While pasteurization killed bacteria, it also destroyed vitamin C. This was eventually resolved by supplementing with onion juice or cooked potatoes. Native Americans helped save some newcomers from scurvy by directing them to eat wild onions. 20th century
By the early 20th century, when Robert Falcon Scott made his first expedition to the Antarctic (1901–1904), the prevailing theory was that scurvy was caused by "ptomaine poisoning", particularly in tinned meat. However, Scott discovered that a diet of fresh meat from Antarctic seals cured scurvy before any fatalities occurred.In 1907, an animal model which would eventually help to isolate and identify the "antiscorbutic factor" was discovered. Axel Holst and Theodor Frølich, two Norwegian physicians studying shipboard beriberi contracted by ships crews in the Norwegian Fishing Fleet, wanted a small test mammal to substitute for the pigeons then used in beriberi research. They fed guinea pigs their test diet of grains and flour, which had earlier produced beriberi in their pigeons, and were surprised when classic scurvy resulted instead. This was a serendipitous choice of animal. Until that time, scurvy had not been observed in any organism apart from humans and had been considered an exclusively human disease. Certain birds, mammals, and fish are susceptible to scurvy, but pigeons are unaffected, since they can synthesize ascorbic acid internally. Holst and Frølich found they could cure scurvy in guinea pigs with the addition of various fresh foods and extracts.
It is thought that in disorders where there is right-to-left shunting or lung malignancy, the megakaryocytes can bypass the breakdown within the pulmonary circulation and enter the systemic circulation. They are then trapped within the capillary beds within the extremities, such as the digits, and release platelet-derived growth factor (PDGF) and vascular endothelial growth factor (VEGF). PDGF and VEGF have growth promoting properties and cause connective tissue hypertrophy and capillary permeability. Diagnosis
When clubbing is observed, pseudoclubbing should be excluded before making the diagnosis. Associated conditions may be identified by taking a detailed medical history—particular attention is paid to lung, heart, and gastrointestinal conditions—and conducting a thorough clinical examination, which may disclose associated features relevant to the underlying diagnosis. Additional studies such as a chest X-ray and a chest CT-scan may reveal otherwise asymptomatic cardiopulmonary disease. Stages
Clubbing is present in one of five stages:
No visible clubbing - Fluctuation (increased ballotability) and softening of the nail bed only. No visible changes of nails. Mild clubbing - Loss of the normal <165° angle (Lovibond angle) between the nailbed and the fold (cuticula). Schamroths window (see below) is obliterated. Clubbing is not obvious at a glance. Moderate clubbing - Increased convexity of the nail fold. Clubbing is apparent at a glance. Gross clubbing - Thickening of the whole distal (end part of the) finger (resembling a drumstick)
Hypertrophic osteoarthropathy - Shiny aspect and striation of the nail and skinSchamroths sign or Schamroths window test (originally demonstrated by South African cardiologist Leo Schamroth on himself) is a popular test for clubbing.