Electrolyte emergencies in the ICU — the drugs, the doses, the onsets, and the things each drug does not do
Based on Koyner, Handbook of Critical Care Nephrology (2021) · NTUH Yunlin Branch
Learning objectives
Koyner Ch 21–24, 49–50 · Ronco Ch 41, 57–58 · Cairo–Bishop 2004 · NICE CG32
The only electrolyte that kills within minutes — and the one where the reflex to treat most often outruns the duty to verify.
There is no reliable conversion factor between pH and serum K⁺. Mineral (non-gap) acidosis shifts potassium out of cells substantially; organic acidosis (lactic, ketoacidosis) and respiratory acidosis do so far less, because the accompanying anion enters the cell with the proton. Never "correct" a measured potassium for pH at the bedside.
Koyner Ch 21 · Palmer BF. Clin J Am Soc Nephrol 2015;10:1050 · Ronco Ch 57
| True hyperkalaemia — mechanism | ICU examples |
|---|---|
| Reduced renal excretion | AKI, AKI on CKD, oliguria, effective volume depletion |
| Hypoaldosteronism / blockade | ACEi, ARB, spironolactone, eplerenone, amiloride, triamterene, heparin, calcineurin inhibitors, trimethoprim, NSAIDs |
| Cellular release | Rhabdomyolysis, tumour lysis, haemolysis, ischaemic gut, burns, succinylcholine |
| Shift out of cells | Mineral acidosis, insulin deficiency, hypertonicity, non-selective β-blockade, digoxin toxicity |
| Load | Stored blood, TPN, tube feeds, K⁺-containing drug diluents, oral supplements |
A whole-blood gas potassium takes 60 seconds and settles the question in almost every case.
Koyner Ch 21 · Palmer BF, Clegg DJ. JAMA 2015;314:2405 · Ronco Ch 57
Peaked T wavesTall, narrow, symmetrical; shortened QT. Earliest and least specific.
P-wave lossFlattening then disappearance; PR prolongation.
QRS wideningBundle-branch-like patterns. This is the danger zone — treat now.
Sine waveQRS merges with T; then bradycardia, idioventricular rhythm, VF or asystole.
ECG changes correlate poorly with the serum potassium. In a retrospective review of hyperkalaemic episodes, strict ECG criteria were insensitive and a substantial proportion of patients with K⁺ above 6.5 mmol/L had no diagnostic changes at all. A normal ECG never makes a potassium of 7 safe, and chronic hyperkalaemia is better tolerated than an acute rise of the same magnitude. Treat the number, the rate of rise and the cause — and give calcium whenever any ECG change is present.
Montague BT et al. Clin J Am Soc Nephrol 2008;3:324 · Koyner Ch 21 · Ronco Ch 57
Protect the membrane — IV calcium if any ECG change or K⁺ > 6.5 mmol/L. Onset 1–3 min, duration 30–60 min. It does not lower potassium by a single mmol.
Shift it into cells — insulin with dextrose (first-line), nebulised salbutamol (additive). Onset 15–30 min, lasts 2–6 h. Total body potassium is unchanged; the number will come back.
Correct a metabolic acidosis — sodium bicarbonate only if the patient is acidaemic and you would have treated the acidosis anyway. Slow, weak, and not a shifting agent at conventional doses.
Excrete it renally — loop diuretic ± saline in a patient who still makes urine. Cheap and rational; no trial shows a reliable acute kaliuresis.
Bind it in the gut — sodium zirconium cyclosilicate or patiromer. Real potassium removal, but hours not minutes: a bridge and a chronic tool, not a resuscitation drug.
Dialyse — the only therapy that removes large amounts fast. Indicated for refractory or recurrent hyperkalaemia, anuric AKI, or ongoing cell lysis.
