Hippocratic fingers: Physiopathology, Epidemiology and Prognosis


Since Hippocrates first described “digital clubbing” in patients with empyema, Hippocratic fingers have been associated with several underlying pulmonary, cardiovascular, neoplastic, infectious, hepatobiliary, mediastinal, endocrine and gastrointestinal diseases.

The appearance of this disease, with no apparent underlying condition, can also occur as an idiopathic form of Mendelian dominant trait.

Clubbing, or hippocratic fingers, is a clinically descriptive term, referring to the uniform bulbous inflammation of the soft tissue of the terminal of the phalange of a digit with the consequent loss of the normal angle between the nail and the nail bed.

The change of the phalanges of the fingers in the form of a thigh or fingernails in the form of a clock crystal (Hippocratic fingers) presents a well-known clinical phenomenon that suggests the presence of various diseases.

Especially those diseases associated with hypoxia, manifested by respiratory and / or cardiac insufficiency, as well as malignant tumors and subacute infective endocarditis.

At the same time, the fact that this clinical phenomenon may accompany other diseases (Crohn’s disease, HIV infection) must also be taken into account.

Hippocratic fingers often appear first than more specific symptoms.

In this sense, the correct interpretation of this clinical sign, complemented by laboratory tests, allows an early and valid diagnosis.

Digital clubbing is classified into primary (ie, idiopathic, hereditary) and secondary forms. Digital clubbing can be symmetrical bilaterally, or it can be unilateral or involves only one finger.

Anatomical considerations, such as the classical measurement of the Lovibond angle or the more recently derived index of the curvature of the nails by Goyal, can usually be identified in a simple physical examination and can be used to identify digital clubbing and to control this dynamics objectively .

Several imaging modalities have been used not only to evaluate the fingers but also to help identify possible clues for their development.

El clubbing

Clubbing is a characteristic of Pachydermoperiostosis, a rare genodermatosis characterized by pachydermia, digital clubbing, periostosis, with a population of affected males.

Although it is usually an autosomal dominant model with incomplete penetrance and variable expression, both autosomal and recessive inheritance have been suggested in some families with relatives who have Pachydermoperiostosis.

Primary hypertrophic osteoarthropathy is a rare hereditary disorder with digital pairing, with formation of new subperiosteal bone and arthropathy.

It has been linked to mutations in the HPGD gene of 15-hydroxy-prostaglandin dehydrogenase (15-PGDH), which causes this.

A mutation was identified in a large Pakistani family with congenital clubbing isolated on the nails.

In another study of homozygous mutations, an intragenic deletion resulting in a mutation was associated with a severe phenotype. A heterozygous carrier of a mutation had isolated digital clubbing.


The specific physiopathological mechanism of digital clubbing remains unknown. Many theories have been proposed, but none has received widespread acceptance as a complete explanation of the phenomenon of digital clubbing.

As Samuel West said in 1897, “Clubbing is one of those phenomena we are all so familiar with that we seem to know more about it than we really can.”

Alterations in the size and configuration of the fingers result from changes in the nail bed, beginning with the increase in interstitial edema at the beginning of the process.

As the musculature advances, the volume of the terminal portion of the finger may increase due to an increase in vascular connective tissue and to the change in vascular connective tissue quality, although some cases have been associated with bone spurs in the terminal phalanx. .

Although clubbing is a common physical finding in many underlying pathological processes, surprisingly, the mechanism of how clubbing occurs is unclear.

Different pathological processes can follow different paths towards a common goal. Many studies have shown an increase in blood flow in the portion of the fingers that have this syndrome.

High resolution magnetic resonance images using a contrast agent in 4 patients with Clubbing and 4 healthy volunteers documented the hypervascularization of the nail bed as binding in affected patients.

Most researchers agree that this is due to an increase in digital distal vasodilation, whose cause is unknown.

The exact mechanism by which increased blood flow produces changes in vascular connective tissue under the nail bed is also unknown.

Epidemiology: Frequency

Idiopathic or primary clubbing is rare, while the occurrence of secondary clubbing depends on the underlying disease.

It has been reported that 89% of patients diagnosed with Pachydermoperiostosis have primary digital dysfunction. This syndrome occurs more often in young males.

Of the patients with idiopathic pulmonary fibrosis, 65% have clinical digital clubbing. In these patients, a higher incidence has been observed in patients with higher levels of smooth muscle proliferation in the lungs.

In 29% of patients with lung cancer it has been reported that clubbing is more common in patients with non-small cell lung carcinoma (35%) than in patients with small cell lung carcinoma (4%).

In 38% of patients with Crohn’s disease, digital discord was reported in 15% of patients with ulcerative colitis and in 8% of patients with proctitis. Clubbing was observed in up to one third of Ugandan patients with pulmonary tuberculosis. It was not associated with stages of HIV infection, or hypoalbuminemia.


The racial predilection of secondary clubbing depends on the racial prevalence of the underlying disease.


The sexual predilection of secondary clubbing of the fingers depends on the prevalence of the underlying disease.

Forecast: Hippocratic fingers

Since this condition is a clinical finding, it is not an independent cause of mortality; However, the mortality associated with the underlying pathology in patients with secondary clubbing varies widely. Morbidity is minimal.

Treating the underlying pathological condition can decrease clubbing or potentially reverse it if it is done early enough.

Once there have been substantial changes in chronic tissues, including increased collagen deposition, it is unlikely. The prognosis of the underlying disease must be determined individually.