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| BRIEF COMMUNICATION |
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| Year : 2019 | Volume
: 6
| Issue : 1 | Page : 72-75 |
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Clubbing: The oldest clinical sign in medicine
Rakesh Agarwal1, Rashmi Baid2, Dhurjati Prasad Sinha1
1 Department of Cardiology, IPGME and R, Kolkata, West Bengal, India
2 Genome Fertility Institute, Kolkata, West Bengal, India
| Date of Submission | 01-Aug-2017 |
| Date of Decision | 01-Sep-2017 |
| Date of Acceptance | 28-Nov-2018 |
| Date of Web Publication | 14-Feb-2019 |
Correspondence Address:
Rakesh Agarwal
IPGME and R and SSKM Hospital, Kolkata, West Bengal
India
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/cjhr.cjhr_68_17
How to cite this article:
Agarwal R, Baid R, Sinha DP. Clubbing: The oldest clinical sign in medicine. CHRISMED J Health Res 2019;6:72-5 |
| Introduction | |  |
Digital clubbing has been regarded as an ominous sign through centuries, often signifying the presence of a dreadful internal illness. Clubbing is described as bulbous uniform swelling of the terminal phalanx of a digit. Proliferation and edema of connective tissue leads to a loss of the normal angle between the nail and the nail bed [Figure 1].[1],[2] Acropachy is another name for clubbing, albeit used rarely. Other synonyms include hippocratic nails, dysacromelia, Trommelschlagel finger, digital hippocratism, watch-glass nails, drumstick fingers, parrot-beak fingers, and serpent head nails. Clubbing is usually acquired and often reversible. Furthermore, clubbing is painless unless associated with hypertrophic osteoarthropathy (HOA).[3] HOA is characterized by periostitis of the long bones, joint pain, and clubbing. It may be primary (autosomal dominant inheritance) or secondary to underlying illness.[4],[5]
We review the history, epidemiology, pathophysiology, clinical features, and significance of this sign of great clinical value in medicine.
| Epidemiology | | |
Exact frequency of clubbing due to various causes remains unknown. It is said to be present in 1% of internal medicine admissions and associated with serious disease in nearly 40%.[6] About 2% of healthy volunteers may have clubbing.[7] Nearly 75%–80% of cases are associated with chronic pulmonary disorders, 10%–15% with cardiovascular disease, 5%–10% with chronic hepatic and gastrointestinal diseases, and finally, 5%–10% with miscellaneous conditions.[1]
| History | | |
Digital clubbing is regarded as the oldest clinical sign in medicine. Clubbing was probably first described by Hippocrates in the 5th century BC in association with chronic empyema. He wrote: “the nails appear curved and the patient suffers as if he had pus inside.”[8] In the late 19th century, Bamberger and Marie named the periosteal proliferation of tubular bones accompanying clubbing as pulmonary HOA.[9],[10] Later on, the suffix “pulmonary” was dropped for obvious reasons.[8]
Rice and Rowland described the ratio of distal phalangeal to interphalangeal depth of >1:1 as a sign of clubbing in 1961. Lovibond described Lovibond's sign in 1938.[5],[11] Schamroth demonstrated obliteration of the diamond-shaped window formed by opposing dorsal surfaces of terminal phalanges in himself, after having suffered from three episodes of infective endocarditis.[12]
| Pathophysiology | | |
No single theory can explain all causes of clubbing. Vascular endothelial growth factor is said to play a key role. Produced in diverse malignancies and stimulated by hypoxia, it is known to induce vascular hyperplasia, edema, and fibroblast or osteoblast proliferation leading to clubbing.[5],[11],[13]
One theory suggests that megakaryocytes and platelet clumps cause clubbing. Megakaryocytes are continually released from the bone marrow and fragment into platelets in the pulmonary capillary bed. In the right-to-left shunts and carcinoma bronchus, these megakaryocytes or megakaryocyte fragments bypass the pulmonary capillaries. Similarly, large platelet clumps form in the great arteries or left side of the heart in conditions such as subacute bacterial endocarditis or subclavian aneurysm. These reach the fingertips through bloodstream and release platelet-derived growth factor which in turn leads to connective tissue hypertrophy and clubbing.[1],[13],[14]
Growth hormone has been implicated as well. A neural mechanism involving the vagal system is consistent with the fact that clubbing might be reversed with vagotomy. This neurocirculatory reflex leads to increased blood flow and consequent clubbing.[1],[13]
