When to intubate in GCS?

GCS ≤ 8 requires intubation for airway protection. The patient cannot protect their own airway at this level of consciousness. Motor score is the most prognostically important component.

What is the best initial fluid for sepsis resuscitation?

Lactated Ringer's (LR) is the preferred resuscitation fluid. The SMART trial (2018) showed balanced crystalloids reduced death, new renal failure, and persistent renal dysfunction compared to normal saline.

When to start vasopressors in septic shock?

Start norepinephrine (first-line vasopressor) if MAP remains < 65 mmHg after initial 30 mL/kg crystalloid resuscitation, or earlier if patient is profoundly hypotensive. Do not delay pressors to complete full fluid resuscitation.

Why can serum uric acid be normal during acute gout?

During acute inflammation, IL-6 increases renal urate excretion and redistributes urate from plasma to tissues. Up to 40% of acute gout flares have normal serum uric acid. Joint aspiration with polarized microscopy is needed for definitive diagnosis.

How do you distinguish lupus flare from infection in SLE?

Key clues: CRP is low/normal in flare but elevated in infection. Complement (C3/C4) drops in flare but is normal/elevated in infection. Procalcitonin is elevated in bacterial infection but normal in flare. Anti-dsDNA rises in flare, stable in infection.

What is the difference between DKA and HHS?

DKA features acidosis (pH 600), hyperosmolality (> 320), and minimal ketosis -typically in Type 2 DM. DKA requires insulin drip; HHS requires aggressive fluid resuscitation first.

When to give tPA in acute ischemic stroke?

IV alteplase (tPA) can be given within 4.5 hours of last known well time in eligible patients. CT head must rule out hemorrhage first. For large vessel occlusion, mechanical thrombectomy can be performed up to 24 hours with favorable imaging.

What antibiotics for community-acquired pneumonia?

Inpatient non-ICU: ceftriaxone + azithromycin. ICU: ceftriaxone + azithromycin (add vancomycin if MRSA risk). Outpatient healthy: amoxicillin. Outpatient with comorbidities: augmentin + azithromycin or respiratory fluoroquinolone. Duration: 5 days if clinically stable for 48 hours.

How to interpret iron studies?

Iron deficiency: low ferritin (< 30), high TIBC, low iron, low transferrin saturation (< 20%). Anemia of chronic disease: normal/high ferritin (acute phase reactant), low TIBC, low iron. A ferritin of 50-100 in an inflamed patient may still represent iron deficiency.

What is the correction rate for hyponatremia?

Correct sodium no more than 8 mEq/L in 24 hours to avoid osmotic demyelination syndrome (ODS). For symptomatic severe hyponatremia with seizures, give 3% hypertonic saline 100-150 mL bolus over 10-20 minutes. If overcorrected, use D5W + DDAVP rescue protocol.

When to start antibiotics in meningitis?

Within 30-60 minutes. Do NOT delay antibiotics for LP or CT. Draw blood cultures, start empiric antibiotics (vancomycin + ceftriaxone ± ampicillin if > 50 or immunocompromised), then perform LP when possible. Dexamethasone should be given before or with the first antibiotic dose.

DOACs vs warfarin in antiphospholipid syndrome?

DOACs are contraindicated in APS. The TRAPS trial (2018) showed rivaroxaban was inferior to warfarin with more thrombotic events in triple-positive APS patients. Warfarin with INR target 2-3 is the standard for APS, indefinitely.

How to manage scleroderma renal crisis?

ACE inhibitors (captopril) are life-saving -start immediately and titrate aggressively. Do NOT hold for rising creatinine. Steroids > 15 mg prednisone per day precipitate scleroderma renal crisis. ARBs are NOT a substitute -evidence is only for ACEi.

What are the 4 pillars of heart failure treatment?

