SUN-617 - Bullous Diabeticorum During Critical Illness in Type 2 Diabetes

Background

Bullous diabeticorum is a rare, spontaneous, noninflammatory blistering disorder in patients with longstanding diabetes. It is underrecognized and may mimic drug eruptions, bullous pemphigoid, or SJS/TEN. Accurate identification is critical in hospitalized patients on multiple new medications, where misdiagnosis may lead to inappropriate treatment changes.

Case Presentation

An 88-year-old man with poorly controlled type 2 diabetes (HbA1c 9.0%), diabetic neuropathy, CAD, and PAD presented with altered mental status, hypotension, and hyperglycemia (glucose >500 mg/dL). Workup revealed elevated beta-hydroxybutyrate, lactic acidosis, and AKI. He was admitted to the ICU for DKA and septic shock from candidemia secondary to pyelonephritis. Management included IV fluids, vasopressors, insulin, corticosteroids, and antimicrobials.

During recovery, he developed abrupt-onset blistering over both feet, including two large tense bullae on the dorsum and posterior heel of the right foot, one on the left dorsum, and several smaller bullae on the distal lower legs. Exam showed bilateral 3+ pitting edema. The bullae were nonhemorrhagic, without surrounding erythema, mucosal involvement, diffuse rash, or epidermal detachment.
Given temporal association with piperacillin–tazobactam and caspofungin, drug eruption was initially suspected. Dermatology, infectious disease, and pharmacy were consulted. Medication review and serial exams were inconsistent with SJS/TEN or drug-induced blistering. Based on acral distribution, tense morphology, lack of inflammation, and longstanding diabetes, bullous diabeticorum was diagnosed. Lesions were managed conservatively with local wound care, edema control, and glycemic optimization, without secondary infection or surgical need.

Discussion

Bullous diabeticorum presents as sudden, painless, tense bullae on the distal extremities, typically the feet. The pathogenesis remains incompletely understood but is thought to involve a combination of diabetic microangiopathy, peripheral neuropathy, impaired dermal–epidermal adhesion, and increased susceptibility to minor trauma.
In this patient, chronic hyperglycemia, acute metabolic derangement, critical illness, and lower-extremity edema likely contributed. Misdiagnosis as a drug eruption can lead to unnecessary discontinuation of essential antimicrobials. Lesion morphology, distribution, and absence of mucocutaneous involvement are key to accurate diagnosis.

Conclusion

Bullous diabeticorum should be included in the differential diagnosis of new-onset acral bullae in patients with diabetes during hospitalization, particularly in the context of hyperglycemic crisis or severe systemic illness. Accurate bedside recognition can prevent unnecessary changes in medical therapy and underscores the systemic impact of chronic dysglycemia.

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