Clubbing

Basics

Description

Digital clubbing is characterized by enlargement of the terminal segments of the fingers and/or the toes due to proliferation of connective tissue between the nail matrix and the distal phalanges.
Clubbing can occur bilaterally or unilaterally.
Clubbing is painless, unless associated with hypertrophic osteoarthropathy.
Digital clubbing and hypertrophic osteoarthropathy represent different stages of the spectrum of the same syndrome.
Digital clubbing was described in the 5th century BC by Hippocrates in a patient with empyema and has been alternatively called Hippocratic fingers, watch-glass nails, or drumstick fingers.

Epidemiology

Clubbing is seen in a wide variety of conditions.
Among cardiac causes are those associated with central cyanosis and right-to-left shunting.
Examples of these heart diseases include:
- Tetralogy of Fallot
- Tricuspid atresia
- Transposition of the great vessels
Pulmonary diseases associated with clubbing include:
- Primary or metastatic pulmonary malignancies
- Mesothelioma
- Pleural tumors
- Cystic fibrosis
- Pulmonary arteriovenous malformations
- Empyema
- Bronchiectasis
- Lung abscess
- Idiopathic pulmonary fibrosis
- Hypersensitivity pneumonitis
- Hepatopulmonary syndrome
- Sarcoidosis
- Asbestosis
Clubbing is relatively rare in COPD and suggests the presence of bronchiectasis or bronchogenic carcinoma.
Clubbing without cyanosis may be seen in patients with certain infectious, gastrointestinal, vascular, neurologic, rheumatologic, neoplastic, and endocrine disorders.
Infectious etiologies are endocarditis, TB, HIV, and chronic parasitic infections.
GI diseases include inflammatory bowel disease (both Crohn disease and ulcerative colitis), celiac sprue, and some forms of liver disease.
POEMS syndrome, lymphoma, nasopharyngeal carcinoma, and hyperthyroidism are also associated with clubbing.
Usually clubbing is symmetric, although unilateral clubbing has been associated with arterial aneurysms, dialysis fistulas, and hemiplegic stroke.

Associated Conditions

Clubbing may occur associated with other musculoskeletal manifestations of hypertrophic osteoarthropathy (HOA):
- HOA is characterized by digital clubbing, periostosis of the tubular bones, and joint effusions. Some patients present with painful arthropathy.
- HOA may occur as a familial form beginning in childhood or as a secondary form, related to any of the diseases previously mentioned.
- HOA is most frequently diagnosed after the patient presents with persistent pain in the extremities. Bony tenderness due to periostitis may be elicited on palpation of the shafts of the long bones.
- The skeletal findings in HOA consist of periosteal elevation and new bone formation, seen primarily in the distal phalanges and long bones.
- Synovial involvement also may lead to pain and swelling of the knees, ankles, wrists, and elbows.
- Occasionally, other joints such as the shoulders, clavicles, and temporomandibular joints also may be involved.
- There may be mononuclear infiltration in adjacent soft tissue. Connective tissue proliferation occurs in the nail bed, giving rise to clubbing, which is seen in virtually all patients.
The etiology and pathogenesis of clubbing and HOA remain unclear:
- A current theory focuses on megakaryocyte or platelet clumps bypassing the lung capillary network and becoming lodged in the peripheral vasculature of the digits. These platelet particles then release vascular endothelial growth factor (VEGF). VEGF promotes the morphologic findings seen in clubbing and HOA. Furthermore, VEGF action is induced by hypoxia and is produced by diverse malignant tumors. Thus, tumor and hypoxic expression of VEGF would also cause clubbing and HOA in the absence of prominent extrapulmonary shunting of blood.
Primary HOA (Touraine-Soulente-Gole syndrome) develops slowly in puberty, is inherited in an autosomal-dominant fashion with variable expression, and is more common in boys than in girls:
- There is marked thickening of the distal extremities as well as clubbing, leading to a spadelike appearance to the hands.
- The face often has a leonine appearance that may mimic acromegaly. Symptoms of bone and joint pain may not occur until 20-30 yr from the onset of the disease.
Secondary HOA is more common than primary HOA and accompanies many of the cardiac and pulmonary diseases discussed in the preceding text:
- HOA may precede the accompanying manifestations of the primary disorder by several months.
- Joint manifestations may be very painful and most commonly involve the metacarpophalangeal and metatarsophalangeal joints, as well as the wrists, ankles, and knees.
- HOA may occur in as many as 5-10% of pulmonary-related malignancies and may progress particularly rapidly in cases of bronchogenic carcinoma.
- Symptoms of HOA may precede pulmonary manifestations when there is underlying lung cancer. Full-blown HOA may occur with cyanotic congenital heart disease.
- Blood tests are normal in patients with HOA, with the exception of a mild increase in the erythrocyte sedimentation rate.
- Joint effusions are small and most commonly noninflammatory when they occur. Periosteal elevation that occurs in the disease produces a characteristic appearance on radiographs of long bones.
- Bone scan imaging detects areas of increased osteoblastic activity and may identify periostitis before it is apparent clinically or on plain films.
HOA is frequently confused with rheumatoid arthritis.
The presence of clubbing is an important clue to the diagnosis. HOA-associated effusions are noninflammatory, as attested to by the absence of rheumatoid factor or antinuclear antibodies.