Guideline-directed medical therapy (GDMT) for HFrEF: (1) ARNI or ACEi/ARB, (2) beta-blocker (carvedilol, metoprolol succinate, or bisoprolol), (3) MRA (spironolactone or eplerenone), (4) SGLT2 inhibitor (dapagliflozin or empagliflozin). All four should be initiated and titrated to target doses.

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EmergentNephrology

Hyponatremia

Na⁺ < 135 mEq/L -the most common electrolyte abnormality in hospitalized patients. The approach is systematic: (1) serum osmolality, (2) volume status, (3) urine studies. Correct slowly -osmotic demyelination syndrome is iatrogenic and devastating.

🔍 Systematic Approach

Step 1 -Serum Osmolality

Serum Osm	Category	Causes
< 275 (low)	Hypotonic (true hyponatremia)	Most cases. Proceed to Step 2.
275–295 (normal)	Isotonic (pseudohyponatremia)	Hyperlipidemia, hyperproteinemia (multiple myeloma). Lab artifact -true Na is normal. Check lipid panel + protein.
> 295 (high)	Hypertonic (translocational)	Hyperglycemia (#1 -correct Na for glucose: add 1.6 mEq/L Na for every 100 mg/dL glucose above 100), mannitol, IV contrast.

Step 2 -Volume Status (for Hypotonic)

Volume Status	Urine Na	Causes	Treatment
Hypovolemic (dry mucous membranes, orthostasis, tachycardia, skin tenting)	< 20: extrarenal losses (GI: vomiting, diarrhea; 3rd spacing: burns, pancreatitis) > 20: renal losses (diuretics, adrenal insufficiency, cerebral salt wasting)	GI losses, diuretics, adrenal crisis, burns	Volume resuscitation with NS. Na will correct as volume is restored. Watch for overcorrection -once ADH stimulus (hypovolemia) is removed, kidneys dump free water rapidly.
Euvolemic (no edema, no orthostasis -hardest to assess)	> 40 (inappropriately concentrated urine)	SIADH (#1), hypothyroidism, adrenal insufficiency, psychogenic polydipsia (Uosm < 100), beer potomania, tea-and-toast	Fluid restriction (SIADH). Treat underlying cause. See SIADH topic for details.
Hypervolemic (edema, JVD, ascites, anasarca)	< 20: CHF, cirrhosis, nephrotic syndrome (effective hypovolemia → ADH release → water retention) > 20: CKD/ESKD (kidneys can't excrete water)	HF, cirrhosis, nephrotic, CKD	Fluid restriction + treat underlying disease. Diuretics for HF/cirrhosis. Dialysis if ESKD.

Step 3 -Key Labs to Order

Serum osmolality (first -classifies the hyponatremia)
Urine osmolality (Uosm < 100 = appropriate dilution → water overload/polydipsia. Uosm > 100 = kidneys inappropriately concentrating → ADH-mediated)
Urine sodium (renal vs extrarenal losses in hypovolemic; confirms SIADH if > 40 in euvolemic)
Serum glucose (correct for hyperglycemia: add 1.6 per 100 above 100)
TSH, AM cortisol (rule out hypothyroidism and adrenal insufficiency before diagnosing SIADH)

🚨 Management

Correction Rates

The danger of hyponatremia treatment is NOT the low sodium -it's correcting too fast. Osmotic demyelination syndrome (ODS) is iatrogenic, irreversible, and devastating. ODS Prevention Study, 2010

Scenario	Max Correction Rate	Treatment
Chronic (> 48h or unknown duration)	≤ 8 mEq/L in 24h (some guidelines use ≤ 10). High-risk for ODS: ≤ 6 mEq/L in 24h.	Fluid restriction (SIADH), NS (hypovolemic), treat underlying cause. Check Na q4–6h.
Acute (< 48h, known onset)	Can correct faster -brain hasn't adapted. Still aim for ≤ 10–12 mEq/L in 24h.	More aggressive treatment acceptable. Still monitor closely.
Symptomatic (seizures, coma, severe AMS)	Immediate goal: raise Na by 4–6 mEq/L in first 6h to stop symptoms. Then ≤ 8 total in 24h.	3% hypertonic saline 100–150 mL IV bolus over 10–20 min. SALSA, 2021 May repeat × 2. ICU. Check Na q2h.

