Acute Kidney Injury & Electrolyte Emergencies
Use trends, urine output and volume assessment to identify reversible injury and dangerous electrolyte disturbances.
Quick revision ↓ Medical Dictionary
01Recognise acute change
Acute kidney injury is identified from a rise in creatinine or reduced urine output over a defined period, interpreted against baseline. A creatinine within the laboratory range can still represent a substantial rise for one patient. Review previous results, fluid losses, sepsis, medicines and obstruction symptoms. Creatinine can lag behind injury, so falling urine output and clinical deterioration should not wait for a dramatic number.
02Find the mechanism
Consider reduced renal perfusion, intrinsic renal disease and urinary obstruction. Examine volume status and perfusion, review urine findings and obtain imaging when obstruction is possible. Haematuria and proteinuria with systemic features may suggest glomerular disease requiring urgent renal input. Do not assume every patient with AKI needs fluids: congestion and intrinsic disease may require a different approach, with careful reassessment after any intervention.
03Address hyperkalaemia
Marked potassium elevation can cause fatal arrhythmia even without classic ECG changes. Assess the patient, obtain an ECG and verify possible sample artefact when appropriate without delaying urgent treatment. Emergency treatment can stabilise the myocardium, shift potassium into cells and remove it from the body; these are distinct goals. Monitor glucose after insulin-based therapy and repeat potassium because redistribution is temporary and rebound can occur.
04Treat sodium disorders carefully
Hyponatraemia assessment considers symptoms, duration, tonicity, glucose and volume status. Severe neurological symptoms require urgent supervised treatment, while overly rapid correction of chronic hyponatraemia risks osmotic demyelination. Hypernatraemia often reflects a water deficit but also needs cause and duration assessment. Use a monitored correction plan with repeated measurements rather than a fixed fluid prescription independent of the patient's physiology.
05Escalate and recover
Refractory hyperkalaemia, severe acidosis, pulmonary oedema and uraemic complications may require urgent renal replacement assessment. Review nephrotoxic drugs and dose adjustments, but make decisions in the clinical context rather than stopping every medicine permanently. Document recovery, repeat kidney function after discharge and assess future CKD risk. A temporary improvement does not remove the need to identify and address the cause.
Hyperkalaemia • Three different treatment goals
| Goal | Principle | Important limitation |
|---|---|---|
| Protect the heart | Calcium when indicated | Does not lower potassium |
| Shift potassium into cells | Insulin-based therapy and other indicated measures | Temporary effect; monitor glucose and potassium |
| Remove potassium | Appropriate elimination strategy; dialysis when required | Choice depends on severity, kidney function and response |
High-Yield Revision
- Compare creatinine with baseline and follow urine output.
- Calcium stabilises the myocardium; it does not remove potassium.
- Electrolyte correction needs a monitored plan.
Common Pitfalls
- Do not assume a normal ECG makes severe hyperkalaemia safe.
- Avoid rapid unmonitored correction of chronic hyponatraemia.
References & Further Reading
Read the relevant guideline sections alongside these original clinical teaching cases. Local pathways, available services and individual patient factors determine care.
Reference review: 27 September 2026. Consult current local protocols for prescribing, procedures and escalation.