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DR12.5 | Cutaneous Adverse Drug Reaction Primary Care — SDL Guide (Part 2)

Primary Care Response to DRESS

A four-panel medical diagram summarizes primary-care management of DRESS: stop the culprit drug, avoid related drugs, investigate organ involvement, refer urgently, and monitor liver and renal function. — **Panel A:** Primary-care pathway showing suspected DRESS, immediate drug cessation, avoidance of same-class drugs, baseline tests, urgent referral, and continued monitoring over weeks. **Panel B:** Human body overview showing multiorgan involvement: skin eruption, liver hepatitis, renal involvement, and eosinophilia. **Panel C:** Baseline investigations showing full blood count for eosinophilia, liver function tests for hepatitis, and renal function tests for renal involvement. **Panel D:** Treatment boundary showing symptomatic skin care with emollients and antihistamines in primary care, and systemic corticosteroids reserved for specialist decision.

DRESS sits at the severe end of the spectrum, and the primary-care response is shaped by the fact that it is a multiorgan disease with a tendency to persist. The immediate steps are to stop the culprit drug at once — and, importantly, to avoid restarting any drug of the same class, because cross-reactivity within a class (notably the aromatic anticonvulsants) is common — and to obtain baseline investigations that reveal the extent of organ involvement: a full blood count for eosinophilia, and liver and renal function tests, since hepatitis is the commonest internal complication. The patient should be kept under observation and the affected skin treated symptomatically with emollients and antihistamines while these results guide the urgency of referral.

The key boundary for the primary-care doctor is that the definitive treatment of DRESS — systemic corticosteroids — is a specialist decision made after the diagnosis is confirmed and organ involvement assessed; it is not something to be started reflexively at first contact. The correct primary-care pathway is therefore: stop the drug, establish baseline organ function, treat the skin symptomatically, refer urgently to a dermatologist or physician, and arrange continued monitoring of liver and renal function because organ inflammation can flare over the following weeks. Recognising that DRESS needs specialist-led systemic therapy, not a quick course of steroids from the clinic, is part of competent primary care.

Stop the culprit drug immediately; avoid the whole drug class (cross-reactivity, e.g. aromatic anticonvulsants).
Baseline investigations: full blood count (eosinophilia), liver and renal function (organ involvement).
Symptomatic skin care: emollients, antihistamines.
Refer urgently: systemic corticosteroids for DRESS are a specialist decision after diagnosis is confirmed.
Continued monitoring: organ function over the following weeks, as DRESS can flare.

SJS/TEN: Burns-Model Stabilisation and Emergency Transfer

Infographic showing SJS/TEN emergency management using a burns-model approach with drug cessation, IV fluids, skin protection, mucosal care, documentation, and urgent transfer. — **Panel A:** SJS/TEN patient with widespread epidermal detachment, denuded skin, heat loss arrows, fluid loss arrows, IV crystalloid infusion, burns-model analogy. **Panel B:** Immediate primary-care sequence: stop culprit drug, secure IV access, crystalloid resuscitation, analgesia, warmth and temperature control. **Panel C:** Skin care with fragile epidermis, non-adherent dressings, gentle handling, no primary-care debridement. **Panel D:** Mucosal involvement: oral erosions requiring nil by mouth and hydration attention; ocular involvement requiring urgent ophthalmology to prevent scarring and blindness. **Panel E:** Transfer and documentation: estimated body surface area detachment, SCORTEN severity, ambulance transfer to burns unit or ICU, no systemic corticosteroids or immunomodulators in primary care.

SJS/TEN is a dermatological emergency, and the primary-care response is built on a single analogy: because the patient has lost the epidermal barrier, manage it like a major burn while arranging urgent transfer to a burns unit or intensive care. The sequence begins, as always, with stopping the culprit drug immediately. Then secure intravenous access and begin fluid resuscitation with crystalloid, because fluid loss through the denuded skin is the immediate threat, just as in a burn. Provide skin and wound care with non-adherent dressings, handling the fragile skin gently and avoiding any debridement at primary-care level. Maintain warmth and temperature control, because the lost barrier cannot regulate heat, and give adequate analgesia, as the raw skin is extremely painful.

The mucosal complications need specific attention: if there is oral mucosal involvement the patient may need to be kept nil by mouth with attention to hydration, and eye involvement demands urgent ophthalmology input because ocular scarring can cause permanent blindness. Throughout, document the estimated body surface area of detachment and, where possible, the SCORTEN severity, which guide the receiving unit. The decisive boundary is that the primary-care doctor does not start systemic corticosteroids or other immunomodulatory therapy — their use in TEN is debated and potentially harmful, and is a specialist decision; the primary-care role is to stabilise, support and transfer. Arrange emergency transfer without delay, continuing fluids and supportive care en route.

A step-by-step flowchart shows primary-care emergency management of suspected SJS/TEN, from recognition and stopping the drug through supportive care, SCORTEN assessment, ophthalmology alert, transfer, and avoiding corticosteroids without specialist advice. — **Panel A:** Decision diamond for suspected SJS/TEN recognition; numbered boxes for stopping culprit drug, IV fluids, non-adhesive dressings, warming and temperature monitoring, analgesia, nil by mouth for oral mucosal involvement, ophthalmology alert, SCORTEN and BSA documentation, emergency transfer to burns unit/ICU, and final warning against systemic corticosteroids or immunomodulators without specialist advice..

