1 / 16

Hepatic Disorders

Hepatic Disorders. Tintinalli’s Ch 83. Acute and Chronic Liver Dz. Most common causes: Hepatitis A, B, C Acetaminophen ingestion (42% of acute liver failure cases annually) Alcoholic liver dz Other Toxins Idiosyncratic drug reactions Autoimmune dz Metabolic hepatobiliary dz.

shen
Download Presentation

Hepatic Disorders

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Hepatic Disorders Tintinalli’s Ch 83

  2. Acute and Chronic Liver Dz • Most common causes: • Hepatitis A, B, C • Acetaminophen ingestion (42% of acute liver failure cases annually) • Alcoholic liver dz • Other • Toxins • Idiosyncratic drug reactions • Autoimmune dz • Metabolic hepatobiliary dz

  3. Pathophysiology • Fibrous scarring mixed w/ hepatocyte regeneration • Replaced with scar tissue • Loss of synthetic & metabolic functions • Increases resistance to blood flow from splanchnic circulation • Portal HTN; portal-systemic shunting (acites -> SBP) • Eventual encephalopathy from accumulation • of neurotoxic substances • Types of hepatobiliary dz: • Hepatocellular • Cholestatic • Immunologic • Infiltrative

  4. Clinical Features • Hepatocellular necrosis: • Anorexia • N/V • Fever • Cholestatic • Jaundice • Pruritis • Clay-colored stools • Dark urine • Intrahepatic/infiltrative • More insidious onset • Slower development of jaundice & other constitutional complaints

  5. Clinical Features Cont. • Chronic liver dz • Abdominal pain; ascites; GI bleeding; fever; AMS • Progressive generalized fatigue • Hepatomegaly with tenderness • +/- jaundice • Sallow complexion • Extremity muscle atrophy • Palmar erythema • Cutaneous spider nevi • Parotid gland enlargement • Testicular atrophy/gynecomastia • Splenomegaly + ascites = portal htn

  6. Labs • Markers of acute hepatocyte injury & death • AST (SGPT); also found in heart, smooth muscle, kidney, brain • ALT (SGOT); more specific marker of injury • Alk phos • Measures of hepatocyte synthetic function • Prothrombin time (PT) • Albumin • Indicators of hepatocyte catabolic activity • Direct bilirubin • Indirect bilirubin • Ammonia (although serum level does NOT correlate well with clinical status)

  7. Labs cont. • Viral hepatitis serology • HAV: IgM anti-HAV detectable at onset of illness • HBV: HBsAg (Hep B surface antigen) measurable BEFORE clinical illness along with elevated transaminases (up to 1-2 months); after about 2 weeks can measure anti-HBc (antibodies to Hep B core antigen) • “window period” • then antibodies to Hep B surface antigen (anti-HBsAg) measureable • HCV: anti-HCV detectable with acute infection

  8. Clinical syndromes • Cirrhosis & complications of End-Stage LiverDz • Primarily supportive tx • Try to eliminate reversible causes of liver injury • Identify & treat complications of liver dysfunction • End-stage liver dz • Loss of hepatic synthetic function • Loss of hepatic degradative capacity • Portal hypertension • Coagulopathies • Variceal hemorrhage • Hepatorenal syndrome • Hepatic encephalopathy

  9. Gastroesophageal varices and hemorrhage • Results as intrahepatic fibrosis increases resistance to blood flow from portal vein to IVC • Gastric & esophageal vessels are thin-walled and prone to bleeding because of their location and lack of supporting connective tissue • Mortality with variceal bleeding high • Clinical features: • Hematemesis/”coffee-ground” emesis • Melena/BRBPR • Lightheadedness/gen. weakness/fatigue • Vital signs may be normal or near normal • Variceal bleeding (even if only suspected) is NOT a contraindication for NGT

  10. GE varices and hemorrhage cont. • Treatment • ABC’s • 2 lg. bore IV’s • Type & screen for PRBC’s and FFP • Endoscopy (banding, sclerotherapy) • Balloon tamponade (not used as much anymore) • Vasoactive drugs • Somatostatin/Octreotide – preferred due to lack of side effects; causes relaxation of mesenteric vascular smooth muscle, reducing portal venous pressure w/out arterial vasospasm; 50mcg IV bolus, then 50 mcg IV/h cont. infusion • Vasopressin/Terlipressin – nonspecific arterial vasoconstriction, reducing inflow through the mesenteric circulation reducing portal pressure • Antibiotics – empiric coverage for enteric organisms (ex: Zosyn)

  11. Blood freely flowing from a varix in the lower esophagus, creating a pool of blood, in a 37 year-old man with alcoholic liver disease. Spurting esophageal varix in a 78 year-old man with portal hypertension caused by colon cancer metastatic to liver. The bleeding caused the varix to decompress and flatten. View on the right shows the jet of blood ricocheting off the opposite esophageal wall.

  12. Ascites and SBP • Results due to chronic portal hypertension, hypoalbuminemia & poor renal excretion of sodium/water • Transportal hydrostatic pressure gradient & decrease intravascular oncotic pressure favors the transit of water into the EXTRAcellular space & peritoneum (ascites/anasarca) • SBP results as normal bowel flora migrates across edematous bowel wall; bacteria able to flourish in media (ascites) because liver fails to produce immunologically active proteins • Clinical features: • Abdominal pain +/- fever (w/ fever, think SBP) • Dyspnea (mostly due to abdominal ascites limiting diaphragmatic movement or hydrothorax through hernias)

  13. Paracentesis: • Dx SBP • Symptomatic relief of abd. pain, dyspnea, anorexia • Can remove 6-9L w/out complication • May want to infuse volume expander (like Hespan or albumin) to reduce renal dysfunction • send ascitic fluid for cell count w/ diff.; glucose; protein; gm. stain; C & S • Dx: WBC ct > 1000/uL or neutrophil ct > 250 uL = SBP • Low glucose or high protein suggests bacterial infxn. • Gm stains/cxs may be negative 30-40% of the time • Can also send for cytology (r/o cancer); albumin; LDH; tumor markers

  14. Hepatorenal Sydrome • Development of acute renal failure in presence of preexisting chronic or acute hepatic failure (pt with no hx of renal dz) • Ideas about causes of renal failure: • Poor renal blood flow • RAAS, cytokines, endothelin • Marker of morbidity • survival of 21 days with aggressive tx • Look for reversible causes of renal failure • Intravascular volume depletion (prerenal azotemia), intrinsic renal dz (drug induced); postrenal obstruction; infection • Tx: terlipressin & albumin cont. infusion to improve outcomes

  15. Hepatic Encephalopathy • Due to accumulation of nitrogenous waste products normally metabolized by the liver • Nitrogenous wastes from dietary sources or protein load from GI bleed; changes in gut flora (antibiotics) • Common after TIPS procedure • Clinical features: • Chronic fatigue/acute lethargy • Asterixis • AMS • Progressive neurologic dysfunction • +/- elevated serum ammonia

  16. Hepatic Encephalopathy cont. • Treatment • Reduce production of nitrogenous wastes • Reducing protein intake and metabolic activity of intestinal bacteria • Lactulose – 20 g (30 mL) PO or 300 mL retention enema q4-6h

More Related