The speed of blood flow within a blood vessel and the rate of delivery of blood to capillaries (perfusion) are the main factors that determine whether dissolved gas is taken up by tissue bubbles or circulation bubbles for bubble growth. Pathophysiology
The primary provoking agent in decompression sickness is bubble formation from excess dissolved gases. Various hypotheses have been put forward for the nucleation and growth of bubbles in tissues, and for the level of supersaturation which will support bubble growth. The earliest bubble formation detected is subclinical intravascular bubbles detectable by doppler ultrasound in the venous systemic circulation. The presence of these "silent" bubbles is no guarantee that they will persist and grow to be symptomatic.Vascular bubbles formed in the systemic capillaries may be trapped in the lung capillaries, temporarily blocking them. If this is severe, the symptom called "chokes" may occur. If the diver has a patent foramen ovale (or a shunt in the pulmonary circulation), bubbles may pass through it and bypass the pulmonary circulation to enter the arterial blood. If these bubbles are not absorbed in the arterial plasma and lodge in systemic capillaries they will block the flow of oxygenated blood to the tissues supplied by those capillaries, and those tissues will be starved of oxygen. Moon and Kisslo (1988) concluded that "the evidence suggests that the risk of serious neurological DCI or early onset DCI is increased in divers with a resting right-to-left shunt through a PFO.
Granuloma faciale  is an uncommon benign chronic skin disease of unknown origin characterized by single or multiple cutaneous nodules, usually occurring over the face. : 836  Occasionally, extrafacial involvement is noted, most often on sun-exposed areas. Diagnosis
Skin biopsy for histopathology: 
Focal LCV, diffuse dermal neutrophilia with leukocytoclasia, tissue eosinophilia & perivascular fibrosis. Differential diagnosis
The disease mimics many other dermatoses and can be confused with conditions, such as sarcoidosis, discoid lupus erythematosus, mycosis fungoides, and fixed drug eruption. Treatment
Topical corticosteroid,
Intralesional corticosteroid,
Dapsone,
Colchicine,
Antimalarial,
Pulse dye laser,
Carbon dioxide laser. History
GF was first described in 1945 by John Edwin Mackonochie Wigley (1892–1962). See also
Cutaneous small-vessel vasculitis
List of cutaneous conditions

References


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