Let's learn the physiological basis behind clubbing

1. Physiology
behind
Clubbing

2. Introduction
• Clubbing was 1st described by Hippocrates nearly 2500 years
ago in a patient with chronic empyema. So, often described
as Hippocratic finger.
• Clubbing, regarded to be the oldest sign in clinical medicine.
• We all know that, normal angle between nail bed & proximal
nail fold is around 160° or less (called as Lovibond’s angle).
But in Clubbing, this angle is > 180°.
Obliteration of this angle between nail and nail bed is the
first sign of clubbing and its most constant feature.

3. Schamroth sign
• Is familiar to us as it is usually done during clinical
assessment of clubbing where placing together dorsal
surfaces of terminal phalanges of similar finger
Gives a distinct diamond shaped window at base of nail
bed (Normal)
Obliteration of this window (Clubbing)
But did you know that, it was named after a cardiologist Leo
Schamroth, who when diagnosed with subacute bacterial
endocarditis noted this finding as one of the earliest signs of
clubbing ? He also reported that the window reappeared 2
months after his endocarditis had been treated successfully.

4. Some conditions associated with clubbing
• Pulmonary diseases (75 - 80%)
Pulmonary malignancy
Chronic pulmonary infections (lung abscess, chronic
empyema, bronchiectasis, cystic fibrosis)
• Cardiovascular diseases (10 - 15%)
Cyanotic congenital heart diseases (Right to left shunts)
Subacute bacterial endocarditis
• Chronic hepatic and gastrointestinal disorders (5 - 10%)
Liver cirrhosis, amebic liver abscess
Chronic infection (ascariasis, malaria)
Chronic inflammation (Inflammatory Bowel Disease)
Neoplasms
• Miscellaneous disorders (5 - 10% )
Endocrine (Thyroid acropachy, hyperparathyroidism)

5. Basis for clubbing
• Megakaryocyte continually emerge from bone marrow but
are normally trapped by pulmonary capillary bed &
fragmented there into platelet before entering systemic
circulation.
• But in neoplastic & inflammatory pulmonary disorders,
pulmonary capillaries are damaged. So, megakaryocyte/
megakaryocyte fragments enter systemic circulation & get
impacted in fingertip circulation, where they release VEGF
(Vascular endothelial growth factor) & PDGF (Platelet
derived growth factor). These growth factors increase blood
flow & connective tissue changes of clubbing.
• This could explain the clubbing associated with pulmonary
disorders. But what about clubbing associated with CVS/GIT
disorders ?

6. • Well, in cyanotic congenital heart diseases, there is right to
left intracardiac shunting of blood, so the pulmonary
capillary bed is bypassed.
So what then ? The rest of the mechanism is same as
described earlier i.e. there is peripheral impaction of
megakaryocyte & platelet clumps, release of VEGF &
PDGF which contribute to clubbing.
• In Subacute bacterial endocarditis, platelets clumps break off
valves & get impacted distally that play a role in clubbing.
• In liver disease, there are multiple small pulmonary
arteriovenous anastomoses that allow large particles through.
• In inflammatory bowel disease, increased circulating
platelets aggregates as well as an increase number of
platelets is noted, that contribute in clubbing.

7. Lets summarize the basis for clubbing

8. References
• https://www.ncbi.nlm.nih.gov/pmc/articles/PMC35
19022/
• https://www.ncbi.nlm.nih.gov/books/NBK366/
• https://pubmed.ncbi.nlm.nih.gov/8344332/