AKI & Electrolyte Emergencies: FRCEM SBA Management Guide

Here's a question worth asking yourself honestly: if a patient arrived with a potassium of 7.2 mmol/L and peaked T waves right now, could you state the exact drug, dose, and sequence without hesitating? Most candidates can describe the idea — calcium, insulin, salbutamol — but stumble on the specifics. And the specifics are exactly what the SBA tests.

AKI and electrolyte emergencies appear in 8–10 FRCEM SBA questions, and they're some of the most protocol-driven content in the entire exam. There's very little clinical judgement involved — mostly, there's a right number, a right drug, and a right sequence. That makes this topic either a guaranteed source of marks or a guaranteed source of frustration, depending on how precisely you've revised it.

This guide covers AKI staging and causes, then works through each major electrolyte emergency — hyperkalaemia (the highest-yield of all of them, with a significant recent UK guideline update), hyponatraemia, calcium disorders, and hypomagnesaemia — with the exact numbers FRCEM expects.

Acute Kidney Injury: Recognition and Staging

AKI questions test two things: can you recognise it using the correct criteria, and do you know what to do about it in the ED.

KDIGO Staging — What FRCEM Tests

NICE recommends detecting AKI in line with the KDIGO (or AKIN/RIFLE) criteria, using a rise in serum creatinine of 26 micromol/litre or more within 48 hours, a 50% or greater rise in creatinine known or presumed to have occurred within the past 7 days, or a fall in urine output to less than 0.5 ml/kg/hour for more than 6 hours.

KDIGO staging:

FRCEM angle: A question gives you a creatinine value and a baseline, then asks for the stage. Know the multipliers (1.5–1.9 / 2.0–2.9 / ≥3) cold — this is a calculation question disguised as a clinical scenario.

The Three Categories of Cause

Every AKI question is really asking: pre-renal, renal, or post-renal?

Pre-renal (most common in the ED): Hypovolaemia, sepsis, heart failure, hepatorenal syndrome — anything reducing renal perfusion. Usually reversible with fluid resuscitation if caught early.

Renal (intrinsic): Acute tubular necrosis (often following a pre-renal insult that wasn't corrected), glomerulonephritis, interstitial nephritis (commonly drug-induced — NSAIDs, antibiotics), rhabdomyolysis.

Post-renal (obstructive): Urinary retention, ureteric obstruction (stones, malignancy), blocked catheter. Always check for a palpable bladder and perform a bladder scan — this is the easiest AKI cause to fix and the easiest to miss.

ED Management Principles

1. Identify and treat the cause — fluid challenge for hypovolaemia, treat sepsis, relieve obstruction (catheterise)

2. Stop nephrotoxic drugs — NSAIDs, ACE inhibitors/ARBs, gentamicin, contrast where avoidable

3. Avoid unnecessary contrast — but per NICE, do not delay iodine-based contrast in a genuine emergency if delaying it carries greater clinical risk than the AKI risk

4. Monitor potassium — AKI is one of the most common causes of hyperkalaemia (see below)

5. Fluid balance — careful reassessment; over-resuscitation in oliguric AKI causes pulmonary oedema

When to Call for Emergency Dialysis: AEIOU

This is a classic FRCEM mnemonic for indications for emergency renal replacement therapy:

• A — Acidosis (severe, refractory metabolic acidosis)

• E — Electrolyte abnormalities (refractory hyperkalaemia despite medical management)

• I — Intoxication (certain dialysable poisons — lithium, methanol, salicylates, ethylene glycol)

• O — Overload (refractory pulmonary oedema/fluid overload)

• U — Uraemia (encephalopathy, pericarditis, uraemic bleeding)

FRCEM testing: A scenario describing refractory hyperkalaemia despite calcium, insulin/dextrose, and salbutamol is asking you to recognise the indication for urgent dialysis — not to repeat medical management indefinitely.

Hyperkalaemia: The Highest-Yield Electrolyte Topic — Updated Guidance

If you take one thing from this article, make it this section. Hyperkalaemia is the most frequently tested electrolyte emergency, and the UK Kidney Association updated its national guidance, which changed several of the specific numbers that older revision resources still teach.

ECG Changes — In Order of Severity

This sequence is tested directly and also tells you how urgently to act:

1. Peaked T waves (earliest change)

2. Flattened P waves / PR prolongation

3. Widened QRS complex

4. Sine wave pattern

5. VF / asystole

Severity Definitions

• Mild: 5.5–5.9 mmol/L

• Moderate: 6.0–6.4 mmol/L

• Severe: ≥6.5 mmol/L, or any level with ECG changes

ECG changes — not the number alone — drive urgency of treatment. A potassium of 6.2 with sine waves is treated as severe regardless of the "moderate" label.

Step 1: Protect the Heart — Calcium

This is where the updated guidance matters most.