Koyner Ch 21 · Ronco Ch 57 · Blumberg A et al. Am J Med 1988;85:507
| Agent | Dose & route | Onset | Duration | Expected ΔK⁺ | What it does not do |
|---|---|---|---|---|---|
| Calcium gluconate 10% | 10–30 mL IV over 2–3 min; repeat at 5 min if ECG changes persist, then hourly while hyperkalaemic | 1–3 min | 30–60 min | None | Does not lower potassium at all — it buys time only |
| Calcium chloride 10% | 10 mL IV via central line (3× the elemental calcium of gluconate) | 1–3 min | 30–60 min | None | Peripheral extravasation causes tissue necrosis |
| Regular insulin + dextrose | 10 units IV with 25 g dextrose (50 mL of 50%); 5 units or 0.1 U/kg if eGFR < 30 or glucose low | 15 min | 4–6 h | 0.6–1.2 mmol/L | Removes nothing; causes hypoglycaemia for hours after |
| Salbutamol nebulised | 10–20 mg over 10 min (10× the bronchodilator dose) | ~30 min | 2–4 h | 0.5–1.0 mmol/L | Not monotherapy — a minority of patients do not respond; tachycardia limits use |
| Sodium bicarbonate 8.4% | 50–100 mmol IV — only with metabolic acidaemia | Hours | — | Unreliable | Does not shift potassium at these doses; adds sodium and volume |
| Furosemide | 40–120 mg IV (higher in CKD), with saline if not congested | 30–60 min | Variable | Unpredictable | Useless in anuria; worsens hypovolaemia if given without volume |
Koyner Ch 21 · Ronco Ch 57 · Allon M et al. Ann Intern Med 1989;110:426 · Allon M, Shanklin N. Am J Kidney Dis 1996;28:508
Hyperkalaemia in digoxin poisoning reflects Na⁺/K⁺-ATPase blockade, and IV calcium has been implicated in irreversible myocardial contracture ("stone heart"). The treatment is digoxin-specific Fab fragments, which also correct the potassium. If you must give calcium in a peri-arrest digoxin patient, give it slowly and only after Fab has been ordered.
Koyner Ch 21–22, 27 · Ronco Ch 57
Capillary glucose at 30 min, 1 h, 2 h, 4 h and 6 h. Recheck potassium at 1 h and 4 h. A single K⁺ at 60 minutes that looks reassuring is the most dangerous number in the chart, because the shift is temporary and the potassium is still in the body.
Insulin and salbutamol act on the same pump. Their effects are additive, not synergistic — combining them is reasonable, but expect roughly the sum of two modest effects, not a rescue.
Koyner Ch 21 · Allon M, Copkney C. Kidney Int 1990;38:869 · Apel J et al. Clin Kidney J 2014;7:248 · Ronco Ch 57
| Agent | Dose | Onset | Evidence & place | Cautions |
|---|---|---|---|---|
| Sodium polystyrene sulfonate | 15–30 g orally or per rectum, usually in sorbitol | Hours; unreliable | Historic data supported chronic use; modern short-term studies show little acute effect on serum K⁺ | Colonic necrosis signal, especially with sorbitol, post-operative ileus and transplant patients; large sodium load |
| Sodium zirconium cyclosilicate | 10 g three times daily for up to 48 h, then 5–10 g once daily | ~1 h; median time to normokalaemia 2.2 h in HARMONIZE | Effective in CKD and dialysis; the most credible "bridge" agent, though ICU-specific trials are lacking | Sodium load and oedema at higher doses; do not give with other oral drugs (separate by 2 h) |
| Patiromer | 8.4 g once daily, titrated weekly | ~7 h | Enables continuation of RAAS inhibitors in heart failure and CKD (OPAL-HK) | Binds magnesium — hypomagnesaemia is the classic adverse effect; constipation |
Binders are a chronic, RAAS-inhibitor-enabling tool that occasionally buys hours in the acute setting. None of them is an emergency drug, and none of them substitutes for calcium, insulin or dialysis in a patient with a wide QRS.
Kosiborod M et al. JAMA 2014;312:2223 (HARMONIZE) · Weir MR et al. N Engl J Med 2015;372:211 (OPAL-HK) · Harel Z et al. Am J Med 2013;126:264.e9 · Koyner Ch 21
A 1 mmol/L bath removes potassium fastest. The association between low-potassium baths and sudden cardiac death comes from the chronic haemodialysis population, not from the ICU; a randomised crossover study found fewer ventricular ectopics with a 1K bath. Choose the bath for the clinical situation, then recheck the potassium 4–6 h after the session ends.
