Hypothesis: is the skin and tissue loss associated with septic purpura fulminans temperature related? Parallels with the anatomical distribution of frostbite.
Purpura fulminans is a life threatening complication of many septic states, most notably meningococcaemia. It can also occur due to congenital deficiency of anticoagulant proteins. The pathophysiology of purpura fulminans is complex and not fully understood, but involves abnormalities of coagulation pathways, damage to vessel walls, and abnormal vasoconstriction which may lead to ischaemia and organ dysfunction. After the acute illness has resolved purpuric lesions may lead to extensive tissue loss and prolonged morbidity. Although vascular beds throughout the body are affected, and lesions can be seen in all areas of the skin, the distribution of permanent lesions is often confined to the peripheries, resulting in amputation of digits, hands and feet, or even limbs. Many pharmacological strategies have been used in attempts to reduce the tissue loss, but as yet none have proved to be consistently safe and effective. The distribution of this tissue loss is remarkably similar to that seen in frostbite, and raises the hypothesis that local temperature may have some contributing effect on the severity of these lesions. Hypothermia is known to be associated with vasoconstriction (in an attempt to preserve core temperature) and abnormalities of coagulation. This generally leads to an anticoagulated state, however the severe vasoconstriction and hypovolaemia associated with the early (pre-resuscitation) phases of acute sepsis results in peripheral skin temperatures approaching ambient. The effect on coagulation at these temperatures is not as well understood, but recent work has suggested increased platelet aggregation, adverse effects on blood rheology and increased intravascular thrombosis at temperatures of 31-34 degrees C. We hypothesise that low temperature leads to worsening of purpuric lesions and that active warming of the peripheries may reduce the tissue loss associated with resolving purpuric illnesses.
Oram
John
J
Anaesthesia and Intensive Care, Leeds General Infirmary, Gt George St., Leeds LS1 3EX, United Kingdom. johnoram1@googlemail.com
Bodenham
Andrew
A
D005627:Frostbite / Q000503:physiopathology*; D006801:Humans; D011695:IgA Vasculitis / Q000209:etiology* / Q000503:physiopathology; D008954:Models, Biological; D018805:Sepsis / Q000150:complications*; D012871:Skin Diseases / Q000209:etiology*; D013696:Temperature