Clubbing refers to the bulbous uniform swelling of the soft tissue of the terminal phalanx of a digit with subsequent loss of the normal angle between the nail and the nail bed.

Finding is based on nail fold angles and phalangeal depth ratios. 1


Digital clubbing may be symmetric bilaterally, or it may be unilateral or involve a single digit. Anatomic considerations, such as the classic measurement of the Lovibond angle or the more recently derived index of nail curvature by Goyal et al[1] , usually can be identified on simple physical examination.

Historical Perspective

Since Hippocrates first described digital clubbing in patients with empyema, digital clubbing has been associated with various underlying pulmonary, cardiovascular, neoplastic, infectious, hepatobiliary, mediastinal, endocrine, and gastrointestinal diseases. Finger clubbing also may occur, without evident underlying disease, as an idiopathic form or as a Mendelian dominant trait.

Congenital Clubbing

cystic_fibrosis, cirrhosis, congenital HD Lung abscess #Ulcerative_colitis Brachial AV fistula #Bronchiectasis Infectious endocarditis/Interstitial lung disease Neoplasia (cancer) #Graves_disease

digital clubbing has been associated with various underlying pulmonary, cardiovascular, neoplastic, infectious, hepatobiliary, mediastinal, endocrine, and gastrointestinal diseases.


Clubbing can be primary (pachydermoperiostosis or hypertrophic osteoarthropathy) or secondary (pulmonary, cardiac, or GI disease or HIV).


Finger clubbing also may occur, without evident underlying disease, as an idiopathic form or as a Mendelian dominant trait.


Many researchers agree that the common factor in most types of clubbing is distal digital vasodilation, which results in increased blood flow to the distal portion of the digits. Whether the vasodilation results from a circulating or local vasodilator, neural mechanism, response to hypoxemia, genetic predisposition, or a combination of these or other mediators is not agreed on currently.

Evidence that favors the presence of a circulating vasodilator derives from the association of clubbing with cyanotic congenital heart disease. Many potential vasodilators, which usually are inactivated as blood passes through the lungs, bypass the inactivation process in patients with right-to-left shunts. Patients with tetralogy of Fallot with substantial shunting have a high incidence of clubbing. After surgical correction diminishes the shunt, the clubbing improves. Also previously observed is clubbing confined to the feet in patients with late untreated patent ductus arteriosus in whom blood from the pulmonary artery bypasses the lungs and is shunted into the descending aorta. In the absence of a shunt, the circulating vasodilator may be produced by the lung tissue, or, possibly, it passes through the pulmonary circulation without becoming inactivated. Proposed vasodilatory factors include ferritin, prostaglandins, bradykinin, adenine nucleotides, and 5-hydroxytryptamine.

A neural mechanism has been proposed with particular consideration of the vagal system. An increased incidence of digital clubbing has been associated with the pathology and disease of vagally innervated organs. Furthermore, regression of clubbing after vagotomy has been reported. Although some factor related to the vagal system is a possible contributor to the development of clubbing, especially clubbing occurring with hypertrophic osteoarthropathy, the hypothesis of a neural mechanism has decreased in popularity because of the lack of evidence of clubbing in neurologic disorders and the presence of clubbing in diseases of organs not innervated by the vagal system.

Hypoxia has been proposed as an alternative explanation for clubbing in cyanotic heart disease and pulmonary diseases. An increase in hypoxia may activate local vasodilators, consequently increasing blood flow to the distal portion of the digits; however, in most cases, hypoxia is absent in the presence of clubbing, and many diseases with noted hypoxia are not associated with clubbing.

Genetic inheritance and predisposition also may play a role in digital clubbing. Hereditary clubbing is observed in 2 forms, including idiopathic hereditary clubbing and clubbing associated with pachydermoperiostosis. The 2 forms are believed to be separate entities. Both demonstrate autosomal dominant inheritance with incomplete penetrance.

More recently, platelet-derived growth factor released from fragments of platelet clumps or megakaryocytes has been proposed as the mechanism by which digital clubbing occurs.[6] The fragments are large enough to lodge in the vascular beds of the fingertips, and, subsequently, they release platelet-derived growth factor. This factor has been shown to have general growth-promoting activity and causes increased capillary permeability and connective tissue hypertrophy.



Clubbing is a feature of pachydermoperiostosis (PDP), a rare genodermatosis characterized by pachydermia, digital clubbing, periostosis, and an excess of affected males.[2] Although usually an autosomal dominant model with incomplete penetrance and variable expression, both autosomal recessive and X-linked inheritance have been suggested in some PDP families.

Primary hypertrophic osteoarthropathy (PHO), a rare hereditary disorder with digital clubbing, subperiosteal new bone formation, and arthropathy, has been linked mutations in the 15-hydroxy-prostaglandin dehydrogenase (15-PGDH) encoding gene HPGD, which causes PHO.[3] A mutation was identified in a large Pakistani family with isolated congenital nail clubbing.[4] In another study of homozygous mutations, an intragenic deletion that results in frameshift and a missense mutation was associated with a severe PHO phenotype. A heterozygous carrier of a stop mutation had isolated digital clubbing.




The treatment is to correct the underlying cause, after which clubbing may resolve.

Rule out secondary clubbing can be caused by many conditions, including:

  • Pulmonary—Idiopathic pulmonary fibrosis, malignancy, asbestosis, COPD, and cystic fibrosis.
  • Cardiac—Congenital heart disease, endocarditis, atrioventricular malformations, or fistulas.
  • GI—Inflammatory bowel disease, cirrhosis, and celiac disease.
  • HIV infection

If negative consider

Primary Clubbing is due to:

      • Primary HOA, also known as pachydermoperiostosis, is an autosomal dominant disorder.
    • Familial clubbing, now thought to be an incomplete form of primary HOA.



A 31-year-old man with congenital heart disease has had these clubbed fingers since his childhood (Figures 51-1 and 51-2). A close view of the fingers shows a widened club-like distal phalanx. He has learned to live with the limitations from his congenital heart disease and his fingers do not bother him at all.

Image not available.

Clubbing of all the fingers in a 31-year-old man with congenital heart disease. Note the thickening around the proximal nail folds. (Courtesy of Richard P. Usatine, MD.)

Image not available.

Close-up view of a clubbed finger. (Courtesy of Richard P. Usatine, MD.)



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