Portal Hypertension

Variceal rupture is what kills them - It is the most common fatal complication of cirrhosis, and bleeding risk tracks with the pressure gradient (above 12 mmHg) and the size of the varices. Anything that spikes portal pressure or venous return can set one off: the hypertensive response to laryngoscopy, straining or bucking on extubation, Valsalva. Blunt the intubation response and plan a smooth, non-coughing emergence.

Treat hypotension with volume before vasoconstrictors - A sudden rise in blood pressure from a bolus of ephedrine can precipitate a variceal bleed. Fluid is the first line. Preload before a neuraxial block and before the abdomen is decompressed or ascites is drained, because both drop preload sharply.

Treat as a full stomach - Ascites and splenomegaly raise intra-abdominal pressure and with it the aspiration risk. In the reported obstetric case this was the specific reason regional anesthesia was chosen over general.

The coagulopathy is mixed and it is real - Parenchymal liver disease impairs synthesis of factors I, II, V, VII and X, while hypersplenism produces thrombocytopenia and pancytopenia. Get a PT/INR, platelet count and albumin — a prolonged prothrombin time with a low albumin is the reliable read on hepatic synthetic function. Correct with FFP and platelets before an invasive procedure. Microvascular bleeding usually needs platelets below 100,000/mm3 and rarely needs them above 50,000/mm3. Note that the pancytopenia of hypersplenism is not reversed by a portosystemic shunt.

Neuraxial needs extra thought - Portal hypertension engorges the extradural veins, so the chance of a bloody tap goes up. The same platelet ranges have been suggested for avoiding neurologic complications, though the true minimum count is undefined. A lateral decubitus position was preferred over sitting in the reported case to reduce that risk.

Set up for transfusion before you need it - Type and cross, large-bore access, FFP and platelets available, and an arterial line for pressure monitoring in a patient who is both coagulopathic and pancytopenic.

Know what precipitates encephalopathy - Hypotension, GI bleeding, hypoxia, hypokalemia, hyponatremia, alkalosis, sedatives, diuretics and surgical stress all push toward it. Check a metabolic panel and correct the electrolytes. Use morphine cautiously because of active metabolites, and benzodiazepines cautiously because of the sedation itself.

Beta blockers cut both ways - Nonselective beta blockers (propranolol, nadolol) are the standing prophylaxis against variceal bleeding and lower portal pressure. During an active bleed they are avoided, because they drop the blood pressure and blunt the compensatory tachycardia you are relying on to read the patient.

Managing an active variceal hemorrhage - Intubate for airway protection; it is recommended before endoscopy and before balloon tamponade, where aspiration pneumonia is the most common complication. Large-bore IVs, blood products, correction of coagulopathy, and empiric antibiotics — a third-generation cephalosporin — since up to two-thirds of patients with variceal bleeding develop an infection, most often spontaneous bacterial peritonitis. Octreotide constricts the splanchnic vessels as an adjunct to endoscopic therapy. TIPS is the salvage route when endoscopy fails.

Shunts trade bleeding for encephalopathy - A TIPS or a surgical portacaval shunt decompresses the portal system but routes portal blood past the liver's metabolic function. Encephalopathy and shunt occlusion within 12 months are the known costs. Expect a shunted patient to be more sensitive to sedatives, not less.

Renal and volume status - Sodium and water retention, azotemia and progressive oliguria mark the slide toward hepatorenal failure. Monitor urine output. The standing ascites regimen of spironolactone plus furosemide sets the electrolytes up badly before you ever see the patient.

Drug handling is unpredictable - Deranged hepatic function alters both metabolism and excretion. Titrate to effect rather than to a weight-based number.

Pregnancy multiplies everything - Variceal bleeding risk in a pregnant patient with portal hypertension is roughly 400 times that of a pregnant patient without it, and up to 78% of those with known varices bleed during pregnancy — peaking in the second trimester when maternal blood volume is maximally expanded and the fetus compresses the IVC. Second-stage pushing raises portal pressure, and diaphragmatic contraction can triple it, so elective cesarean or a vacuum- or forceps-assisted vaginal delivery under epidural is generally recommended. Minimize oxytocics and avoid ergometrine, which force large blood volumes toward the IVC and the varices. Look for a splenic artery aneurysm on the ultrasound and Doppler report — rupture in pregnancy is catastrophic.

Portal hypertension is a raised pressure gradient between the portal venous system and the hepatic vein or inferior vena cava. Normal is 5 mmHg or less. A hepatic venous pressure gradient of 6 mmHg or more defines it, above 10 mmHg it becomes clinically significant, and above 12 mmHg is where varices bleed. Two forces build it. Resistance to portal flow rises — most often intrahepatic from cirrhosis, through stellate-cell activation, fibrosis, regenerative nodules and sinusoidal constriction — and inflow rises from splanchnic vasodilation driven by nitric oxide, prostacyclin and TNF, which also produces a hyperdynamic, high-output circulation.

Because the portal system has no valves, pressure backs up into portosystemic collaterals: gastroesophageal varices draining to the azygos vein, caput medusae, gastro-renal shunts. Splenomegaly with hypersplenism follows, and with it the thrombocytopenia, ascites and encephalopathy that make these patients hard to anesthetize.