Tuesday, July 7, 2015

“My Eyes Are Yellow!”

“My Eyes Are Yellow!”

Case presentation: 
A 48-year-old female presents to the emergency department with the chief complaint: “My
eyes are yellow!” 
Yellow Eye , Icterus 

She denies other clinical symptoms. Her physical examination is remarkable only for scleral icterus and jaundice (illustrated). No abdominal tenderness or hepatomegaly is detected

Question: Which of the following statements is true?

A. Her scleral icterus effectively rules out hemolysis as a cause of her condition
B. Normal to mildly elevated transaminases with an elevated alkaline phosphatase and conjugated
bilirubin would suggest extrinsic bile duct compression in this patient
C. The presence of Courviosier’s sign suggests an infectious etiology in this patient
D. The lack of abdominal pain effectively rules out pancreatic cancer as a cause of her condition
E. Excessive beta-carotene ingestion is a potential cause of this patient’s condition

note the lower bulbar conjunctiva is yellow 

Answer: B
Jaundice secondary to hyperbilirubinemia
Discussion: Jaundice is the yellowish discoloration of the skin, mucous membranes, and sclerae caused by hyperbilirubinemia. Jaundice is not usually clinically apparent unless the serum bilirubin is above 3 mg/dL. It can be sign of many medical conditions ranging from the benign to the potentially fatal.
Jaundice results from a dysfunction in bilirubin metabolism at either the prehepatic, intrahepatic, or posthepatic phase. Bilirubin itself is produced from the metabolism of heme, which largely comes from breakdown of red blood cells.
The fi rst step in the diagnosis of jaundice is determining the type of hyperbilirubinemia. Blood should be analyzed for levels of conjugated and unconjugated bilirubin.
If the hyperbilirubinemia is primarily unconjugated, a disorder of bilirubin metabolism should be suspected. Increased bilirubin production that occurs from hemolysis, ineffective erythropoiesis, massive transfusion, or the resorption of a large hematoma can exceed the liver ’ s conjugation process. Decreased hepatocellular uptake can be caused by drugs such as rifampin. Decreased conjugation is responsible for Gilbert ’ s or Crigler – Najjar syndrome and is the cause of physiologic jaundice of the newborn.

If the hyperbilirubinemia is predominantly conjugated, the etiology is likely to be secondary to liver disease, cholestasis, extrinsic bile duct compression, Dubin – Johnson or Rotor ’ s syndrome. Alanine aminotranferase and aspartate aminotransferase elevation suggests intrinsic liver disease or a cholestatic process. Normal to mildly elevated transaminases with an elevated alkaline phosphatase
and gamma - glutamyltransferase suggests extrinsic bile duct compression. Etiologies of intrinsic
liver disease include hepatitis, cirrhosis, hepatotoxins, metabolic disorders of the liver such as Wilson ’ s disease, HELLP syndrome, and infi ltrative diseases such as amyloidosis and metastatic carcinoma. Cholestatic diseases include graft-versus-host disease, primary biliary cirrhosis, and drugs such as erythromycin and chlorpromazine.

Extrinsic obstruction of the bile ducts can be caused by cholelithiasis and cholecystitis, primary sclerosing cholangitis, postsurgical strictures, neoplasms of the pancreatic head and biliary tract, and pancreatitis. Initial imaging of the right upper quadrant can be done with either computed tomography or ultrasound scanning. Further work-up should be directed by the outcome of initial
laboratory values and abdominal imaging. Scleral icterus is more sensitive than jaundice for the
detection of hyperbilirubinemia because of the high concentration of elastin in the sclera, which has a high affinity for bilirubin. Courvoisier’s sign is painless enlargement of the gallbladder that represents extrinsic compression of the biliary tree; however, it is present in less than a third of patients with biliary obstruction. The classic diagnosis associated with painless jaundice is pancreatic carcinoma. Excessive beta-carotene ingestion does not cause scleral icterus. Lack of scleral icterus can clinically differentiate pseudo-jaundice caused by beta-carotene from jaundice. Cholestatic jaundice can also present with generalized pruritis as the primary complaint. 



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