home Education, Physical Examination Pathophysiology of Digital Clubbing (Hippocratic Fingers)

Pathophysiology of Digital Clubbing (Hippocratic Fingers)

 

Digital Clubbing of a patient with emphysema.
http://sayitaduran.com/social-work-dissertation-help/ Digital Clubbing of an 83-year-old patient with emphysema.

enter see url What is digital clubbing?

http://fionadalwood.com/business-plan-writers-vancouver-bc/ Clubbing is a clinically descriptive term, referring to the bulbous uniform swelling of the soft tissue of the distal part of the fingers and toes with subsequent loss of the normal angle between the nail and the nail bed. The nail plate is enlarged and excessively curved, with a greater than 180° widening of the angle between the proximal nail fold and the nail plate.

 

finger-clubbing-diagram1
Lovibond angle.

get link History of Digital Clubbing

First described by Hippocrates in the first century BC, clubbing may be congenital or acquired. Acquired clubbing is uncommon and has been associated with various chronic diseases. It is associated with cardiovascular, neoplastic, hepatobiliary, osteopathic and gastrointestinal diseases, however, in 80% of cases it is associated with pulmonary diseases. It may be symmetric bilaterally, or it may be unilateral or involve a single digit. Anatomic considerations, usually can be identified on simple physical examination and can be used to identify digital clubbing and to monitor this dynamic process objectively. It can measured and diagnosed with the Lovibond angle. Normally, the nail plate has an angle of about 160°. In clubbing, the nail plate can be greater than 180° as shown in the image.

 

Digital Clubbing of a patient with emphysema.
Digital Clubbing of an 83-year-old patient with emphysema.

http://cantat.amu.edu.pl/?diversity-in-new-york-essay Pathophysiology

The pathophysiologic mechanism of digital clubbing remains unknown, however, many theories have been proposed. Alterations in size and configuration of the clubbed digit result from changes in the nail bed beginning with increased interstitial edema. As clubbing progresses, the volume of the fingertips or toes may increase because of an increase in the vascular connective tissue  and change in quality of the vascular connective tissue. Bone spurs on the terminal phalanx may also form.

Different pathological processes may follow different pathways to a common end resulting in clubbing. Several studies show an increased blood flow with  nail bed hypervascularization in the clubbed portion of the finger. Most researchers agree that this results from an increase in distal digital vasodilation, the cause of which is unknown.

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Evidence that favors the presence of a circulating vasodilator derives from the association of clubbing with cyanotic congenital heart disease. Many potential vasodilators, which usually are inactivated as blood passes through the lungs, bypass the inactivation process in patients with right-to-left shunts. Patients with tetralogy of Fallot with substantial shunting have a high incidence of clubbing. After surgical correction diminishes the shunt, the clubbing improves. Also previously observed is clubbing confined to the feet in patients with late untreated patent ductus arteriosus in whom blood from the pulmonary artery bypasses the lungs and is shunted into the descending aorta. In the absence of a shunt, the circulating vasodilator may be produced by the lung tissue, or, possibly, it passes through the pulmonary circulation without becoming inactivated. Proposed vasodilatory factors include ferritin, prostaglandins, bradykinin, adenine nucleotides, and 5-hydroxytryptamine.

Digital Clubbing of a patient with emphysema.
Digital Clubbing of an 83-year-old patient with emphysema.

Genetic inheritance and predisposition also may play a role in digital clubbing. Hereditary clubbing is observed in 2 forms, including idiopathic hereditary clubbing and clubbing associated with pachydermoperiostosis. The 2 forms are believed to be separate entities. Both demonstrate autosomal dominant inheritance with incomplete penetrance.

The theory of platelet-derived growth factor (PDGF) released from megakaryocytes and platelet emboli has been proposed as the mechanism by which digital clubbing occurs. These emboli are trapped in the tiny vascular beds of the fingertips where they release platelet-derived growth factor (PDGF). This factor promotes fibrovascular proliferation increasing capillary permeability and connective tissue hypertrophy. Megakaryocytes and clumps of platelets are not normally found in arterial circulation. They have a large size which prevents them from passing through pulmonary capillaries when they are released from bone marrow.

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In conditions where platelets may clump in the arterial circulation or bypass the pulmonary capillaries, they can reach the systemic circulation and become trapped in the terminal capillaries of the fingers and toes. Damage to pulmonary capillaries from various lung disorders can have the same effect.

 

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