Dermatology — Drug Eruptions and the Unwell Patient with a Rash, NMC MBBS licence examination syllabus (Nepal Medical Council).
Most drug rashes are a nuisance. A few are the first sign that the patient is about to become critically ill.
The first dermatology chapter covered the conditions patients come to a clinic with. This one covers the rashes a doctor is most likely to cause or to miss — which is where the harm in dermatology actually happens.
A widespread red rash a week or two into a course of antibiotics is common, usually self-limiting, and usually needs nothing more than stopping the drug and explaining.
What matters is being able to spot the small number that are not that. Four features change the situation entirely:
Identifying which drug caused a reaction is a matter of timing, and the intuitive answer is often wrong.
A first exposure takes time to sensitise the immune system. So a rash appearing today may be caused by a drug started a week or two ago rather than the one started yesterday. Assuming the newest drug is the culprit can leave the real cause in place.
On re-exposure the reaction is faster and more severe. This is why a documented drug allergy is never re-prescribed "to see whether it really was that drug" — the test can produce a far worse reaction than the original.
Pressing a glass against a rash separates two mechanisms. A rash that blanches is dilated blood vessels — the pattern of most viral exanthems and drug rashes. A rash that does not blanch is blood that has left the vessels.
A non-blanching rash in an unwell patient means treat for meningococcal disease immediately — antibiotics first, investigations after. You do not need the diagnosis confirmed to start, and the delay involved in confirming it is what kills.And the rash is a late sign. A patient with meningococcal sepsis can be critically ill before any rash appears, so its absence is not reassurance. Waiting to see whether a rash develops before treating is waiting too long.
Non-blanching purpura in a patient who is well is a different problem — it raises low platelets, clotting disorders, vasculitis, and in children Henoch–Schönlein purpura. Still needs investigation, but not the same emergency response.
Topical steroids are among the most useful drugs in general practice and among the most poorly prescribed, in both directions.
Too strong, for too long, in the wrong place. Skin thins, stretch marks form, and blood vessels become visible. The face and flexures absorb far more than thick skin elsewhere, so a preparation that is safe on a palm can cause visible damage on a cheek.
Too weak, for too short a time. This is at least as common. The eczema never comes under control, the patient concludes that steroids do not work, and they stop using them — often reinforced by widespread anxiety about steroid use. An under-treated inflammatory skin disease causes more harm than a properly used steroid.
The error that is purely ours, though: putting a steroid on a rash that has not been diagnosed. On a fungal infection, a steroid removes the inflammation — so the rash looks better briefly — while the fungus spreads unchecked, producing an altered appearance that is harder to recognise afterwards.
So the prescription needs instructions: where to apply it, how much, how often, and for how long. A tube handed over without those produces one of the two errors above.
Generalised itch with nothing to see on the skin is a systemic question, not a dermatological one. Consider liver disease, kidney failure, thyroid disease, iron deficiency, lymphoma, and drugs.
The trap is that scratching creates its own findings. Excoriations, thickened skin and secondary infection are all consequences of the itch, and it is easy to treat them as though they were the diagnosis. Ask what came first — the itch or the rash.
And ask who else at home is itching. Scabies is the commonest missed cause of persistent itch, it is often not visible in an early or well-washed patient, and it cannot be cured by treating one person while their household remains infested. That question takes five seconds and changes management completely.
Urticaria — raised itchy weals that come and go, with individual lesions lasting hours rather than days. The key clinical division is whether there is angioedema involving the lips, tongue or throat, which threatens the airway and is managed as covered in the emergencies chapter. Weals that persist unchanged for days, or that bruise as they fade, are not ordinary urticaria and need review.
A rash in an immunosuppressed patient behaves differently. Infections that would be trivial otherwise can disseminate, and the usual inflammatory signs may be muted — so a patient on chemotherapy, on long-term steroids, or with advanced HIV deserves a lower threshold for assuming a rash is serious.
No surface area thresholds, steroid potency names or quantities appear here: classifications differ between systems and formularies, and a junior classifying severity is doing the wrong task. Escalate instead, and use your national formulary.
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