The production of ketones is strongly regulated by insulin and an absolute or relative lack of insulin underlies the pathophysiology of ketoacidosis. Insulin is a potent inhibitor of fatty acid release, so insulin deficiency can cause an uncontrolled release of fatty acids from adipose tissue. Insulin deficiency can also enhance ketone production and inhibit peripheral use of ketones. This can occur during states of complete insulin deficiency (such as untreated diabetes) or relative insulin deficiency in states of elevated glucagon and counter-regulatory hormones (such as starvation, heavy chronic alcohol use or illness).Acetoacetic acid and β-hydroxybutyrate are the most abundant circulating ketone bodies. Ketone bodies are acidic; however, at physiologic concentrations, the bodys acid/base buffering system prevents them from changing blood pH. Management
Treatment depends on the underlying cause of the ketoacidosis. Diabetic ketoacidosis is resolved with insulin infusion, intravenous fluids, electrolyte replacement and supportive care. Alcoholic ketoacidosis is treated with intravenous dextrose and supportive care and usually does not require insulin. Starvation ketoacidosis can be resolved with intravenous dextrose with attention to electrolyte changes that can occur with refeeding syndrome. Epidemiology
Certain populations are predisposed to develop ketoacidosis including people with diabetes, people with a history of prolonged and heavy alcohol use, pregnant women, breastfeeding women, children, and infants. People with diabetes that produce very little or no insulin are predisposed to develop ketoacidosis, especially during periods of illness or missed insulin doses.
Erythema multiforme (EM) is a skin condition that appears with red patches evolving into target lesions, typically on both hands.It is a type of erythema possibly mediated by deposition of immune complexes (mostly IgM-bound complexes) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure. It is an uncommon disorder, with peak incidence in the second and third decades of life. The disorder has various forms or presentations, which its name reflects (multiforme, "multiform", from multi- + formis). Target lesions are a typical manifestation. Two types, one mild to moderate and one severe, are recognized (erythema multiforme minor and erythema multiforme major). Erythema multiforme was first described by von Hebra in 1860. Signs and symptoms
The condition varies from a mild, self-limited rash (E. multiforme minor) to a severe, life-threatening form known as erythema multiforme major (or erythema multiforme majus) that also involves mucous membranes. Consensus classification:
Erythema multiforme minor—typical targets or raised, edematous papules distributed acrally
Erythema multiforme major—typical targets or raised, edematous papules distributed acrally with involvement of one or more mucous membranes; epidermal detachment involves less than 10% of total body surface areaStevens–Johnson syndrome and toxic epidermal necrolysis used to be considered part of the erythema multiforme spectrum, but that is no longer the case.The mild form usually presents with mildly itchy (but itching can be very severe), pink-red blotches, symmetrically arranged and starting on the extremities. It often takes on the classical "target lesion" appearance, with a pink-red ring around a pale center.