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156 PORTAL HYPERTENSION

156 PORTAL HYPERTENSION
Harrison’s Manual of Medicine

156

PORTAL HYPERTENSION

Esophagogastric Varices
Hepatic Encephalopathy
Bibliography

An increase in portal vein pressure due to anatomic or functional obstruction to blood flow in the portal venous system. Normal portal vein pressure is 5–10 mmHg. Indicators of portal hypertension are (1) intraoperative portal vein pressure of >30 cm saline, (2) intrasplenic pressure of >17 mmHg, (3) wedged hepatic vein pressure of >4 mmHg above IVC pressure.
CLASSIFICATION   See Table 156-1.

Table 156-1 Pathophysiologic Classification of Portal Hypertension

CONSEQUENCES   (1) Increased collateral circulation between high- pressure portal venous system and low-pressure systemic venous system: lower esophagus/upper stomach (varices, portal hypertensive gastropathy), rectum (varices, portal hypertensive colopathy), anterior abdominal wall (caput Medusae; flow away from umbilicus), parietal peritoneum, splenorenal; (2) increased lymphatic flow; (3) increased plasma volume; (4) ascites; (5) splenomegaly, possible hypersplenism; (6) portosystemic shunting (including hepatic encephalopathy).
ESOPHAGOGASTRIC VARICES
Bleeding is major life-threatening complication; risk correlates with variceal size above minimal portal venous pressure >12 mmHg and presence on varices of “red wales.” Mortality correlates with severity of underlying liver disease (hepatic reserve), e.g., Child-Turcotte classification (Table 156-2).

Table 156-2 Classification of Cirrhosis According to Child and Turcotte

DIAGNOSIS   Esophagogastroscopy: procedure of choice for acute bleeding. Upper GI series: tortuous, beaded filling defects in lower esophagus. Celiac and mesenteric arteriography: when massive bleeding prevents endoscopy and to evaluate portal vein patency (portal vein also may be studied by ultrasound with Doppler and MRI).

TREATMENT
See Chap. 22 for general measures to treat GI bleeding.
Control of Acute Bleeding Choice of approach depends on clinical setting and availability.
1.   Endoscopic band ligation or sclerotherapy—procedure of choice (not always suitable for gastric varices); band ligation is now preferred because of lower complication rate and possibly greater efficacy—application of bands around “pseudopolyp” of varix created by endoscopic suction; sclerotherapy involves direct injection of sclerosant into varix; >90% success rate in controlling acute bleeding; complications (less frequent with band ligation than sclerotherapy)—esophageal ulceration and stricture, fever, chest pain, mediastinitis, pleural effusions, aspiration.
2.   Intravenous vasopressin up to 0.1–0.4 U/min until bleeding is controlled for 12–24 h (50–80% success rate, but no effect on mortality), then discontinue or taper (0.1 U/min q6–12h); add nitroglycerin up to 0.6 mg SL q 30 min, 40–400 µg/min IV, or by transdermal patch 10 mg/24 h to prevent coronary and renal vasoconstriction. Maintain systolic bp >90 mmHg. Octreotide 50–250 µg bolus + 50–250 µg/h IV infusion as effective as vasopressin with fewer serious complications.
3.   Blakemore-Sengstaken balloon tamponade: can be inflated for up to 24–48 h; complications—obstruction of pharynx, asphyxiation, aspiration, esophageal ulceration. Due to risk of aspiration, endotracheal intubation should be performed prior to placing Blakemore-Sengstaken tube. Generally reserved for massive bleeding, failure of vasopressin and/or endoscopic therapy.
4.   Transjugular intrahepatic portosystemic shunt (TIPS)—radiologic portacaval shunt, reserve for failure of other approaches; risk of hepatic encephalopathy (20–30%), shunt stenosis or occlusion (30–60%), infection.
Prevention of Recurrent Bleeding
1.   Repeated endoscopic band ligation or sclerotherapy (e.g., q2–4 weeks) until obliteration of varices. Decreases but does not eliminate risk of recurrent bleeding; effect on overall survival uncertain but compares favorably to shunt surgery.
2.   Propranolol or nadolol—nonselective beta blockers that act as portal venous antihypertensives; most effective in well-compensated cirrhotics; generally given in doses that reduce heart rate by 25%.
3.   Splenectomy (for splenic vein thrombosis).
4.   TIPS—regarded as useful “bridge to” liver transplantation in pt awaiting a donor liver who has failed on pharmacologic therapy.
5.   Portosystemic shunt surgery: portacaval (total decompression) or distal splenorenal (Warren) (selective; contraindicated in ascites; ? lower incidence of hepatic encephalopathy). Alternative procedure—devascularization of lower esophagus and upper stomach (Sugiura). Surgery is now generally reserved for pts with compensated cirrhosis (Child’s class A) who fail nonsurgical therapy (e.g., band ligation). Liver transplantation should be considered in appropriate candidates. (A previous portosystemic shunt does not preclude subsequent liver transplantation, though best to avoid portacaval shunts in transplant candidates.)
Prevention of Initial Bleed Recommended for pts at high risk of variceal bleeding—large varices, “red wales.” Beta blockers appear to be more effective than sclerotherapy; role of band ligation uncertain.

