Fluid and Electrolyte Disorders: Fluids and Sodium

behaves like free water (distributes everywhere, mostly ICF).

D5W

stays in ECF (¼ plasma, ¾ interstitial).

normal saline

live intravascular—at least initially.

colloids (5% albumin)

select all that apply:

what are the three ways to estimate adult maintenance needs (baseline water to match normal losses in a stable patient, not shock)?

1. Holliday-Segar

2. adjusted Holliday-Segar

3. weight-and-age-based

select all that apply:

where do we get information to determine fluid volume status?

1. patient interviews

2. physical assessment and vitals

3. weight changes

4. laboratory values

5. nurse and physician notes

select all that apply:

what are patient characteristics in fluid deficit that would affect fluid balance?

1. vomiting/diarrhea

2. ostomy output

3. burns

4. heavy sweating

5. poor intake

6. unintentional weight loss

7. medicines

8. diet

select all that apply:

what are patient characteristics in fluid overload that would affect fluid balance?

1. heart failure

2. ESRD

3. cirrhosis

4. medicines

5. diet

dry mucosa, ↓turgor, sunken eyes, outs > ins, weight loss, oliguria. orthostasis (↓BP/↑HR), BUN/Cr >15-20, ↑Hct from hemoconcentration.

deficit (hypovolemia)

edema/ascites, weight gain, ins > outs, crackles/rales, pulmonary edema/effusions, elevated JVP, ↑BP.

overload (hypervolemic)

44-yo, post-chemo, 5 days diarrhea, BP 70/50, HR 120, dark urine

hypovolemic

distribute into the ECF; isotonic ones expand plasma reasonably well. examples: NS (0.9% NaCl), LR, Plasma-Lyte, D5W, ½NS.

crystalloids

5% albumin: behaves like plasma expander → ~1 L stays intravascular right away. 25% albumin: hyperoncotic—can pull interstitial water into plasma. evidence hasn't shown mortality magic over crystalloids for routine resuscitation. use selectively (e.g., cirrhosis with large-volume paracentesis, refractory edema with low albumin, or when you specifically want oncotic pull). avoid HES (renal injury).

colloids

chloride-heavy → large volumes can cause hyperchloremic metabolic acidosis and renal vasoconstriction. cheap, everywhere, fine in small/moderate doses; watch Cl.

normal saline

balanced. lactate → bicarb in liver. gentler acid-base profile; classic for resuscitation, burns, GI losses, pancreatitis.

Lactated Ringer's

very plasma-like; buffers → bicarb. also "balanced."

Plasma-Lyte

hypotonic; spreads into ICF/ECF → maintenance, not rescue.

½NS (0.45%)

free water after metabolism → use for hypernatremia or gentle maintenance.

D5W

hypertonic; pulls water out of cells → use for severe symptomatic hyponatremia or raised ICP with tight monitoring.

3% NaCl

have less Na than plasma, so water distributes ICF + ECF and swells cells a bit. good for maintenance and hypernatremia. not good for hypotension/shock (they don't stay intravascular). D5W distribution: ~67% ICF / 33% ECF (only ~8% of the liter shows up as plasma).

hypotonic solutions

once the dextrose is metabolized, D5W behaves like pure water. it spreads ⅔ into cells (ICF ≈ 667 mL) and ⅓ outside cells (ECF ≈ 333 mL). only ~83 mL ends up intravascular.

so what: amazing for hypernatremia (you're replacing water), terrible for _______________ (it doesn't stay in the tank). avoid in acute brain swelling—free water worsens cerebral edema.

resuscitation

stomach fluid is Na ~60, Cl ~130, K ~15, HCO₃ 0 mEq/L. you're literally losing acid (H⁺) and a ton of chloride, with some sodium/potassium.

losing gastric fluid → metabolic alkalosis + chloride depletion + volume depletion.

replacement principle: give chloride back and some K⁺, while refilling ECF: ½NS (0.45% NaCl) + 10-20 mEq KCl/L to approximate the composition.

