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

Liked this post? Download the app on your smart phone and sign up

Subscribe to Blog via Email

Enter your email address to subscribe to this blog and receive notifications of new posts by email.

to catch future pearls right into your inbox, all for free!


  1. Williams JW, Simetl DL. Does this patient have ascites? How to divine fluid in the abdomen. JAMA 1992;267: 2645-48.
  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.
  3. Cummings S, Papadakis M, Melnick J, et al. The predictive value of physical examinations for ascites. West J Med 1985;142:633-36.
  4. Fitzgerald FT. Physical diagnosis versus modern technology. A review. West J Med 1990;152:377-82.
  5. CDC. Assessment for ascites. Accessed November 13, 2019.
My patient with jaundice complains of abdominal fullness. How useful is the history or physical exam when assessing for ascites?

Why does my patient with alcoholic cirrhosis have macrocytic anemia?

Macrocytic anemia is commonly due to folate or vitamin B12 (cobalamin) deficiency.1 Deficiency in these vitamins can be related broadly to poor intake, poor absorption, or drug interference. In patients with chronic excess alcohol consumption, both intake and/or absorption of these vitamins may be affected.

Although folate deficiency is increasingly rare in many developed countries due to mandatory folate fortification of flour and uncooked-grain, alcohol use can be associated with malnourishment severe enough to causes folate deficiency. In addition, alcohol itself can alter folate metabolism and absorption.  More specifically, chronic alcohol consumption has been shown to be associated with decreased folate absorption by the small intestine, altered intrahepatic processing and distribution between the systemic and enterohepatic folate circulations as well as increased folate urinary excretion. 2 Though uncommon,3 alcohol can also be associated with a food B12 malabsorption process, whereby despite adequate intake, B12 is not released or absorbed from food. 4

But what if serum folate and B12 levels return as normal in our patient with macrocytosis? It turns out that alcohol consumption, independent of folate or B12 deficiency, may also cause macrocytosis. 5 Though the exact mechanism is unknown, it may be related to alcohol’s direct toxicity or that of its metabolites; alcohol is oxidized to acetaldehyde, which affects membranes of red blood cells (RBCs) and their precursors by forming adducts with erythroid proteins,6 and interfering with cell division.7 Interestingly, alcohol-related macrocytosis may appear before anemia is detected and can resolve within 2-4 months of abstinence.

In addition to alcohol, cirrhosis itself may be associated with macrocytic anemia caused by lipid deposition on RBC membranes.1

See also a related pearl at   


  1. Hoffbrand V, Provan D. ABC of clinical haematology: macrocytic anaemias. BMJ 2011;314(7078):430–430.
  2. Medici V, Halsted CH. Folate, alcohol, and liver disease. Mol Nutr Food Res 2013;57(4):596–606.
  3. Bode C, Bode CJ. Effect of alcohol consumption on the gut. Best Pract Res Clin Gastroenterol [Internet] 2003;17(4):575–92.
  4. Dali-Youcef N, Andrès E. An update on cobalamin deficiency in adults. QJM 2009;102(1):17–28.
  5. Savage DG, Ogundipe A, Allen RH, Stabler SP, Lindenbaum J. Etiology and diagnostic Evaluation of macrocytosis. Am J Med Sci [Internet] 2000;319(6):343–52.
  6. Latvala J, Parkkila S, Melkko J, Niemelä O. Acetaldehyde adducts in blood and bone marrow of patients with ethanol-induced erythrocyte abnormalities. Mol Med 2001;7(6):401–5.
  7. Wickramasinghe SN, Malik F. Acetaldehyde causes a prolongation of the doubling time and an increase in the modal volume of cells in culture. Alcohol Clin Exp Res 1986;10(3):350–4.


Contributed by Kim Schaefer, Harvard medical student, Boston, MA

Liked this post? Sign up under MENU and catch future pearls right into your inbox!



Why does my patient with alcoholic cirrhosis have macrocytic anemia?

Should my patient with cirrhosis and esophageal varices be considered for partial splenic embolization?


Although limited, the weight of the evidence suggests that patients with cirrhosis and esophageal varices may benefit from partial splenic embolization (PSE).

