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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

Synonyms: hippocratic nails, hippocratic fingers (first described by Hippocrates)

This describes an increase in the soft tissue around the end of the fingers and toes.The swelling is painless and usually bilateral, unless a localised vascular abnormality exists. There is no change to the underlying bone. The nail base eventually becomes convex and extends halfway up the nail.

Clubbing is thought to result from changes to the volume of interstitial fluid and increased blood flow to the area but the exact pathophysiology remains unknown.[1]

Primary clubbing may be idiopathic or be a feature of an inherited condition. Secondary clubbing may be caused by a wide range of diseases.

Causes of Clubbing[1]
  • Pachydermoperiostosis (also known as primary hypertrophic osteoarthropathy) - characterised by periostosis, 89% of patients also have clubbing.[2]
  • Familial clubbing.[3]
  • Hypertrophic osteoarthropathy (a syndrome which also includes chronic proliferative periostitis of the long bones and joint swelling).
Pulmonary disease
Cardiac disease
Gastrointestinal diseaseSkin disease
  • Bureau-Barrière-Thomas syndrome (digital clubbing associated with palmoplantar keratoderma).
  • Fischer's syndrome (keratosis palmaris et plantaris, hair hypoplasia, onycholysis and onychogryphosis).
  • Palmoplantar keratoderma (diffuse patches on the palms and soles).
Miscellaneous conditions

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Pachydermoperiostosis is a rare disease.The exact incidence is unknown. American studies report that it is more common in African Americans than in whites. The male-to-female ratio is roughly 7:1. Men tend to be affected more severely than women, in whom the disease may go undetected. The condition typically appears during childhood and progresses over the subsequent 5-20 years, after which it stabilises.[2]

The epidemiology of secondary clubbing depends on the cause.


The patient may notice a swelling of the distal portion of the fingers or toes but the onset is usually so gradual as to make this a rare occurrence. Even more rarely, the patient may notice some discomfort, because most clubbing is painless. The majority of clubbing is detected by doctors as part of a routine examination for other presenting symptoms.

Clubbing has been described as a bulbous fusiform enlargement of the distal portion of a digit. It is commonly bilateral but may be unilateral and can affect a single digit. Both fingers and toes can be affected.

As clubbing progresses, the angle between the nail and the nail base (called the Lovibond angle) becomes obliterated. Normally, the angle is less than or equal to 160°. With increasing convexity of the nail, the angle becomes greater than 180°. In early clubbing, the nail may feel springy instead of firm when palpated and the skin at the base of the nail may become smooth and shiny.

In individuals without clubbing, if two opposing fingers are placed together, a diamond-shaped window will appear. In clubbing, this window is obliterated and the distal angle formed by the two nails becomes wider. This is known as Schamroth's window test.

Pseudo-clubbing - this is overcurvature of the nails in both the longitudinal and transverse axes, with preservation of a normal Lovibond angle.[4] The main features of pseudo-clubbing seen in one study were asymmetrical finger involvement and acro-osteolysis. Whilst these were present in the majority of cases they were also present in some cases of clubbing, so could not be said to be pathognomonic. Pseudo-clubbing may be seen in chronic renal failure, hyperparathyroidism, sarcoidosis, scleroderma, subungual haematoma and chromosome deletion.[5] 

Laboratory investigations

These will depend on the underlying conditions suggested by the overall clinical picture.


This is not usually required to diagnose clubbing but plain radiographs of the digits may help to elucidate the cause. Osteolysis is often seen in patients with congenital cyanotic heart disease, whilst bone hypertrophy suggests a pulmonary condition.[1]
Other modalities sometimes employed in clinical and research settings include technetium-99m scanning to assess bone loss, thermography and positron emission tomography (PET) scanning.

CT and MRI scanning of other areas may be required to assist in diagnosing the underlying primary cause.

This will be dictated by the underlying disease process.

Clubbing is potentially reversible if the underlying condition is treated early enough but the changes may be irreversible once collagen deposition has set in.

Further reading & references

  • Seifert W, Kuhnisch J, Tuysuz B, et al; Mutations in the prostaglandin transporter encoding gene SLCO2A1 cause primary hypertrophic osteoarthropathy and isolated digital clubbing. Hum Mutat. 2012 Apr;33(4):660-4. doi: 10.1002/humu.22042. Epub 2012 Feb 24.
  • Mukherjee A, Bhattacharyya P, Saha I, et al; Evaluation of a simple bedside tool developed to measure different parameters of clubbing. Lung India. 2011 Jul;28(3):228-9.
  1. Schwartz AR et al, Clubbing of Nails, Medscape, Feb 2012
  2. Goyal S et al; Pachydermoperiostosis, Medscape, Dec 2011
  3. Horsfall F; Congenital Familial Clubbing of the Fingers and Toes Can Med Assoc J. 1936 February; 34(2): 145û149
  4. Farzaneh-Far A; Images in clinical medicine. Pseudoclubbing. N Engl J Med. 2006 Apr 13;354(15):e14.
  5. Santiago MB, Lima I, Feitosa AC, et al; Pseudoclubbing: Is It Different from Clubbing? Semin Arthritis Rheum. 2008 Mar 29.

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Laurence Knott
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
1971 (v22)
Last Checked:
Next Review:
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