GI losses

sodium content ≈ plasma, so they stay in the ECF and don't swell/shrink cells. distribution per liter: ~250 mL plasma, 750 mL interstitial (0 mL ICF). use: resuscitation (perfusion problem) and replacement of losses (bile, pancreatic, small-bowel).

isotonic solutions

all ECF, with ~250 mL of each liter actually boosting intravascular volume. so what: will raise BP more than D5W for the same liter. watch for hyperchloremic metabolic acidosis if you pour on big volumes.

normal saline

duodenum/ileum/bile/pancreas are Na ~140-ish, Cl 75-104, K ~5, and (key!) bicarbonate is high (pancreas ~115, bile ~35, ileum ~30). losing these secretions → non-anion gap metabolic acidosis (bicarb loss) + ECF depletion.

replacement principle: return volume + bicarb equivalents and K⁺, without drowning them in chloride.

best fits: _______________; their lactate/acetate → bicarbonate), plus potassium. NS is okay in moderation, but can worsen hyperchloremic acidosis if used exclusively for large volumes. consider custom acetate/bicarb-containing fluids or bicarb if acidemia is severe.

balanced crystalloids (LR or Plasma-Lyte

more Na than plasma (≈513 mEq/L); lives in ECF and pulls water out of cells. use cases: severe symptomatic hyponatremia (seizure, coma, impending herniation): give 100 mL over ~10 min, recheck, repeat up to ×3 to get an initial +4-6 mEq/L bump, then slow the roll.

raised ICP/cerebral edema (per neuro/ICU protocols). hard lines: cap total correction ≤8 mEq/L per 24 h (≤4-6 if high ODS risk).

3% NaCl

vomiting / NG suction (stomach = low Na, high Cl, K, no HCO₃):

refill ECF and give chloride: NS (for alkalosis + hypotension) then ½NS + KCl to mirror ongoing losses; replete K⁺.

diarrhea / small bowel / pancreatic/biliary (bicarb-rich)

replace volume + bicarb precursors: LR/Plasma-Lyte + K⁺; consider bicarb if pH is low.

hypernatremia (free water loss)

D5W or enteral water; correct ≤10-12 mEq/24 h.

shock/perfusion problem

LR/Plasma-Lyte (or NS if that's what's available), bolus and reassess.

JJ is a 44-year-old female presents to clinic complaining of fatigue. she just finished chemo and reports diarrhea for 5 days. BP 70/50, HR 120, urine is dark and concentrated. labs pending.

based on her fluid status, which of the following IV solutions would be indicated for use in JJ?

isotonic

the major extracellular cation and the main driver of serum osmolality. rough osmolality = 2×__________ + glucose/18 + BUN/2.8

sodium

normal Na 135-145 mEq/L, but the level mostly reflects ___________, not total body sodium.

water balance

too much water relative to Na

hyponatremia

too little water relative to Na

hypernatremia

kidneys reabsorb almost all filtered Na (they can waste or retain as needed), which is why __________________ (water hormone) often dictates the serum Na you see.

ADH

serum Na

hyponatremia

osmotic trigger: rising serum osmolality → __________ up → kidneys hold water.

non-osmotic triggers: low BP/low effective arterial volume (HF, cirrhosis), pain, nausea, stress, meds (SSRIs, carbamazepine, opioids) → __________ up even if osmolality is low.

___________ causes free-water reabsorption in the collecting duct and stimulates thirst. that combo dilutes Na.

ADH

the most common electrolyte issue in the hospital; you'll see it constantly.

higher risk: very young/very old, post-op, menstruating/postpartum people, CNS/lung disease, cancer, and folks on thiazides/SSRIs/carbamazepine. why we care: associated with falls, fractures, longer LOS, and mortality—even when "mild."

hyponatremia

brain hasn't adapted → water rushes into neurons → cerebral edema → headache, vomiting, seizures, herniation risk. you can (and should) correct faster up front.

acute hyponatremia

brain extrudes solutes to adapt → fewer symptoms, but if you raise Na too quickly → osmotic demyelination syndrome (ODS).

chronic hyponatremia

symptoms of hyponatremia are mostly neurologic because hypotonic serum pushes water into brain cells. severity tracks with: absolute Na (lower = worse), and speed of fall (fast drops hit harder). moderate: headache, nausea, fatigue, mild confusion. severe: vomiting, _________, cardio-respiratory distress, deep somnolence, coma (GCS ≤8).

