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Clinical Sign: Clubbing THIEME Clinical Rounds e1 Clinical Sign: Clubbing Maddury Jyotsna1 Jagan Mohan Tharakan2 1 Department of Cardiology, Nizam’s Institute of Medical Sciences Address for correspondence Prof.MadduryJyotsna,MD,DM,FACC, (NIMS), Punjagutta, Hyderabad, Telangana, India FESC, FICC, Department of Cardiology, Nizam’s Institute of Medical 2 Department of Cardiology, Sree Chitra Tirunal Institute for Medical Sciences (NIMS), Punjagutta, Hyderabad 500082, Telangana, India Sciences and Medical College,Thiruvananthapuram, Kerala, India (e-mail: [email protected]). Indian J Cardiovasc Dis Women-WINCARS 2017;2:e1–e9. Background Although usually an autosomal dominant model with incom- Since Hippocrates first described digital clubbing in patients plete penetrance and variable expression, both autosomal with empyema, digital clubbing has been associated with recessive and X-linked inheritance have been suggested in various underlying pulmonary, cardiovascular, neoplastic, some PDP families. infectious, hepatobiliary, mediastinal, endocrine, and gastro- intestinal diseases. Finger clubbing also may occur, without Secondary Clubbing evident underlying disease, as an idiopathic form or as a Secondary clubbing occurs due to multiple systemic causes mendelian dominant trait. described in the following text. Definition Method of Examination “Clubbing” is a clinically descriptive term, referring to the Anatomic considerations, such as the classic measurement of bulbous uniform swelling of the soft tissue of the terminal the Lovibond angle or the more recently derived index of nail phalanx of a digit with subsequent loss of the normal angle curvature by Goyal et al, usually can be identified on simple between the nail and the nail bed. physical examination and can be used to identify digital clubbing and to monitor this dynamic process objectively.1 Classification Various imaging modalities have been used not only to eval- uate clubbing but also to help identify possible clues to its Digital clubbing is classified into primary (i.e., idiopathic, development. Details of physical examination are given below. hereditary) and secondary forms. Digital clubbing may be symmetric bilaterally, or it may be unilateral or involve a Pathophysiology single digit. The specific pathophysiologic mechanism of digital clubbing Primary Clubbing remains unknown. Many theories have been proposed, yet Primary hypertrophic osteoarthropathy (PHO), a rare her- none have received widespread acceptance as a comprehen- editary disorder with digital clubbing, subperiosteal new sive explanation for the phenomenon of digital clubbing. As bone formation, and arthropathy, has been linked mutations stated best by Samuel West in 1897, “Clubbing is one of those in the 15-hydroxy-prostaglandin dehydrogenase (15-PGDH) phenomena with which we are all so familiar that we appear encoding gene HPGD, which causes PHO. A mutation was to know more about it than we really do.” identified in a large Pakistani family with isolated congenital Alterations in size and configuration of the clubbed digit nail clubbing. In another study of homozygous mutations, an result from changes in the nail bed, beginning with increased intragenic deletion that results in frameshift and a missense interstitial edema early in the process. As clubbing pro- mutation was associated with a severe PHO phenotype. A gresses, the volume of the terminal portion of the digit heterozygous carrier of a stop mutation had isolated digital may increase because of an increase in the vascular con- clubbing. nective tissue and change in quality of the vascular connec- Clubbing is a feature of pachydermoperiostosis (PDP), a tive tissue, although some cases have been associated with rare genodermatosis characterized by pachydermia, digital spurs of bone on the terminal phalanx. Different pathologic clubbing, periostosis, and an excess of affected males. processes may follow different pathways to a common end. DOI https://doi.org/ Copyright © 2017 Women in Cardiology 10.1055/s-0037-1607321. and Related Sciences e2 Clinical Sign: Clubbing Jyotsna, Tharakan Many studies have shown increased blood flow in the the fingertips, and, subsequently, they release platelet-derived clubbed portion of the finger. High-resolution magnetic growth factor. This factor has been shown to have general resonance imaging (MRI) using a contrast agent showed growth-promoting activity and causes increased capillary nail bed hypervascularization as linked with clubbed nails. permeability and connective tissue hypertrophy.2 Most researchers agree that this results from an increase in distal digital vasodilation, the cause of which is unknown. Epidemiology Also unknown is the exact mechanism by which increased blood flow results in changes in the