Stop the culprit drug immediately.
Burns-model care: IV fluids (crystalloid) for skin losses; non-adherent dressings, gentle handling, no debridement; warmth and temperature control; analgesia.
Mucosal care: nil by mouth if oral involvement; urgent ophthalmology for eye involvement.
Assess and document: BSA of detachment and SCORTEN.
Do NOT start systemic corticosteroids/immunomodulators in primary care — specialist decision.
Arrange emergency transfer to a burns unit/ICU, continuing care en route.

SELF-CHECK

A patient with toxic epidermal necrolysis (about 35% BSA detachment) presents to a primary health centre. Which action is NOT appropriate at the primary-care level?

A. Stop the culprit drug immediately

B. Begin intravenous fluid resuscitation and gentle wound care

C. Start high-dose systemic corticosteroids before transfer

D. Arrange urgent ophthalmology input and emergency transfer to a burns unit

Reveal Answer

Answer: C. Start high-dose systemic corticosteroids before transfer

Starting systemic corticosteroids in TEN is a specialist decision — their benefit is debated and they may be harmful — and is NOT the primary-care doctor's role. The correct primary-care actions are to stop the drug, give burns-model supportive care (fluids, wound and mucosal care, analgesia, warmth), and arrange urgent transfer.

Differential and Investigations in Primary Care

A four-panel medical diagram compares SJS/TEN, SSSS, erythema multiforme, and DRESS while summarizing primary-care investigations and referral-level biopsy. — **Panel A:** Primary-care decision pathway showing suspected SJS/TEN, suspected DRESS, likely mimics, mucosal erosions, facial edema, eosinophilia, body surface area estimate, urgent referral. **Panel B:** Skin cross-sections comparing TEN full-thickness epidermal necrosis with subepidermal separation versus SSSS superficial intraepidermal split; epidermis, dermis, split level, mucosal erosion absent in SSSS. **Panel C:** Clinical differential insets showing erythema multiforme target lesions, DRESS morbilliform rash with facial edema, and SJS/TEN dusky rash with blistering and oral mucosal erosions. **Panel D:** Primary-care investigations showing full blood count, eosinophilia, liver function, renal function, electrolytes, clinical body surface area grading, and referral-centre skin biopsy.

Correct primary-care management depends on not confusing a severe drug reaction with its mimics, since the treatment paths diverge sharply. The most important differential of TEN is staphylococcal scalded skin syndrome (SSSS), a toxin-mediated condition that mainly affects young children, produces a more superficial split with perioral crusting, and — crucially — does not cause the true mucosal erosions of SJS/TEN; SSSS needs antistaphylococcal antibiotics, not burns-type care for an immune reaction. Erythema multiforme, with its classic target lesions and frequent association with herpes simplex, is usually a milder, more limited condition that should not be over-treated as TEN. A widespread morbilliform drug rash with fever and a swollen face should prompt thought of DRESS rather than a simple exanthem.

The investigations available at primary-care level are modest but useful. A full blood count can reveal the eosinophilia of DRESS; basic biochemistry (liver and renal function, electrolytes) detects organ involvement and the metabolic disturbance of extensive skin loss; and clinical estimation of body surface area grades SJS/TEN. Definitive tests such as skin biopsy (to confirm the level of the epidermal split and distinguish TEN from SSSS) are usually performed at the referral centre. The primary-care doctor's task is to use simple clinical discrimination and the available bedside and basic laboratory clues to reach a working diagnosis, treat accordingly, and refer — not to await a tissue diagnosis before acting.

Three-panel labeled comparison of SJS, SSSS, and erythema multiforme highlighting lesion morphology, mucosal involvement, Nikolsky sign, and epidermal cleavage level. — **Panel A:** Drug-induced SJS: atypical target lesions, mucosal erosions, positive Nikolsky sign, skin detachment, full-thickness epidermal necrosis, subepidermal split.. **Panel B:** SSSS: young child, diffuse erythema, superficial flaccid blisters, perioral crusting, no true mucosal erosions, positive Nikolsky sign, superficial intraepidermal split at stratum granulosum.. **Panel C:** Erythema multiforme: classic three-zone target lesions, acral distribution, limited mucosal involvement, post-HSV trigger, no widespread epidermal detachment.. **Bottom strip:** Key distinctions: drug trigger vs staphylococcal toxin vs HSV trigger; severe mucosal erosions vs spared mucosa vs limited mucosa; subepidermal detachment vs superficial intraepidermal cleavage vs localized interface reaction..

SSSS: young children, superficial split, perioral crusting, no true mucosal erosions — needs antibiotics, not burns care.
Erythema multiforme: target lesions, often post-herpes, usually limited — do not over-treat as TEN.
DRESS: morbilliform rash + fever + facial oedema — think DRESS, not simple exanthem.
Primary-care tests: FBC (eosinophilia), biochemistry (organ/metabolic), BSA estimation; biopsy at referral centre.