Blumberg A et al. Am J Med 1988;85:507 · Blumberg A et al. Nephrol Dial Transplant 1997;12:1629 · Pun PH et al. Kidney Int 2011;79:218 · Koyner Ch 21
Koyner Ch 21 · Lin SH et al. Arch Intern Med 2004;164:1561 · Kamel KS, Halperin ML. Curr Opin Nephrol Hypertens 2011;20:547
| Route / formulation | Dose | Expected effect | Rules |
|---|---|---|---|
| Oral KCl (preferred) | 40–60 mmol per dose | Raises serum K⁺ by 1–1.5 mmol/L | Safest and fastest for a patient with a working gut; nausea limits larger doses |
| IV KCl — peripheral | 10 mmol/h, concentration ≤ 40 mmol/L | ~0.1 mmol/L per 10 mmol given | Higher concentrations cause phlebitis and pain; dilute in saline, not dextrose — dextrose triggers insulin and drives K⁺ back into cells |
| IV KCl — central | Up to 20 mmol/h | As above, faster | Continuous ECG monitoring and hourly-to-2-hourly levels. Rates of 20–40 mmol/h are described in extremis and demand a dedicated nurse |
| Potassium phosphate | 15 mmol phosphate carries ~22 mmol potassium | Corrects both deficits | Ideal when phosphate is also low; count the potassium it delivers and never co-infuse with calcium |
Intracellular magnesium depletion removes the block on ROMK and causes obligate renal potassium wasting. Until magnesium is replaced, every ampoule of potassium you give is excreted. Check and replace magnesium first, then potassium — and remember that shift-related hypokalaemia (thyrotoxic or hypokalaemic periodic paralysis) rebounds to dangerous hyperkalaemia if replaced aggressively.
Koyner Ch 21, 24 · Huang CL, Kuo E. J Am Soc Nephrol 2007;18:2649 · Hamill RJ et al. Crit Care Med 1991;19:694
One number matters in the ICU, the formula everyone quotes does not work there, and most low calcium needs no drug at all.
~50% ionised (active), ~45% protein-bound (chiefly albumin), the rest complexed to citrate, phosphate, sulfate and bicarbonate. Only 0.1% of body calcium is in the extracellular fluid.
Alkalaemia increases albumin binding and lowers ionised calcium with an unchanged total; acidaemia does the reverse. Sepsis alters both albumin and binding affinity. Total calcium can be normal while ionised calcium is dangerously low.
Citrate chelates ionised calcium by design — in massive transfusion, apheresis and regional citrate anticoagulation on CRRT. In liver failure citrate clearance falls and the total-to-ionised calcium ratio rises (Lecture 09 — KRT II).
Payne RB et al. Br Med J 1973;4:643 · Slomp J et al. Crit Care Med 2003;31:1389 · Koyner Ch 22 · Ronco Ch 58
Koyner Ch 22 · Zivin JR et al. Am J Kidney Dis 2001;37:689 · Egi M et al. Crit Care Med 2011;39:314 · Desai TK et al. Am J Med 1988;84:209
Exceptions where repletion is reasonable: citrate-driven hypocalcaemia during massive transfusion or CRRT, and dialysis-related falls.
Forsythe RM et al. Cochrane Database Syst Rev 2008;CD006163 · Collage RD et al. Crit Care Med 2013;41:e352 · Aberegg SK. Chest 2016;149:846 · Koyner Ch 22
Humoral hypercalcaemia of malignancy — squamous carcinomas, renal cell, breast. PTHrP raises bone resorption and distal tubular calcium reabsorption. PTH is suppressed.
Direct bone invasion and cytokine-driven osteoclast activation — myeloma, breast cancer, diffuse marrow infiltration.
Extrarenal 1-α-hydroxylase in lymphoma and granulomatous disease (sarcoid, tuberculosis, fungal). This is the subgroup that responds to glucocorticoids.
Calcium activates the calcium-sensing receptor on the thick ascending limb, inactivating NKCC2 — a natriuresis and a nephrogenic diabetes insipidus from aquaporin-2 downregulation. The patient becomes volume-deplete, GFR falls, calcium excretion falls, and calcium rises further.
Koyner Ch 22, 50 · Rosner MH, Dalkin AC. Clin J Am Soc Nephrol 2012;7:1722 · Ronco Ch 58
Isotonic saline — 200–300 mL/h until volume replete, then titrate to urine output 100–150 mL/h. Reduce to 75–150 mL/h in hypoalbuminaemic patients with advanced malignancy. Onset immediate; typically lowers calcium 1–2 mg/dL. It does not stop bone resorption.
