EDAITUTOR
ED Briefs · Nephrology v1.0 Educational use only

Acute Kidney
Injury

AKI is a syndrome, not a diagnosis. — treat the sick-now threats, then work out why the kidney is failing, not just that it is.

Sick now?Perfusion / parenchyma / plumbingWhat can I reverse?
Adult retrieval — ARV (VIC)

Call early when the patient may need dialysis, ventilation, vasopressors or urgent urological decompression beyond local capability. Continue serial K⁺, ECG, glucose and acid–base monitoring during transfer prep. Confirm destination with local protocols and the retrieval service.

The creatinine is the alarm, not the emergency

Treat the complications before you classify the AKI: hyperkalaemia, pulmonary oedema, severe acidaemia, uraemic complications, obstruction. A normal creatinine does not exclude early AKI (it lags the insult), and a normal ECG does not exclude dangerous hyperkalaemia. And “pre-renal” is not shorthand for “give litres”.

Start here — pick the presentation, or read the three questions
AKI + sepsisCase 1 · resuscitate first AKI + vomiting / diarrhoeaCase 2 · volume-responsive AKI + long lie / fallCase 3 · rhabdomyolysis AKI + a nephrotoxic drugNSAID · ACEi/ARB · contrast AKI + high potassiumthe sick-now threat AKI + retention / anuriaexclude obstruction

Three questions, in order

  • 1. Is the patient sick now? — hyperkalaemia, oedema, acidaemia, uraemia. Treat before staging.
  • 2. Why is the kidney failing? — perfusion, parenchyma or plumbing?
  • 3. What can I reverse or stop? — volume, obstruction, sepsis, nephrotoxic drugs.

Two reframes that recur

  • Pre-renal ≠ give fluid. Assess perfusion and congestion; low urine output can mean venous congestion or obstruction.
  • Dialysis is driven by complications and trajectory, not by an isolated creatinine.
Q1 · Sick now? K⁺ ≥6.5 / ECG change · pulmonary oedema · severe acidaemia · uraemic complication · anuria → treat in parallel, before staging
Q2 · Perfusion / parenchyma / plumbing? dry or shocked? · obstructed (bladder scan)? · intrinsic insult (urinalysis, CK, systemic features)? → the mechanism drives everything
Q3 · Reverse & protect treat the cause · stop nephrotoxins · relieve obstruction · avoid further injury
◯ the spineSick-now → mechanism → reverse. Everyone can read what AKI is; the ED job is spotting the killable complication and the reversible cause fast.
Sick now? — the threats that come before classification

Immediate physiological threats

  • Hyperkalaemia — K⁺ ≥6.5, rapid rise, ECG change or weakness
  • Severe / worsening metabolic acidaemia
  • Pulmonary oedema or respiratory failure
  • Shock, sepsis or ongoing haemorrhage
  • Uraemic encephalopathy, pericarditis, seizures, bleeding
  • Anuria or rapidly falling urine output
  • Dialysable poisoning · tumour lysis

Time-critical causes not to miss

  • Infected obstructed system / pyonephrosis — source control is time-critical
  • Bilateral obstruction, or obstruction of a solitary kidney
  • Rapidly progressive GN / pulmonary–renal syndrome
  • Thrombotic microangiopathy
  • Rhabdomyolysis
  • Renal vascular occlusion · aortic pathology · abdominal compartment syndrome
🔴 before stagingDo not wait for AKI staging to treat dangerous potassium, shock or pulmonary oedema. Escalation follows trajectory, physiology and local capability — not the creatinine value.
Perfusion, parenchyma, plumbing — three questions, not three labels

PPerfusion

dry, shocked—or congested
  • GI losses, haemorrhage, sepsis, over-diuresis → may improve with correction
  • But congestion counts too: cardiorenal / right-heart failure — raised JVP, B-lines → more fluid worsens AKI
assess fluid responsiveness AND tolerance

PParenchyma

intrinsic insult
  • ATN, GN, vasculitis, interstitial nephritis, TMA, rhabdomyolysis, tumour lysis
  • Urinalysis is mandatory: blood + protein (esp. with hypertension, no obstruction) → nephritic — call renal
  • CK for rhabdomyolysis
blood + protein = cannot-miss

PPlumbing

obstruction
  • Blocked catheter, retention/BPH, bilateral ureteric obstruction, pelvic malignancy, stone in solitary kidney
  • Bladder scan / post-void residual early
  • Anuria or fluctuating output → think obstruction
decompress infected obstruction <12h
🔴 the trap“Pre-renal AKI” is not shorthand for “give litres”. Low urine output may reflect venous congestion, intrinsic injury or obstruction. Give fluid only when perfusion / fluid-responsiveness supports it, in small reassessed aliquots — then re-check BP, work of breathing, B-lines, JVP, urine output and lactate after each.

