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Life-Threatening Electrolyte Abnormalities
| Disorder | Symptoms | Causes | Treatment |
| Hypo-K+ | Weakness | Entry into cells: alkalosis, insulin, b-agonist | Treat concurrent hypomag |
| K+ < 3.5 | EKG changes: ST depression, U waves, low T | GI losses | Address cause |
| Arrhythmias: bradycardia, AV block, VT, VF, torsades (with hypo-Mg) | Urinary loss: diuretics, mineralocorticoid excess, DKA, RTA, low Mg, amphoB | Replete to >4mg/dL: max IV rate 20 mEq/hr –requires central line | |
| Refeeding syndrome | K 3.5-4.0: 10mEq to by 0.1 | ||
| K 3.0-3.5: 20mEq to by 0.1 | |||
| K 2.5-3.0: 30mEq to by 0.1 | |||
| K 2.0-2.5: 50mEq to by 0.1 | |||
| Hyper-K+ | Weakness | Release from cells: acidosis, low-insulin, tissue death, exercise, b-blocker, digitalis, succinylcholine | IVF resuscitation if volume-down |
| K+ > 5.1 | EKG changes: | Hypoaldosteronism (ACE-I, heparin, critical illness) | CaCl 500 – 1,000mg IV over 2-3 min |
| peaked T, | Kidney injury (acute or chronic) | 10u reg insulin + 1amp (50 mL) D50 | |
| long PR, | Albuterol continuous neb | ||
| wide QRS, | NaHCO3 (minimal effect) | ||
| low P, | Loop or thiazide diuretic | ||
| sine wave | HD | ||
| Kayexalate—caution—can cause bowel necrosis | |||
| Hypo-Mg2+ | HypoK, hypoCa, tetany, weakness, coma, arrhythmias: torsades, afib | GI loss, pancreatitis, chronic PPI, EtOH, hyperCa, meds (loops, thiazides, aminoglycosides, amphoB, pentamidine), refeeding | Do not give excessive Mg (IV or PO) if pt has ileus |
| Mg2+ < 1.5 | magnesium sulfate 1-2g IV | ||
| replete to >2 mg/dL | |||
| Hyper-Mg2+ | Hyporeflexia, hypotension, somnolence, paralysis, | Renal failure | Normal saline and loop diuretics if intact kidney fxn, but… |
| Mg2+ > 2.5 | EKG changes: long PR, heart block | Increased gut uptake | Will almost always require HD, as rarely develops unless severe renal dysfunction |
| Iatrogenic | |||
| Hypo-Ca2+ | Tetany, seizures, hypotension, long QT, anxiety, psychosis | Hypo-PTH, PTH resistance, vit D def/resist, drugs (phenytoin, foscarnet, bisphosphonates, calcitonin, citrate—in blood products), hypoMg | Correct for hypoalbuminemia |
| Ca2+ < | Check ionized calcium | ||
| iCa < | Calcium gluconate 1-2g over 20 min | ||
| Correct hypomag | |||
| Hyper-Ca2+ | Obtundation, arrhythmias, renal failure | Hyperparathyroid, PTHrP, bone resorption, decreased excretion, excess vitamin d | NS until euvolemic then titrate to UOP > 100 mL/hr |
| Ca2+ > 11 | Calcitonin 4-8 IU/kg IM q6-12h | ||
| Bisphosphonates | |||
| HD | |||
| Hypo-PO43- | Encephalopathy, weakness, dysphagia, decreased cardiac contractility, ileus | Refeeding, insulin, resp alkalosis, catecholamines, b-agonists, hyperparathyroid, poor intake, phos-binders, diarrhea, Fanconi syndrome, corticosteroids | Oral repletion preferred |
| PO43- < | For severe (phos < 1mg/dL) 0.6 mmol/kg IBW IV over 6 hr | ||
| Correct underlying cause | |||
| Hyper- PO43- | Mostly related to concurrent hypercalcemia | Renal failure, Transcellular shifts: rhabdo, tumor lysis, met acidosis, insulin deficiency | Correct underlying cause |
| PO43- > | Phos binders | ||
| Saline+acetazolamide | |||
| HD | |||
| Hypo – Na | Altered Mental Status | Rapid decrease in plasma sodium concentration (either by acute hyponatremia or rapid correction of chronic hypernatremia) allows water to move into cells and causes cerebral edema and herniation | Hypovolemic: volume (always 0.9% NaCl, 154mEq Na) |
| Seizures if severe | Hypervolemic: diuretics | ||
| Symptoms of ODS are delayed (2-6 days) and permanent | EtOH, liver disease, malnutrition, hypokalemia, Na < 120 mEq/L, rate of change >10-20 mEq over 24 hrs (day change more important than hourly) | Euvolemic: vaptans (anti-V2 receptor), salt (NaCl tabs, hypertonic NaCl, loop diuretic) | |
| Hypovolemic: vomiting, diarrhea, hemorrhage, adrenal insufficiency | If symptomatic (seizing) give 3% NaCl 100cc boluses q10 min (up to 3x) until seizures stop and Na by 4-6 mEq/L then hold for 6h (note: old references may say 12mEq/L/hr but newer recs more conservative d/t risk of ODS) | ||
| Euvolemic: SIADH, polydipsia, low cortisol, hypothyroid | |||
| Hypervolemic: CHF, cirrhosis, nephrosis | If known acute (developed in < 48 hr) can treat quickly | ||
| If chronic or unknown, go slow (4-6 mEq/24h) | |||
| If overcorrected (>8 mEq/L/day +risk factors for ODS or >12 without), give D5W + desmopressin (DDAVP) | |||
| Hyper – Na | Altered mental status | Almost always due to hypovolemia | Hypervolemic: hypertonic Na administration or hyperaldosteronism/Cushing’s |
| Hypovolemic: | |||
| Symptoms of ODS are delayed (2-6 days) and permanent | Rapid increase in plasma sodium (either by acute hypernatremia or rapid overcorrection of chronic hyponatremia) causes osmotic demyelination syndrome (ODS, syndrome formerly known as central pontine myelinolysis) | Check urine osms: | |
| If > 800 mOsm/kg, ADH normal. Check urine volume: | |||
| If < 800 mL/day, ¯ intake or insensible losses | |||
| If < 800 mOsm/kg, give DDAVP | |||
| If no response to DDAVP, nephrogenic diabetes insipidus | |||
| If nl response to DDAVP, central diabetes insipidus | |||
| Treat: go by 0.5 mEq/l/hr (faster if acutely symptomatic; overcorrection less concerning) |