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- Acute cholecystitis
- Acute cholangitis
- Splenic Infarction
- Lab evaluation of liver disease
Cholelithiasis (gall stones)Very common / 10-20% of patients > 65 yrs (only 10% develop symptoms within 10 yrs) Acute calculus >>> chronic calculus >> acute acalculus > chronic acalculus Presentation: biliary colic (epigastric pain, often after meals, may radiate to right shoulder, last about 1-4 hrs) Labs: elevated alk phos, elevated bilirubin (> 3g/dL suggests common duct stone) Complications: obstruction (cystic or common bile duct) may lead to gallstone pancreatitis, cholangitis biliary fistula (necrosis) gallstone ileus (erosion into bowel – 98% caused by gall stones) Treatment (see acute cholecystitis): do not treat asymptomatic gallstones (if symptomatic, consider cholecystectomy, lithotripsy is 2nd line) / 40% recur within 6 weeks Cholesterol (Fat (cholesterol), Female 3:1, Fertile, > Forty, Familial, Hispanic) Risk factors: women 3:1, increasing age, obesity, Hispanic, familial mixed type (cholesterol, bile, Ca, protein) — most common stone(s) aggregate, smooth / chronic cholecystitis / growth by accretion supersaturation 7 α-hydroxylase deficiency (↓ bile salt pool) / obesity cholesterol secretion nidus, nucleation secreted glycoprotein as nidus / deficiency of anti-nucleating factor calcium pigment calcium and bile / normal gall bladder / multiple, small, sharp black hemolysis, increased unconjugated bilirubin in bile brown bacterial cholangitis, increased unconjugated bilirubin in bile (due to bacterial hydrolysis) often in intra/extra hepatic ducts / malnourishment Acute cholecystitisless common than chronic (often superimposed on chronic) Presentation: severe RUQ pain (Murphy’s sign—pain with inspiration on palpation of RUQ), fever, leukocytosis, enlarged gallbladder, prior h/o pain Imaging: Ultrasound: 90% with stones, gallbladder wall thickening, distended gall bladder, pericholecystic fluid MRCP ERCP, IOC or PTC (percutaneous transhepatic cholangiography) KUB shows 20% of stones
Organisms: E. coli, klebsiella, bacteroides, Enterococcus, pseudomonas Emphysematous cholecystitis: Clostridium perfringens and diabetics / may perforate (5%)
acute cholecystitis (operate after antibiotics and decreased temperature) ascending cholangitis (very serious, STAT operation) pancreatitis (usually from small stones) obstruction (pt with jaundice) Treatment: cefoxitin (anaerobes), gentamicin (GNR) Chronic cholecystitis 90-95% with stones / rarely typhoid fever / mucosal atrophy or ulceration, fibrosis, Rokitansky-Aschoff projections, calcification or porcelain gall bladder / can happen in people who don’t have gall bladder (stones formed in ducts) Presentation: chronic indigestion, large fatty meals aggravate (CCK stimulated contraction) Treatment: symptomatic cases treated with cholecystectomy, (rarely) shock-wave lithotripsy, litholytic drugs Acute cholangitisPresentation: Charcot’s triad fever, jaundice, RUQ pain / Raynaud’s pentad: add hypotension, mental status changes / and elevated WBC Ultrasound: may see evidence of obstruction CT scan
CXR: may see sympathetic effusion (left) Treatment: if stable, can give abx such as Unasyn 3 g q 6 until patient is ‘cooled off’ and then the obstruction must be relieved either by ERCP or IOC; if patient unstable, must do emergent ERCP or IOC (w/ sphincterotomy or tube placement) Carcinoma of gall bladder (usually incurable) 1 in 50,000 / if discovered incidentally, 5 yr survival 50%, if symptomatic, 1 year survival of 5% / associated with chronic cholecystitis / finding of porcelain gall bladder carries 25% risk of progression to carcinoma and requires open cholecystectomy (because cannot risk having it be malignant and rupture) / liver and lymph mets / adenocarcinoma (80%), anaplastic (10%), squamous (5%) Carcinoma of extra-hepatic biliary apparatus (usually incurable) men / 5yr survival of 10% ampulla of Vater (soft, papillary), common duct (hard, infiltrative), confluence of hepatic and common duct (Klatskin tumor) / obstructive jaundice (first sign), upper abdominal pain, hepatomegaly Risk factors: ulcerative colitis, sclerosing cholangitis, clonorchis sinensis infection Diagnosis: U/S, CT, ERCP or PTC Spleen 25% with accessory spleen Splenic InfarctionDiagnosis: DPL (diagnostic peritoneal lavage), U/S, CT Treatment: repair or remove based on amount damaged / observe (especially in children, who get post-splenectomy sepsis) Note: don’t forget to give the vaccines for Hib vaccine, pneumococcus and N. meningitis Indications for splenectomy ITP + spherocytosis, bleeding and diseased states (EBV, malaria, trauma) distal pancreatectomy failed medical therapy of autoimmune hemolytic anemia GI Surgery (more) Anastomoses of bowel segments / must remove bacteria (bowel prep solutions) in order to increase wound healing (some authors suggest decontamination with polymyxin, tobramycin, vancomycin, and amphotericin B) Pimp anatomy: Marginal artery of Drummond, anastomosis of Riolan Liver [Liver Function Tests] Hepatitis Viral Hepatitis (HAV, HBV, HCV) (hepatitis labs) Alcoholic hepatitis Autoimmune hepatitis Non-alcoholic fatty liver disease Biliary System Gall Bladder (cholelithiasis, cholecystitis, cholangitis) Biliary Cirrhosis (PBC), Sclerosing Cholangitis (PSC) alpha-1-antitrypsin, Wilson’s, Hemochromatosis Cirrhosis (ascites, SBP) Portal cirrhosis / Post-necrotic cirrhosis / Portal venous hypertension Liver Neoplasia Liver Transplant focal nodular hyperplasia hepatocellular adenoma hepatocellular carcinoma Lab evaluation of liver diseaseLab error rate usually about (3-4%) serum bilirubin (see pediatric) jaundice when serum bilirubin above 3mg/dL / high serum levels may correlate to severity of chronic liver disease / G-6-PD patients (black) may have disproportionately high bilirubin (hemolysis) 5mg/dl and PT > 4 seconds (50% mortality) in patients with acute alcoholic hepatitis causes of unconjugated bilirubinemia include hemolysis, impaired hemoglobin synthesis, genetic defect of bilirubin transport into hepatocyte –
unconjugated BR is bound to albumin and cannot be filtered / early indicator for liver disease (even before jaundice / pyridium and phenothiazide give false positive results urine urobilinogen absence on dipstick indicated biliary obstruction / elevation may mean liver injury (impaired re-uptake of serum urobilinogen) or hemolysis / can be an early marker for liver damage
rarely used / antibiotics may suppress bacterial conversion of bilirubin to urobilinogen albumin not early or sensitive due to 14-20 day half-life, large stores / can be decreased from renal loss great marker for severe, chronic liver disease / good response to therapy will see a rise above 3g/dl prothrombin time (PT) [11-13] useful in assessing prognosis of severe acute/chronic liver disease / 2, 7, 9, 10 / PTT may also be elevated in severe liver disease Hepatocellular aminotransferase (AST/ALT) [10-40] absolute level of no prognostic value (mainly used as an early indicator) / AST (heart, liver, muscle, kidney, some pancreas/spleen) / ALT (many tissues, highest in liver, some in kidney) / AST reaches higher levels than ALT in non-hepatic injury / AST over 400 units/liter is liver or skeletal muscle, an MI above 200u/l would be severe and obvious / acute liver injury may reach 400-1000u/l, obstruction will not be over 400u/l / values may drop from 1000 to 300 in just 3-5 days (masking previously high levels) 80% alcoholic liver disease (AST > ALT) – alcoholics are PBP deficient (this is a false-phenomenon also seen with fatty liver associated with pregnancy) ALT – cytosol / injured cell releases enzymes into circulation male > female, higher in winter, Hispanic/native American higher, increased weight, married > single / ALT reaction measures activity (step 1 requires PBP, step 2 uses NADH, measures NAD production) / test results can vary based on many factors (including drugs and solutes in the patients blood sample) AST – in organelles? Similar reaction, but not dependent on PBP Only ⅔ of increased AST with liver disease (type B and O blood has increased activity)
very sensitive, not selective (pancreas, heart, lungs, kidney) / elevated by drugs (ethanol, phenobarbital, phenytoin) and diabetes, some drugs increase hepatocyte membrane (releases GGT into circulation) / may confirm AP / inhibited by gestational hormones (non-informative in pregnant women) Other enzymes LAP and 5’-NT only in liver and placenta (not bone) / may confirm AP / many false negatives LDH – may rise moderately in several liver diseases (mild in obstructive) / marked increases may result from liver mets Other tests (not often used) bromosulphopthalein BSP, indocyanine green, meg-x, aminopyrine, caffeine Hepatitis Labs Viral Hepatitis Labs (see micro) [diagram] [diagram] Autoimmune Hepatitis Labs ANA, ASMA, LKM-1, AMA lab values can show large variability even from the same lab anti-ANA used with SMA to diagnose “lupoid hepatitis” (unrelated to SLE) ASMA chronic active hepatitis (60%), biliary cirrhosis (10%) / transient rise with EBV LKM-1 rare type of autoimmune hepatitis (not having ANA or SMA) – type II AMA 100% of primary biliary cirrhosis (M2 fraction) 25% chronic active hepatitis (M4) alpha-fetoprotein endoderm derived (peak at 12 weeks gestation) / malignant HCC or germ cell tumors (>1000ng/ml) others include pancreas, gall bladder / used to follow progression, not for diagnosis Complications/Findings of Liver Failure/Cirrhosis Decreased hepatic function neurological: encephalopathy (confusion, somnolence, coma) from elevated ammonium coagulopathy: increased PT (lack of clotting factors) hypoglycemia lactic acidosis jaundice estrogen metabolism decreased (spider angiomas, redistribution of hair, etc.) Ascites (see Ddx below) Presentation: dyspnea, umbilical hernia Mechanisms: hydrostatic, oncotic (decreased albumin) / SAAG usually high in mixed cases / portal vs. malignant (can tap more fluid off safely with malignant ascites because hemodynamics are less likely to be embarrassed) SAAG (serum ascites albumin gradient = serum albumin – ascitic albumin) [more Ddx] > 1.1 g/dL: cirrhosis, portal vein thrombosis, Budd-Chiari, CHF, constrictive pericarditis, urinary extravasation, hypothyroidism, Meig’s, hydronephrosis < 1.1 g/dL: peritoneal infection, peritoneal carcinomatosis, pancreatic ascites, bowel obstruction or infarction, serositis (e.g. SLE), nephrotic syndrome Physical exam: JVD/pulsatile liver / KUB ground glass w/ centrally located bowel loops Note: all new or unexplained cases of ascites should undergo paracentesis (may rule in infectious/tuberculous, primary hepatoma or malignant seeding / you should inoculate cultures at bedside Hepatic hydrothorax Negative inspiratory pressure causes buildup of ascitic fluid through small diaphragmatic holes Treatment: same as ascites except avoid tube thoracostomy because this will just pull more fluid into pleural space / refractory cases can consider VATS to correct any defect or pleurodesis Nephrogenic ascites diagnosis of exclusion / intractable ascites with resultant cachexia / mechanism is multifactorial (i.e. unclear) / occurs from 20 months pre to 70 months post-initiation of dialysis from ESRD / dialysis associated hypotension may be a harbinger / M:F 2:1 / survival ~ 10 months / best treatment is bilateral nephrectomy with renal transplant / some benefit from CAPD, or peritoneovenous shunt Varices (see GI bleed) esophageal, hemorrhoidal, caput medusae (ammonia bypasses liver and reaches CNS causing hepatic encephalopathy)
