My patient with jaundice complains of abdominal fullness. How useful is the history or physical exam when assessing for ascites?

Even in the age of ultrasound, history and physical exam can be useful in assessing for ascites.

History is a good place to start. Of all the questions we often ask when we suspect ascites (eg, increasing abdominal girth, weight gain and ankle swelling), lack of report of ankle swelling is probably the most helpful in excluding ascites (negative likelihood ratio [LR-], 0.1 in a study involving men), followed by no increase in abdominal girth (LR-, 0.17). Conversely, patient reported ankle swelling or increasing abdominal girth may be helpful in suspecting ascites (LR+ 4.12 and 2.8, respectively). 1

Of the various physical signs and maneuvers, absence of peripheral edema is highly associated with the lack of ascites, followed by lack of shifting dullness or fluid wave (LR-, 0.2, 0.3, 0.4, respectively). The presence of a fluid wave may be the most helpful in suspecting ascites, followed by peripheral edema, and shifting dullness (LR+ 6.0, 3.8, 2.7, respectively). 1  Relatively high sensitivities have been reported for shifting dullness (83-88%), while relatively high specificities have been reported for the fluid wave test (82-90%).2,3 An elevated INR may also improve the positive predictive value of shifting dullness and fluid waves.4

So if you don’t get a history of ankle edema and find no evidence of peripheral edema or shifting dullness on exam, the likelihood of ascites is pretty low. On the other hand, if you find a positive fluid wave, you can be pretty sure that the patient has ascites.

Of course, the actual likelihood of detecting ascites also depends on several other factors, including your pre-test probability and the volume of the ascites in the abdominal cavity, with at least ~500 ml of ascites necessary before it can be detected on exam (vs ~100 ml for ultrasound). 2,5

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References

  1. Williams JW, Simetl DL. Does this patient have ascites? How to divine fluid in the abdomen. JAMA 1992;267: 2645-48. https://jamanetwork.com/journals/jama/fullarticle/397285
  2. Cattau EL, Benjamin SB, Knuff TE, et al The accuracy of the physical examination in the diagnosis of suspected ascites. JAMA 1982;247:1164-66. https://www.ncbi.nlm.nih.gov/pubmed/7057606
  3. Cummings S, Papadakis M, Melnick J, et al. The predictive value of physical examinations for ascites. West J Med 1985;142:633-36. https://www.ncbi.nlm.nih.gov/pubmed/3892916
  4. Fitzgerald FT. Physical diagnosis versus modern technology. A review. West J Med 1990;152:377-82. https://www.ncbi.nlm.nih.gov/pubmed/2190412
  5. CDC. Assessment for ascites. https://www.cdc.gov/dengue/training/cme/ccm/Assess%20for%20Ascites_F.pdf. Accessed November 13, 2019.
My patient with jaundice complains of abdominal fullness. How useful is the history or physical exam when assessing for ascites?

What is the association between sepsis and jaundice in patients without biliary obstruction?

Up to 20% of cases of jaundice in community hospitals may be due to sepsis and bacterial infections, often occurring within a few days of onset of bacteremia or even before other clinical features of infection become apparent. 1 

Although biliary obstruction as the cause of jaundice is usually suspected, many patients lack extrahepatic cause for their jaundice. Gram-negative bacteria (eg, E. coli) are often the culprit with intraabdominal or urinary tract infection, pneumonia, endocarditis, and meningitis sources also often cited. Hyperbilirubinemia (often 2-10 mg/dl) is commonly associated with elevated alkaline phosphatase and mild aminotransferases elevations, and usually resolves with treatment of infection.1

Although factors such as increased bilirubin load from hemolysis, hepatocellular injury, and drugs (eg, penicillins and cephalosporins) may play a role, cholestasis—likely due to cytokines such as tumor necrosis factor (TNF)α— is the predominant cause. 1  

Interestingly, anti-TNF-α antibodies block reduction in bile flow and bile salt excretion in laboratory animals2

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References

  1. Chand N, Sanyal AJ. Sepsis-induced cholestasis. HEPATOLOGY 2007;45: 230-240. https://aasldpubs.onlinelibrary.wiley.com/doi/full/10.1002/hep.21480
  2. Whiting J, Green R, Rosenbluth A, Gollan J. Tumor necrosis factor-alpha decreases hepatocyte bile salt uptake and mediates endotoxin-induced cholestasis. HEPATOLOGY 1995;22:1273-1278. https://www.deepdyve.com/lp/wiley/tumor-necrosis-factor-alpha-decreases-hepatocyte-bile-salt-uptake-and-J9rdeMQBpF
What is the association between sepsis and jaundice in patients without biliary obstruction?

Why doesn’t excessive ingestion of carrots cause yellow discoloration of the sclera?

Great question! “Carotenoderma” refers to the yellow discoloration of the skin caused by increased serum carotenoids1.  Carotenoids are absorbed by passive diffusion from the gastrointestinal tract which are partially metabolized in the intestinal mucosa and liver to vitamin A, and then transported in the plasma into the intercellular lipids of stratum corneum of the skin which has a high affinity for carotene1,2.

The maximal accumulation of carotenoids occurs in areas with an abundance of sweat glands (eg, the palms, soles, nasolabial folds). In the absence of strateum corneum, the sclera is spared!

Of note, there are many causes of carotenoderma besides excessive ingestion of carrots.  Among foods, increased ingestion of tomatoes, tangerines, red palm oil, and squash may also be responsible1,2

Systemic diseases associated with increase in serum carotenoids (possibly related to decreased conversion to vitamin A, hyperlipidemia, or other factors) include hypothyroidism, diabetes mellitus, anorexia nervosa, nephrotic syndrome, and liver disease.

References 

  1. Horev L, Ramot Y, Klapholz L. Yellow feet in a patient with breast and thyroid carcinoma, due to oral intake of turmeric. Drug Saf-Case Rep 2015;2:4.https://link.springer.com/article/10.1007/s40800-015-0006-4
  2. Maharshak N, Shapiro J, Trau H. Carotenoderma-a review of the literature. Int J Dermatol 2003;42:178-181. http://onlinelibrary.wiley.com/doi/10.1046/j.1365-4362.2003.01657.x/epdf

 

Contributed by Clara Yang, Medical Student, Harvard Medical School

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Why doesn’t excessive ingestion of carrots cause yellow discoloration of the sclera?