The UK Kidney Association's updated guideline recommends that IV calcium chloride is the preferred calcium salt in cardiac arrest or peri-arrest, while IV calcium gluconate should be used for all other patients with ECG signs of hyperkalaemia.

Following an MHRA review into underdosing concerns, the recommended dose of calcium gluconate increased: 30 ml of 10% calcium gluconate IV over 10 minutes is now the recommended initial dose — a notable increase from the 10 ml often cited in older teaching.

Key points:

• Calcium does not lower serum potassium — it stabilises the cardiac membrane and protects against arrhythmia while other treatments take effect

• Repeat ECG after calcium administration to confirm effect

• If ECG changes persist, the dose can be repeated

• Use with caution in patients on digoxin — calcium can potentiate digoxin toxicity

Step 2: Shift Potassium Into Cells — Insulin/Glucose

For severe hyperkalaemia (K⁺ ≥6.5 mmol/L), the updated guideline recommends insulin-glucose infusion: 10 units of soluble insulin in 25 g of glucose by IV infusion.

Critical monitoring point: Delayed hypoglycaemia is a well-recognised complication. Monitor capillary glucose at 0, 15, and 30 minutes, then hourly for up to 6 hours. If pre-treatment glucose is low (<7 mmol/L), a 10% glucose infusion may be needed afterward to prevent hypoglycaemia.

Adjuncts to shift potassium:

• Nebulised salbutamol (10–20 mg) — additional potassium-lowering effect, used alongside insulin/glucose, not instead of it

• IV sodium bicarbonate — only if significant metabolic acidosis is present; not a routine hyperkalaemia treatment on its own

Step 3: Remove Potassium From the Body

• Dialysis — definitive treatment, especially in AKI/CKD with refractory hyperkalaemia

• Potassium binders (e.g. sodium zirconium cyclosilicate / patiromer) — onset over hours, not for acute severe hyperkalaemia, but increasingly used as an adjunct in the modern pathway

• Calcium resonium — largely superseded; slow onset, not appropriate for acute management

The Updated Hyperkalaemia Algorithm — Summary

FRCEM trap: If a question option says "10 ml of 10% calcium gluconate" as the correct first step, that reflects the older dosing. The current recommended dose is 30 ml. Similarly, "50 units of insulin in 50 ml of 50% dextrose" overstates the glucose load relative to current guidance (10 units / 25 g).

For the broader resuscitation context — including hyperkalaemia as one of the 4Hs reversible causes of cardiac arrest — see the FRCEM SLO 3 resuscitation guide.

Hyponatraemia

Hyponatraemia questions test two things: assessing volume status to find the cause, and knowing when (and how) to use hypertonic saline.

Assess Volume Status First

• Hypovolaemic: vomiting, diarrhoea, diuretics, Addison's — give isotonic saline cautiously

• Euvolaemic: SIADH (common causes: malignancy, CNS pathology, pneumonia, certain drugs — SSRIs, carbamazepine), hypothyroidism, adrenal insufficiency

• Hypervolaemic: heart failure, cirrhosis, nephrotic syndrome — fluid restriction, treat underlying cause

Severe Symptomatic Hyponatraemia: Hypertonic Saline

For severe symptoms — seizures, significantly reduced GCS, signs of cerebral oedema — regardless of chronicity, this is a medical emergency.

Management: 150 ml of 3% hypertonic saline IV over 10–20 minutes, which can be repeated up to a total of 3 boluses (or until symptoms improve), aiming for an initial rise in serum sodium of approximately 4–6 mmol/L.

Critical safety point — overcorrection risk: Once symptoms improve or the target rise of 4–6 mmol/L is reached in the first hour, stop further hypertonic saline boluses. The overall correction rate should not exceed 10 mmol/L in 24 hours (some sources use 8 mmol/L as the more conservative ceiling) — overcorrection risks osmotic demyelination syndrome (ODS), a devastating and often irreversible complication.

FRCEM testing: A scenario presents a seizing patient with sodium 112 mmol/L. The correct answer is 150 ml 3% hypertonic saline as a bolus — not slow correction with normal saline, and not free water restriction (which has no role in the acute emergency setting).

Calcium Disorders

Hypercalcaemia

Most common ED cause: malignancy (bone metastases, myeloma, PTHrP-secreting tumours) and primary hyperparathyroidism.

Symptoms — "bones, stones, groans, and psychiatric moans": bone pain, renal stones/AKI, abdominal pain/constipation, confusion.

Management of severe hypercalcaemia (typically >3.0–3.5 mmol/L or symptomatic):

1. IV fluids (0.9% saline) — rehydration is first-line; promotes renal calcium excretion

2. IV bisphosphonate (e.g. zoledronic acid) — once rehydrated; takes 2–4 days for full effect, so this addresses the underlying cause while fluids manage the acute crisis

3. Calcitonin — rapid onset but short-lived effect, used for very severe/symptomatic cases as a bridge

FRCEM trap: Don't select bisphosphonate alone as the "immediate" management — fluids come first, and bisphosphonates take days to work.

