A 58-year-old Indian male presents with acute onset diffuse erythema and fine scaling involving >90% of his body surface area, as shown by the structure marked **A** in the diagram. He reports fever, tachycardia, and severe pruritus. His past medical history includes poorly controlled psoriasis for which he had recently discontinued oral methotrexate due to financial constraints. On examination, he has peripheral edema, alopecia, and nail dystrophy. Which of the following is the MOST LIKELY systemic complication requiring immediate management in this patient?
A. Spontaneous bacterial peritonitis from ascites
B. Fluid and electrolyte loss leading to dehydration and hypovolemic shock
C. Acute myocardial infarction from coronary vasospasm
D. Acute renal failure from direct glomerulonephritis
Explanation
Why "Fluid and electrolyte loss leading to dehydration and hypovolemic shock" is right
Erythroderma (confluent erythema and scaling involving >90% BSA) is a dermatologic emergency with mortality of 3–64% depending on etiology. The defining pathophysiology of erythroderma includes massive FLUID AND ELECTROLYTE LOSS through the damaged skin barrier, leading to dehydration, hypovolemia, and shock. This is one of the four cardinal systemic complications (along with hypothermia, high-output cardiac failure, and secondary infection) that drive mortality. In this case, the patient's recent methotrexate withdrawal precipitated psoriasis-to-erythroderma transformation—a classic trigger—and his acute presentation with fever, tachycardia, and edema reflects the acute fluid shifts and electrolyte derangement characteristic of erythroderma. Immediate IV fluid and electrolyte correction is a cornerstone of management (Bolognia Dermatology 5e).
Why each distractor is wrong
Acute myocardial infarction from coronary vasospasm: While erythroderma can cause HIGH-OUTPUT CARDIAC FAILURE (from increased metabolic demand and fluid shifts), acute MI from vasospasm is not a recognized systemic complication of erythroderma. Cardiac complications are secondary to volume overload and metabolic stress, not primary coronary events.
Spontaneous bacterial peritonitis from ascites: Ascites is not a feature of erythroderma. Although protein loss (hypoalbuminemia) occurs, it does not cause ascites or peritonitis. This is a complication of cirrhosis, not erythroderma.
Acute renal failure from direct glomerulonephritis: While acute kidney injury can occur in severe erythroderma from dehydration and prerenal mechanisms, direct glomerulonephritis is not a recognized pathophysiologic feature. Renal complications are secondary to hypovolemia and electrolyte disturbance, not immune-mediated glomerular disease.
High-YieldNEET PG
Erythroderma mortality stems from FLUID/ELECTROLYTE LOSS, HYPOTHERMIA, HIGH-OUTPUT CARDIAC FAILURE, PROTEIN LOSS, and SECONDARY INFECTION—remember these five for any erythroderma question.
Bolognia Dermatology 5e; British Journal of Dermatology Guidelines
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