Fluid: no oedema → challenge; oedema → don't reflex-load

  • No pulmonary or peripheral oedema + adequate perfusion → give a fluid challenge. One published ED approach (EM Cases): Ringer's lactate 1 L bolus, then 150 mL/h, aiming urine output ≥50 mL/h (≥200 mL/h in rhabdomyolysis).
  • Give in reassessed aliquots — re-check BP, work of breathing, B-lines, JVP, urine output and lactate; balanced fluid (RL) is generally preferred over saline.
  • Oedema with adequate perfusion → furosemide, not fluid. Furosemide 1 mg/kg IV (1.5 mg/kg if already on it). Also think pulmonary–renal syndromes (anti-GBM, ANCA vasculitis, lupus) — look for arthritis, purpura, Raynaud's.
  • Diuretics treat congestion, not the parenchymal injury — don't use them just to convert oliguric to non-oliguric AKI.
◯ don't over-orderTests that rarely change ED management: the BUN:creatinine ratio is not reliable for separating pre-renal from renal AKI, and urine electrolytes / FENa are rarely useful in the ED (hard to interpret without inpatient workup) — the exception is suspected hepatorenal syndrome. The urine dipstick (blood + protein) and a post-void residual are the two that do change what you do.
Nephrotoxic & contributing drugs — hold, don't reflexively stop forever
DrugWhyED action
NSAIDsAfferent vasoconstriction — worsens perfusionHold
ACE inhibitor / ARBEfferent vasodilation — harmful during hypoperfusion; hyperkalaemiaHold during the acute insult
DiureticsWorsen genuine hypovolaemiaHold if truly volume-depleted; keep for congestion
MetforminAccumulation → lactic acidosis riskHold in significant AKI
SGLT2 inhibitorEuglycaemic ketoacidosis in acute illnessHold during severe acute illness
Aminoglycosides / other nephrotoxinsDirect tubular toxicityReview, adjust or stop; check levels
Iodinated contrastContrast-associated AKI (risk overstated)Don't withhold essential imaging — optimise haemodynamics, use local pathway
◯ noteWithholding is usually temporary and documented, with a restart/review plan — not indiscriminate permanent cessation. Also review every drug for renal dose adjustment and accumulation.
KDIGO staging — useful, but one creatinine can't stage it
KDIGO criteria (any one defines AKI)
Creatinine rise ≥26.5 µmol/L (0.3 mg/dL) within 48 h
Creatinine rise to ≥1.5× baseline within 7 days
Urine output <0.5 mL/kg/h for >6 h
◯ caveatStaging needs a baseline and a trajectory. A single value under-stages the patient if creatinine is still rising, and creatinine lags the insult — early AKI may show first as oliguria, hyperkalaemia or acidosis. The 2026 KDIGO AKI/AKD update is in draft (awareness only, not yet final).
Hyperkalaemia — UKKA 2023 teaching values, verify local protocol
AimUKKA teaching value
Protect the myocardium (ECG changes present)Calcium gluconate 10% 30 mL IV over 10 min, or calcium chloride 10% 10 mL IV over 5 min. Calcium chloride preferred in arrest/peri-arrest.
Shift K⁺ intracellularlySoluble insulin 10 units IV with 25 g glucose (= 50 mL of 50%) — for K⁺ ≥6.5 (suggested 6.0–6.4). Glucose dose depends on the BSL — see pearls.
Prevent hypoglycaemiaIf pre-treatment glucose <7 mmol/L → 10% glucose 50 mL/h for 5 h after insulin–glucose.
Adjunct shiftNebulised salbutamol 10–20 mg — not monotherapy for severe hyperkalaemia.
Remove K⁺Sodium zirconium cyclosilicate (formulary-dependent) — does not replace dialysis when life-threatening.
MonitorK⁺ at ~1, 2, 4, 6, 24 h. Glucose every 30 min ×2 h, then hourly to ≥6 h after insulin–glucose.

Two reversals worth knowing

  • No routine IV bicarbonate purely as K⁺-shifting therapy
  • No routine calcium resonium for acute hyperkalaemia

And a normal ECG does not exclude dangerous hyperkalaemia — treat by level, trajectory and clinical state, not only by the presence of peaked T waves. For K⁺ ≥6.0, get an urgent 12-lead; continuous monitoring for K⁺ ≥6.5 or ECG change.

