Clubbing of the Nails Workup

Updated: Mar 18, 2020
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: William D James, MD  more...
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Workup

Laboratory Studies

Because clubbing typically is secondary to an underlying pathological process, perform pertinent laboratory studies for primary medical disorders that are suggested clinically.

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Imaging Studies

Radiographic changes in patients with digital clubbing vary and include bone dissolution, bone formation, or no change in the bone of the distal phalanx. The types of changes may depend on the underlying pathological processes, as well as the duration of the processes. The severity of soft tissue changes in clubbed digits has not been found to correlate with the type of bone change or the degree of radiographic change. Probably, the lysis of bone predominates in the digits of patients with congenital cyanotic heart disease, while hypertrophy predominates in the digits of patients with clubbing secondary to pulmonary conditions. As an alternate view, hypertrophy may occur earlier in the process of clubbing, and, eventually, it may change to osteolysis as the process becomes chronic.

Technetium Tc 99m skeletal imaging with good-quality views may be helpful in determining the presence and extent of bone changes in clubbed digits, which show increased uptake of the radionuclide. The increased, intense, symmetric uptake typically is localized to the nail beds and may result from increased blood flow and changes in the surrounding soft tissues.

Thermography is another imaging modality being studied for use in diagnosis and monitoring of patients with digital clubbing. [43] Patients may show increased temperature in the distal digits, which can be attributed to an increase in blood flow secondary to vasodilation. Not all patients with clubbing have positive thermographic results.

Positron emission tomography also has been used to study the glucose metabolism of clubbed digits. [44] An increased signal, indicating increased glucose metabolism, has been demonstrated in the distal part of the clubbed fingers. These changes are not seen in fingertips with normal morphology. The increase in signal supports the theory that clubbing is caused by the presence of a factor (eg, platelet-derived growth factor) that increases cellular metabolism.

Other imaging studies, such as computed tomography or magnetic resonance imaging, may be helpful in evaluating the patient for the primary pathological process causing the clubbing. Use of high-frequency ultrasound imaging has also been advocated for the diagnosis of clubbing. [45] Ultrasound in primary hypertrophic osteoarthropathy may show echogenic tissue surrounding the long bones, likely a reflection of edema and inflammatory tissue. [46]

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Histologic Findings

Microscopically, the collagen fibrils and cells are separated by a distance greater than that seen in histologically normal specimens. This increased separation results in a less dense nail bed matrix. Primitive fibroblasts are seen with large nuclei, basophilic cytoplasm, and long reticular processes. Increased and scattered extravascular lymphocytes and, less often, a moderately increased number of tissue eosinophils also are noted in the nail beds of some specimens. The periosteum of the nail bed may be thickened with increased vascular penetration.

Eventually, increased collagen is laid down in all types of chronic clubbing. The mat of collagen fibers may be abnormally thick and dense. The walls of the vascular components increase in thickness and are encased in a thick fibrous sheet. At this stage of clubbing, the histologic and morphologic changes probably are irreversible.

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