CHAPTER 84 TINTINALLI

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CHAPTER 84TINTINALLIS EMERGENCY
MEDICINEROBERT MOOSALLY, DO

• JAUNDICE

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PATHOPHYSIOLOGY

• CLINICAL MARKER OF A DEFECT IN METABOLISM
  EXCRETION OF BILIRUBIN
• NOT HARMFUL EXCEPT IN NEONATES
• YELLOWISH DISCOLORATION OF SCLERA, SKIN MUCOUS
  MEMB.
• CAUSED BY DEPOSITION OF BILE PIGMENTS
• HYPERBILIRUBINEMIA (SERUM BILIRUBIN gt 2.0-2.5
  ml/dl)
• TWICE UPPER LIMITS OF NORMAL
• USUALLY 1ST NOTICED IN SCLERA
• SCLERA HAS A LOT OF ELASTIN
• ELASTIN HAS HIGH AFFINITY FOR BILIRUBIN
• IF SKIN IS GREEN, THEN INDICATES
• LONG STANDING JAUNDICE
• (BILIRUBIN ? BILIVERDIN)
• CAN BE CONFUSED WITH PEOPLE WHO EAT TOO MANY
  CARROTS OR HAVE HEMOCHROMATOSIS (NEITHER WILL
  DISCOLOR SCLERA)

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• HYPERBILIRUBINEMIA
• OVERPRODUCTION OF BILIRUBIN IN
  RETICULOENDOTHELIAL SYSTEM
• FAILURE OF HEPATOCYTE UPTAKE
• FAILURE OF HEPATOCYTE TO CONJUGATE OR EXCRETE
  BILIRUBIN
• OBSTRUCTION OF BILIARY EXCRETION INTO INTESTINE
• 2 TYPES
• UNCONJUGATED-PRODUCTION EXCEEDS ABILITY FOR LIVER
  TO PROCESS IT OR DEFECT IN THE UPTAKE BY THE
  LIVER (SO YOUR SERUM LEVELS WILL RISE)
• Ex HEMOLYSIS HEMOLYTIC ANEMIA TRANSFUSION
  REACTION INBORN ERRORS OF METABOLISM
• CONJUGATED-LIVER PRODUCES BUT CANNOT PROCESS DUE
  TO A METABOLIC DEFECT OR INTRINSIC/EXTRINSIC
  OBSTRUCTION
• Ex CONGENITAL DEFECT, INFLAMMATION, MASS
  LESION, GALLSTONES-gtCHOLEST
  ASIS
• TABLE 84-1 (TINTINALLIS)

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CLINICAL PICTURE

• FAMILY HISTORY/RECURRENT MILD JAUNDICE THAT
  RESOLVES SPONTANEOUSLY
• THINK FAMILIAL DISORDERS OF BILIRUBIN METABOLISM
• Ex GILBERT (MOST COMMON FORM), ROTOR,
  CRIGLER-NAJJAR, DUBIN-JOHNSON SYNDROMES
• SICKLE CELL DZ. WILL DEVELOP CHRONIC JAUNDICE
  WITH ONGOING HEMOLYSIS (IF ABD. PAIN, FEVER,
  VOMITING ACUTE CHOLEY/BILIARY OBSTRUCTION)
• ACUTE JAUNDICE
• YOUNG PERSON
• VIRAL HEPATITIS (RUQ PAIN HEPATOMEGALY), MAY
  NOT HAVE PRURITIS
• TOXIC CAUSES LIKE ACETAMINOPHEN, HALOTHANE,
  METHYLDOPA, ISONIAZID OR PHENYTOIN OCPS,
  ANABOLIC STEROIDS CHLORPROMAZINE CAN CAUSE
  CHOLESTASIS, HEPATIC NECROSIS FROM AMANITA
  MUSHROOMS, CARBON TETRACHLORIDE PHOSPHORUS

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• ACUTE JAUNDICE CONT.
• HEPATIC OR BILE DUCT OBSTRUCTION
• ALCOHOLIC LIVER DZ/CIRRHOSIS-WEAKNESS, PERIPHERAL
  MUSCLE WASTING, ASCITES, SPIDER ANGIOMATA,
  PRURITUS, SXS OF PORTAL HTN
• FEVER, VOMITING, RUQ TENDERNESS
• ASTERIXIS, FETOR HEPATICUS, ENCEPHALOPATHY
  INDICATE ADVANCED DZ
• ACUTE CHOLANGITISABD. PAIN, JAUNDICE, VOMITING,
  FEVER, RUQ TENDERNESS
• CHOLECYSTITIS ALONE WILL NOT PRODUCE
• JAUNDICE
• MALIGNANCYPAINLESS JAUNDICE,
• WT. LOSS, EPIGASTRIC MASS
• IF NODULAR LIVER, THEN METASTATIC DZ
• CHFHEPATOMEGALY, PEDAL EDEMA
• JVD S3 GALLOP

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LABS

• SERUM BILIRUBIN (TOTAL DIRECT)
• ALT
• AST
• ALK PHOS
• U/A (LOOK FOR BILRUBIN/UROBILINOGEN)
• CBC
• PT
• AMYLASE/LIPASE

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• UNCONJUGATED HYPERBILIRUBINEMIA
• BILIRUBIN WILL BE SLIGHTLY ELEV.
• gt85 WILL BE INDIRECT FORM
• TIGHTLY BOUND TO ALBUMIN SO YOU WILL NOT SEE THIS
  TYPE IN THE URINE
• ALT/AST NORMAL
• CBC WILL SHOW ANEMIA/HEMOLYSIS
• NEED TO DO COOMBS TEST TO DETERMINE

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• CONJUGATED BILIRUBINEMIA
• WATER SOLUABLE SO WILL APPEAR IN URINE (EVEN WITH
  LOW SERUM CONCENTRATIONS)
• UROBILINOGEN WILL BE ABSENT IF SIGNIFICANT
  CHOLESTASIS
• IF AST/ALT/ALK PHOS NORMAL, THEN JAUNDICE IS FROM
  SEPSIS, IN-BORN ERRORS OF METABOLISM, PREGNANCY
• IF AST/ALT/ALK PHOS ABNORMAL, THEN LIVER IS THE
  PROBLEM

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• CAN PROCEED TO OTHER LABS DEPENDING ON WHAT YOUR
  PRIMARY INVESTIGATION REVEALS..
• HEPATOCELLULAR DZ THEN GET SEROLOGIC VIRAL
  STUDIES
• ALCOHOLIC LIVER DZ THEN GET PLATELET COUNT AND
  SERUM ALBUMIN LEVELS TO DETERMINE EXTENT OF
  INJURY
• IF EVERYTHING NEG. THEN LIVER BX

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IMAGING

• US
• GALLSTONES
• DILATED EXTRAHEPATIC BILIARY DUCTS
• MASSES IN LIVER, PANCREAS OR PORTAL AREA
• CT
• F/U STUDY IF INCONCLUSIVE US

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DISPOSITION

• IF JAUNDICE AND STABLE GO HOME
• SECURE FOLLOW UP
• IF ANYTHING ELSE COMES UP IN YOUR INVESTIGATION,
  THEN ADMIT
• /- SURGERY CONSULT