Educational draft · awaiting clinical reviewUse Rapid for revision, not patient-care decisions. Check current national and local guidance and the BNF or BNFC before acting.
2 min synopsisUK scopeSources checked 27 Aug 2026Clinical review pending
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Escalate
Haemodynamic AKI with shock, active haemorrhage, septic hypoperfusion, myocardial ischaemia, severe heart failure or rapidly progressive pulmonary oedema requires immediate resuscitation and senior critical-care or specialty input; a low urine output must not prompt indiscriminate fluid when the patient is congested.
Synopsis
Distinguish true intravascular depletion from low effective arterial circulation and venous congestion, restore renal perfusion safely, and prevent haemodynamic AKI from becoming structural injury.
Pre-renal AKI reflects reduced glomerular filtration from impaired perfusion without necessarily implying whole-body dehydration; haemorrhage, sepsis, low cardiac output and cirrhotic vasodilatation can produce different haemodynamic phenotypes.
Effective filtration depends on systemic pressure, renal blood flow and glomerular arteriolar tone. NSAIDs impair prostaglandin-mediated afferent dilatation, while ACE inhibitors and ARBs reduce angiotensin-mediated efferent constriction.
Diuretics can compound salt and water loss, creating the familiar ACE inhibitor or ARB plus diuretic plus NSAID risk combination, particularly during intercurrent illness.
Key red flags
External volume loss
Vomiting, diarrhoea, fever, burns, polyuria, poor intake or haemorrhage with weight loss, thirst, postural symptoms, tachycardia and low filling signs favours true depletion. Older adults and people taking beta blockers may lack classic tachycardia.
Investigation priorities
01
Supine and standing observations with perfusion examinationFirst step
Identify haemodynamic compromise and quantify response to initial resuscitation.
Management branches
DepletionTreat probable intravascular loss
A compatible history and examination indicate hypovolaemia without pulmonary or systemic congestion.
1. Control ongoing losses, obtain urgent blood tests and cross-match when bleeding is possible, and establish reliable observations and urine measurement.
2. Give a locally approved isotonic crystalloid bolus, or blood products through the haemorrhage pathway when appropriate, with a pre-specified reassessment time.
Key medicines
Isotonic crystalloid resuscitationUse a protocol-sized bolus for suspected hypovolaemia and reassess after each administration; frailty, cardiac failure and renal congestion usually require smaller increments and closer observation.
Noradrenaline through a critical-care protocolTitrate by trained critical-care staff to an individual haemodynamic target after appropriate initial volume assessment; concentration, access and rate follow the local vasoactive infusion policy.
National guidance is shown before implementation-dependent detail. Typical adult dose examples remain subject to patient factors, contraindications and the live BNF or specialist protocol. Source check completed 27 Aug 2026; clinical approval remains outstanding.