Stop the contributors — calcium and vitamin D supplements, thiazides, lithium, calcium-containing antacids and dialysate. Loop diuretics only if hypervolaemic: they retard volume repletion and the practice is unproven.
Calcitonin 4 IU/kg IM or SC every 12 h (up to 8 IU/kg every 6–12 h if inadequate at 24 h). Onset within 6 h, falls of 1–2 mg/dL. Tachyphylaxis by 48 h — it is a bridge to a bisphosphonate, never a treatment on its own.
Zoledronic acid 4 mg IV over ≥ 15 min — most potent, but onset is 48–72 h. Superior to pamidronate for hypercalcaemia of malignancy. Avoid in severe AKI; use pamidronate 60 mg over 4–6 h instead, and expect prolonged action in kidney impairment.
Denosumab 120 mg SC — anti-RANKL, not renally cleared, so the agent of choice when eGFR is low or bisphosphonate has failed. Watch for profound and prolonged hypocalcaemia in advanced CKD; check calcium and magnesium repeatedly.
Glucocorticoids (e.g. prednisone 40–60 mg/day) for 1,25-(OH)₂-vitamin-D–mediated hypercalcaemia — lymphoma, sarcoidosis, vitamin D intoxication. Ineffective in PTHrP-driven disease.
Haemodialysis against a low- or zero-calcium bath — for hypercalcaemic crisis with coma, anuric AKI, or when saline cannot safely be given. Effective and immediate, but purely temporising: the bone keeps releasing calcium until the tumour is treated.
Koyner Ch 22, 50 · Major P et al. J Clin Oncol 2001;19:558 · LeGrand SB et al. Ann Intern Med 2008;149:259 · Camus C et al. Intensive Care Med 1996;22:116
The electrolyte nobody calls about — and the one that keeps a patient on the ventilator.
High-dose mannitol causes factitious hypophosphataemia by assay interference. Interpret a low phosphate cautiously in a neurocritical care patient on mannitol before infusing potassium phosphate.
Koyner Ch 23 · Aubier M et al. N Engl J Med 1985;313:420 · Demirjian S et al. Nephrol Dial Transplant 2011;26:3508 · Zazzo JF et al. Intensive Care Med 1995;21:826
| Serum phosphate | IV dose (potassium or sodium phosphate) | Infusion time | Notes |
|---|---|---|---|
| 2.3–3.0 mg/dL (0.74–0.96 mmol/L) | 0.16 mmol/kg | 6 h | Oral or enteral repletion is reasonable if the gut works |
| 1.6–2.2 mg/dL (0.51–0.71 mmol/L) | 0.32 mmol/kg | 6 h | Recheck 2–4 h after the infusion finishes |
| ≤ 1.5 mg/dL (≤ 0.48 mmol/L) | 0.64 mmol/kg | 6 h | Severe; expect to repeat. Weight-based dosing over 6 h achieved > 75% correction with few episodes of overshoot |
| Active haemolysis or rhabdomyolysis | 15 mmol single dose | 2 h | The only setting where faster correction is justified |
Count the cation. 15 mmol of potassium phosphate delivers ~22 mmol of potassium — dangerous in AKI; use sodium phosphate when potassium is normal or high. Never run phosphate through the same line as calcium (precipitation). Faster infusion causes transient hyperphosphataemia, hypocalcaemia, ECG changes and AKI. On CRRT, consider a phosphate-containing replacement or dialysate (1 mmol/L) rather than chasing the level with boluses.
Taylor BE et al. J Am Coll Surg 2004;198:198 · Koyner Ch 23 · Geerse DA et al. Crit Care 2010;14:R147
Carbohydrate after starvation triggers an insulin surge that drives phosphate, potassium and magnesium into cells, into an already depleted body. The phosphate falls on day 1–3 of feeding, and the patient arrests, seizes or fails to wean.
NICE CG32, Nutrition support for adults (2006, updated 2017) · Koyner Ch 15, 23 · Marinella MA. J Intensive Care Med 2005;20:155
AKI and CKD dominate. Hospitalised patients with hyperphosphataemia had a mean eGFR of 22 vs 93 mL/min/1.73 m² and higher mortality (11% vs 2%). Hypoparathyroidism raises phosphate with preserved GFR.
Tumour lysis, rhabdomyolysis, haemolysis, lactic acidosis and DKA. These are the three ICU emergencies that combine hyperphosphataemia with the nephrotoxin that caused it.