FOAMed pearls — calcium (LITFL / EMCrit)

  • Calcium protects the myocardium; it does NOT lower K⁺. It buys time — a shift (insulin–glucose ± salbutamol) and removal must follow.
  • Indication is myocardial protection: give for ECG changes — bradycardia / conduction defect, QRS widening, sine wave, or arrest. Usually not for peaked T waves alone.
  • Consider even without ECG changes if K⁺ >6.5 and rapidly rising, or with coexisting acidaemia / cardiac disease (controversial but reasonable).
  • Suspected digoxin toxicity: give calcium cautiously and slower — 1 g of 10% calcium gluconate in 100 mL over 15–30 min (not 5 min).

FOAMed pearls — the shift (EM Cases)

  • Glucose dose depends on the starting BSL — insulin is fixed at 10 units:
    • BSL low or normal (< ~14 mmol/L): give 50 g glucose = 2 × 50 mL of 50% (2 amps D50W), not 1 — 25 g leaves many patients hypoglycaemic (EM Cases, on systematic review). Or a 10% glucose infusion per UKKA.
    • BSL already high (> ~14 mmol/L): give insulin alone, hold the dextrose, and recheck glucose — adding 50 g would worsen hyperglycaemia.
  • Whichever route, keep monitoring glucose per the UKKA schedule — hypoglycaemia can occur late.
  • Salbutamol is an adjunct, not monotherapy — additive with insulin–glucose, never relied on alone for severe hyperkalaemia.
  • Recheck K⁺ and repeat the ECG after treatment — the shift is temporary; if the driver (AKI, drugs, tissue breakdown) persists, K⁺ rebounds.
Rhabdomyolysis — when to look, and what the CK means

When to send a CK

  • Any one risk factor: trauma / crush / compartment, extreme exertion, hyperthermia, found down / long lie
  • Any one symptom: muscle pain, weakness, vomiting, dark urine
  • CK peaks at 24–72 h — may be low early, so serial CKs matter if the insult is recent
  • Urine myoglobin has little ED role (half-life 2–3 h — a negative at 4–6 h misleads)
  • If CK >1000: add calcium, phosphate, VBG to gauge severity / dialysis risk

Fluids & targets

  • IV Ringer's lactate, titrated to a higher urine output target: ≥200 mL/h (vs ≥50 mL/h in general AKI)
  • Trend CK and creatinine to guide disposition
  • Watch K⁺, Ca, PO₄ — crush + AKI drives hyperkalaemia (see the hyperkalaemia section)
  • Look for compartment syndrome; remove ongoing compression
CK (IU/L)Approach
<1000Oral fluids usually adequate if CK not trending up and McMahon low.
1000–5000IV Ringer's lactate; trend CK & creatinine — the trajectory decides disposition.
>5000IV RL + admission; ~50% progress to AKI. Consider dialysis if McMahon ≥6.
◯ score & dischargeThe McMahon score (age, sex, creatinine, Ca, CK, phosphate, bicarbonate) estimates severity and dialysis need — MDCalc →. Safe discharge (per EM Cases experts): cause identified and reversed, CK <1000 and down-trending, creatinine normalised, and reliable to continue oral fluids at home.
Imaging — choose wisely — POCUS first; formal imaging for a small subset

POCUS first

  • Volume: IVC, JVP, lungs (B-lines) — guides the fluid-vs-decongestion decision
  • Obstruction: post-void residual, hydronephrosis, ureteric jets — absent jets ≈ 90% PPV for obstruction
  • Often obviates formal renal imaging — but accuracy is operator-dependent

Formal (radiology) imaging — reserve for

  • No improvement with fluid challenge (pre-renal less likely), and
  • Normal urine dip (intra-renal less likely), and
  • Post-void residual <100 mL (BPH less likely), or
  • Obvious bilateral hydronephrosis on POCUS
looking for bilateral ureteric obstruction — pelvic malignancy, lymphoma, stone in a solitary kidney
🔴 pitfallDon't attribute AKI to a ureteric stone. Unless the patient has a solitary kidney, nephrolithiasis rarely causes AKI — a single obstructed kidney with a normal contralateral one won't raise the creatinine. If the creatinine is up, look for another cause.
When to dialyse & when to call — complications, not a creatinine

!Urgent — with AKI

AEIOU — refractory to medical Rx
  • E — refractory severe hyperkalaemia, esp. with conduction abnormality
  • A — refractory severe metabolic acidosis (commonly pH <7.2, when bicarbonate has failed)
  • O — refractory pulmonary oedema unresponsive to diuretics (a mandatory indication)
  • U — uraemic complications: encephalopathy, pericarditis, bleeding
“refractory” = medical therapy has failed, judged on rate, ECG effect & persistence

