Erythema Multiforme (EM)

Tell it apart from SJS and TEN first - This is the decision that sets the whole plan. EM has typical symmetric acral targets of three concentric zones, spares the trunk, and heals without scarring; even EM major stays under 10% body surface area. Stevens-Johnson syndrome (SJS) involves up to 10% of body surface area with asymmetric, predominantly axial target-like lesions of only two concentric zones and purpuric evolution, is usually drug-driven, and can progress to toxic epidermal necrolysis (TEN) — EM does not. If what you are looking at is axial, purpuric, and atypical, stop calling it EM and manage the patient as SJS/TEN.

Look in the mouth before you commit to an airway - Mucosal lesions start as bullae and turn quickly into painful erosions. Thick hemorrhagic crusts cover the lips and a fibrin-whitish coating lines the cheeks, palate, and genital mucosa. Do a direct oral exam preop — crusted, eroded mucosa bleeds and sloughs under a blade. Where the mouth is involved, a video laryngoscope buys the view without the leverage of a direct blade, and generous lubrication and an unhurried technique matter more than speed.

Mucosal involvement is where the pain is - Skin lesions are not painful, and some patients report burning instead. The mucosal erosions hurt. That points analgesia at the mouth and means oral airways, bite blocks, NG tubes, and TEE probes all cause real damage and real pain in a patient with oral involvement.

Hunt the trigger before you pick a drug - HSV-1 and HSV-2 and Mycoplasma pneumoniae lead the infectious causes; penicillins, cephalosporins, macrolides, sulfonamides, anti-tuberculosis agents, and antipyretics lead the drug list, and all offending drugs must be stopped immediately. Read the medication list against that list before choosing surgical prophylaxis — the antibiotic you would reach for by habit may be the one that caused this.

Cough and dyspnea point to the lungs - Pulmonary signs in EM usually reflect the Mycoplasma pneumoniae that triggered it. Get a chest x-ray; interstitial infiltrate is the finding. You are then anesthetizing someone with an active atypical pneumonia, not just a rash.

Volume and electrolytes - Extensive skin involvement causes dehydration, and painful mouth erosions make eating hard enough that patients lose weight. Check a basic metabolic panel — electrolytes are altered when the patient is dry or has developed renal failure. Correct the deficit before induction instead of chasing hypotension afterward. Blood work may also show mild leukocytosis, neutropenia, and mild anemia.

Keep them warm - Severe EM is managed like a burn, and these patients get hypothermic. Warming blanket, warmed IV fluids, a warm room from the start. Do not wait for the core temperature to fall before you act.

Access and asepsis - In severe cases central lines are avoided specifically to lower infection risk, and strict asepsis is the standard. Site peripheral access through unaffected skin, secure it without adhesive over lesions, and treat every line as a portal in a patient whose barrier is gone. Bacterial superinfection is one of the two things that turns EM dangerous; severe mucosal involvement is the other.

Protect the eyes deliberately - Ocular mucosa is involved and eye complications occur in up to 20% of patients — uveitis, conjunctivitis, scarring, panophthalmitis, and permanent blindness. Many already have dry eye and corneal scarring. Use ointment rather than taping across inflamed lids, and get an ophthalmology opinion before elective surgery when the eyes are involved.

Strictures change what you pass - Healing mucosa forms synechiae and strictures of the esophagus, urethra, vagina, and anus. An esophageal stricture changes how an NG tube or TEE probe goes down — expect resistance, and do not force anything.

Elective surgery waits out the acute phase - Severe cases go to the ICU. Debridement is avoided while lesions are still progressing, and re-epithelialization takes 7 to 21 days; healing runs 2 to 3 weeks for EM minor and 4 to 6 weeks for EM major, with mucosal lesions always slower. Recurrences are under 5% and mainly herpes-driven, so there is nothing to gain from operating electively during an active outbreak.

Know who does badly - Patients with HIV, on corticosteroids, otherwise immunosuppressed, after bone marrow transplant, and with lupus are predisposed to EM. Poor prognostic factors are renal dysfunction, prior bone marrow transplant, visceral involvement, and advanced age. Check a creatinine and review the transplant and immunosuppression history — those move your threshold for postponing.

Prophylaxis in the sick patient - Deep venous thrombosis and stress ulcer prophylaxis are recommended in severe EM. Confirm with the primary team exactly what the patient is receiving before any neuraxial technique is planned.

Erythema multiforme (EM) is an acute, sometimes recurrent cutaneous and mucosal hypersensitivity reaction. CD8 T lymphocytes and macrophages flood the dermo-epidermal junction and release cytokines that kill keratinocytes, producing a vacuolar interface dermatitis and, in advanced lesions, epidermal necrosis with subepidermal blisters. Herpes simplex virus (HSV) types 1 and 2 and Mycoplasma pneumoniae are the commonest triggers; drugs including penicillins, cephalosporins, macrolides, sulfonamides, anti-tuberculosis agents, and antipyretics account for the majority of cases overall. The classic lesion is the target — under 3 cm, three concentric rings, symmetric and acral on the palms, dorsa of the hands, feet, and extensor limbs, with the trunk usually spared. Mucous membranes are involved in 2 to 10% of patients, most often the mouth.