seizures

water stays, Na looks low.

antidiuretic hormone

severe symptoms (seizure, coma, impending herniation): this is an emergency. 3% NaCl 100 mL IV over ~20 min, recheck; repeat up to 3 times until symptoms abate or Na rises ~5 mEq/L. then slow down and stay under the 24-h ceiling.

acute or symptomatic hyponatremia

GI losses, diuretics

clues: dry patient, tachy/orthostasis, Uosm >100, UNa

hypovolemic hyponatremia

SIADH, hypothyroid, adrenal insuff., low-solute diet/beer potomania

clues: normal exam, Uosm >100, UNa >30; check TSH, AM cortisol, meds (SSRIs, carbamazepine, opioids), pain/nausea. treatment: fluid restriction (often ≤1-1.2 L/day, or urine output + insensible ~500 mL).

increase solute: urea PO, salt tablets + loop diuretic to dump electrolyte-free water.

vaptans (tolvaptan) for select, resistant inpatient cases—use with protocol and frequent Na checks. low-solute diets (beer potomania): give protein/solute, avoid rapid auto-correction → consider DDAVP clamp early.

euvolemic hyponatremia

HF, cirrhosis, CKD

clues: edema, ascites/JVD; Uosm >100, UNa

hypervolemic hyponatremia

65-yo man, hard to arouse, appears to be seizing, Na 110 mEq/L.

severe hyponatremia symptoms. a 3% NaCl situation.

weight-based rate to raise Na by 1 mEq/L/hr in an 80-kg patient?

80 mL/hr of 3% NaCl.

first question in ANY low Na:

what's the serum osmolality?

if glucose is high, sodium looks falsely low. correct Na roughly by:

+0.016 × (glucose - 100)

second step in low sodium:

use sOsm to pick the correct branch

plasma is concentrated by another osmole pulling water out of cells, diluting Na. common causes: hyperglycemia, mannitol. fix the cause (e.g., treat the high glucose, stop/reverse mannitol). don't chase the Na directly.

hypertonic hyponatremia

"pseudo-hyponatremia" from lab artifact when very high lipids or proteins occupy volume in old measurement methods. address the lipid/protein issue; Na itself isn't truly low in water phase.

isotonic hyponatremia

this is true, clinically important hyponatremia. next step: determine volume status (hypovolemic, euvolemic, hypervolemic) with history, exam, urine studies. that steers therapy.

hypotonic hyponatremia

start with serum osmolality. calculate or measure it: sOsm = 2 × Na + Glucose/18 + BUN/2.8. then sort the patient into one of three buckets:

all of the above

sodium looks low only because there's a ton of other osmoles in blood (usually glucose, sometimes mannitol/glycerol). these pull water out of cells into the ECF → dilutes Na. total body sodium is normal.

key clue: very high glucose or mannitol infusion.

treatment: fix the cause (insulin for hyperglycemia, stop mannitol/other hypertonic agents). you don't need hypertonic saline.

hypertonic hyponatremia

called "pseudo-hyponatremia." lab artifact from a very large non-water fraction in serum (e.g., severe hypertriglyceridemia, marked hyperproteinemia, or lipid/protein infusions). the sodium in the aqueous phase is actually normal.

treat the underlying condition. if the patient needs fluids for volume, give isotonic saline (0.9% NaCl); do not chase the sodium number with hypertonic solutions.

isotonic hyponatremia

the common, clinically important type.

next step: determine volume status (hypovolemic, euvolemic, hypervolemic) to guide therapy.

hypotonic hyponatremia

serum osmolality < 275 mOsm/kg means the plasma is dilute: this is the common, true form of hyponatremia.

then sort patients by ECF volume status:

hypovolemic (volume depleted)

euvolemic

hypervolemic

hypotonic hyponatremia

if they are hypotonic and look volume depleted, you're in the _______________ box:

both Na and water are down, but Na is down more → low serum Na. volume contraction triggers ADH (vasopressin) and thirst → kidneys retain water and patients often drink hypotonic fluids → hyponatremia worsens.

