Descriptions of cyanopathia or Morbus caeruleus (cyanosis) have populated medical literature since the time of Hippocrates, although the actual pathophysiology behind its development eluded physicians until the advent of objective anatomy and physiology. Morgagni, “accurate anatomist,” philosopher, and one of the fathers of contemporary medicine, is often credited with having first described cyanosis (in association with stasis due to pulmonic stenosis [1761]),(1) however, it was actually deSenac, personal physician to King Louis XV (and the first to elucidate the relationship between atrial fibrillation and mitral stenosis), who first described the pathophysiology of cyanosis (albeit not entirely correctly!) in 1749.(2) It was not until over 2 centuries later, however, that Christen Lundsgaard actually quantified the amount of deoxygenated hemoglobin that was required to produce that bluish discoloration that produces the clinical finding of cyanosis.(2)Features of Cyanosis
Cyanosis is an abnormal bluish discoloration of the skin and mucous membranes; it is caused by high levels of deoxygenated (reduced) hemoglobin (or its derivatives) circulating within the superficial dermal capillaries and subpapillary venous plexus (not, as commonly taught, the deeper arteries and veins).(1) Hypoxemia, not to be confused with hypoxia (which reflects tissue oxygenation), is the deficient oxygenation of blood that leads to cyanosis.(3)
Whether or not cyanosis is apparent to the human eye depends on dermal thickness, cutaneous pigmentation, and state of the cutaneous capillaries.(4) In light of this, cyanosis is best appreciated in areas of the body where the overlying epidermis is thin and the blood vessel supply abundant, such as the lips, malar prominences (nose and cheeks), ears, and oral mucous membranes (buccal, sublingual); it is better appreciated in fluorescent lighting.(1)
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— Sarah M. McMullen, MD, Ward Patrick, MD
This article originally appeared in the March 2013 issue of The American Journal of Medicine.