Osmotic Demyelination Syndrome (ODS)

Occurs 2–6 days after overcorrection -not immediately
Central pontine myelinolysis → "locked-in syndrome" (quadriplegia, inability to speak/swallow, preserved consciousness)
Risk factors for ODS: chronic hyponatremia (> 48h), alcoholism, malnutrition, hypokalemia (correct K⁺ simultaneously -K⁺ correction counts toward Na correction!), liver disease, Na < 105
If overcorrecting (Na rising too fast): (1) D5W infusion (free water to re-lower Na), (2) DDAVP 2 mcg IV q8h (clamp urine output → stop Na from rising further), (3) target: bring Na back within safe correction range

🔄 Updated Practice: Old teaching: correct sodium no more than 10-12 mEq/L in 24 hours. Updated: the recommended limit is now ≤8 mEq/L in any 24-hour period for patients at high risk for osmotic demyelination syndrome (ODS) -chronic hyponatremia (>48h), alcoholism, malnutrition, hypokalemia, liver disease. For truly acute hyponatremia (<48h, e.g., exercise-associated, postoperative), faster correction is safe. If overcorrected: give back free water (D5W) and consider desmopressin (DDAVP) 2 mcg IV to re-lower sodium.

Danger point: hypovolemic hyponatremia corrected with NS. Once volume is restored, the ADH stimulus disappears → kidneys suddenly excrete massive free water → Na shoots up rapidly → osmotic demyelination syndrome (ODS) risk. Prevention: anticipate it, cap correction ≤ 8 mEq/L in any 24h period in high-risk patients (chronic hyponatremia, alcoholic, malnourished, liver disease, hypokalemia). If overshooting: D5W infusion ± DDAVP 2 mcg IV to re-lower Na into the safe range.

Swipe for more examples

📋 Case 1, SIADH from SCLC

Patient: 68F with SCLC, found lethargic, Na⁺ 118 mEq/L.

Step 1 -Is this real? Serum osm: 248 (< 280 = true hypoosmolar hyponatremia). Not pseudohyponatremia.

Step 2 -Assess volume status:

Exam: Mucous membranes moist, no edema, no JVD, skin turgor normal → euvolemic
Urine Na: 45 mEq/L (> 40 = kidneys wasting Na → SIADH)
Urine osm: 520 (> 100 = kidneys concentrating inappropriately → SIADH)
TSH: normal. AM cortisol: normal (rules out hypothyroid and adrenal insufficiency)

Diagnosis: SIADH from SCLC (paraneoplastic ADH secretion)

Step 3 -Treatment:

Symptomatic (lethargic) → 3% hypertonic saline 100 mL IV bolus over 10 min. Recheck Na in 2h.
Na went 118 → 121 (+3 in 2h) -good. Symptoms improving.
Target: correct ≤ 8 mEq/L in first 24h (risk of osmotic demyelination if faster)
Fluid restriction 1L/day for maintenance
If refractory SIADH: tolvaptan (Samsca) 15mg PO daily (check Na q6h -potent)

📋 Case 2, Beer Potomania

Patient: 48M heavy beer drinker (12+ beers/day), found confused. Na⁺ 108 mEq/L. No edema. Uosm 58 (maximally dilute).

Diagnosis: Beer potomania, massive free water intake with minimal solute intake → kidneys cannot excrete the water load despite maximally dilute urine.

Treatment:

STOP free water intake. Normal saline is usually sufficient (not hypertonic) because once solute intake resumes, kidneys correct rapidly.
Monitor Na q2h closely.
If correcting > 8 mEq/day → give DDAVP 2 mcg IV q8h + D5W to slow correction.

