Desmopressin
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Direct answer
Desmopressin (DDAVP, 1-deamino-8-D-arginine vasopressin) is a synthetic vasopressin analogue selective for V2 receptors, producing antidiuresis without the V1-mediated vasoconstriction, and with a longer action than native vasopressin. It is the drug of choice in central (cranial) diabetes insipidus — nephrogenic diabetes insipidus does not respond, which itself differentiates the two — and is also used in primary nocturnal enuresis and to raise factor VIII and von Willebrand factor in haemophilia A and mild type 1 von Willebrand disease. Its principal hazard is water retention with dilutional hyponatraemia, so evening fluid restriction is mandatory in enuresis use.
What you must remember
- Receptor pharmacology: V2-selective agonism increases water reabsorption through aquaporin-2 channels in the collecting duct; absent V1 activity means no pressor effect, unlike vasopressin used in shock or variceal bleeding.
- Central diabetes insipidus: first-line therapy by oral, sublingual or intranasal route; a desmopressin challenge that fails to concentrate urine indicates nephrogenic disease, where thiazides, amiloride or NSAIDs are used instead.
- Primary nocturnal enuresis: oral desmopressin at bedtime with fluid restriction one hour before and eight hours after the dose; it is rapidly effective but relapse on stopping is common, so behavioural therapy remains central.
- Haemostatic use: releases stored factor VIII and von Willebrand factor from endothelium, useful in mild haemophilia A, mild type 1 von Willebrand disease, ureamic platelet dysfunction and before minor surgery or dental work — avoiding blood products.
- Exceptions in von Willebrand disease: it is ineffective and potentially harmful in type 2B (may aggravate thrombocytopenia) and useless in type 3 (no stores to release).
- Routes: oral and sublingual melts, intranasal spray (avoided when congested), subcutaneous or intravenous for surgical or diagnostic settings.
- Adverse effects: hyponatraemia with water intoxication (headache, nausea, seizures) is the key toxicity — check sodium if symptoms develop and restrict fluids; nasal congestion, flushing and abdominal pain also occur.
Common confusion
The classic distinction is central versus nephrogenic diabetes insipidus: desmopressin corrects central disease completely, while nephrogenic disease (lithium, hypercalcaemia, hypokalaemia, demeclocycline) needs dietary sodium restriction, thiazides or amiloride instead. Students also mix up desmopressin with vasopressin or terlipressin — V1 activity makes those drugs vasoconstrictors for shock and variceal bleeding, unsuitable as daily antidiuretics.
Exam-focused takeaway
Stems typically describe polyuria and polydipsia after pituitary surgery that responds to a nasal spray, a child with bedwetting treated at bedtime with fluid restriction, or a mildly affected haemophiliac dentally prepared without factor concentrate. Hyponatraemia in a patient on the drug is the standard toxicity question. Expect a one-step diagnostic question where failure to respond to desmopressin defines nephrogenic disease, and contraindication recall in von Willebrand type 2B.
Frequently asked questions
Why does desmopressin not work in nephrogenic diabetes insipidus?
The V2 receptors or aquaporin pathway in the collecting duct is defective or blocked (as with lithium), so the drug has no target to act upon.
How is desmopressin used in enuresis?
Orally at bedtime with restricted evening fluids; it reduces nights wet immediately, but relapse after stopping is common without adjunctive behavioural measures.
How does desmopressin help haemophilia A?
It releases endogenous factor VIII and von Willebrand factor from endothelial stores, raising levels two- to four-fold in mild disease and minor procedures.
In which von Willebrand types is desmopressin contraindicated?
Type 2B, where it can worsen thrombocytopenia by releasing abnormal high-affinity multimers, and type 3, where no stores exist.
What is the most important adverse effect of desmopressin?
Dilutional hyponatraemia from water retention; evening fluid restriction and sodium monitoring when symptomatic prevent water intoxication.