Hypocalcaemia

Causes: hypoparathyroidism (including post-thyroidectomy), vitamin D deficiency, pancreatitis, rhabdomyolysis, massive blood transfusion (citrate toxicity), severe hypomagnesaemia (impairs PTH release/action — correct magnesium first or calcium replacement won't work).

Signs: Chvostek's sign (facial twitch on tapping facial nerve), Trousseau's sign (carpal spasm with BP cuff inflation), tetany, seizures, prolonged QTc.

Management: IV calcium gluconate (not calcium chloride peripherally — chloride is more tissue-irritant and can cause severe extravasation injury). Check and correct magnesium alongside calcium.

Hypomagnesaemia

Often overlooked, but tested because of its relationship with both potassium and calcium.

Why it matters: Hypomagnesaemia causes renal potassium wasting — hypokalaemia that won't correct despite potassium replacement is a classic sign of coexisting hypomagnesaemia. It also impairs PTH secretion, causing hypocalcaemia.

ECG effects: Prolonged QT, predisposition to torsades de pointes (also the first-line treatment for torsades regardless of baseline magnesium level — IV magnesium sulphate 2 g).

Management: IV magnesium sulphate. FRCEM rule: if a question presents refractory hypokalaemia despite adequate potassium replacement, the next step is to check and correct magnesium.

Common FRCEM Mistakes

1. Using outdated calcium gluconate doses for hyperkalaemia The current recommended dose is 30 ml of 10% calcium gluconate over 10 minutes — not 10 ml. This update is recent enough that many question banks and notes haven't caught up.

2. Forgetting that calcium doesn't lower potassium Calcium protects the myocardium. Insulin/glucose (and salbutamol) are what actually shift potassium intracellularly. Both are needed — calcium alone is not definitive treatment.

3. Missing delayed hypoglycaemia after insulin/glucose Glucose monitoring must continue for up to 6 hours after insulin-glucose infusion — hypoglycaemia can occur well after the infusion finishes.

4. Overcorrecting hyponatraemia Stop hypertonic saline once symptoms improve or sodium has risen 4–6 mmol/L. Continuing boluses to "normalise" sodium rapidly risks osmotic demyelination syndrome.

5. Treating hypocalcaemia without checking magnesium If magnesium is low, calcium replacement alone won't correct the hypocalcaemia — PTH release remains impaired until magnesium is corrected.

6. Missing post-renal AKI A blocked catheter or urinary retention is the most easily reversible cause of AKI — and the most commonly missed on a busy take. Bladder scan should be routine in unexplained AKI.

7. Calling bisphosphonate the "immediate" treatment for hypercalcaemia IV fluids come first. Bisphosphonates take days to lower calcium, even though they're essential for sustained control.

Put Your Knowledge to the Test

Reading about guideline updates is one thing, but applying them under time pressure against expert-level distractors is exactly how the FRCEM SBA tests your clinical reasoning.

Can you spot the difference between an initial treatment and a definitive one? Do you know exactly when to withhold calcium gluconate in a crashing patient?

Stop passively reading and start actively testing your exam technique. Our comprehensive FRCEM SBA question bank covers every single curriculum topic — from these tricky electrolyte emergencies to complex trauma, toxicology, and beyond.

👉 Take a Free Demo Quiz or Register to Unlock the Full Question Bank

Study Strategy

This topic rewards memorising exact numbers more than almost any other area of the FRCEM curriculum — there's relatively little ambiguity once you know the protocol.

Priority order:

1. Hyperkalaemia — the updated calcium gluconate dose (30 ml of 10%) and insulin-glucose regime (10 units/25g) are the highest-yield specific facts in this entire guide

2. AKI staging — KDIGO multipliers (1.5–1.9× / 2.0–2.9× / ≥3×)

3. Severe hyponatraemia — 150 ml 3% hypertonic saline, 4–6 mmol/L target, stop on improvement

4. AEIOU for emergency dialysis indications

5. Hypercalcaemia sequence — fluids before bisphosphonate

6. Hypomagnesaemia as the cause of refractory hypokalaemia/hypocalcaemia

This topic pairs naturally with the RCEM clinical guidelines cheat sheet, since the hyperkalaemia dosing update is exactly the kind of recent change that older question banks haven't reflected yet.

AKI and electrolyte emergencies are number-driven, protocol-based, and highly predictable — which makes them some of the most efficient marks to secure in your final revision weeks. Get the updated hyperkalaemia doses exactly right, know the KDIGO multipliers, and understand the hypertonic saline ceiling for hyponatraemia, and this topic stops being a weak spot.

For SLO-mapped questions covering AKI and electrolyte emergencies with detailed, guideline-referenced explanations, register with StudyFRCEM.