Clubbing is the bulbous swelling of the terminal part of the fingers and the toes with an increase in the soft tissue mass, and increased anteroposterior as well as transverse diameter of the nails due to proliferation of subungual connective tissue.
Normal angle between the skin and the nail bed is 160 degree. It is also called as lovibond angle Obliteration of this angle is an early sign of clubbing.There is also increase in the soft tissue of distal part of the fingers and toes.This is manifested as biconvexity of nail and the bulbous distal portion of fingers.
In normal nails when the thumb nails are placed in opposion There is a lozenge shaped gap .In clubbing this gap is obliterated called as Schamroth's window test or sign.
What is the basic mechanism of clubbing?
Arterial hypoxemia and neurohumeral stimulus produces hypervascularity and opening up of anastamotic channels in the nail bed which lead to overgrowth of soft tissue.This is the basic mechanism of clubbing
Why the pulp tissue is increased in clubbing ?
Pulp tissue is increased due to
There are several theories to explain clubbing
Hereditary' predisposition - an autosomal gene of variable penetrance has been detected.
Vasodilators such as prostaglandins, bradykinins, 5-HT may be responsible for the development of clubbing. In bronchogenic carcinoma, vasodilator substances which are normally detoxified by lungs enters unaltered into systemic circulation
There is trapping of megakaryocytes and platelet clumps with local release of platelet-derived growth factor (PDGF) and other cytokines which increase the capillary permeability (latest and most acceptable theory). Arterial hypoxemia and neurohumeral stimulus produces hypervascularity and opening up of anastamotic channels in the nail bed which lead to overgrowth of soft tissue.
Possible mechanism of clubbing
The different hypothesis are
Normal angle between the skin and the nail bed is 160 degree. It is also called as lovibond angle Obliteration of this angle is an early sign of clubbing.There is also increase in the soft tissue of distal part of the fingers and toes.This is manifested as biconvexity of nail and the bulbous distal portion of fingers.
In normal nails when the thumb nails are placed in opposion There is a lozenge shaped gap .In clubbing this gap is obliterated called as Schamroth's window test or sign.
What is the basic mechanism of clubbing?
Arterial hypoxemia and neurohumeral stimulus produces hypervascularity and opening up of anastamotic channels in the nail bed which lead to overgrowth of soft tissue.This is the basic mechanism of clubbing
Why the pulp tissue is increased in clubbing ?
Pulp tissue is increased due to
- Proliferation of subungual connective tissue.
- Interstitial oedema.
- Dilatation of arterioles and capillaries.
There are several theories to explain clubbing
Hereditary' predisposition - an autosomal gene of variable penetrance has been detected.
Vasodilators such as prostaglandins, bradykinins, 5-HT may be responsible for the development of clubbing. In bronchogenic carcinoma, vasodilator substances which are normally detoxified by lungs enters unaltered into systemic circulation
There is trapping of megakaryocytes and platelet clumps with local release of platelet-derived growth factor (PDGF) and other cytokines which increase the capillary permeability (latest and most acceptable theory). Arterial hypoxemia and neurohumeral stimulus produces hypervascularity and opening up of anastamotic channels in the nail bed which lead to overgrowth of soft tissue.
Possible mechanism of clubbing
The different hypothesis are
- Anoxia- It is the most important theory which leads to opening up of deep arteriovenous fistula of the terminal phalanges. Fallot's tetralogy is an example
- Toxic - Example is SBE.
- Reflex theory- Vagotomy often improves the clubbing in bronchogenic carcinoma.
- Metabolic causes - Example is thyrotoxicosis.
- Humoral theory- Increased growth hormone, parathormone, bradykinin. eg. acromegaly. Pressure changes between the radial and digital arteries.
- Reduced ferritin (may escape oxidation in lungs and leads to dilatation of arteriovenous anastomosis by entering into systemic circulation) may play an important role (recent view).