⚠️ DANGER: These patients auto-correct too fast once admitted and beer is stopped. The kidneys suddenly have enough solute to excrete free water → Na shoots up.

Key lesson: Beer potomania corrects itself dangerously fast when you admit the patient and stop beer. DDAVP rescue may be needed to SLOW correction.

📋 Case 3, SIADH from SSRI

Patient: 72F started on sertraline 3 weeks ago, presents with nausea and confusion. Na⁺ 122 mEq/L. Euvolemic.

Labs: Uosm 580 (inappropriately concentrated). Urine Na 65. TSH and cortisol normal.

Diagnosis: Classic SIADH from SSRI.

Treatment:

Fluid restriction 1–1.2 L/day (first-line for SIADH).
If not improving → salt tabs 1–2 g TID + loop diuretic (furosemide 20 mg, forces dilute urine).
Consider stopping sertraline or switching to a less SIADH-prone antidepressant.
Avoid hypertonic saline unless symptomatic (seizures, severe AMS).

Key lesson: Always check the med list for SIADH causes. SSRIs are the #1 medication cause. Fluid restriction is first-line, not hypertonic saline.

Related Topics

Acid-Base DisordersCalciphylaxis (Calcific Uremic Arteriolopathy)Chronic Kidney Disease (CKD)Contrast-Induced NephropathyDialysis IndicationsHypernatremia

🧪 Workup

Diagnostic Workup -Hyponatremia

Systematic approach: (1) Serum osmolality → (2) Volume status → (3) Urine studies. Do NOT diagnose SIADH without first ruling out hypothyroidism and adrenal insufficiency.

Test	Rationale	Key Values / Interpretation
Serum osmolality	First step -classifies the hyponatremia.	< 275 = hypotonic (true hyponatremia -proceed to step 2). 275-295 = isotonic (pseudohyponatremia -check lipids, protein). > 295 = hypertonic (hyperglycemia -correct Na: add 1.6 mEq/L per 100 mg/dL glucose above 100).
Urine osmolality	Distinguishes ADH-mediated from water overload.	< 100 mOsm/kg = kidneys appropriately diluting (polydipsia, beer potomania, tea-and-toast). > 100 = ADH-mediated (inappropriate concentration → SIADH, hypovolemia, hypervolemia).
Urine sodium	Differentiates renal from extrarenal sodium losses in hypovolemic states; confirms SIADH in euvolemic.	UNa < 20 = extrarenal losses (GI, third-spacing) or effective hypovolemia (CHF, cirrhosis). UNa > 40 in euvolemic state = SIADH. UNa > 20 in hypovolemic = renal losses (diuretics, adrenal insufficiency).
Volume status (clinical)	Essential physical exam -guides entire differential and treatment.	Hypovolemic (orthostasis, dry mucous membranes, tachycardia) → NS. Euvolemic → SIADH workup. Hypervolemic (edema, JVD, ascites) → CHF/cirrhosis/nephrotic.
TSH	Hypothyroidism is a reversible cause -must exclude before diagnosing SIADH.	Severe hypothyroidism → decreased free water clearance → hyponatremia. Treat thyroid disease first.
AM cortisol	Adrenal insufficiency mimics SIADH (euvolemic, high UNa). Must exclude before SIADH diagnosis.	AM cortisol < 3 = adrenal insufficiency likely. 3-15 = indeterminate → ACTH stimulation test. > 15 = AI unlikely.
Serum glucose	Correct Na for hyperglycemia (translocational hyponatremia).	Corrected Na = measured Na + 1.6 × [(glucose - 100) / 100]. If corrected Na is normal → not true hyponatremia.

