AKI & Electrolyte Emergencies for FRCEM SBA: A Practical Guide for Emergency Medicine Doctors


What Are AKI & Electrolyte Emergencies and Why Do They Matter in the ED?


Acute kidney injury (AKI) is a sudden decline in kidney function over hours–days, leading to reduced urine output and/or a rise in serum creatinine. NICE NG148 uses criteria equivalent to KDIGO: a ≥50% rise in creatinine within 7 days or oliguria <0.5 ml/kg/hr for >6 hours in adults, among others. (NICE)


Electrolyte emergencies are acute, potentially life-threatening disturbances in serum electrolytes, especially:


These problems are bread-and-butter ED medicine and perfect for FRCEM SBA: the exam loves numbers-heavy stems where you must interpret U&Es, ECGs and choose the correct, guideline-aligned “next best step”.


How AKI & Electrolyte Emergencies Appear in the FRCEM SBA Exam


Expect SBAs built around:


  • Diagnosis / recognition
    • Interpreting KDIGO/NICE criteria to decide if AKI is present and how severe it is. (NICE)
    • Spotting dangerous hyperkalaemia (e.g. K⁺ ≥6.5 mmol/L or ECG changes). (UK Kidney Association)
    • Identifying severe symptomatic hyponatraemia vs chronic/asymptomatic. (Clinical Knowledge Summaries)
    • Recognising hypercalcaemia of malignancy patterns.


  • Initial investigation choice


  • First-line management
    • Fluid resuscitation vs restriction (AKI, hypovolaemic vs hypervolaemic hyponatraemia).
    • Hyperkalaemia bundle: IV calcium, insulin–dextrose, nebulised salbutamol ± potassium binders and dialysis. (UK Kidney Association)
    • Hypercalcaemia: IV fluids + IV bisphosphonates (e.g. zoledronic acid). (Gloucestershire Hospitals Trust)


  • Complications / red flags
    • AKI → pulmonary oedema, refractory hyperkalaemia, metabolic acidosis.
    • Hyponatraemia → seizures, reduced GCS.
    • Hyperkalaemia → wide QRS, sine wave, VF arrest.
    • Hypercalcaemia → arrhythmias, AKI.


Typical formats:

  • Chunky U&E panels and VBG results.
  • ECG descriptions (“tall tented T waves, flattened P waves”).
  • Guideline-style “single best next step” questions.


Example micro-scenario:

A 79-year-old man with sepsis and poor oral intake has creatinine rising from 90 to 160 μmol/L over 2 days, urine output 0.3 ml/kg/hr. K⁺ 6.8 mmol/L, ECG shows broad QRS with peaked T waves. What is the most appropriate immediate treatment?


Core Concepts You Must Know About AKI & Electrolyte Emergencies


Definitions & Key Criteria


AKI – NICE/KDIGO concepts (NICE)


AKI is present if any of:

  • Increase in serum creatinine ≥26 μmol/L within 48 hours, or
  • Increase in serum creatinine to ≥1.5 times baseline within the last 7 days, or
  • Urine output <0.5 ml/kg/hr for >6 hours (adult).


You don’t need to quote all KDIGO stages in the exam, but know:


  • AKI 1 – mild rise or modest oliguria.
  • AKI 2–3 – bigger creatinine rises, prolonged oliguria/anuria → higher risk, likely needs senior/nephrology input.


Hyperkalaemia (adult) – RA/UKKA: (UK Kidney Association)


  • Mild: K⁺ 5.5–5.9 mmol/L
  • Moderate: 6.0–6.4 mmol/L
  • Severe: ≥6.5 mmol/L or any level with ECG changes


Hyponatraemia – NICE/European guideline: (Clinical Knowledge Summaries)


  • Na⁺ <135 mmol/L; classify by severity and symptomatology: 
    • Mild: 130–134
    • Moderate: 125–129
    • Severe: <125, especially if acute/symptomatic.


Also classify by volume status (hypovolaemic, euvolaemic, hypervolaemic) and chronicity (acute <48 h vs chronic).