A 2006 small randomized-controlled trial comparing PSE and endoscopic ligation vs. endoscopic ligation alone in patients with cirrhosis, thrombocytopenia and esophageal varices reported reduced risk of recurrence of varices, progression to variceal bleeding and death over a mean follow-up of 4.8 years. 1

A 2016 meta-analysis of PSE in the management of gastroesophageal variceal hemorrhage arrived at a similar conclusion with respect to reducing the risk of recurrence of varices, variceal hemorrhage and mortality. 2 The studies included in this meta-analysis, however, were small with only 1 randomized-controlled trial (RCT) in the series.

A 2019 small retrospective of patients undergoing transjugular intrahepatic portosystemic shunt (TIPS) placement with or without PSE found a significant benefit in primary shunt patency (period between placement and first shunt dysfunction), but not secondary shunt patency (period between placement and permanent shunt dysfunction) or mortality over a 5-year follow-up.3

Adverse effects of PSE include post-embolization syndrome—a constellation of symptoms such as fever, pain, and nausea/vomiting— reported in 78%-100% of patients. More severe complications up to 15%-30% may also occur with PSE, particularly when around 70% or more of splenic volume is embolized. These complications include pleural effusion/ascites, spontaneous bacterial peritonitis, pulmonary embolism, liver failure, portal vein thrombosis and splenic abscesses which may develop between 10 days to 3 months following the procedure.  Up to 6% of patients undergoing PSE may die of the procedure-related complications. 4-6  

For these reasons, careful selection of patient for PSE and limiting the extent of splenic necrosis to 50% with close monitoring of clinical and ultrasound follow-up, particularly in patients with a volume of splenic necrosis >50%,  have been suggested.6


Fun fact: Did you know that splenic embolization was first performed by Frank E. Maddison of Madison, Wisconsin, in 1973 using autologous clot to treat recurrent gastrointestinal hemorrhage arising from esophageal varies?


Liked this post? Sign up under MENU and catch future pearls right into your inbox!



  1. Ohmoto K, Yoshioka N, Tomiyama Y, et al. Improved prognosis of cirrhosis patients with esophageal varices and thrombocytopenia treated by endoscopic variceal ligation plus partial splenic embolization. Digestive Diseases and Sciences 2006;51:352-58.
  2. Wang P, Liu R, Tong L, et al. Partial splenic embolization has beneficial effects for the management of gastroesophageal variceal hemorrhage. Saudi J Gastroenterol 2016;22:399-406.
  3. Wan Y-M, Li Y-H, Xu Z-Y, et al. Comparison of TIPS alone and combined with partial splenic embolization (PSE) for the management of variceal bleeding. European Radiology 2019;
  4. N’Kontchou G, Seror O, Bourcier V, et al. Partial splenic embolization in patients with cirrhosis: efficacy, tolerance, and long-term outcome in 32 patients. Eur J Gastroenterol Hepatol 2005;17:179-84.
  5. Hadduck TA, McWilliams JP. Partial splenic artery embolization in cirrhotic patients. World J Radiol 2014;28:6:160-168.
  6. Smith M, Ray CE. Splenic artery embolization as an adjunctive procedure for portal hypertension. Semin Intervent Radiol 2012;29:135-39.
  7. Maddison FE. Embolic therapy of hypersplenism. Invest Radiol 1973;8:280-281.


Contributed in part by Theodore R. Pak, MD, PhD, Mass General Hospital, Boston, Massachusetts.

Should my patient with cirrhosis and esophageal varices be considered for partial splenic embolization?

Should I continue nadolol in my patient with cirrhosis and refractory ascites?

Under certain circumstances, you may need to! Although nonselective beta blockers (NSBBs), such as nadolol and propranolol, have been the cornerstone of medical treatment of portal hypertension in preventing variceal bleeding in patients with cirrhosis for decades, recent reports of their association with worsening survival, increased risk of hepatorenal syndrome and acute kidney injury in patients with refractory ascites or spontaneous bacterial peritonitis [SBP]) 1,2 have added controversy to their routine use in end-stage cirrhosis.