PROGNOSIS (AND SURGICAL RISK)   Correlated with Child and Turcotte classification (see Table 156-2).
HEPATIC ENCEPHALOPATHY
A state of disordered CNS function associated with severe acute or chronic liver disease; may be acute and reversible or chronic and progressive.
CLINICAL FEATURES   Stage 1: euphoria or depression, mild confusion, slurred speech, disordered sleep, asterixis (flapping tremor). Stage 2: lethargy, moderate confusion. Stage 3: marked confusion, sleeping but arousable, inarticulate speech. Stage 4: coma; initially responsive to noxious stimuli, later unresponsive. Characteristic EEG abnormalities.
PATHOPHYSIOLOGY   Failure of liver to detoxify agents noxious to CNS, i.e., ammonia, mercaptans, fatty acids, g-aminobutyric acid (GABA), due to decreased hepatic function and portosystemic shunting. Ammonia may deplete brain of glutamate, an excitatory neurotransmitter, to form glutamine. False neurotransmitters also may enter CNS due to increased aromatic and decreased branched-chain amino acid levels in blood. Endogenous benzodiazepine agonists may play a role. Blood ammonia most readily measured marker, although may not always correlate with clinical status.
PRECIPITANTS   GI bleeding (100 mL = 14–20 g of protein), azotemia, constipation, high-protein meal, hypokalemic alkalosis, CNS depressant drugs (e.g., benzodiazepines and barbiturates), hypoxia, hypercarbia, sepsis.

TREATMENT
Remove precipitants; reduce blood ammonia by decreasing protein intake (20–30 g/d initially, then 60–80 g/d, vegetable sources); enemas/cathartics to clear gut. Lactulose (converts NH3 to unabsorbed NH4+, produces diarrhea, alters bowel flora) 30–60 mL PO qh until diarrhea, then 15–30 mL tid-qid prn titrated to produce 3–4 loose stools/d. In coma, give as enema (300 mL in 700 mL H2O). Lactilol, a second-generation disaccharide that is less sweet than lactulose and can be dispensed as a powder, is not yet available in U.S. In refractory cases, add neomycin 0.5–1 g PO bid, metronidazole 250 mg PO tid, or vancomycin 1 g PO bid. Unproven: IV branched-chain amino acids, levodopa, bromocriptine, keto-analogues of essential amino acids. Flumazenil, a short-acting benzodiazepine receptor antagonist, may have a role in management of hepatic encephalopathy precipitated by benzodiazepine use. Liver transplantation when otherwise indicated.

Bibliography

For a more detailed discussion, see Chung, RT, Podolsky DK: Cirrhosis and Its Complications, Chap. 299, p. 1754; in HPIM-15.

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