Sodium-phosphate enemas and bowel preparations — a 250 mL dose contains up to 32 g of phosphorus. In the elderly, in gut dysmotility and in CKD this has caused phosphate levels above 40 mg/dL, profound hypocalcaemia and death.
Koyner Ch 23 · Haider DG et al. PLoS One 2015;10:e0133426 · Ori Y et al. Arch Intern Med 2012;172:263 · Tan HK et al. Int J Artif Organs 2001;24:186
A cation you cannot measure properly, that controls two other cations you keep failing to correct.
| Situation | Regimen |
|---|---|
| Torsades de pointes | MgSO₄ 2 g (16 mEq) IV over 15 min, then 1 g (8 mEq) hourly. Give it regardless of the serum level. |
| Severe symptomatic (< 1 mEq/L with arrhythmia, seizure or neuromuscular signs) | 2 g over 5–10 min (over 1 h if not immediately life-threatening), then 4–6 g (32–48 mEq) per day for 3–5 days to refill intracellular stores |
| Mild to moderate, gut working | Magnesium oxide 400 mg two to three times daily — limited by diarrhoea, which itself wastes magnesium |
| Cardiac arrest | Not recommended routinely (ACLS 2018, Class III: no benefit). Reserve for torsades. |
Koyner Ch 24 · Tzivoni D et al. Circulation 1988;77:392 · Gu WJ et al. Trials 2012;13:41 · Panchal AR et al. Circulation 2018;138:e740
| Serum Mg²⁺ (mg/dL) | Clinical picture |
|---|---|
| 1.7–2.4 | Normal |
| ~4.8 and above | Loss of deep tendon reflexes — the first and most reliable clinical sign; check it before every dose escalation |
| 5–8 | Nausea, vomiting, flushing, headache, somnolence, hypotension |
| 12–15 | AV block, bradycardia, QRS widening, muscle weakness and paralysis — including the respiratory muscles |
| > 15 | Cardiac and respiratory arrest |
Stop the magnesium. Give 1 g IV calcium gluconate as the physiological antidote — it blocks the toxic effect within minutes but does not remove magnesium. Saline with a loop diuretic if kidney function is intact. Dialysis for kidney failure or severe symptoms; intermittent haemodialysis lowers magnesium fastest, but consider CKRT afterwards when a gut reservoir of magnesium citrate or laxative continues to be absorbed.
Koyner Ch 24 · Clark BA, Brown RS. Am J Nephrol 1992;12:336 · Bokhari SR et al. Am J Med Sci 2018;355:390
Fluid given in the first hours is worth more than any drug given later — and the calcium you are tempted to replace will come back to hurt you.
Points from age, female sex, initial creatinine, calcium < 7.5 mg/dL, CK > 40,000 U/L, phosphate, bicarbonate < 19 mmol/L, and an aetiology other than seizure, syncope, exercise, statin or myositis.
Score < 5 → 2.3% risk of KRT or death (97% negative predictive value). Score > 10 → 61.2%. Use it to decide who needs an ICU bed and aggressive fluids, not to withhold them.
Koyner Ch 49 · McMahon GM et al. JAMA Intern Med 2013;173:1821 · Bosch X et al. N Engl J Med 2009;361:62 · Clarkson PM et al. Med Sci Sports Exerc 2006;38:623
Third-spacingNecrotic muscle sequesters litres of fluid — profound hypovolaemia with a normal-looking weight.
VasoconstrictionRAAS and sympathetic activation, plus myoglobin scavenging nitric oxide locally.
Cast nephropathyMyoglobin precipitates with Tamm–Horsfall protein in concentrated, acidic tubular fluid; obstruction raises intraluminal pressure.
Heme toxicityATP depletion, oxidative stress and lipid peroxidation in the proximal tubule.
Koyner Ch 49 · Zager RA. Kidney Int 1996;49:314 · Vanholder R et al. J Am Soc Nephrol 2000;11:1553
Stop the muscle injury — remove the crush, stop the statin, treat the seizures, cool the hyperthermia, reverse the ischaemia, correct hypophosphataemia and hypokalaemia (both can cause rhabdomyolysis).
Isotonic crystalloid, immediately — 0.9% saline or a balanced solution. In crush injury, start during extrication at 1,000 mL/h for the first 2 h, then halve if extrication runs long; 3–6 L/day is reasonable when close monitoring is impossible. Target urine output > 200 mL/h until CK is clearly falling.