This is because patients with end-stage cirrhosis may be highly dependent on their cardiac output (particularly the heart rate) in maintaining an adequate arterial blood pressure 3-5 and the negative inotropic and chronotropic effects of NSBBs blunt this compensatory mechanism. The result is a drop in the cardiac output that may be particularly significant in the presence of conditions already associated with hypotension, such as sepsis, spontaneous bacterial peritonitis (SBP), or hemorrhage, further increasing the risk of renal hypoperfusion and hepatorenal syndrome.3

Although 2 meta-analysis studies failed to find an association between NSBBs and increased mortality among patients with cirrhosis and ascites, 6,7 serious concerns over the adverse effects of these drugs in at least a subset of patients has not waned.  Some have recommended reducing NSBB dose or discontinuing treatment in patients with refractory ascites or SBP and any of the following parameters: 4

  • Systolic blood pressure <90 mmHg
  • Serum creatinine >1.5 mg/dL
  • Hyponatremia <130 mmol/L

Similar recommendations were made by a 2015 consensus conference on individualizing the care of patients with portal hypertension.

In the absence of randomized-controlled studies, it seems prudent to proceed with more caution when using NSBBs in patients with end-stage cirrhosis and watch closely for any signs of hypotension or renal function deterioration.


  1. Serste T, Njimi H, Degre D, et al. The use of beta-lackers is associated with the occurrence of acute kidney injury in severe hepatitis. Liver In 2015;35:1974-82.
  2. Mandorfer M, Bota S, Schwabl P, et al. Nonselective beta blockers increase risk of hepatorenal syndrome and death in patients with cirrhosis and spontaneous bacterial peritonitis. Gastroenterol 2014;146:1680-90.
  3. Garcia-Tsao G. The use of nonselective beta blockers for treatment of portal hypertension. Gastroenterol Hepatol 2017;13: 617-19.
  4. Reiberger T, Mandorfer M. Beta adrenergic blockade and decompensated cirrhosis. J Hepatol 2017;66: 849-59.
  5. Giannelli V, Lattanzi, Thalheimer U, et al. Beta-blockers in liver cirrhosis. Ann Gastroenterol 2014;27:20-26.
  6. Facciorusso A, Roy S, Livadas S, et al. Nonselective beta-blockers do not affect survival in cirrhotic patients with ascites. Digest Dis Sci 2018;63:1737-46.
  7. Njei B, McCarty TR, Garcia-Tsao G. Beta-blockers in patients with cirrhosis and ascites: type of betablocker matters. Gut 206;65:1393-4.
  8. De Franchis R. Expanding consensus in portal hypertension. Report of the Baveno VI Consensus Workshop: stratifying risk and individualizing care for portal hypertension.  J Hepatol 2015;63:743-52.  

If you like this post, sign up under MENU and get future pearls straight into your mailbox! 

Should I continue nadolol in my patient with cirrhosis and refractory ascites?

Should I avoid intravenous furosemide for management of ascites in my patient with cirrhosis?

Generally, yes! IV furosemide for treatment of ascites in patients with cirrhosis should be avoided for couple of reasons.

First, in contrast to patients with congestive heart failure in whom the absorption of oral furosemide may be impaired due to bowel wall edema, patients with cirrhosis and ascites appear to absorb oral furosemide efficiently, similarly to that of control patients.1   Another reason for avoiding IV furosemide in this setting is the possibility of a significant drop in the GFR with its attendant rise in BUN and serum creatinine, clinically resembling a picture of hepatorenal syndrome.2

Although the mechanism of the adverse effect of IV furosemide on the renal function of patients with cirrhosis is not totally clear, furosemide-induced vasoconstriction, not intrasvascular volume depletion due to sodium wasting, seems to play an important role.3

Nevertheless, certain situations may necessitate the use of IV furosemide in patients with cirrhosis and ascites, such as in single doses to help identify patients who will be responsive to diuretics, and in patients in need of prompt diuresis such as those with concurrent pulmonary edema. In a somewhat reassuring study, a single dose of 80 mg IV furosemide reliably identified cirrhotic patients with ascites responsive to diuretics, without a significant risk of deteriorating renal function.3



  1. Sawhney VK, Gregory PB, Swezey SE, et al. Furosemide disposition in cirrhotic patients. Gastroenterology 1981; 81: 1012-16.
  2. Daskalopoulos G, Laffi G, Morgan T, et al. Immediate effects of furosemide on renal hemodynamics in chronic liver disease with ascites. Gastroenterology 1987;92:1859-1863.
  3. Spahr, L., Villeneuve, J., Tran, H. K., & Pomier-Layrargues, G. Furosemide-induced natriuresis as a test to identify cirrhotic patients with refractory ascites. Hepatology 2001;33:28-31.