Hypercalcaemia – typical cut-offs: (Gloucestershire Hospitals Trust)


  • Normal adjusted Ca²⁺ ≈ 2.2–2.6 mmol/L
  • Mild: 2.6–3.0 mmol/L
  • Severe: ≥3.0 mmol/L, especially if symptomatic (confusion, dehydration, arrhythmia).


Hypocalcaemia (exam-level):


  • Corrected Ca²⁺ <2.1 mmol/L; consider acute symptomatic hypocalcaemia in post-thyroid/parathyroid surgery, massive transfusion, pancreatitis.



Assessment & Investigations


AKI – ED assessment


  • History: volume loss (vomiting, diarrhoea, diuretics), sepsis, nephrotoxins (ACEi/ARB, NSAIDs, contrast, aminoglycosides), obstruction (urinary symptoms, retention, BPH).
  • Examination: volume status, bladder palpable, lung bases (fluid overload).
  • Investigations: 
    • U&Es, creatinine, bicarbonate, lactate.
    • Urinalysis – blood, protein, casts.
    • Bladder scan; consider urgent renal tract ultrasound if obstruction suspected. (NICE)


Hyperkalaemia


  • Recheck K⁺ if unexpected.
  • 12-lead ECG + continuous monitoring – essential in moderate/severe or symptomatic cases.
  • Look for: peaked T waves, flattened P waves, PR prolongation, wide QRS, sine-wave pattern. (UK Kidney Association)
  • Identify triggers: AKI, medications (ACEi/ARB, spironolactone, trimethoprim), metabolic acidosis, rhabdomyolysis.


Hyponatraemia


  • History: fluid intake, diuretics, SSRIs, antiepileptics, heart failure, liver disease, malignancy, CNS/pulmonary disease (SIADH).
  • Exam: volume status – JVP, oedema, mucous membranes, postural BP.
  • Investigations: 
    • Serum Na⁺, osmolality, U&Es, glucose, cortisol, TFTs.
    • Urine sodium and osmolality to classify SIADH vs hypovolaemic/hypervolaemic causes. (Clinical Knowledge Summaries)


Calcium disorders


  • Ask about malignancy, bone pain, fractures, kidney stones, polyuria, polydipsia, vitamin D supplements, thiazides.
  • Corrected Ca²⁺, phosphate, PTH, U&Es, ECG (shortened QT in hypercalcaemia, prolonged QT in hypo).


Initial ED Management


AKI – ED priorities (NICE NG148): (NICE)


  1. ABCDE – manage sepsis and shock early.
  2. Optimise intravascular volume (balanced crystalloids or 0.9% NaCl depending on situation).
  3. Stop or avoid nephrotoxins (ACEi/ARB, NSAIDs, contrast) if safe to hold.
  4. Treat underlying cause – e.g. antibiotics for sepsis, relieve obstruction (catheter, urology).
  5. Monitor U&Es, urine output, lactate; early nephrology referral for severe AKI (Stage 3), refractory hyperkalaemia, pulmonary oedema, or suspected intrinsic renal disease.


Hyperkalaemia – RA/UKKA/UK practice: (UK Kidney Association)


For K⁺ ≥6.5 mmol/L or ECG changes, treat as medical emergency:


  1. Membrane stabilisation
    • IV calcium (e.g. calcium gluconate 10% 10 mL IV over 2–5 min); repeat if ECG changes persist.
  2. Shift K⁺ into cells
    • Insulin–dextrose: e.g. 10 units soluble insulin in 25 g glucose IV.
    • Nebulised salbutamol (e.g. 10–20 mg via nebuliser) if not contraindicated.
  3. Remove K⁺ from body
    • Loop diuretics if fluid-loaded and kidneys working.
    • Potassium binders (patiromer, sodium zirconium cyclosilicate) often via specialist/renal guidance.
    • Urgent dialysis for refractory or life-threatening hyperkalaemia (especially in severe AKI or CKD).
  4. Continuous ECG & repeat K⁺ levels.


