Electrolyte & Fluid Replacement

The mainstay of pre-renal AKI: isotonic fluid is both therapeutic and diagnostic — if renal function improves with volume, the cause was perfusion. Given cautiously, watching for overload, because the same patient flips to fluid restriction once oliguric. The electrolyte side carries the emergencies: potassium-shifting therapy for hyperkalemia, buffers for metabolic acidosis, phosphate binders — and normal saline is the named fluid for contrast prophylaxis and post-obstructive diuresis support.

The other half of crisis treatment, given alongside the steroid rather than after it: 1000 mL of isotonic saline immediately, or 5% glucose in isotonic saline where hypoglycemia is present so volume and glucose are corrected together — up to 2–3 litres as urgently as possible, and in children a 20 mL/kg bolus repeatable to 60 mL/kg within an hour for shock. The electrolytes largely correct themselves once cortisol and volume are restored, but must be monitored, and hyperkalemia with ECG change still needs its own treatment sequence. In the subacute phase saline continues at a slower rate for 24–48 hours, and fludrocortisone is started only once the saline stops — while it is running, the salt load is covering the mineralocorticoid need. Long-term the same class becomes dietary: liberal salt intake, adequate sodium in the diet, and increased electrolyte-containing fluids during illness.

Correct deficiencies and electrolyte losses — malabsorption treatment "targets correcting deficiencies, treating the underlying cause, avoiding triggers (typically dietary), and treating symptoms"; prolonged intractable diarrhea can cause life-threatening electrolyte disturbances.

First-line and before insulin: isotonic 0.9% NaCl reverses an osmotic-diuresis deficit of up to 10–15% of body weight; potassium added to the fluids pre-empts insulin-induced hypokalemia (total-body deficit 3–6 mmol/kg despite the normal-looking serum value); and dextrose joins the fluids once glucose falls below ~250 mg/dL so the insulin can keep running until the gap closes.

Warmed fluids, not electrolytes. StatPearls (Hypothermia): "Warmed intravenous fluids, typically 38 to 42 °C, are useful for preventing additional heat loss and treating volume depletion, although they provide only modest rewarming when used alone." Routine electrolyte replacement is not a drowning treatment — "Electrolyte disturbances are uncommon unless hypothermia is present."

Replacing what purging and refeeding remove. For the volume-depletion alkalosis of bulimia, "saline administration is indicated in addition to the cessation of the purging behavior" — and "these patients require monitoring for signs of volume overload." In refeeding, potassium, phosphate and magnesium are repleted to the standard of care and checked every 12 hours for the first 3 days in high-risk patients, with feeding held if levels are severely low. Thiamine 100 mg is given before dextrose-based solutions.

In a ruptured ectopic, fluid is the bridge to the operating room, not the treatment. The treatment is surgical hemostasis, and everything given before it is aimed at keeping the patient alive long enough to reach it. The sourced approach is damage-control resuscitation, which has three named strategies. Permissive hypotension targets a systolic pressure of 90 mm Hg, "accepting a short period of suboptimal end-organ perfusion" until the hemorrhage is controlled — a deliberately lower target than instinct suggests, because pushing pressure up before the bleeding is stopped pushes clot off the bleeding vessel. Hemostatic resuscitation "pushes for early use of blood products rather than an abundance of crystalloids in order to minimalize the metabolic derangement, resuscitation-induced coagulopathy, and the hemodilution that occurs with crystalloid resuscitation." And balanced ratios favour 1:1:1: a recent study found "no significant difference in mortality at 24 hours or 30 days between ratios of 1:1:1 and 1:1:2," but "patients who received the more balanced ratio of 1:1:1 were less likely to die due to exsanguination in 24 hours and were more likely to achieve hemostasis." The disorder-side caution is the one that changes practice at the bedside: crystalloid excess drives metabolic derangement, coagulopathy and hemodilution. Volume alone dilutes the clotting factors a bleeding patient still has. The triad being worked against is acidosis, hypothermia and coagulopathy, which is why products and fluids are warmed rather than merely given fast. What is not here matters too: no fetched source names a vasopressor for this setting, and the sourced answer to hypotension in a ruptured ectopic is blood and a surgeon. Fluid composition, tonicity and electrolyte pharmacology belong to the class page.

The definitive fix for every deficit on this page — but each replacement carries its own safety rule: oral or diluted, pump-controlled IV KCl for hypokalemia (never IV push, ≤10–20 mEq/h, cardiac monitor above 10), IV calcium gluconate for symptomatic hypocalcemia (and as the membrane stabilizer in hyperkalemia and the antidote in hypermagnesemia), IV magnesium sulfate for hypomagnesemia and torsades, isotonic crystalloids for volume deficit, and 3% saline only for severe symptomatic hyponatremia under the correction-speed cap.