Monitor for the fluid you cannot give — anuric patients, the elderly and those with cardiac disease will become overloaded. Reassess volume status hourly; once anuria is established, fluid stops helping.
Sodium bicarbonate — theoretically prevents cast formation and heme redox cycling, but an RCT in doxylamine-induced rhabdomyolysis showed no difference in AKI. Reserve it for acidaemia; if used, target urine pH > 6.5 and watch calcium fall further.
Mannitol — no demonstrated benefit over volume alone, and nephrotoxic at high cumulative doses. Loop diuretics only to augment urine flow once volume-replete, with no evidence they prevent AKI.
KRT for the usual indications: refractory hyperkalaemia, refractory acidaemia, volume overload, uraemia. No role for prophylactic dialysis to clear myoglobin. If KRT is needed, high-flux or continuous therapy removes myoglobin better; high-cutoff membranes clear more but cost albumin and protein-bound drugs.
Koyner Ch 49 · Sever MS, Vanholder R. Clin J Am Soc Nephrol 2013;8:328 · Brown CV et al. J Trauma 2004;56:1191 · Zeng X et al. Cochrane Database Syst Rev 2014;CD008566
Hypocalcaemia in rhabdomyolysis is caused by calcium depositing into damaged muscle, not by loss. As the muscle heals, that calcium is released and 1,25-(OH)₂ vitamin D production rises, producing rebound hypercalcaemia and, if you have loaded the patient, metastatic calcification. Do not treat the early hypocalcaemia unless the patient is symptomatic — tetany, seizure, arrhythmia — or unless it is needed as membrane protection against hyperkalaemia.
Fluid resuscitation makes injured muscle swell. A limb that becomes tense and painful after resuscitation, with rising CK despite adequate volume, needs compartment pressures measured and a surgical opinion. The same logic applies to the abdomen: measure bladder pressure in a tense abdomen (Lecture 02 — Renal Hemodynamics).
Akmal M et al. J Clin Endocrinol Metab 1986;63:137 · Koyner Ch 49 · Bosch X et al. N Engl J Med 2009;361:62
The only electrolyte emergency in this lecture you can usually schedule — and therefore the only one you should never be surprised by.
| Laboratory TLS — 2 or more, from 3 days before to 7 days after therapy | Threshold |
|---|---|
| Uric acid | ≥ 8 mg/dL (476 µmol/L) or 25% rise from baseline |
| Potassium | ≥ 6.0 mmol/L or 25% rise |
| Phosphate | ≥ 4.5 mg/dL (1.45 mmol/L) in adults (≥ 6.5 in children) or 25% rise |
| Calcium | ≤ 7.0 mg/dL (1.75 mmol/L) or 25% fall |
| Clinical TLS — laboratory TLS plus one | Definition |
|---|---|
| Kidney | Creatinine ≥ 1.5 × the institutional upper limit of normal |
| Cardiac | Arrhythmia or sudden death not attributable to a drug |
| Neurological | Seizure not attributable to a drug |
The 2011 refinements are worth knowing: require two abnormalities simultaneously, drop the 25% criterion, and count any symptomatic hypocalcaemia as clinical TLS.
Cairo MS, Bishop M. Br J Haematol 2004;127:3 · Cairo MS et al. Br J Haematol 2010;149:578 · Howard SC et al. N Engl J Med 2011;364:1844 · Koyner Ch 50
Do not alkalinise the urine. Raising urine pH from 5 to 7 increases urate solubility more than tenfold, but it simultaneously drives calcium-phosphate and xanthine precipitation in the tubules and worsens hypocalcaemia by increasing albumin binding. It is no longer recommended. Do not routinely replace calcium in TLS — the calcium-phosphate product is already high, and giving calcium invites metastatic deposition. Treat calcium only for symptoms or arrhythmia, and lower the phosphate instead. Start KRT early: the threshold is lower than in other AKI, and CKRT at high effluent rates is preferred when potassium and phosphate rebound after intermittent sessions.