gastric mucosa is weakened by portal hypertension and more likely to bleed Peritonitis usually from perforation of abdominal viscus, but portal HT is the first cause of spontaneous peritonitis in adults (may have more insidious onset, lack of peritoneal signs) / 50% mortality / more than 250 PMNs/mL Hepatorenal syndrome Unrelenting renal failure because of liver failure Types of Cirrhosis Portal cirrhosis alcohol / portal tract to portal tract, tract to central vein / small, pseudo-lobules (regenerating tissue, no intralobular structures) Post-necrotic cirrhosis chronic active hepatitis and autoimmune hepatitis / patchy distribution (piecemeal necrosis) / irregular broad bands of fibrosis / variable sized nodules / also called portal triaditis Biliary Cirrhosis portal tract to portal tract / central veins are spared Portal venous hypertension [diagram of portacaval anastomoses] Pre-portal: portal vein thrombosis, schistosomiasis Sinusoidal: HCV, HBV, alcohol Post-portal: Budd-Chiari, pericarditis, renal failure Budd-Chiari occluded IVC/hepatic vein / polRV?, pregnancy, HCC / SAAG > 1.1 Fibrocongestive splenomegaly greater in post-necrotic, hemolysis, pigment gall stones Hepatitis (Hepatocellular) Viral: hepatitis virus A - G / CMV / EBV / Yellow Fever Bacteria: Coxiella, TB Parasites: Echinococcus Drugs: Antibiotics: rifampin, PZA, INH, macrolides CNS: phenytoin, VPA, carbamazepine, antipsychotics, pemoline, methyldopa, MAO inhibitors Other: PTU, indomethacin, diclofenac, halothane Toxins: EtOH, Neoplasms: Other: alpha-1-antitrypsin, Wilson’s, Hemochromatosis Alcoholic hepatitis heavy alcohol consumption / Mallory’s hyaline / neutrophilic infiltrate / fatty change, hydropic change, fibrosis around central vein / AST:ALT > 2 / < 300 AST Non-alcoholic fatty liver disease (NAFLD) 20% of US adults (1 in 30 develop cirrhosis or less commonly HCC, ESLD requiring transplant) Risk factors: obesity, type 2 DM, hyperlipidemia Diagnosis: biopsy is only way to tell prognosis and r/o other diseases / LFT’s may not correlate / macrovesicular accumulation of fat (fatty deposits) Treatment: ?gemfibrozil, vitamin E, thiazolinediones (promising but trials underway 11/06) / too rapid wt loss is actually harmful Non-alcoholic steatohepatitis (NASH) progression/complication of NAFLD but when hepatocyte necrosis occurs Acute Fatty Liver of Pregnancy – microvesicular fat Reye’s Syndrome – microvesicular fat Granulomatis hepatitis in AIDS may not be able to produce impressive granulomas Acetaminophen toxicity Ingestion of 10g or more Mechanism: increased p450 metabolism (NAPQI formation) and depletion of glutathione stores (leads to NAPQI persistence) Labs: LFTs reaction to normal dose markedly increased AST / moderately increased ALT / AST:ALT > 2 / increased to markedly increased PT / huge overdose normal initially, later markedly increased AST and ALT Treatment: N-acetylcysteine should be started within first 10 hrs, continued 72 hrs Ischemic hepatitis – bile duct obstruction Hypotension Sudden, very high rise of AST 24-48 hrs peak Rapid normalization within 7-10 days after reperfusion Concomitant renal impairment
increase in LFT’s with smaller increase in alkaline phosphatase peak ~2 weeks, then decline even with continued TPN / reversible
steatohepatitis (common) / can lead to fibrosis (discontinue, cycle, reduce calories and/or supplement with small amount of enteral nutrition) cholestasis and hepatic fibrosis (uncommon) Biliary sludge (50% > 6 wks, ~100% > 3 months) Gallstones (acalculus and calculus cholecystitis) From decreased bile flow and gallbladder stasis (can try CCK, pulsed amino acids, small enteral feedings) Download 3.95 Mb. Share with your friends:
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