Hyponatraemia – ED management: (Clinical Knowledge Summaries)


  • Severe symptomatic (seizures, reduced GCS) hyponatraemia (often Na⁺ <120): 
    • Treat with hypertonic saline (e.g. 3% NaCl) in small boluses aiming to raise Na⁺ by 4–6 mmol/L in the first 6 hours, not exceeding ~8–10 mmol/L in 24 hours, to avoid osmotic demyelination (check local protocol).
    • Continuous monitoring, ICU/HDU input.


  • Mild–moderate, asymptomatic or chronic: 
    • Treat underlying cause and adjust fluids: 
      • Hypovolaemic → isotonic crystalloid.
      • Euvolaemic (e.g. SIADH) → fluid restriction; consider medications (e.g. vaptans) via specialist. (Clinical Knowledge Summaries)
      • Hypervolaemic (HF, cirrhosis) → fluid + salt restriction, diuretics, heart failure/ liver optimisation.


Calcium disorders – emergency hypercalcaemia: (Gloucestershire Hospitals Trust)


  • Acute severe hypercalcaemia (≥3.0 mmol/L or symptomatic): 
    1. IV fluids – 0.9% NaCl to correct dehydration (careful in HF).
    2. IV bisphosphonate – e.g. zoledronic acid 4 mg IV over at least 15 min (adjusted if severe renal impairment).
    3. Consider calcitonin (regional variation) for faster, short-lived Ca²⁺ reduction.
    4. Treat precipitating cause (malignancy, excess vitamin D, hyperparathyroidism).


  • Acute symptomatic hypocalcaemia: 
    • IV calcium gluconate, treat cause (e.g. post-thyroidectomy, massive transfusion, pancreatitis).


Red Flags and Pitfalls


Red flags:


  • AKI + pulmonary oedema or refractory hyperkalaemia → urgent renal / ICU.
  • K⁺ ≥6.5 or ECG changes → treat now, not after ward round. (UK Kidney Association)
  • Hyponatraemia with seizures or reduced GCS → hypertonic saline under senior guidance. (European Society of Endocrinology)
  • Hypercalcaemia with confusion, dehydration, AKI → urgent fluids + bisphosphonate.


Exam pitfalls FRCEM loves:


  • Correcting chronic hyponatraemia too fast → osmotic demyelination.
  • Using normal saline for SIADH (worsens hyponatraemia).
  • Forgetting IV calcium in life-threatening hyperkalaemia.
  • Failing to stop nephrotoxic drugs in AKI.
  • Missing post-renal obstruction as cause of AKI (no bladder scan, no ultrasound when indicated). (NICE)


Special Populations


  • Elderly/frail – more prone to AKI and HHS/Na⁺ issues; fluid balance is very fine.
  • Paediatrics – different thresholds and fluid regimens for hyperkalaemia and hyponatraemia; always use paediatric-specific guidance. (watch.nhs.uk)
  • Pregnancy – AKI causes differ (pre-eclampsia, HELLP, hyperemesis); hyperkalaemia & hyponatraemia management needs obstetric input.


Common FRCEM SBA Traps Related to AKI & Electrolyte Emergencies


“Question writers love to test the difference between X and Y…”


  • Hyperkalaemia with normal ECG
    • Trap: Ignoring K⁺ 6.8 because the ECG “looks okay”.
    • Fix: RA/UKKA: K⁺ ≥6.5 is severe and still needs active treatment; ECG changes just increase urgency. (UK Kidney Association)


  • Treating SIADH with 0.9% NaCl
    • Trap: Giving normal saline to euvolaemic SIADH (worsens Na⁺).
    • Fix: SIADH is usually fluid restriction ± other measures; use saline cautiously based on expert guidance. (European Society of Endocrinology)


  • Over-rapid correction of chronic hyponatraemia
    • Trap: Driving Na⁺ up >10–12 mmol/L in 24 hours.
    • Fix: Aim for slow correction and stop/slacken if rising too quickly; consider desmopressin to prevent over-correction in some cases. (European Society of Endocrinology)


  • Assuming all AKI is “pre-renal”
    • Trap: Giving endless fluid to a patient with AKI from obstruction or intrinsic GN.
    • Fix: Take a proper history, examine, do urinalysis + bladder scan + ultrasound when indicated. (NICE)


  • Delaying hypercalcaemia treatment
    • Trap: Waiting for full malignancy work-up before treating Ca²⁺ 3.4 mmol/L and confusion.
    • Fix: Severe/symptomatic hypercalcaemia requires urgent fluids ± bisphosphonate now, then full work-up. (Gloucestershire Hospitals Trust)


High-Yield Clinical Patterns for AKI & Electrolyte Emergencies in the ED


Classic Presentation – AKI with Hyperkalaemia


Age: 79-year-old manBackground: CKD 3, HF, ACEi + spironolactoneSymptoms: Reduced oral intake, diarrhoea, breathlessnessObs: HR 110, BP 95/60, RR 24, SpO₂ 94% RALabs: Urea 25 mmol/L, creatinine 220 μmol/L (baseline 110), K⁺ 6.7 mmol/L, HCO₃⁻ 16 mmol/LECG: Peaked T waves, broad QRS


FRCEM angle: recognise AKI with severe hyperkalaemia → give IV calcium + insulin–dextrose + fluids + nephro consult.


Classic Presentation – Symptomatic Hyponatraemia


Age: 62-year-old womanBackground: Small-cell lung cancer, on chemoSymptoms: Headache, confusion, vomiting, had a tonic–clonic seizure in EDObs: HR 96, BP 140/80, RR 18, SpO₂ 98% RALabs: Na⁺ 112 mmol/L, serum osmolality low, urine osmolality high, urine Na⁺ 55 mmol/L


Pattern suggests acute symptomatic SIADH-related hyponatraemia → hypertonic saline in ICU/HDU with tight correction window, then onc/endo involvement.


Classic Presentation – Hypercalcaemia of Malignancy


Age: 70-year-old manBackground: Metastatic lung cancerSymptoms: Polyuria, polydipsia, constipation, confusionLabs: Adjusted Ca²⁺ 3.2 mmol/L, creatinine 180 μmol/L, PTH suppressed


ED answer: IV 0.9% saline to rehydrate + IV zoledronic acid ± short-term calcitonin, admit under oncology/medicine. (Gloucestershire Hospitals Trust)


Dangerous Mimics

  • Pseudohyperkalaemia – haemolysed sample; repeat before panicking (unless ECG bad).
  • Pseudohyponatraemia – hyperglycaemia or high lipids/proteins; check serum osmolality. (Clinical Knowledge Summaries)
  • AKI vs CKD – longstanding anaemia, small kidneys on ultrasound, known low eGFR history.


How to Revise AKI & Electrolyte Emergencies Efficiently for the FRCEM SBA


Use Question Banks First, Then Guidelines


  1. Do blocks of AKI + electrolyte SBAs: 
    • U&Es, ECG changes, fluid regimes, hyperkalaemia bundles, hyponatraemia correction, hypercalcaemia management.
  2. Then read targeted sections of: 
    • NICE NG148 – Acute kidney injury: prevention, detection and management (ED-side recognition, investigation and referral). (NICE)
    • Renal Association/UKKA hyperkalaemia guideline – thresholds and treatment bundles. (UK Kidney Association)
    • Local/NICE CKS hyponatraemia guidance – especially for fluid strategies and correction limits. (Clinical Knowledge Summaries)
    • Emergency hypercalcaemia guidelines (Endocrine Society & UK oncology/acute oncology resources). (Gloucestershire Hospitals Trust)


Build Mini-Notes or Flashcards from Mistakes


For each wrong AKI/electrolyte question, capture:

  • What the stem was really about
    • “Hyperkalaemia with normal ECG,”
    • “Chronic hyponatraemia – rate of correction,”
    • “Post-renal AKI vs pre-renal.”
  • Your error
    • Misread K⁺ threshold, forgot ECG, picked wrong fluid, ignored obstruction.
  • One-liner rule
    • “K⁺ ≥6.5 or ECG changes = IV calcium + insulin–dextrose + salbutamol + consider dialysis.” (UK Kidney Association)
    • “In chronic hyponatraemia, correct Na⁺ by ≤8–10 mmol/L in 24 h to avoid osmotic demyelination.” (European Society of Endocrinology)
    • “Always look for obstruction in unexplained AKI – bladder scan + ultrasound when indicated.” (NICE)