Rehydration — without overdoing it. Heat exhaustion and cramps: "oral rehydration with water or an electrolyte-containing drink can commence on-site"; the Yellow Book adds fluids "containing glucose and salt." Heat stroke: "Adequate rehydration is essential, although rapid correction of sodium abnormalities should be avoided"; many need intensive care to replace losses. "Care should be taken not to overhydrate patients," especially with reduced cardiac function. Salt: NIOSH says "Avoid salt tablets" for heat cramps; the Yellow Book notes "Salt tablets swallowed whole can cause gastrointestinal irritation and vomiting." Not used: antipyretics — "Antipyretics have no role in the treatment of heat stroke and may cause hepatic toxicity"; dantrolene — "does not improve outcomes"; diuretics for heat edema — "There is no role for diuretic medications for heat edema."

IV fluids, electrolytes and thiamine. "Initial inpatient management focuses on stabilizing the patient through aggressive intravenous (IV) fluid therapy and correcting electrolyte abnormalities. Thiamine and multivitamin supplementation are crucial to prevent neurological complications." Thiamine goes before or with any dextrose — "Carbohydrate administration increases thiamine requirements and can worsen thiamine deficiency." Correct potassium and magnesium; low levels also call for ECG monitoring if ondansetron is used. When feeding restarts, watch phosphate, potassium and magnesium for refeeding syndrome.

The first and dominant therapy — profound dehydration and hyperosmolality, not glucose, are the killers here. 0.9% NaCl or balanced crystalloid at 500–1,000 mL/h for the first 2–4 h, replacing ~50% of the ~9 L deficit in the first 8–12 h and the rest over 24–48 h (smaller 250-mL boluses for older adults and heart/kidney failure). Fluids alone drop glucose about 50–70 mg/dL/h before any insulin. Potassium is part of the job: K⁺ < 3.5 → replace 10–20 mmol/h and postpone insulin; 3.5–5.0 → add 10–20 mmol per liter of fluid; > 5.0 → none, recheck in 2 h. 0.45% saline only if osmolality won’t decline despite adequate fluids and insulin.

Warmed IV fluids and glucose in hypothermia. "Warmed intravenous fluids, typically 38 to 42 °C, are useful for preventing additional heat loss and treating volume depletion, although they provide only modest rewarming when used alone." Cold diuresis causes volume depletion. "Documented or strongly suspected hypoglycemia should be treated with oral glucose if the patient can safely swallow or with intravenous dextrose when indicated." Warm drinks only for a conscious person — never alcohol.

Alkaline hydration to prevent and treat tumor lysis syndrome in bulky, high-LDH disease.

Isotonic saline first for hypercalcemia — "Vigorous saline hydration, an integral part of hypercalcemia therapy, should be initiated promptly," avoiding overhydration in heart failure.

The backbone of two syndromes. TLS prevention: aggressive IV hydration at 3–3.5 L/m²/day (or 4–5 L/day) targeting urine output ≈ 2 mL/kg/h, started 48 hours before chemo and continued 48 hours after — dilutes and flushes the solute load before crystals form. Hypercalcemia: isotonic saline at 200–300 mL/h titrated to urine output > 100 mL/h is the first treatment — it rehydrates, restores GFR, and promotes calciuresis. One trap: in TLS, replace calcium only for symptomatic hypocalcemia — IV calcium feeds calcium-phosphate precipitation and worsens the AKI.

Calcium here is nutritional adequacy, not a treatment for osteoporosis — it is the substrate every antiresorptive and anabolic agent needs, and the deficiency that makes those drugs dangerous. The Bone Health and Osteoporosis Foundation 2022 targets are banded by age and sex: 1,000 mg/day for men aged 50–70, and 1,200 mg/day for women aged 51 and over and men aged 71 and over, with an upper limit of 2,000–2,500 mg/day. Food first is the sourced rule: "Increasing dietary calcium is the first-line approach, but calcium supplements should be used when an adequate dietary intake cannot be achieved" — and the gap is real, since average US intake is only 600 to 800 mg/day. On the cardiovascular question, the newest and highest-tier source settles it toward safety: BHOF 2022 reports that "a large systematic review and meta-analysis including RCTs and cohort studies found no evidence that calcium with or without vitamin D increased cardiovascular disease," with the VITAL study finding no adverse effects. Name the controversy if a patient raises it; do not tell them supplements cause heart attacks. The genuine caution is hypocalcemia before an antiresorptive — calcium and 25-hydroxyvitamin D are measured and corrected before the first bisphosphonate or denosumab dose.

Three roles, all first-line. (1) IV calcium for symptomatic or severe hypocalcemia — "Calcium gluconate 1 to 2 g (90 to 180 mg elemental calcium) or calcium chloride 1 g (270 mg elemental calcium) can be administered over 10 to 20 minutes, followed by continuous infusion if hypocalcemia persists"; gluconate is preferred for a lower risk of tissue necrosis if it extravasates; give it with cardiac monitoring and never through the same line as bicarbonate or phosphate. Beware the numbers: "a 10 cc vial of 10% calcium gluconate has 1 g of calcium gluconate but only 93 mg of elemental calcium." (2) Oral calcium for hypoparathyroidism and after neck surgery — "Calcium carbonate (40% elemental calcium) and calcium citrate (21% elemental calcium) are the most commonly used preparations," divided into 2 to 3 doses; carbonate "is better absorbed with food" and needs acid, while citrate "can be taken with or without food, and gastric pH does not affect absorption." (3) 0.9% saline for hypercalcemia — the first step, until urine output is adequate and the patient euvolemic.