Contributed by Sam Miller, MD, Mass General Hospital, Boston, MA.


Should I avoid intravenous furosemide for management of ascites in my patient with cirrhosis?

My patient with cirrhosis has a large right sided pleural effusion with only a small amount of ascites. Could this effusion still be related to his cirrhosis?

Yes! Although we often associate pleural effusions in patients with cirrhosis with the presence of large ascites, some patients present with hepatic hydrothorax even in the absence of significant ascites.1-3  

In fact, in a study involving 77 patients with hepatic hydrothorax, 49% had minimal or small and 9% had no detectable ascites!1  Interestingly, nearly three-quarters of patients in this study had right sided pleural effusion with 10% having bilateral and 17% having left sided effusion only. Hepatic hydrothorax without ascites as the first sign of liver cirrhosis has also been reported.2

Although the mechanism(s) behind hepatic hydrothorax is not fully clear, the passage of peritoneal fluid into the pleural cavity through defects in the tendinous portion of the diaphragm assisted by negative intrathoracic pressure during inspiration is commonly favored. 1-3  

Supportive evidence includes a number of studies involving intraperitoneal injection of air, dyes or technetium 99 m-sulfur colloid that have demonstrated the trans-diaphragmatic flow of ascites into the pleural cavity. 1-4  In the absence of ascites, a complete equilibrium between the amount of ascites produced and its flow into and reabsorption by the pleural cavity is assumed.1,2

Bonus Pearl: Did you know that although most patients with hepatic hydrothorax have a transudative pleural effusion according to Light’s criteria, 1 study showed that 18% of patients may meet the Light’s criteria for an exudative effusion? 5,6


If you liked this post, sign up under MENU and catch future pearls right into your inbox!


  1. Badillo R, Rockey DC. Hepatic hydrothorax: Clinical features, management, and outcomes in 77 patients and review of the literature. Medicine 2014;93:135-142.
  2. Kim JS, Kim CW, Nam HS, et al. Hepatic hydrothorax without ascites as the first sign of liver cirrhosis. Respirology Case Reports 2016;4:16-18.
  3. Rubinstein D, McInnes IE, Dudley FJ. Hepatic hydrothorax in the absence of clinical ascites: diagnosis and management. Gastroenterology 1985;88:188-91.
  4. Holt KA, Oliviera E, Rohatgi PK. Hepatic hydrothorax demonstration by Tc-99 sulfur colloid ascites scan. Clin Nucl Med 1999;24:609. 
  5. Light RW. New treatment for hepatic hydrothorax? Ann Am Thorac Soc 2016;13:773-74.
  6. Bielsa S, Porcel JM, Castellote J, et al. Solving the Light’s criteria misclassification rate of cardiac and hepatic transudates. Respirology 2012;17”721-726.
My patient with cirrhosis has a large right sided pleural effusion with only a small amount of ascites. Could this effusion still be related to his cirrhosis?

My patient with cirrhosis has hypohonia and cogwheel rigidity. Is there a connection between cirrhosis and Parkinson’s disease?

There is a high prevalence of extra-pyramidal or Parkinson-like (PL) clinical findings in patients with cirrhosis. In fact, over 75% of patients with cirrhosis may exhibit PL signs, such as tremor, rigidity, and akinesia, with 88% also showing hyperintensity in the globus pallidus of basal ganglia on T1-weighted brain MRI.1

What’s even more interesting is the similarity between PL clinical and MRI findings among patients with cirrhosis and those with Manganese (Mn) toxicity.2,3 More specifically, similar MRI findings involving the globus pallidus have been reported in Mn-exposed workers, patients with cirrhosis, and those undergoing total parenteral nutrition with excessive Mn replacement. 4 These observations seem more than coincidental as 67% of patients with cirrhosis have been reported to have elevated blood Mn concentrations, with significantly higher levels in patients with previous portacaval anastomoses or transjugular intrahepatic portosystemic shunt (TIPS).1

Mn-induced parkinsonism is distinguishable from classic Parkinson’s disease in several ways, including the absence of Lewy bodies, more frequent dystonia, and less resting tremor.5 Also, remember that Mn-induced PL disease does NOT respond to L-dopa, a drug used to treat early stages of PD. 5 This finding can be explained by the fact that, in contrast to Parkinson’s disease where many of the dopamine-producing cells in the substantia nigra of the brain degenerate resulting in dopamine deficiency, in Mn-induced PL disease the problem is release of dopamine into synapses not its production.5

Bonus Pearl: Did you know that due to its paramagnetic properties, manganese can be effectively seen by MRI!