hypovolemic hypotonic hyponatremia

urine is concentrated (often Uosm > 450 mOsm/kg) because ADH is on. urine sodium helps find the cause: uNa < 30 mEq/L (extrarenal losses): the kidneys are trying to conserve salt.

think GI losses (vomiting, diarrhea, ostomies/fistulas), skin losses (sweat, burns), or third spacing (pancreatitis, bowel obstruction, sepsis, muscle injury).

uNa > 30 mEq/L (renal losses): the kidneys are losing salt.

think thiazide diuretics, adrenal insufficiency, renal disease, or cerebral salt wasting.

hypovolemic hypotonic hyponatremia

select all that apply:

what is treatment for hypovolemic hypotonic hyponatremia?

1. refill the vascular space and turn off the ADH drive.

2. use isotonic crystalloid

3. check serum Na frequently

4. keep the daily Na rise ≤ 8-10 mEq/L

↑ total body water with normal (or slightly ↓) total body Na. you won't see edema or obvious volume depletion.

euvolemic hypotonic hyponatremia

typical screening labs

urine Osm ≥100 mOsm/kg and Urine Na ≥20-30 mEq/L → kidneys aren't diluting urine → think SIADH, adrenal insufficiency, or hypothyroidism.

urine Osm

euvolemic hypotonic hyponatremia

why does euvolemic hyponatremia happen?

serum osmolality falls → normally __________________ should be suppressed, allowing free-water excretion (dilute urine).

in SIADH, it is inappropriately high despite low osmolality → water reabsorption in the collecting duct → concentrated urine (↑ urine Osm), low urine volume, and dilutional hyponatremia—without frank edema.

ADH (vasopressin)

persistent or intermittent ADH activity when osmo/volume cues should be shutting it off.

SIADH

select all that apply:

what are some causes of SIADH?

1. meningitis

2. SAH

3. tumors and head trauma

4. pain and anxiety

5. severe nausea.

6. pneumonia, TB, abscess

7. ectopic ADH

8. severe hypothyroidism

9. secondary adrenal insufficiency

10. medications

select all that apply:

what are the medications associated with SIADH?

1. antidepressants

2. anticonvulsants

3. antipsychotics/antiemetics

4. anticancer

5. chlorpropamide

6. opioids

7. MDMA

8. NSAIDs and acetaminophen

9. ACE-Is

10. vasopressin analogs

select all that apply:

how do you recognize SIADH?

1. low serum Osm

2. inappropriately concentrated urine

3. urine Na ≥30 mEq/L

4. clinically euvolemic

select all that apply:

how would we treat SIADH?

1. treat the cause

2. fluid restriction

3. salt tablets ± loop diuretic if needed

select all that apply:

how will we treat euvolemic hypotonic hyponatremia?

1. treat underlying causes

2. fluid restriction

3. if refractory SIADH: consider vasopressin

select all that apply:

what are the two categories of vasopressin receptor agents?

1. demeclocycline

2. vaptans

tetracycline that reduces renal response to ADH. downsides: hepatic metabolism; photosensitivity, nausea, nephrotoxicity.

demeclocycline

ADH receptor blockers → cause aquaresis (water diuresis without losing much Na)

vaptans

total body water ↑↑ and total body Na ↑, but water rises more.

hypervolemic hypotonic hyponatremia

edema (expanded interstitial ECF) but low effective circulating volume in the arteries. that low effective volume triggers RAAS + non-osmotic ADH release, so the body retains more water than salt → dilutional hyponatremia. typical uNa

hypervolemic hypotonic hyponatremia

select all that apply:

how do we treat hypervolemic hypotonic hyponatremia?