Volume is the first thing given and the least of what is needed. Immediate stabilization in abruption is quoted as "intravenous fluids, supplemental oxygen, and continuous maternal and fetal monitoring," with blood typed and cross-matched and access established, because "careful management of fluids and circulatory volume is vital." The disorder-side caution is the whole teaching point: crystalloid is a bridge, not the treatment. Excess crystalloid causes resuscitation-induced coagulopathy, and the disorder-side consequence is specific to this page: in a patient who is already consuming fibrinogen inside her uterus, diluting what is left makes the coagulopathy worse — so excess crystalloid is an iatrogenic precipitant of deterioration, not a neutral holding measure. The balanced product ratio, the argument for early products over volume, and the lethal triad of acidosis, hypothermia and coagulopathy are owned by the shock and disseminated intravascular coagulation pages — cross-link rather than carrying a second copy of them, and note that the reason those pages matter here is obstetric: this bleed consumes clotting factors inside the uterus while it is still enlarging itself. Blood-bank activation is a named team step: type and cross, then activate the massive transfusion protocol. In previa this planning happens antenatally, because patients "should consent for possible blood transfusions" before any bleed. Fluid composition, tonicity and electrolyte pharmacology belong to the class page.

Pre-hydration before IVIG — "Ensure adequate hydration in patients before administration" (label); StatPearls lists "saline for pre-hydration."

The first drug of shock: crystalloids are first-line for volume — available, cheap, minimally allergenic — with balanced crystalloids preferred over 0.9% saline (SSC; large saline volumes cause hyperchloremic metabolic acidosis). Only ~20–25% of a bolus stays intravascular, so resuscitation takes volume (sepsis: 30 mL/kg within 3 hours, SSC) and every bolus demands a reassessment for overload. The exception is hemorrhage: crystalloid is a bridge only — blood products 1:1:1 and bleeding control are the therapy.

The fluid itself is the therapy, and the direction reverses between the two disorders. In severe symptomatic hyponatremia — seizures, obtundation, delirium — 3% hypertonic saline (osmolality 513 mOsm/kg) is given as 100 mL intravenous boluses over 10 minutes as needed, targeting a rise of 4 to 6 mEq/L in the first 4 hours, because that increment is what reduces the severity of neurologic symptoms; the SIADH-specific literature describes a slower 100 mL bolus over 3–4 hours for the non-emergent case. Less urgent hyponatremia is managed with oral salt tablets or intravenous saline, sized by the arithmetic sodium deficit = total body water × (desired − current sodium), where total body water is weight in kg × 0.6 for men and children and × 0.5 for women and older adults. In DI the same class means plain water and free-water repletion: "it is essential to replete fluid losses in all DI, as some patients may have thirst impairment and will not respond adequately to water intake." After pituitary surgery, mild DI — urine output under 4–6 L/day with serum sodium under 150 mEq/L — is managed with oral fluid replacement, escalating to 5% dextrose and then desmopressin only if it does not resolve. Hypertonic saline has one more role here: it is the infusion paired with plasma copeptin in the modern diagnostic test for DI.

The most powerful ("high-ceiling") diuretics — they work even in kidney failure. Watch potassium, volume, and hearing.

First-line for hypertension — a milder diuretic acting further down the nephron. Remember the four metabolic highs — glucose, lipids, uric acid and calcium — and that the calcium rise comes from retention (opposite of loops).

Weak diuretics that preserve potassium instead of wasting it — the defining danger is hyperkalemia. Two mechanisms; spironolactone also lowers heart-failure mortality.

Two diuretic groups that are used mostly for something other than edema: the carbonic anhydrase inhibitors acetazolamide and methazolamide (glaucoma, altitude sickness) and the osmotic diuretic mannitol (raised intracranial or intraocular pressure). Watch for metabolic acidosis, low potassium and serious sulfonamide reactions with the first group, and for fluid overload, kidney injury and electrolyte swings with mannitol.

Tolvaptan blocks vasopressin’s V2 receptor in the kidney so the body sheds free water and serum sodium rises (Samsca, for hyponatremia), and it slows kidney decline in polycystic kidney disease (Jynarque). The two brands carry different boxed warnings: correcting sodium too fast, and serious liver injury.

Gut-acting drugs that bind potassium in the intestine so it leaves in the stool. Their onset is delayed, so they are not emergency treatment for life-threatening hyperkalemia. Watch for low potassium, the sodium they carry (sodium polystyrene sulfonate, Lokelma), low magnesium (Veltassa) and their effects on other oral drugs.