vascular connective Frequency tissue under the nail bed. Whether the vasodilation results Idiopathic or primary clubbing is rare, while the occurrence from a circulating or local vasodilator, neural mechanism, of secondary clubbing depends on the underlying disease. response to hypoxemia, genetic predisposition, or a combi- Primary digital clubbing has been reported to occur in 89% nation of these or other mediators is not agreed on currently. of patients diagnosed with PDP.3 This syndrome most often Evidence that favors the presence of a circulating vasodi- occurs in young males. lator derives from the association of clubbing with cyanotic Of patients with idiopathic pulmonary fibrosis, 65% have congenital heart disease. Many potential vasodilators, which clinical digital clubbing. In these patients, an increased usually are inactivated as blood passes through the lungs, occurrence has been shown in patients with higher grades bypass the inactivation process in patients with right-to-left of smooth muscle proliferation in the lungs. shunts. Patients with tetralogy of Fallot (TOF) with substantial Clubbing has been reported in 29% of patients with lung right-to-left shunting have a high incidence of clubbing. After cancer and is observed more commonly in patients with surgical correction eliminates the right-to-left shunt, the non–small-cell lung carcinoma (35%) than in patients with clubbing improves. Also previously observed is clubbing con- small cell lung carcinoma (4%). fined to the feet in patients with late untreated patent ductus Digital clubbing was reported in 38% of patients with arteriosus (PDA) in whom blood from the pulmonary artery Crohn’s disease, 15% of patients with ulcerative colitis, and bypasses the lungs and is shunted into the descending aorta. In 8% of patients with proctitis. Clubbing was observed in up to the absence of a shunt, the circulating vasodilator may be one-third of Ugandan patients with pulmonary tuberculosis. It produced by the lung tissue, or, possibly, it passes through the was not associated with stage of human immunodeficiency pulmonary circulation without getting inactivated. Proposed virus (HIV) infection, extensive disease, or hypoalbuminemia. vasodilatory factors include ferritin, prostaglandins, bradyki- nin, adenine nucleotides, and 5-hydroxytryptamine. History A neural mechanism has been proposed with particular The development of clubbing usually is gradual enough that consideration of the vagal system. An increased incidence of many patients are unaware of its presence; however, some digital clubbing has been associated with the pathology and patients may report swelling of the distal portion of the disease of vagally innervated organs. Furthermore, regres- digits, which may be bilateral or unilateral or may involve a sion of clubbing after vagotomy has been reported. Although single digit. Although clubbing typically is painless, it rarely some factor related to the vagal system is a possible con- may present with pain in the fingertips. Rapid postoperative tributor to the development of clubbing, especially clubbing resolution of clubbing in a few days was described in a occurring with hypertrophic osteoarthropathy (HOA), the patient with aortic and mitral valve replacement due to hypothesis of a neural mechanism has decreased in popu- infective endocarditis. HOA may occur as an isolated calca- larity because of the lack of evidence of clubbing in neuro- neal periostitis bilaterally. logic disorders and the presence of clubbing in diseases of organs not innervated by the vagal system. Physical Examination Hypoxia has been proposed as an alternative explanation Clubbing is a clinical finding characterized by bulbous fusi- for clubbing in cyanotic heart disease and pulmonary dis- form enlargement of the distal portion of a digit (►Fig. 1). eases. An increase in hypoxia may activate local vasodilators, When the profile of the distal digit is viewed, the angle consequently increasing blood flow to the distal portion of made by the proximal nail fold and nail plate (Lovibond the digits; however, in most cases, hypoxia is absent in the angle) typically is less than or equal to 160 degrees.4 In presence of clubbing, and many diseases with noted hypoxia clubbing, the angle flattens out and increases as the severity are not associated with clubbing. of the clubbing increases. If the angle is greater than Genetic inheritance and predisposition also may play a 180 degrees, definitive clubbing exists. An angle between role in digital clubbing. Hereditary clubbing is observed in 160 and 180 degrees falls in a gray area and may indicate two forms, including idiopathic hereditary clubbing and early stages of clubbing or a pseudoclubbing phenomenon. clubbing associated with PDP. The two forms
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