| Eliciting the Sign | | |
Clubbing usually first develops in the thumb and forefinger. Early clubbing may be detected using the “floating nail” sign and the “profile sign.”[1]
Floating nail sign is demonstrated by applying pressure at the root of the nail plate. Normally, pressure produced no movement there. There is a movement toward the bone in clubbing. The profile sign refers to increased angle between the nail plate and skin overlying the proximal part of the distal phalanx (Lovibond's angle). The angle increases over 180° compared to normal angle of <160°. Obliteration of the angle between nail and nail bed is the first sign of clubbing and is a constant feature.[1],[3],[5]
Schamroth sign entails placing the two thumbs of a patient's hands back to back with the two fingertips and interphalangeal joints aligned. Normally, a diamond-shaped area is apparent. With clubbing, this empty space is lost. This sign has a high value in differentiating clubbing from pseudoclubbing.[1],[5],[12]
In late stages, the nail assumes an abnormally convex appearance known as the “watch crystal” nail. Later still, the entire distal phalanx becomes enlarged and bulbous and resembles a drumstick.[1]
Clubbing is said to have four grades:
- Fluctuation is positive due to the increased proliferation of cells at the nail base with obliteration of onychodermal angle
- Grade 1+ – increased anteroposterior and transverse diameters of nails
- Grade 2+ – increase in pulp tissue resulting in Parrot's beak or drumstick appearance
- Grade 3+ – HOA.[15]
With HOA, the patient may complain of deep pain over the distal extremities, worse at night, and on dependency. There may be tenderness, warmth, reddening, or brawny edema over the distal long bones, particularly the shins. Later autonomic changes such as flushing, sweating, or blanching may be noted in the affected hands and feet.[1],[4]
| Clinical Significance | | |
Clubbing or HOA may provide the first clinical indication of an underlying serious illness. However, it is easily overlooked on routine clinical examination. The development of clubbing takes years though occasionally it develops suddenly.[5] The causes are enumerated in [Table 1]. Clubbing may occasionally be unilateral only [Table 2] or unidigital [Table 3].[1],[11],[13],[16] Differential clubbing refers to clubbing present in the toes but not in the fingers and may be seen in coarctation of the aorta or patent ductus arteriosus with reversal of shunt.[15],[16]
While clubbing may be seen in any type of lung cancer, it frequently occurs with squamous and adenocarcinomas and less frequently with small cell carcinoma. It is very important to consider other symptoms of HOA along with clubbing, because 90% adults with the complete, nonfamilial HOA syndrome have or will develop a malignancy![5],[17]
Tuberculosis (TB) in isolation does not cause clubbing though it is said to occur with cavitating TB, in pulmonary TB/HIV co-infection, and with supervening bronchiectasis.[7],[11] In a Ugandan study, 30% patients affected with sputum-positive pulmonary TB and only 2% of healthy volunteers had clubbing. However, it was shown to be unrelated to concomitant HIV disease, radiographic extent of disease, and nutritional status, as assessed by albumin levels. Poor performance status and a history of prior TB were associated with clubbing.[7]
Pseudoclubbing of a single digit has been said to occur with subungual tumor, pseudocyst, or osteoid osteoma.[5] Generalized pseudoclubbing can be seen with any disease-causing acro-osteolysis.[18]
| Prognosis | | |
Clubbing has been considered to be a poor prognostic sign, meaning the illness is in an advanced stage.[8] This has been shown in patients with sickle cell anemia, pulmonary fibrosis, asbestosis, cystic fibrosis, Graves' disease, hypersensitivity pneumonitis, and TB.[5],[7],[8],[19] However, the prognosis of clubbing is dependent on the underlying process too. Treatment of the primary disease often leads to the complete resolution of clubbing and is currently the only recognized treatment for clubbing. This has been shown with Crohn's disease, pleural tumors, hepatopulmonary syndrome with transplant, as well as whipworm antimicrobial therapy.[5],[8]
New onset of clubbing in a patient with chronic obstructive pulmonary disease usually implies the development of bronchogenic carcinoma provided associated bronchiectasis and lung abscess has been ruled out. Similarly, development of clubbing with cyanosis in patients with congenital acyanotic diseases usually implies a reversal of shunt and poor prognosis.
