Acute myeloid leukaemia — Rapid

Synopsis

Recognise acute myeloid leukaemia, confirm lineage and defining genetics urgently, stabilise cytopenic and hyperleukocytic emergencies and select biology- and fitness-led treatment with measurable residual disease follow-up.

Suspect AML with unexplained cytopenias, circulating blasts, recurrent infection, bleeding, bone pain or gingival and skin infiltration; a normal total white-cell count does not exclude it.
First-line tests are urgent FBC and expert blood film, coagulation and fibrinogen, renal, liver, urate, LDH, calcium, phosphate, cultures and group samples.
Confirm with bone-marrow aspirate and trephine, flow cytometry, karyotype or FISH and a rapid molecular panel; some defining genetic AML diagnoses do not require 20% blasts.
Always create an emergency APL branch: send rapid PML::RARA testing and begin oral tretinoin immediately if morphology suggests APL.
Intensive versus non-intensive treatment is based on physiological fitness, frailty, organ function, genetics and patient goals—not chronological age alone.
Fit adults receive a current UK protocol using induction and consolidation with genotype-directed additions; exact cytarabine and anthracycline schedules are centre and trial specific.
Adults unsuitable for intensive chemotherapy may receive azacitidine plus venetoclax when commissioned and appropriate, with mandatory tumour-lysis, CYP3A and prolonged-cytopenia management.
FLT3, NPM1, CEBPA, TP53 and other lesions influence prognosis, targeted treatment and transplant decisions; obtain adequate diagnostic material before non-essential steroids or chemotherapy.
Measurable residual disease after induction and consolidation refines relapse risk and transplant strategy; morphological remission alone is not the whole response.
Leukapheresis is not routine AML treatment and must never delay hydroxycarbamide or definitive therapy; use it only for selected symptomatic leucostasis through apheresis expertise.

Key red flags

Fever, rigors, hypotension, hypoxia or confusion with neutropenia is a haematological emergency requiring empiric broad-spectrum antibiotics within the local sepsis pathway.

Dyspnoea, hypoxaemia, headache, confusion, focal deficit, priapism or retinal change with a very high myeloid count suggests leucostasis and requires immediate cytoreduction planning.

Bleeding, bruising, low fibrinogen or prolonged coagulation with abnormal promyelocytes suggests APL; tretinoin and aggressive blood support must begin on morphological suspicion.

Hyperkalaemia, hyperphosphataemia, hypocalcaemia, rising urate or creatinine before or after therapy indicates tumour lysis and requires continuous cardiac and metabolic escalation.

Hyperleukocytic emergency

Hypoxaemia, confusion, headache, focal deficit, priapism or retinal haemorrhage with high blasts suggests leucostasis rather than a harmless laboratory count.

APL warning

Bleeding, low fibrinogen and abnormal promyelocytes demand immediate tretinoin and PML::RARA testing before final classification.

Investigation priorities

First-line: FBC and expert blood filmFirst stepFirst line

Identify blasts, cytopenias and morphology that changes emergency care.

Management branches

Suspected AMLStabilise while preserving diagnosis

Blasts, unexplained cytopenias or an AML emergency is identified.

Send FBC, film, coagulation, fibrinogen, lysis, infection and group tests and obtain urgent blood or marrow diagnostic material.
Treat sepsis, bleeding and lysis immediately; start tretinoin on APL suspicion and cytoreduce symptomatic hyperleukocytosis with haematology.
Complete integrated morphology, flow, cytogenetic and molecular classification before the definitive MDT regimen.

Key medicines

Azacitidine with venetoclaxGive azacitidine 75 mg/m² subcutaneously on days 1–7 of each 28-day cycle and venetoclax orally 100 mg day 1, 200 mg day 2 and 400 mg from day 3 when no interacting inhibitor requires reduction.Classify tumour-lysis risk, hydrate and lower urate; strong CYP3A inhibitors require major venetoclax dose reduction and are contraindicated during some ramp contexts. Perform early marrow assessment to distinguish aplasia from persistent AML and adjust post-remission duration through protocol. Avoid pregnancy and breastfeeding.

HydroxycarbamideFor urgent AML cytoreduction give a specialist protocol dose commonly 50–100 mg/kg/day orally in two or three divided doses, adjusted frequently to count, renal function and definitive-treatment timing.It is not curative and must not delay APL-specific tretinoin or induction. Monitor FBC and lysis chemistry at least daily, use renal adjustment and safe handling, and avoid in pregnancy unless life-saving specialist benefit clearly outweighs fetal risk.

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