  1. Spahr L, Butterworth RF, Fontaine S, et al. Increased blood manganese in cirrhotic patients: relationship to pallidal m agnetic resonance signal hyperintensity and neurological symptoms. Hepatology 1996;24:1116-1120.
  2. Hauser RA, Zesiewicz TA, Rosemurgy AS, et al. Manganese intoxication and chronic liver failure. Ann Neurol 1994;36:871-75.
  3. Krieger S, Jaub M, Jansen O, et al. Neuropsychiatric profile and hyperintense globus pallidus on T1-weighted magnetic resonance images in liver cirrhosis. Gastroenterol 1996;111:147-55.
  4. Lucchini R, Albini E, Placidi D, et al. Brain magnetic resonance imaging and manganese exposure. Neurotoxicity 2000;21:769-75.
  5. Kwakye GF, Paoliello MMB, Mukhopadhyay S, et al. Manganese-induced parkinsonism and Parkinson’s disease: Shared and distinguishable features. Int J Environ Res Public Health 2015;12;7519-40.

Don’t forget to sign up under menu to get future pearls right into your mailbox!

My patient with cirrhosis has hypohonia and cogwheel rigidity. Is there a connection between cirrhosis and Parkinson’s disease?

Why is my hospitalized patient with alcohol withdrawal syndrome so thrombocytopenic?

Although thrombocytopenia associated with chronic alcoholism may be related to complications of cirrhosis (eg, platelet sequestration in spleen due to portal hypertension, poor platelet production, and increased platelet destruction) (1), it may also occur in the absence of cirrhosis due to the direct toxic effect of alcohol on platelet production and survival (2).

In a prospective study of patients ingesting the equivalent of a fifth or more daily of 86 proof whiskey admitted for treatment of alcohol withdrawal—without evidence of severe liver disease, infection or sepsis— 81% had initial platelet counts below 150,000/µl, with about one-third having platelet counts below 100,000 µl (as low as 24,000/ul) (3).
In most patients, 2-3 days elapsed before the platelet count began to rise significantly, peaking 5-18 days after admission. Others have also reported that platelet counts rise within 5-7 days and normalize in a few weeks after alcohol withdrawal (1); bleeding complications have been uncommon in this setting.
Perhaps even more intriguing is the report of the association between thrombocytopenia in early alcohol withdrawal and the development of delirium tremens or seizures (sensitivity and specificity ~ 70%, positive predictive value less than 10% but with a negative predictive value of 99%) (4)! In fact, the authors suggested that, if their findings are corroborated, a normal platelet count could potentially be used to identify patients at low risk of alcohol withdrawal syndrome and therefore outpatient therapy. 

1. Mitchell O, Feldman D, Diakow M, et al. The pathophysiology of thrombocytopenia in chronic liver disease. Hepatic Medicine: Evidence and Research 2016;8 39-50.

2. Cowan DH. Effect of alcoholism on hemostasis. Semin Hematol 1980;17:137-47.

3. Cowan DH, Hines JD. Thrombocytopenia of severe alcoholism. Ann Intern Med 1971;74:37-43.

4. Berggren U, Falke C, Berglund KJ, et al. Thrombocytopenia in early alcohol withdrawal is associated with development of delirium tremens or seizures. Alcohol & Alcoholism 2009;44:382-86.

If you like this pearl, sign up under menu and receive future pearls right into your mailbox!

Why is my hospitalized patient with alcohol withdrawal syndrome so thrombocytopenic?

Should my patient with suspected alcoholic hepatitis undergo liver biopsy?

