Nail clubbing

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Clubbing
Acopaquia.jpg
Clubbing
ICD-10 R68.3
ICD-9 781.5

In medicine, nail clubbing[1] (also known as drumstick fingers and watch-glass nails)[1] is a deformity of the fingers and fingernails associated with a number of diseases, mostly of the heart and lungs.[2]:656 Hippocrates was probably the first to document clubbing as a sign of disease, and the phenomenon is therefore occasionally called Hippocratic fingers.

Idiopathic clubbing can also occur, as 60% of cases have no associated underlying disease.[3]

Signs and symptoms[edit]

Front and side views of nail clubbing

Clubbing develops in five steps:[4]

  1. Fluctuation and softening of the nail bed (increased ballotability)
  2. Loss of the normal <165° angle (Lovibond angle) between the nailbed and the fold (cuticula)
  3. Increased convexity of the nail fold
  4. Thickening of the whole distal (end part of the) finger (resembling a drumstick)
  5. Shiny aspect and striation of the nail and skin

Schamroth's test or Schamroth's window test (originally demonstrated by South African cardiologist Leo Schamroth on himself)[5] is a popular test for clubbing. When the distal phalanges (bones nearest the fingertips) of corresponding fingers of opposite hands are directly opposed (place fingernails of same finger on opposite hands against each other, nail to nail), a small diamond-shaped "window" is normally apparent between the nailbeds. If this window is obliterated, the test is positive and clubbing is present.

Diagnosis[edit]

Clubbing of the fingernail: The red line shows the outline of a clubbed nail.

When clubbing is encountered in patients, doctors will seek to identify its cause. They usually accomplish this by obtaining a medical history—particular attention is paid to lung, heart, and gastrointestinal conditions—and conducting a clinical examination, which may disclose associated features relevant to a diagnosis. Additional studies such as a chest X-ray and a chest CT-scan may also be performed.[4]

Disease associations[edit]

Although many diseases are associated with clubbing (particularly lung diseases), the reports are fairly anecdotal. Prospective studies of patients presenting with clubbing have not yet been performed, and hence there is no conclusive evidence of these associations.

Isolated clubbing[edit]

Clubbing is associated with:

Nail clubbing is not associated with chronic obstructive pulmonary disease (COPD). Therefore, in patients with COPD with significant degrees of clubbing, a search for signs of bronchogenic carcinoma (or other causes of clubbing) might be indicated.[4]

HPOA[edit]

Main article: Periosteal reaction
Bone scan of a patient with HPOA

A special form of clubbing is hypertrophic pulmonary osteoarthropathy, known in continental Europe as Pierre Marie-Bamberger syndrome. This is the combination of clubbing and thickening of periosteum (connective tissue lining of the bones) and synovium (lining of joints), and is often initially diagnosed as arthritis. It is commonly associated with lung cancer.

Primary HPOA[edit]

Primary hypertrophic ostoarthropathy is HPOA without signs of pulmonary disease. This form has a hereditary component, although subtle cardiac abnormalities can occasionally be found. It is known eponymously as the Touraine-Solente-Golé syndrome. This condition has been linked to mutations in the gene on the fourth chromosome (4q33-q34) coding for the enzyme 15-hydroxyprostaglandin dehydrogenase (HPGD); this leads to decreased breakdown of prostaglandin E2 and elevated levels of this substance.[10]

Pathophysiology[edit]

The exact cause for sporadic clubbing is unknown, with numerous theories as to its cause. Vasodilation (distended blood vessels), secretion of growth factors (such as platelet-derived growth factor and hepatocyte growth factor) from the lungs, and other mechanisms have been proposed. The discovery of disorders in the prostaglandin metabolism in primary osteoarthropathy has led to suggestions that overproduction of PGE2 by other tissues may be the causative factor for clubbing.[10] That is to say, up-regulation of PGE2 has been implicated as a possible etiology of nail clubbing.[citation needed]

Epidemiology[edit]

The exact frequency of clubbing in the population is not known. A 2008 study found clubbing in 1% of all patients admitted to a department of internal medicine. Of these, 40% turned out to have significant underlying disease of various causes, while 60% had no medical problems on further investigations and remained well over the subsequent year.[3]

See also[edit]

References[edit]

  1. ^ a b Rapini, Ronald P.; Bolognia, Jean L.; Jorizzo, Joseph L. (2007). Dermatology: 2-Volume Set. St. Louis: Mosby. ISBN 1-4160-2999-0. 
  2. ^ Freedberg, et al. (2003). Fitzpatrick's Dermatology in General Medicine. (6th ed.). McGraw-Hill. ISBN 0-07-138076-0.
  3. ^ a b Vandemergel X, Renneboog B (July 2008). "Prevalence, aetiologies and significance of clubbing in a department of general internal medicine". Eur. J. Intern. Med. 19 (5): 325–9. doi:10.1016/j.ejim.2007.05.015. PMID 18549933. 
  4. ^ a b c Myers KA, Farquhar DR (2001). "The rational clinical examination: does this patient have clubbing?". JAMA 286 (3): 341–7. doi:10.1001/jama.286.3.341. PMID 11466101. 
  5. ^ Schamroth L (February 1976). "Personal experience". S. Afr. Med. J. 50 (9): 297–300. PMID 1265563. 
  6. ^ Sridhar KS, Lobo CF, Altman RD (1998). "Digital clubbing and lung cancer" (PDF). Chest 114 (6): 1535–37. doi:10.1378/chest.114.6.1535. PMID 9872183. 
  7. ^ Epstein O, Dick R, Sherlock S (1981). "Prospective study of periostitis and finger clubbing in primary biliary cirrhosis and other forms of chronic liver disease". Gut 22 (3): 203–6. doi:10.1136/gut.22.3.203. PMC 1419499. PMID 7227854. 
  8. ^ Naeije R (March 2003). "Hepatopulmonary syndrome and portopulmonary hypertension". Swiss Med Wkly 133 (11–12): 163–9. PMID 12715285. 
  9. ^ -724565997 at GPnotebook
  10. ^ a b Uppal S, Diggle CP, Carr IM, et al. (June 2008). "Mutations in 15-hydroxyprostaglandin dehydrogenase cause primary hypertrophic osteoarthropathy". Nat. Genet. 40 (6): 789–93. doi:10.1038/ng.153. PMID 18500342.