Ronco Ch 41 · Koyner Ch 50 · Coiffier B et al. J Clin Oncol 2008;26:2767 · Howard SC et al. N Engl J Med 2011;364:1844
The therapy we prescribe creates the deficiencies we then spend the night correcting — so prescribe both together.
| Lost on CKRT | Why it matters | What to prescribe |
|---|---|---|
| Phosphate | Hypophosphataemia in over 50% of patients, up to 65% at high effluent rates; nearly double the rate of prolonged respiratory failure | Phosphate-containing replacement fluid or a dialysate with phosphate 1 mmol/L; otherwise scheduled IV repletion, daily levels |
| Potassium | Standard solutions contain 0–4 mmol/L; a patient started for hyperkalaemia is hypokalaemic 24 h later | Move to a potassium-containing bag rather than chasing with boluses; check at least daily and after any bag change |
| Magnesium | Freely filtered and unbound; deficiency perpetuates hypokalaemia and arrhythmia | Scheduled IV magnesium sulfate; target the upper half of the normal range in arrhythmic patients |
| Calcium | Citrate anticoagulation lowers ionised calcium by design; solution calcium of 2.5 vs 3.5 mmol/L changes the balance markedly | Systemic calcium infusion per the citrate protocol; ionised calcium on the circuit and the patient (Lecture 09 — KRT II) |
| Amino acids, water-soluble vitamins, trace elements | 10–15 g/day of amino acid loss is typical; thiamine, folate, vitamin C, selenium, zinc and copper are all removed | Increase protein delivery toward 1.5–2.5 g/kg/day and supplement water-soluble vitamins and trace elements (Lecture 03 — Fluids & Diuretics for the fluid side) |
On continuous therapy, electrolyte replacement is prophylaxis, not rescue. Write the replacement into the CRRT order set on day 0 and review it every time the effluent dose changes.
Koyner Ch 15, 23–24 · Demirjian S et al. Nephrol Dial Transplant 2011;26:3508 · Yang Y et al. Crit Care 2013;17:R205 · Ronco Ch 57–58
78 M, day 3 of a urinary sepsis admission. Oliguric AKI, on lisinopril and spironolactone at home, both continued. Nurse calls with a "wide complex" rhythm on the monitor.
Write the first five orders, in order, with doses. Which of them actually lowers the potassium?
Think 60 seconds · answer on the next slide
Protect · 0–3 minCalcium gluconate 10% 10–30 mL IV; repeat at 5 min if the QRS is still wide. Buys 30–60 min.
Shift · 15–30 minInsulin 5 U + 25 g dextrose, then 10% dextrose 75 mL/h. Salbutamol 10–20 mg nebulised alongside.
Subtract · same hourStop the ACE inhibitor, spironolactone and every potassium-containing fluid; recount the tube feed.
Remove · < 2 hCall for a dialysis catheter. In oliguric AKI nothing else removes potassium at the required rate.
Everything on rungs 1–3 is a loan against time, repayable within hours. The potassium will rebound about 6 h after dialysis and sooner after insulin wears off. Decide who is doing the 4-hour recheck before you leave the bedside.
Koyner Ch 21 · Ronco Ch 57 · Blumberg A et al. Nephrol Dial Transplant 1997;12:1629
34 M, trapped under machinery for 5 hours, extricated 90 minutes ago. Both thighs swollen and tense. Dark urine in the catheter bag.
He is hypocalcaemic and asymptomatic. Do you replace the calcium? What is your fluid order, and what will make you call for KRT?
Think 45 seconds · discuss in pairs
Koyner Ch 49 · Sever MS, Vanholder R. Clin J Am Soc Nephrol 2013;8:328 · McMahon GM et al. JAMA Intern Med 2013;173:1821
26 M, bulky abdominal disease, LDH 3,400 U/L. Received allopurinol and IV saline before chemotherapy. Now confused, with a rising creatinine.
Does he meet criteria for clinical TLS? What do you give, what do you check first, and what do you deliberately withhold?
Hands up — then name the one test you must have before the drug goes up
A 62-year-old on furosemide and a proton pump inhibitor has K⁺ 3.0 mmol/L with U waves. You give 40 mmol of KCl centrally over 2 hours. The repeat potassium is 3.1 mmol/L. Magnesium has not been checked.
A. Give another 40 mmol of KCl · B. Check and replace magnesium before more potassium · C. Give sodium bicarbonate to shift potassium out of cells · D. Switch to oral potassium and wait 24 hours
Hands up — then say which drug in his list is the culprit
References & further reading
Questions & discussion — bring the worst potassium you have ever treated.
Next: Lecture 07 — Acid-Base Disorders & DKA