1. stop offending meds

2. fluid restriction ≤1-1.5 L/day

3. sodium restriction

4. loop diuretics

5. consider vaptans

6. treat the underlying disease

water restriction + solute (salt/urea) ± loop; fix cause; vaptan if refractory.

euvolemic (SIADH)

fluid & Na restriction + loop; fix HF/cirrhosis/nephrosis; vaptan if needed.

hypervolemic

watch rate of Na rise with any therapy to avoid _________________.

osmotic demyelination

if sOsm > 290 mOsm/kg = ______________ hyponatremia. usually something osmotically active in plasma (e.g., high glucose, mannitol) pulls water out of cells → dilutes Na⁺.

hypertonic

if sOsm 275-290 = ___________________ hyponatremia. lab artifact from hyperlipidemia/hyperproteinemia or lipid/protein infusions. treat underlying issue; Na⁺ in the aqueous phase is actually normal.

isotonic (pseudo)

if sOsm < 275 = _______________ hyponatremia → go to step 2.

hypotonic (true)

if ____________, determine volume status. think "what's the ECF doing?" use exam + urine studies.

hypotonic

↓TBW, but more ↓Na⁺

clues: volume depletion (orthostasis, dry mucosa), concentrated urine.

urine Na⁺ < 30 mEq/L → extrarenal losses (GI loss, third-spacing, burns, sweat).

urine Na⁺ > 30 mEq/L → renal losses (thiazides, adrenal insufficiency, salt-wasting).

treatment: isotonic fluids (0.9% NaCl, LR, Plasmalyte); stop diuretics; give steroids if adrenal insufficiency.

hypovolemic hypotonic

slightly ↑TBW, normal total Na⁺

big bucket: SIADH (most common), also severe hypothyroidism or secondary adrenal insufficiency; sometimes primary polydipsia/low-solute intake.

typical labs for SIADH: urine Osm > 100 mOsm/kg and urine Na⁺ > 20-30 mEq/L (kidney is in "water-reabsorbing" mode).

treatment: treat cause (stop offending drug, manage cancer/infection, replace thyroid or steroids if needed) + fluid restriction (often

euvolemic hypotonic

↑↑TBW, ↑Na⁺ but water gain ≫ Na⁺

causes: heart failure, cirrhosis, nephrotic syndrome, advanced kidney disease.

urine Na⁺ may help: often < 20 mEq/L in cirrhosis/nephrosis; > 20 in intrinsic kidney failure.

treatment: sodium + fluid restriction, loop diuretics, treat the underlying disease; consider vaptans selectively.

hypervolemic hypotonic

fix the osmole (insulin for hyperglycemia; stop mannitol).

hypertonic

isotonic fluids; remove cause; give steroids if adrenal insufficiency

hypovolemic

fluid restriction ± loop diuretic + salt; address cause; consider urea; refractory → vaptan or demeclocycline (rarely used).

euvolemic

Na⁺/fluid restriction + loop diuretic; concentrate parenteral nutrition if applicable; vaptans in select refractory cases.

hypervolemic

in symptomatic/acute hyponatremia, give _____________ to control symptoms, but limit total correction to ~8-10 mEq/L in 24 h (≤18 mEq/L in 48 h) to prevent osmotic demyelination.

3% NaCl

a patient has hypotonic hyponatremia and is on carbamazepine. what subtype?

euvolemic

serum Na >145 mEq/L.

always hyperosmolar: there's too little water relative to solute, so plasma osmolality is high.

when it happens: often during poor fluid intake or excessive water losses.

who's at risk: infants, comatose/ICU patients, and frail/elderly people who can't access or sense thirst well.

why it's serious: mortality is high, especially with acute rises (up to ~75% in adults) and still substantial when chronic.

hypernatremia

brain can't adapt quickly → more dramatic symptoms.

acute (≤24-48 hr) hypernatremia

brain accumulates "organic osmolytes" to hold onto water → fewer symptoms, but this adaptation means over-rapid correction later can cause cerebral edema

chronic (>48 hr) hypernatremia

hypertonic plasma pulls water out of neurons → neurons _____________ → neurologic symptoms. severity tracks with how high the Na is and how fast it rose.

shrink

lethargy, weakness, confusion, restlessness, irritability.

mild to moderate hypernatremia symptoms

muscle twitching, seizures, coma, even death.

severe/rapid rise symptoms of hypernatremia

select all that apply:

how do we treat hypernatremia?

1. relieve symptoms if present

2. normalize Na safely

3. stop ongoing fluid losses

4. replace the free-water deficit

5. avoid complications from correcting too fast