Clubbing of the fingers or toes (also called acropachy) refers to certain changes in fingernails or toenails that occur due to an underlying condition. These changes can include:
- softening of the nail beds, which makes the nails seem to float instead of being attached
- an increase in the angle between the cuticle and the nail
- enlarging or bulging of the tip of the finger, which may also be red and warm
- downward curving of the nail
CLUBBING MAY BE HEREDITARY OR CAUSED DUE TO CERTAIN ACQUIRED CONDITIONS.
IT MAY BE UNILATERAL OR BILATERAL OR OCCUR IN ONE FINGER OR ALL FINGERS.
DIFFERENT PATTERN OF CLUBBING TELLS US ABOUT DIFFERENT UNDERLYING CONDITIONS,
EG. UNILATERAL CLUBBING IS MOSTLY CAUSED BECAUSE OF ANEURYSM OF AORTA.
UNDERLYING CAUSES OF CLUBBING:
- lung cancer
- heart defects at birth
- chronic lung infections
- heart chamber and heart valve infections
- celiac disease (an autoimmune disease of the small intestine that prevents it from absorbing gluten from food)
- cirrhosis of the liver
- Graves’ disease (an autoimmune disease that causes the thyroid gland to overproduce hormones)
- several types of cancer, including liver and gastrointestinal cancers
copied from http://www.healthline.com/symptom/finger-clubbing
BUT WHY DOES THE ABOVE CONDITION LEAD TO CLUBBING ?
Clubbing occurs because of increase in soft tissue mass under the nail plate. This occurs due to decreased amount of oxygen in blood. Exact mechanism of how decreased blood oxygen causes clubbing is unknown.
BUT HERE ARE THE PROPOSED HYPOTHESIS
Shneerson (1981) reviews the four most likely mechanisms underlying clubbing. They include a circulating vasodilator, tissue hypoxia, a neurocirculatory reflex, and genetic factors. For acquired clubbing, the most likely mechanism postulates a neurocirculatory reflex, leading to increased blood flow through multiple arteriovenous shunts in the distal phalanges. Increased blood flow then leads to tissue hypertrophy and hyperplasia on a nutritional basis. The evidence for this mechanism is threefold: (1) clubbing may resolve after vagotomy; (2) disturbances of the vasculature such as arteriovenous fistulae and aneurysms are associated with its development; and (3) Racoceanu (1971) and others have demonstrated increased blood flow to digitial capillaries in acquired clubbing.
Flavell (1956) first proposed the neurocirculatory reflex theory to explain hypertrophic osteoarthropathy, after he observed that severing the vagus nerve could reverse it even when the underlying lung cancer was unresectable. According to this theory, there is a reflex in which afferent impulses travel by the vagus nerve from the inciting focus (such as a lung tumor) to the central nervous system. The efferent limb of the proposed reflex is unknown, but presumably some humoral substance or neural impulse mediates the vascular changes, leading to hypertrophy of the fibroconnective tissues. Others have supported such a mechanism by observations that the visceral organs in which associated diseases occur are all innervated by the glossopharyngeal or vagus nerves.
Strong support for this theory has also come from a study by Gold and colleagues (1979). They studied a unique case of unilateral clubbing secondary to a posttraumatic aneurysm of the ulnar artery, which resolved after resection of the aneurysm. Using the contralateral hand of the otherwise healthy patient, they conducted detailed studies of the microcirculation by Doppler flow recordings, differential pulse pressure measurements, angiography, measurements of reactive hyperemia, and differential capillary blood gas determinations. They interpreted their findings of increased blood flow, decreased peripheral resistance, and increased oxygenation to support the neurocirculatory reflex mechanism. They postulated that the efferent limb of the reflex was cholinergic fibers of the autonomic sympathetic innervation of digital arteriovenous shunts.
However, different mechanisms may cause acquired and hereditary clubbing. Some workers have found that digital capillary blood flow, measured by washout of krypton-85 solution, is increased in acquired clubbing but normal in hereditary clubbing. An alternative explanation for this finding may be that in hereditary clubbing the condition has been studied only after the condition has stopped progressing; the physiologic findings might be similar in the active phase