| Conclusion | | |
The value of clubbing as a distinct clinical sign with all its remarkable features always makes an interesting discussion. Its value as a window to internal medicine cannot be over exaggerated. It has mesmerized clinicians for centuries and rightly so. With contemporary research and literature and with on new understandings of its pathogenesis, newer therapies in the form of antiplatelet and anticytokine therapy may someday be useful in treatment of clubbing. Till then, we can but marvel at its clinical utility and rich heritage.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
| References | | |
| 1. | McPhee SJ. Clubbing. In: Walker HK, Hall WD, Hurst JW, editors. Clinical Methods: The History, Physical, and Laboratory Examinations. 3 rd ed., Ch. 44. Boston: Butterworths; 1990. Available from: http://www.ncbi.nlm.nih.gov/books/NBK366/. [Last accessed on 2018 Dec 26].  |
| 2. | Lyons AS, Petrucelli RJ. Medicine: An Illustrated History. New York: Abrams INC Publishers; 1978. p. 216. |
| 3. | Myers KA, Farquhar DR. The rational clinical examination. Does this patient have clubbing? JAMA 2001;286:341-7. |
| 4. | Martínez-Lavín M, Matucci-Cerinic M, Jajic I, Pineda C. Hypertrophic osteoarthropathy: Consensus on its definition, classification, assessment and diagnostic criteria. J Rheumatol 1993;20:1386-7. |
| 5. | Spicknall KE, Zirwas MJ, English JC 3 rd. Clubbing: An update on diagnosis, differential diagnosis, pathophysiology, and clinical relevance. J Am Acad Dermatol 2005;52:1020-8. |
| 6. | Vandemergel X, Renneboog B. Prevalence, aetiologies and significance of clubbing in a department of general internal medicine. Eur J Intern Med 2008;19:325-9. |
| 7. | Ddungu H, Johnson JL, Smieja M, Mayanja-Kizza H. Digital clubbing in tuberculosis – Relationship to HIV infection, extent of disease and hypoalbuminemia. BMC Infect Dis 2006;6:45. |
| 8. | Martinez-Lavin M. Exploring the cause of the most ancient clinical sign of medicine: Finger clubbing. Semin Arthritis Rheum 2007;36:380-5. |
| 9. | Boyer-Duck E, Dajer-Fadel WL, Hernández-Arenas LÁ, Macías-Morales MP, Rodríguez-Gómez A, Romo-Aguirre C, et al. Pierre-Marie-Bamberger syndrome and solitary fibrous tumor: A rare association. Asian Cardiovasc Thorac Ann 2018;26:154-7. |
| 10. | Chakraborty RK, Sharma S. Hypertrophic Osteoarthropathy, Secondary. In: StatPearls. Treasure Island (FL): StatPearls Publishing; 2018. Available from: https://www.ncbi.nlm.nih.gov/books/NBK513342/. [Last updated on 2018 Jul 09]. |
| 11. | Schamroth L. Personal experience. S Afr Med J 1976;50:297-300. |
| 12. | |
| 13. | Dickinson CJ, Martin JF. Megakaryocytes and platelet clumps as the cause of finger clubbing. Lancet 1987;2:1434-5. |
| 14. | Gantait K. Idiopathic clubbing – A typical presentation. J Assoc Physicians India 2012;60:116. |
| 15. | Rao BN. Clinical Examination in Cardiology. New Delhi: Elsevier; 2014. |
| 16. | Kurzrock R, Cohen PR. Cutaneous paraneoplastic syndromes in solid tumors. Am J Med 1995;99:662-71. |
| 17. | Santiago MB, Lima I, Feitosa AC, Braz Ade S, Miranda LG. Pseudoclubbing: Is it different from clubbing? Semin Arthritis Rheum 2009;38:452-7. |
| 18. | Adekile AD. Arterial oxygen tension, haemoglobin F and red cell 2, 3 diphosphoglycerate in sickle cell anaemia patients with digital clubbing. Ann Trop Paediatr 1989;9:165-8. |
| 19. | Marrie TJ, Brown N. Clubbing of the digits. Am J Med 2007; 120:940-1. |
[Figure 1]
[Table 1], [Table 2], [Table 3]
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