a bleed will go. A hepatic venous pressure gradient above 20 mmHg predicts rebleeding and higher mortality.

Anything that spikes portal or venous pressure can rupture a varix - the hypertensive response to laryngoscopy, straining and coughing on emergence, retching, and abrupt vasoconstrictor boluses. Blunt the intubation and plan a smooth extubation.

Treat hypotension with volume first - fluid before ephedrine or other vasoconstrictors. A sudden rise in blood pressure can precipitate a variceal bleed.

Full stomach until proven otherwise - active bleeding fills the stomach with blood, and ascites plus splenomegaly raise intra-abdominal pressure. RSI with a cuffed tube and large-bore suction at the head of the bed.

Coagulopathy comes from two directions - the failing liver stops synthesizing clotting factors (factor V and VII deficiency described, occasionally true prothrombin deficiency) and hypersplenism drops the platelets. Type and cross early, get an arterial line, and have products in the room.

Neuraxial deserves a hard look - check INR and platelet count first. Portal hypertension also engorges the extradural veins, so a bloody tap is more likely; the lateral decubitus position lowers that risk compared with sitting.

Hold the beta blocker in an active bleed - nonselective beta blockade is standard prophylaxis, but during hemorrhage it lowers blood pressure and blunts the compensatory tachycardia you are relying on.

Anesthesia for banding - band ligation beats sclerotherapy for both bleeding and medium-to-large nonbleeding varices, and it is repeated every 1 to 4 weeks until the varices are eradicated. Plan for a series of shared-airway cases in a patient with a full stomach.

Balloon tamponade means secure the airway first - a Sengstaken-Blakemore or Minnesota tube is a temporizing bridge to TIPS when endoscopy fails, and most patients are already intubated. If not, intubate before placement. The serious complications are airway obstruction, esophageal rupture, and aspiration pneumonitis.

Expect infection - as many as two-thirds of patients with variceal bleeding develop an infection, most commonly spontaneous bacterial peritonitis, UTI, or pneumonia. Antibiotic prophylaxis is part of the resuscitation, not an afterthought.

Bleeding clouds the sensorium - hepatic encephalopathy commonly complicates a variceal bleed, and sedatives make it worse. Go light and expect slow emergence.

The pregnant patient with varices - the risk of variceal bleeding is dramatically higher than in pregnancy without portal hypertension. Minimize oxytocics and avoid ergometrine, since forceful uterine contraction squeezes a large volume into the IVC and up into the varices. Postpartum hemorrhage rates run 7% to 26% on top of coagulopathy and thrombocytopenia.

Esophageal varices are dilated submucosal veins in the distal esophagus that connect the portal and systemic circulations. They form in response to portal hypertension, most often from cirrhosis. The portal system carries over 1,500 mL/min and has no valves, so resistance anywhere between the splanchnic vessels and the right heart raises pressure and drives flow retrograde into collaterals. Normal portal pressure is 5 to 10 mmHg; with obstruction it can reach 15 to 20 mmHg. The gastroesophageal collaterals draining into the azygos vein enlarge into a congested submucosal plexus of tortuous distal esophageal veins.

When those veins rupture, the bleeding is massive — variceal hemorrhage is the most common fatal complication of cirrhosis. Bleeding risk tracks with the degree of portal hypertension (above 12 mmHg) and the size of the varices.