Diagnosis

Signs and Symptoms á

The normal angle between the fingernail and the nail base is ~160 degrees and has a firm feeling on palpation. As clubbing progresses, the angle between the nail and its base increases to 180 degrees (and sometimes more) as the nail base becomes swollen and edematous.
The nail base in the individual with clubbing has a spongy or swollen feeling on palpation. The nail itself may have a convex appearance in advanced clubbing, although this should not be confused with the curved nails sometimes seen in normal individuals. An important distinguishing feature is that the normal nail will have a preserved angle between the nail and its base, whereas the truly clubbed individual will not.
The diagnosis of clubbing is made solely by physical exam. The softening of tissue at the nail base can be felt on palpation. The skin around the cuticle is noted to take on a smooth and shiny appearance. Although quantification of clubbing has been accomplished using various techniques, including plaster casts and "shadowgrams"Ł of the digital profile, the methods have not replaced bedside diagnosis in standard clinical practice.

Treatment

General Measures

Most fundamental to the treatment of both clubbing and HOA is the identification and care of the underlying disorder with which they are associated.
Both may regress or resolve with identification and proper therapy of the related condition.

Medication

NSAIDs can be beneficial for treating pain from osteoarthropathy.
Bisphosphonates and octreotide can be used to relieve symptoms in refractory HOA cases.

Additional Reading

1Atkinson áS, Fox áS. Vascular endothelial growth factor (VEGF)-A and platelet-derived growth factor (PDGF) play a central role in the pathogenesis of digital clubbing. J Pathol. 2004;203:721-728. á[View Abstract]2Braunwald áE, Gilliland áB. In: Harrison's Principles and Practice of Internal Medicine, 13th ed. New York: McGraw-Hill, 1994;182-183, 1705-1706.3Braunwald áE. In: Heart Disease. Philadelphia: WB Saunders, 1997.4Dickinson áCJ, Martin áJF. Megakaryocytes and platelet clumps as the cause of finger clubbing. Lancet. 1987;ii:1434-1435.5Fishman áA. In: Pulmonary Diseases and Disorders. New York: McGraw-Hill, 1988;352-354.6Garske áL, Bell áS. Pamidronate results in symptom control of hypertrophic pulmonary osteoarthropathy in cystic fibrosis. Chest. 2002;121;1363-1364. á[View Abstract]7Hansen-Flaschen áJ, Nordberg áJ. Clubbing and hypertrophic osteoarthropathy. Clin Chest Med. 1987;8:287-299. á[View Abstract]8Martinez-Lavin áM. Exploring the cause of the most ancient clinical sign of medicine: Finger Clubbing. Semin Arthritis Rheum. 2007;36(6):380-385. á[View Abstract]9Myers áK, Farquhar áD. Does this patient have clubbing? JAMA. 2001;286:341-347. á[View Abstract]10Spicknall áK, Zirwas áM, English áJ. Clubbing: An update on diagnosis, differential diagnosis, pathophysiology, and clinical relevance. J Am Acad Dermatol. 2005;52(6):1020-1028. á[View Abstract]

Home

Erectile Dysfunction

Doctor123.org