A. Introduction. A curious relationship exists between certain systemic disorders and the shape of the fingertips: some diseases cause the tips of the phalanges to become enlarged, or “clubbed.”
a. Clubbing is defined as a bulbous enlargement of the connective tissue in the distal phalanges of the fingers and toes. Clubbing can be physiologic or pathologic and is an important clinical sign.
b. Hypertrophic osteoarthropathy is a distinct, more advanced stage of clubbing that is characterized by:
i. Periosteal new bone formation (especially of the long bones)
ii. Symmetric arthritis-like changes in various joints
iii. Neurovascular changes of the hands and feet (leading to paresthesias, erythema, or sweating)
iv. Excess vascular endothelial growth factor release, which is hypothesized to be the etiologic agent of clubbing
B. Clinical Manifestations of Clubbing
a. The thumb and index finger are typically affected first.
b. Clubbing is usually symmetric; however, it may be unilateral in certain vascular disorders (e.g., aortic arch anomalies, subclavian artery aneurysms, patent ductus arteriosus, local vascular disease). Unilateral or asymmetric clubbing should prompt consideration of these conditions.
c. Clubbing is usually a radual, painless process; however, some patients will complain of a dull aching in the fingertips. Pain is not necessarily a sign of pathology.
d. In general, there are three stages in clubbing:
i. During the initial stage, the most difficult stage to appreciate, the nail bed becomes spongy.
The best way to assess whether a patient’s nail bed is spongy is to compare it with your own nail of the same finger.
ii. During the next stage, the angle made by the nail and the dorsum of the distal phalanx increases when viewed from the side. Normally, this angle is less than 180°, but in patients with clubbed fingers, the angle exceeds 180°. Schamroth’s sign can be helpful in confirming this increased angle. In patients without clubbing, when the dorsal surfaces of distal digits of similar fingers are placed together, a diamond-shaped opening appears at the bases of the nails. Schamroth noted that in patients who have mild clubbing, this opening is obliterated. Looking for this sign can help demonstrate the presence of clubbing but does not help in differentiating the cause.
iii. During the final stage, the overall shape of the digit is visibly altered.
i. Pulmonary disease. Approximately 75% of patients with acquired clubbing have pulmonary disease.
1. Chronic obstructive lung disease
2. Lung abscess
5. Cancer (usually primary lung cancer)
ii. Cardiac disease. Approximately 10% of patients with acquired clubbing have cardiac disease.
1. Congenital cyanotic heart disease
2. Subacute bacterial endocarditis
3. Heart failure (especially right-sided heart failure associated with pulmonary disease)
iii. Gastrointestinal disease. Approximately 10% of patients with acquired clubbing have gastrointestinal disease.
1. Inflammatory bowel disease
3. Gastric, colon, or esophageal cancer
iv. Miscellaneous causes
3. Local vascular diseases (leading to unilateral clubbing)
b. Hereditary. Clubbing caused by hereditary factors is indistinguishable morphologically from clubbing caused by acquired disease. However, hereditary clubbing generally develops during childhood and persists for life, and it is often associated with a family history of clubbing.
Patients of African American descent may exhibit mild clubbing unrelated to any pathologic process.
D. Approach to the Patient. For patients with acquired clubbing, an exhaustive search for the underlying causes is unnecessary; however, looking for potentially treatable and reversible diseases is worthwhile. If the patient gives a history compatible with hereditary clubbing, no further evaluation is usually necessary.
a. Patient history. The history should focus on eliciting information about pulmonary symptoms, constitutional symptoms (e.g., fever, weight loss, night sweats, bloody diarrhea), signs (e.g., jaundice, nervousness, tremulousness), alcohol and tobacco use, and family history.
b. Physical examination. The examination should be focused on finding evidence of pulmonary, cardiac, gastrointestinal, or thyroid disease.
c. Diagnostic tests. A complete blood count (CBC), a chest radiograph, an electrocardiogram (EKG), blood gas analysis, serum thyroid-stimulating hormone (TSH) levels, and stool samples (to search for occult blood) may be useful.
E. Treatment. Clubbing usually does not require treatment; rather, the underlying disease process should be identified and addressed. However, if the patient complains of pain in the nail beds, nonsteroidal antiinflammatory medications can be considered.
Suggested Further Readings
Ciment AJ, Ciment L. Regression of clubbing after treatment of lung cancer. N Engl J Med 2016;375:1171.Find this resource:
Dickinson CJ. The aetiology of clubbing and hypertrophic osteoarthropathy. Eur J Clin Invest 1993;23:330–8. (Classic Article.)Find this resource:
Marrie TJ, Brown N. Clubbing of the digits. Am J Med 2007;120:940–1.Find this resource: