Severe hyperkalaemia with conduction delay in advanced CKD, fluid overload and an existing non-dialysis central line
A 62-year-old woman with diabetic kidney disease (CKD stage 5, eGFR 8 mL/min/1.73 m², not yet on dialysis) presents after 3 days of vomiting and poor oral intake. She is drowsy but rousable. Blood pressure 168/92 mmHg, pulse 52/min, SpO₂ 94% on room air, bibasal crackles, raised JVP, bilateral pedal oedema, and a weight gain of 3 kg over one week. ECG shows peaked T waves, PR interval 0.24 s, QRS 130 ms, and absent P waves in V1. Potassium is 7.6 mmol/L, bicarbonate 11 mmol/L, urea 210 mg/dL, creatinine 8.9 mg/dL, sodium 128 mmol/L, glucose 190 mg/dL, venous pH 7.18. She has no arteriovenous fistula. A non-tunnelled right internal jugular line inserted 36 hours ago by the admitting team is still in situ. Platelets are 88 × 10⁹/L. She takes sodium bicarbonate 500 mg three times daily; no potassium-sparing drugs.
1. Set out the first 30 minutes of management in order, and state which measures you would withhold in this particular patient.
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This is a pre-arrest ECG (QRS 130 ms, no P waves) - membrane stabilisation comes first.
- IV calcium gluconate 10 mL of 10% over 5–10 minutes under continuous ECG monitoring, repeated if the QRS remains wide at 5 minutes. Onset is 1–3 minutes, duration 30–60 minutes; it protects the myocardium but does not lower potassium. Calcium chloride is more sclerosing and should not be given peripherally.
- Insulin 10 units with 25 g dextrose IV, then monitor glucose hourly - the hypoglycaemia risk is substantial in renal failure because insulin clearance is reduced.
- Nebulised salbutamol 10–20 mg as an adjunct; watch for tachycardia in a patient who may have ischaemia.
- Continuous cardiac monitoring, IV access, and simultaneous preparation for urgent dialysis - the definitive therapy for this potassium.
Withheld or de-emphasised here:
- Sodium bicarbonate: her acidosis is respiratory-compensated renal acidosis at pH 7.18, and she is already on oral bicarbonate and volume-overloaded; 50 mmol IV adds sodium and volume, can cause hypocalcaemia and tetany, and is reserved for pH <7.1–7.2 in a non-overloaded patient.
- Potassium binders (sodium zirconium cyclosilicate, patiromer) should not be relied on as the urgent measure; onset is 1–4 hours and they are a bridge only.
- Do not give potassium-containing fluids, NSAIDs or ACE inhibitors, and do not treat the drowsiness as a sedative effect without excluding uraemia.
2. Justify dialysing now, and give the dialysis prescription - access, membrane, dialysate, anticoagulation given platelets 88 × 10⁹/L - plus the things you would deliberately avoid.
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Indications converge: hyperkalaemia refractory to medical therapy with conduction delay, oliguric acute-on-chronic kidney failure (urea 210 mg/dL with encephalopathy), refractory volume overload and severe acidosis. Dialysis is not a rescue after failed medical therapy here - it is the definitive treatment and should be started as soon as access is obtained.
Access: the existing 36-hour non-tunnelled internal jugular line was not placed for dialysis, is likely too short for adequate blood flow, and its sterility is unknown. Insert a dedicated non-tunnelled dialysis catheter under ultrasound guidance in the right internal jugular vein, preserving the left side and the non-dominant arm veins for future fistula creation. Avoid subclavian access because of venous stenosis risk; a femoral line is an acceptable temporary alternative.
Prescription: high-flux dialyser; blood flow 200–250 mL/min; dialysate potassium 2 mmol/L (zero or 1 mmol/L risks post-dialysis hypokalaemia and arrhythmia); bicarbonate-buffered dialysate; dialysate temperature 36 °C; modest ultrafiltration of 1–2 L in the first session with sequential removal thereafter.
Anticoagulation: heparin-free with intermittent saline flushes given platelets of 88 × 10⁹/L (not severe thrombocytopenia, but systemic heparin is avoidable); if the circuit clots, regional citrate is preferable to systemic heparin provided liver function is adequate.
Deliberately avoid: rapid solute removal and large ultrafiltration volumes in the first session (dialysis disequilibrium and intradialytic hypotension), subclavian cannulation, and forgetting that potassium rebounds after dialysis as it shifts out of cells.
3. Twelve hours later potassium is 6.2 mmol/L and she is more breathless with SpO₂ 89% on room air. How do you interpret this and what do you do?
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Interpretation: this is not a single problem.
- Rebound hyperkalaemia is expected after a single session in a catabolic, acidotic patient with residual intracellular stores; 6.2 mmol/L still requires an ECG and, if conduction is abnormal, calcium gluconate.
- Worsening hypoxia has a short differential that must be worked through actively: fluid overload from the 3 kg gain with inadequate ultrafiltration; procedure-related complications of the new line (pneumothorax, haemothorax, haematoma) - which is why a post-insertion chest radiograph and examination are mandatory; hospital-acquired pneumonia or aspiration given her drowsiness and vomiting; and possibly pulmonary haemorrhage in a patient with platelets of 88 × 10⁹/L.
Immediate steps: ABC assessment, ECG, arterial blood gas, chest radiograph, bedside ultrasound of lungs and pleural spaces, and review of the dialysis record (net ultrafiltration achieved, circuit clotting, catheter blood flow).
Management: stabilize the potassium (calcium if ECG changes, insulin-dextrose, salbutamol), treat the hypoxia with oxygen and, if the cause is pulmonary oedema, escalate ultrafiltration in the next session rather than giving more fluid; if pneumothorax, drain. Abandon any plan for a one-off dialysis - she needs daily sessions and definitive planning for a functioning arteriovenous fistula, because this cycle will recur.