IUrgent — without AKI

intoxication
  • Lithium
  • Toxic alcohols (ethylene glycol, methanol)
  • Metformin-associated lactic acidosis
  • Salicylate
a dialysable toxin can be the whole indication, independent of the creatinine

∅NOT (yet) an indication

what doesn't earn dialysis
  • KDIGO stage 3 alone, without a complication
  • Sepsis without complicated AKI
  • A number alone — urea, creatinine or K⁺ in isolation
non-urgent: persistent severe AKI, oliguria/anuria >72 h — a considered, not reflex, decision
◯ evidence & timingAbsent an urgent indication, severe AKI can often be observed initially — even with oliguria. Nearly half of stage 3 AKI managed with delayed initiation never need dialysis (STARRT-AKI: no benefit to early/routine RRT). Let diuretic-refractory symptomatic fluid overload, not a creatinine, prompt the RRT conversation. Consult nephrology for inadequate response, no clear cause, stage 3+, pre-existing CKD stage 4+, or likely RRT — and don't wait for a full AEIOU set to make the call.
Outside adult ED scope — different physiology, different pathway

Paediatric AKI / DKA

Weight-based fluids and drug doses, and in DKA the fluid logic inverts — cautious rehydration for cerebral-oedema risk, not aggressive loading. Use your paediatric DKA / AKI pathways and Starship / RCH guidance. Retrieval for children is PIPER (VIC), not ARV.

Pregnancy-related AKI

Baseline creatinine is lower in pregnancy, so a “normal” value may already be abnormal. Drug and imaging choices change, and pre-eclampsia / HELLP, obstetric haemorrhage and hyperemesis are specific drivers. Involve O&G early and use local obstetric pathways.

Three worked cases — three mechanisms; tap to expand
Case 1 · 70M, back pain + fever, BP 80/50, on a beta-blocker, dipstick Leu/Nit+septic AKI
Impression: septic AKI from a likely infected urinary source — shock is the driver, AKI is the alarm. The trapHR 90 on a beta-blocker is a masked tachycardia. BP 80/50 + confusion + fever is shock; don't be reassured by the rate. Sick-nowResuscitate: reassessed crystalloid aliquots (assess response and tolerance), early antimicrobials, source control. Check K⁺, gas, lactate; ECG if hyperkalaemia possible. Key decisions
  • Is the urinary tract obstructed as well as infected? An infected obstructed system needs decompression — antibiotics alone are inadequate → bladder scan, urology, ultrasound within 6 h if pyonephrosis suspected.
  • Stop/hold nephrotoxic and hypotension-contributing drugs; hold the newly-started agent if implicated.
DispositionAdmission ± critical care; nephrology if AKI is stage 2–3 or not responding. Retrieval (ARV) early if RRT/vasopressors/decompression exceed local capability.
Case 2 · 30F, vomiting + diarrhoea 48 h, dry, last urine last nightvolume-responsive
Impression: pre-renal / volume-responsive AKI from GI losses — the case where recognising it before it becomes ATN is the win. AssessmentDry mucous membranes, tachycardia, oliguria support hypovolaemia — but still check for congestion and confirm fluid responsiveness before loading. Key decisions
  • Reassessed crystalloid aliquots, re-checking perfusion, work of breathing, B-lines and urine output — not an automatic large volume.
  • Urinalysis anyway — don't close on “dehydration” without excluding blood+protein, obstruction or a drug cause.
  • Hold contributing drugs (ACEi/ARB, NSAIDs, diuretics) during the acute phase.
DispositionMay be dischargeable only if AKI is mild and improving, cause clearly reversible, K⁺/acid–base safe, oral intake restored, with a documented medication plan and early repeat renal function.
Case 3 · 84M, unwitnessed fall + ~12 h long lie, lives alonerhabdomyolysis
Impression: AKI from rhabdomyolysis after a prolonged lie — and the parallel question of why he fell. Sick-nowCheck K⁺ urgently (crush + AKI → hyperkalaemia), ECG, gas, CK, calcium, phosphate. Look for compartment syndrome and pressure injury. Key decisions
  • Appropriate crystalloid while avoiding overload; monitor K⁺, Ca, PO₄ and CK trajectory. Treat the cause (remove ongoing compression).
  • Work up the fall: sepsis, cardiac, neurological, medication, hypoglycaemia — the long lie is a consequence, not the whole story.
  • Frailty + lives alone changes disposition and social risk.
DispositionAdmission; nephrology/critical care if hyperkalaemia is refractory, AKI is advanced or RRT looks likely.

ED AI Tutor · ED Reference Series · v1.0 · for clinicians and trainees. Always follow local protocols and senior clinician oversight.