High-yield map
Key points before the detail
- 01
Always interpret a blood gas with the sample type, oxygen device/FiO2 and clinical trajectory.
- 02
A near-normal pH with markedly abnormal PaCO2 and bicarbonate may represent a mixed disorder.
- 03
AKI is defined by change from baseline creatinine and/or urine output; oliguria below 0.5 mL/kg/hour is clinically important.
- 04
Postoperative oliguria is a sign to assess, not an automatic indication for repeated fluid boluses or diuretics.
A reproducible blood-gas sequence
| Step | Question |
|---|---|
| 1 | Is the sample arterial or venous, and what oxygen/ventilatory support is being given? |
| 2 | Is there acidaemia or alkalaemia? |
| 3 | Does PaCO2 explain a primary respiratory process? |
| 4 | Does bicarbonate/base excess explain a primary metabolic process? |
| 5 | Is compensation plausible, or is there a mixed disorder? |
| 6 | What do oxygenation, lactate, electrolytes and the clinical trend add? |
Use the anion gap to classify metabolic acidosis
A common calculation is sodium minus chloride plus bicarbonate: Na − (Cl + HCO3). A raised gap suggests accumulation of unmeasured anions such as lactate, ketones, toxins or retained acids in renal failure. A normal-gap hyperchloraemic acidosis commonly reflects bicarbonate loss or chloride-rich fluid administration. Use the local laboratory range; hypoalbuminaemia can lower the baseline gap.
Electrolytes: recognise danger before memorising replacement rates
| Pattern | Why it matters | First principle |
|---|---|---|
| Hyperkalaemia | Can cause conduction abnormalities and fatal arrhythmia | Repeat/confirm when appropriate, obtain ECG, stop potassium sources and initiate the current emergency protocol if clinically significant. |
| Hyponatraemia | Rapid or severe falls can cause cerebral oedema and seizures | Assess symptoms, chronicity, volume state and cause; correction limits and hypertonic therapy require protocolised monitoring. |
| Hypokalaemia / hypomagnesaemia | Predispose to arrhythmia and weakness | Identify losses/drugs and replace using local route/rate/monitoring policy. |
| Hypocalcaemia | Can occur with massive transfusion and other critical illness | Interpret ionised calcium where relevant and treat clinically important abnormalities according to the active protocol. |
Detect AKI by change, not by one creatinine
NICE NG148 advises detecting AKI using any of the recognised changes in adults: serum creatinine rise of 26 micromol/L or more within 48 hours; 50% or greater rise from a known/presumed baseline within the previous 7 days; or urine output below 0.5 mL/kg/hour for more than 6 consecutive hours. A patient can therefore have important AKI while the absolute creatinine remains within a laboratory reference range.
- Review previous creatinine and the time course.
- Measure and trend urine output where clinically indicated.
- Review haemodynamics, fluid balance, nephrotoxic exposures and recent contrast/medication.
- Look for obstruction, especially with retention, pelvic disease, solitary kidney or hydronephrosis risk.
- Urinalysis and targeted imaging/laboratory tests help separate pre-renal, intrinsic and post-renal mechanisms.
Postoperative oliguria: ask why
Reduced urine output can reflect hypovolaemia, haemorrhage, sepsis, reduced cardiac output, vasodilation, renal parenchymal injury, obstruction or physiological postoperative hormonal responses. Repeated fluid loading can worsen pulmonary oedema when the patient is not fluid depleted.
Active recall
Close the notes and answer these
Try each question from memory before revealing the answer. These public prompts are a small preview of the integrated retrieval system inside SurgAtlas.
01Give one creatinine-based NICE criterion for AKI.
A serum creatinine rise of at least 26 micromol/L within 48 hours, or a rise of 50% or more from baseline within 7 days.
02What urine-output threshold is used in NICE adult AKI detection?
Less than 0.5 mL/kg/hour for more than 6 consecutive hours.
03Why should postoperative oliguria not trigger automatic fluid loading?
Oliguria has multiple causes, including pump failure, sepsis, intrinsic AKI and obstruction; excess fluid can harm a patient who is not volume depleted.
Sources & editorial basis
References & editorial basis
- SurgAtlas production chapter — Acid-Base, Electrolytes and Acute Kidney Injury. Primary SurgAtlas source. Guideline-dependent statements in this public lesson were separately checked against the current authoritative sources listed below.
- NICE NG148 — Acute kidney injury: prevention, detection and management. Current UK AKI detection criteria, risk assessment, investigations and management principles. Source ↗
This lesson is derived from the corresponding SurgAtlas production teaching material. Where the source makes current management or guideline claims, the public lesson uses the cited contemporary guidance. It is written for education and examination preparation, not as patient-specific clinical advice.
Editorial details
Medical Doctor (MD) · MRCS Part A · Physician · Surgical Educator
SurgAtlas is an educational resource. For patient care, verify current national guidance, local antimicrobial and transfusion policies, specialty pathways and individual patient factors.
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