Although a characteristic clinical history and biochemical pattern of liver injury can strongly suggest the diagnosis of alcoholic hepatitis (AH), a definitive diagnosis is confirmed with liver biopsy only. In fact, in 30% of patients clinically diagnosed as having AH, a liver biopsy may lead to an alternative diagnosis.1Understandably, many physicians are reluctant to proceed with biopsy in this fragile patient population given the associated risks, notably bleeding. For this reason, most patients with AH are clinically diagnosed without a liver biopsy. However, there are certain instances in which a biopsy can be helpful, including when:2

  • Diagnosis of AH is in doubt
  • Suspicion for another disease process that may be contributing in parallel to AH is high
  • Obtaining prognostic data or identification of advanced hepatic fibrosis or cirrhosis in AH is desired

Thus, liver biopsy findings may influence short- and long-term management in AH. For these reasons, the European Association for the Study of the Liver recommends consideration of a liver biopsy in patients with AH.3 To minimize the bleeding risk, the transjugular approach is preferred.

If you liked this post, sign up under MENU and catch future pearls straight into your mailbox!!


  1. Mookerjee RP, Lackner C, Stauber R, et al. The role of liver biopsy in the diagnosis and prognosis of patients with acute deterioration of alcoholic cirrhosis. J Hepatol 2011; 55:1103-1111 Link
  2. Altamirano J, Miquel R, Katoonizadeh A, et al. A histologic scoring system for prognosis of patients with alcoholic hepatitis. Gastroenterology 2014;146: 1231-1239. PDF
  3. European Association for the Study of Liver. EASL clinical practical guidelines: management of alcoholic liver disease. J Hepatol 2012; 57:399-420. PDF

Contributed by Jay Luther, MD, Gastrointestinal Unit, Mass General Hospital, Boston, MA.

Should my patient with suspected alcoholic hepatitis undergo liver biopsy?

What is the significance of Terry’s or Lindsay’s nails in my hospitalized patient?

Terry’s nails were first described in 1954 in patients with hepatic cirrhosis (prevalence 82%, majority related to alcohol abuse) (1). Since then, they have been reported in a variety of other conditions, including adult-onset diabetes mellitus (AODM), chronic congestive heart failure, chronic renal failure, pulmonary tuberculosis, and Reiter’s syndrome (2).

A 1984 study found Terry’s nails in 25% of hospitalized patients (3).  In this study, cirrhosis, chronic congestive heart failure, and AODM were significantly associated with Terry’s nails, while pulmonary tuberculosis, rheumatoid arthritis and cancer were not. The presence of Terry’s nails may be particularly concerning in patients 50 y of age or younger as it increases the relative risk of cirrhosis, chronic congestive heart failure or AODM by 5-fold (18-fold for cirrhosis alone) in this age group (3).

Terry’s nails should be distinguished from Lindsay’s nails or “half and half” nails. Although both nail abnormalities are characterized by an opaque white proximal portion, Terry’s nails have a thinner distal pink to brown transverse band no more than 3 mm wide (3) (Fig 1), while the same anomaly is wider and occupies 20%-60% of the nail bed in Lindsay’s nails (Fig 2). Of interest, Lindsay’s nails have been reported in up to 40% of patients with chronic kidney disease (4,5).


1. Terry R. White nails in hepatic cirrhosis. Lancet 1954;266:757-59. 
2. Nia AM, Ederer S, Dahlem K, et al. Terry’s nails: a window to systemic diseases. Am J Med 2011;124:603-604. 
3. Holzberg M, Walker HK. Terry’s nails: revised definitions and new correlations. Lancet 1984;1(8382):896-99. 
4. Pitukweerakul S, Pilla S. Terry’s nails and Lindsay’s nails: Two nail abnormalities in chronic systemic diseases. J Gen Intern Med 31;970. 
5. Gagnon AL, Desai T. Dermatological diseases in patients with chronic kidney disease 2013;2:104-109.

Figure 1. Terry’s nails in a patient with end-stage liver disease

Figure 2. Lindsay’s nails in a patient with chronic kidney disease

If you liked this post, SELRES_9060f380-b0ce-41bb-b812-fe2595cb3460SELRES_4b9ffe76-4732-435c-a61e-cb3aba28fef9SELRES_055e8f9c-d15f-4b5c-8ddc-c9eb04539366sign upSELRES_055e8f9c-d15f-4b5c-8ddc-c9eb04539366SELRES_4b9ffe76-4732-435c-a61e-cb3aba28fef9SELRES_9060f380-b0ce-41bb-b812-fe2595cb3460 on the P4P home page and receive future pearls delivered directly into your mailbox!

What is the significance of Terry’s or Lindsay’s nails in my hospitalized patient?