Description
Portal hypertension is a clinical syndrome defined by a hepatic vein pressure gradient (HVPG) greater than 5 mm Hg, and is associated with encephalopathy, ascites, splenomegaly, and gastrointestinal varices. In individuals with cirrhosis, portal hypertension is the primary cause of serious complications and death. Noncirrhotic portal hypertension (NCPH), a disease where portal hypertension develops even in the absence of cirrhosis, is another possibility. The objective is to identify and describe the severity of portal hypertension in both NCPH and cirrhotic portal hypertension. However, knowledge of the underlying pathophysiological and etiological characteristics is crucial for understanding portal hypertension diagnosis and treatment.
Résumé
- The presentation covers portal hypertension, defining it as a pathologic increase in portal venous pressure, leading to collaterals that bypass the liver. The gold standard for diagnosis is the hepatic venous pressure gradient (HVPG), with clinically significant portal hypertension indicated by an HVPG greater than 10 mmHg. Causes are categorized as pre-hepatic, intra-hepatic (pre-sinusoidal, sinusoidal, post-sinusoidal), and post-hepatic, with cirrhosis being the most common.
- The pathophysiology involves increased intrahepatic resistance due to structural changes and increased vascular tone. Clinical manifestations include esophageal varices, gastropathy, GI bleeds, splenomegaly, ascites, and liver cell dysfunction features like encephalopathy and jaundice. Complications can extend to the lungs, heart, kidneys, and brain. Evaluation includes invasive (hepatic venous pressure gradient) and non-invasive methods (blood biomarkers, imaging, elastography, endoscopy).
- Management of varices includes screening, primary prophylaxis, acute bleed management, and secondary prophylaxis. Primary prophylaxis involves non-selective beta-blockers (carvedilol preferred) or endoscopic variceal ligation. Acute variceal bleeds are managed with vasoactive drugs (terlipressin), antibiotics, resuscitation, and endoscopic intervention (banding or sclerotherapy). Salvage therapies include balloon tamponade, self-expanding metal stents, TIPS, and surgery.
- Management of ascites involves sodium restriction and diuretics (spironolactone and furosemide). Refractory ascites may require large volume paracentesis with albumin infusions, and potentially TIPS or liver transplant. Newer modalities include midodrine, terlipressin, rifaximin, and SGLT2 inhibitors. The goal is to address the underlying cause, manage complications, and improve the patient's quality of life.
Exemple de certificat
À propos des intervenants
Dr Rajat Bansal
Gastro-entérologue consultant et endoscopiste thérapeutique à l'hôpital Indraprastha Apollo, New Delhi.
Divulgation financière
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