Non-burn dermatologic emergencies, although less common than burn injuries, are associated with high morbidity and mortality due to the extensive loss of the skin barrier. These conditions often mimic burn-related pathophysiology and demand urgent, multidisciplinary care. Optimal outcomes are typically achieved at specialised burn centres, but limited availability means that initial evaluation and management usually take place in non-specialised settings.
A recent review aims to provide intensivists with a practical framework for triaging and managing these emergencies while awaiting transfer.
Patients with significant skin loss face numerous systemic complications, including fluid and electrolyte imbalance, thermoregulatory failure, high metabolic demand, and increased susceptibility to infection. Conditions such as toxic epidermal necrolysis (TEN), pemphigus vulgaris (PV), and purpura fulminans (PF) are among the most severe and often require rapid transfer to burn centres. Triage criteria include epidermal detachment approaching 25% of body surface area (BSA), mucosal or airway involvement, and signs of systemic decompensation. In cases where the treating facility lacks resources or expertise, transfer should still be prioritised even if criteria are not met.
A systematic approach to management begins with a comprehensive history and physical exam, emphasising BSA estimation, symptom progression, medication exposure, and mucosal involvement. Medication review is essential, with discontinuation of non-critical drugs. BSA estimation tools such as the Lund-Browder diagram and rule of nines may be used.
Airway involvement, particularly in TEN or PV, markedly increases mortality risk. Evaluation should include video laryngoscopy and, if available, fiberoptic nasal endoscopy. Early intubation is critical when airway compromise is suspected. Non-adhesive methods for securing endotracheal tubes are preferred to avoid further mucosal injury.
Fluid resuscitation is necessary to counter increased transepidermal water loss, which can reach 3–4 litres daily in patients with >50% BSA involvement. Though the Parkland formula is used in burns, non-burn skin failure typically requires ~30% less fluid due to preserved capillary integrity. Crystalloids are standard, although no superiority over colloids has been demonstrated.
Nutritional support is equally important, given elevated metabolic demand and impaired absorption. Energy requirements start at 1500–2000 kcal/day, increasing up to 3500–4000 kcal. High-protein enteral feeding (2–3 g/kg/day) is recommended. If oral intake is insufficient, feeding tubes should be promptly initiated.
Loss of thermoregulation mandates maintaining an ambient room temperature around 30°C. External warming should avoid direct contact with denuded skin.
Wound care is central to reducing infection-related mortality. Gentle cleansing, appropriate ointments (e.g., petroleum jelly, antibiotics, or corticosteroids), and layered dressing techniques are emphasised. The goal is to promote healing while preventing trauma and infection.
Stevens-Johnson Syndrome (SJS) and Toxic Epidermal Necrolysis (TEN) are rare but severe skin reactions, often triggered by medications or infections. Both conditions involve the immune system attacking the skin and mucous membranes, leading to symptoms like fever, flu-like signs, and painful blistering. The primary difference between them lies in the extent of skin involvement: SJS affects less than 10% of the body surface area, while TEN affects more than 30%.
Medications are the leading cause of SJS and TEN, with 80–95% of TEN cases attributed to drug reactions. Notable drugs include:
- Antibiotics (e.g., sulfonamides, penicillins)
- Anticonvulsants (e.g., carbamazepine, lamotrigine, phenytoin)
- Nonsteroidal anti-inflammatory drugs (NSAIDs)
- Allopurinol
- Antiretrovirals (e.g., nevirapine)
Infections, such as those caused by Mycoplasma pneumoniae, can also trigger these conditions.
Certain genetic factors increase susceptibility. For instance, the HLA-B1502 allele is linked to carbamazepine-induced SJS/TEN in some Asian populations, and HLA-B5801 is associated with allopurinol-induced reactions. Individuals with HIV have a significantly higher risk—up to 1,000 times greater—of developing SJS/TEN, possibly due to immune system alterations.
Diagnosis involves clinical evaluation, medical history, and sometimes skin biopsies. Immediate discontinuation of the offending drug is crucial. Treatment typically requires hospitalisation, often in intensive care or burn units, focusing on supportive care to manage symptoms and prevent complications like infections.
The severity of SJS and TEN varies. SJS has a mortality rate of approximately 4.8%, while TEN's rate is around 19.4% Early recognition and prompt medical intervention are vital for improving outcomes.
Non-burn dermatologic emergencies require prompt recognition, systematic management, and early transfer to burn centres when indicated. Given the lack of standardised triage protocols, this review offers evidence-based strategies to guide initial care and optimise outcomes for critically ill patients with severe skin involvement.
Source: Ann Am Thorac Soc
Image Credit: iStock