Mix Text-Based and Image-Based Questions

  • Use data tables (U&Es, gas, osmolality) as the main pattern-recognition training.
  • Include ECG screenshots for hyperkalaemia and prolonged QT.
  • Include ultrasound/bedsides images when AKI is due to obstruction or volume issues.


How StudyMedical Covers AKI & Electrolyte Emergencies in Its FRCEM SBA Question Bank


Within StudyMedical, AKI and electrolyte emergencies sit across the Renal/Endocrine/Resuscitation bits of the RCEM 2021 curriculum, so you can slice them multiple ways:

  • Curriculum-mapped AKI SBAs
    • Pre-renal vs intrinsic vs post-renal, sepsis-induced AKI, contrast-associated AKI, obstruction and nephrotoxin cases – all with full vitals and U&Es.
  • Electrolyte emergency SBAs
    • Hyperkalaemia cases spanning K⁺ 5.8–7.8 with varying ECG changes and different underlying drivers.
    • Hyponatraemia stems that force you to decide hypertonic saline vs fluid restriction vs isotonic crystalloid.
    • Calcium disorder cases tied to malignancy, hyperparathyroidism, and iatrogenic causes.
  • Image- and data-based questions
    • ECGs showing hyperkalaemic changes or long QT, simple ultrasound/CT descriptions for obstructive AKI, and serial U&Es to track response to therapy.
  • Guideline-referenced explanations
    • Explanations that explicitly reference NICE NG148, RA/UKKA hyperkalaemia guidelines, hyponatraemia and hypercalcaemia guidance so you’re automatically revising UK practice while doing questions. (NICE)


FAQs About AKI & Electrolyte Emergencies in the FRCEM SBA


How often do AKI and electrolyte emergencies appear in the FRCEM SBA exam?


Very regularly. They’re common in real ED practice and map neatly to multiple SLOs (renal, endocrine, resus), so examiners love them.


What’s the single most important thing to remember about these topics for the exam?


Interpret the numbers in context (U&Es, osmolality, ECG) and then apply the correct UK guideline-driven bundle (hyperkalaemia treatment, hyponatraemia correction limits, AKI investigations).


Are there any must-know guidelines related to AKI & electrolytes?


Yes:


How many AKI- and electrolyte-related questions should I aim to do before the exam?


Aim for at least 40–60 focused SBAs spanning AKI, hyperkalaemia, hyponatraemia and Ca²⁺ disorders, plus plenty of mixed “medical take” questions.


Key Takeaways: AKI & Electrolyte Emergencies for FRCEM in 5 Bullet Points

  • AKI: use creatinine change + urine output to diagnose and always look for sepsis, volume, nephrotoxins, obstruction. (NICE)
  • Hyperkalaemia: K⁺ ≥6.5 or ECG changes → IV calcium + insulin–dextrose + salbutamol, then remove K⁺ and call renal early. (UK Kidney Association)
  • Hyponatraemia: treat based on symptoms, volume status and chronicity, and never correct chronic cases too quickly. (Clinical Knowledge Summaries)
  • Calcium disorders: severe/symptomatic hypercalcaemia needs IV fluids + IV bisphosphonate and malignancy work-up. (Gloucestershire Hospitals Trust)
  • The fastest way to master them is interpret–decide–treat drills via SBAs plus a quick pass through the core guidelines.


Ready to Test Yourself on AKI & Electrolyte Emergencies?


AKI, hyperkalaemia, hyponatraemia and calcium disorders are:


  • Common in the ED,
  • Highly dangerous if mismanaged, and
  • Rich in exam-friendly numbers and patterns.


Understanding the key patterns plus hammering FRCEM-style SBAs will make these questions feel like free marks.