Clubbing

Clubbing is one of those signs which is picked up on a clinical examination and has a vital importance. Many clinicians tend to quiz you regarding clubbing, its theories and the evaluation in detail. Let us now throw some light on the simplicity of clubbing and its interesting realm. 

Clubbing can be defined as the selective bullous enlargement of the distal segments of the fingers and toes due to proliferation of connective tissue, particularly on the dorsal surface. There is increased sponginess of the soft tissue at the nail bed. It is also called HIPPOCRATIC FINGERS, DRUMSTICK FINGERS or WATCH GLASS NAILS. 

Degrees of clubbing: 

Grade 1 – Fluctuation of the nail bed. 

Grade 2 – Obliteration of the Lovibond angle.

Grade 3 – Parrot beak appearance or drum stick appearance.

Grade 4 – Hypertrophic Osteo Arthropathy (HOA).

Some literatures tend to split the grade 3 into 2 separate counterparts and mention 5 grades. However this is the universally accepted grading.

Clubbing is a condition not completely explained. The etiopathogenesis of clubbing is liked to theories. The theories are mentioned below.

Clubbing is believed to be a secondary response to a humoral substance causing vasodilatation at the finger tips.

Neurogenic theory: It has been shown by studies that a vagotomy causes a symptomatic improvement in the HOA, thus allowing us to infer that a vagal stimulus(from a tumour site) via neural reflexes can lead to proliferation of connective tissue at the distal extremities. This theory was unable to explain why conditions like CCHD and aneurysms cause clubbing.

Humoral theory: Normally the lung throws out all the soluble substances by inactivation. But in case of lung problems, these substances reach the systemic circulation in the active state and they stimulate the changes seen in HOA (Prostaglandins, ferritin, bradykinin and growth hormone). However this theory suffered a setback because normal levels of thee metabolites were found in HOA cases.  

Role of platelets: Normally megakaryocytes and large platelets get destroyed in the lung. In cases where these is a lung pathology or CCHD or right to left shunts, these platelets escape and reach distal extremities. Here they interact with the endothelial cells and release platelet derived growth factor (PDGF) post activation. PDGF and other mediators then activate the fibroblasts and transforming growth factor β (TGF-β) which lead to collagen production and connective tissue laying down ultimately giving rise to clubbing and HOA. This theory is supported by the evidence that plasma levels of von Willebrand factor were elevated in HOA cases. Further platelet clumps were demonstrated in infected heart valves, walls of aneurysms and valve grafts.

Hypoxia: Hypoxia is suggested to be a stimulus for HOA. Hypoxia leads to opening of deep arterio-venous shunts and fistulae which increase blood flow to the extremities and leads to hypertrophy.

Why is there clubbing?

Causes:

Clubbing is associated with diseases of the lung, heart, GIT, endocrine system and miscellaneous diseases. The simple way of remembering few causes of clubbing are:

C – Congenital Cyanotic Heart Disease, Cystic fibrosis, Crohn’s disease, Cholangiolitic cirrhosis,

L – Lung abscess, Lipoid pneumonia,

U – Ulcerative colitis,

B – Bronchiectasis, Bronchogenic carcinoma,

B – Biliary cirrhosis,

I – Infective endocarditis, idiopathic pulmonary fibrosis

N – Neoplasms of lung, liver, esophagus, small & large bowel.

G – Grave’s disease (thyroid acropachy)

Other: Mesothelioma, Tuberculosis, Empyema, Atrial myxoma, Eisenmenger’s physiology, Hepato-pulmonary syndrome, Myxoedema, Acromegaly, Diffuse fibrosing alveolitis, Hydatid cysts (Lung), Syringomyelia etc.

Miscellaneous causes : Hereditary, Idiopathic.

Unilateral clubbing: Pancost tumour, subclavian and innominate artery aneurysm.

Unidigital clubbing: Trauma, gout (tophi), sarcoidosis.

Upper limb clubbing only: Heroin addicts (phlebitis)

Lower limb clubbing only: Infected abdominal aneurysms and patent ductus arteriosus.

Assessment of clubbing:

Clinical methods to assess clubbing is done by:

Simple examination:

The nail bed fluctuation is elicited by stabilising the finger between the index finger of of both the hands such that the nail can be balloted between the two fingers. Now, either by using the thumb at the distal margin of the nail or by using one index finger the nail is balloted to check for fluctuation.

The obliteration of Lovibond angle can be assessed clinically by looking tangentially to observe for the angle between the cuticle and the proximal nail. (Normal angle = 15^o from the skin or 160-165^o from the nail).

Schamroth’s sign: Normally when the two fingers ae held together with the nails facing each other, a diamond shaped space is seen at the level of the proximal nail fold. Obliteration of this space indicates clubbing and is called as Schamroth’s +.

Thickness of the digit at the base of the nail compared to the thickness at the distal interphalangeal joint also indicates clubbing.

Objective method: Diameter of the digit at the base of the nail and at the distal interphalangeal joint is taken and their ratio calculated. If the sum of the individual ratios is >10 then it signifies clubbing.

In grade 3 – the characteristic appearance of the nail itself can indicate clubbing.

In grade 4 – deep seated aching pain, inability to move the wrist joint, swellings at the wrist area are characteristic.

Clubbing is a presentation which resolves with treatment of the underlying cause. Usually no other treatment is required. In severe cases a vagotomy or a percutaneous block of th evagus can improve symptoms. Analgesics, NSAID’s and aspirin may help alleviate the symptoms in severe cases.