💊 Medications

Drug Therapy -Hyponatremia

Drug	Dose	Route	Indication	Key Notes
3% Hypertonic saline	100-150 mL IV bolus over 10-20 min. May repeat × 2 (max 3 boluses).	IV	Severe symptomatic hyponatremia (seizures, coma, severe AMS)	ICU setting. Goal: raise Na by 4-6 mEq/L in first 6h to stop symptoms. Check Na q2h. Rapid intermittent bolus is as effective and safer than continuous infusion SALSA, 2021.
Fluid restriction	1-1.5 L/day (all PO and IV fluids combined)	-	SIADH (first-line), hypervolemic hyponatremia (HF, cirrhosis)	Effective if urine osmolality is not extremely high. Poor compliance limits effectiveness. Calculate free water clearance to predict response.
NaCl tablets (salt tabs)	1-3 g PO TID	PO	Chronic SIADH (with or without loop diuretic)	Often combined with furosemide 20 mg daily -the diuretic promotes free water excretion while salt tabs replenish sodium. Effective outpatient strategy.
Furosemide	20-40 mg PO daily	PO	Combined with salt tabs for chronic SIADH	Impairs urinary concentration → promotes electrolyte-free water excretion. Only effective when combined with adequate sodium intake (salt tabs).
Tolvaptan (Samsca)	15 mg PO daily (may increase to 30-60 mg)	PO	Refractory SIADH or hypervolemic hyponatremia not responding to fluid restriction	V2 receptor antagonist ("vaptan") -blocks ADH at collecting duct → aquaresis (free water loss). Must initiate inpatient. Check Na q6h for first 24h. Hepatotoxicity risk -do not use > 30 days. Do NOT use in hypovolemic hyponatremia.
Demeclocycline	300-600 mg PO BID	PO	Alternative for chronic SIADH (if tolvaptan not available/tolerated)	Tetracycline that induces nephrogenic DI. Slow onset (3-5 days). Nephrotoxic -avoid in liver disease. Largely replaced by tolvaptan.
DDAVP (desmopressin)	2 mcg IV q8h	IV	ODS rescue -given when Na is overcorrecting too rapidly	Clamps urine output → stops further Na correction. Combine with D5W (3-6 mL/kg/hr) to actively re-lower Na. Target: bring correction rate back to ≤ 8 mEq/L in 24h.
D5W (5% dextrose)	3-6 mL/kg/hr	IV	ODS rescue -free water to re-lower sodium if overcorrecting	Used with DDAVP. The dextrose is metabolized, leaving free water. Start immediately if Na rising > 8-10 mEq/L in 24h.

📋 On Rounds

Why does correcting hypokalemia matter in hyponatremia?

Potassium is osmotically active and contributes to the Na correction rate. When you give IV KCl, K⁺ enters cells and Na⁺ comes out (to maintain electrochemical balance via the Na⁺/K⁺-ATPase). This means every mEq of K⁺ you give raises the serum Na by approximately the same amount as giving a mEq of Na. If you're correcting hypokalemia aggressively alongside hyponatremia, the Na may rise faster than you expect.

A urine osmolality of 50 mOsm/kg in a hyponatremic patient tells you what?

The kidneys are doing their job -maximally diluting urine. This means ADH is appropriately suppressed and the kidneys are trying to excrete free water. The hyponatremia is from water intake exceeding the kidney's diluting capacity. Differential: psychogenic polydipsia (> 15–20 L/day overwhelms even normal kidneys), beer potomania (low solute intake → low obligate urine output → can't excrete enough water), tea-and-toast diet (same mechanism).

You are correcting hyponatremia and realize you've already gone up 10 mEq in 18 hours. What do you do?

ODS rescue protocol -act immediately: (1) Stop all hypertonic saline and salt tabs, (2) Give D5W at 3-6 mL/kg/hr (free water to re-lower sodium), (3) Give DDAVP 2 mcg IV q8h (makes kidneys retain free water, prevents further correction). (4) Recheck Na q2h until it falls back to the safe correction rate (≤ 8 mEq/24h, some experts say ≤ 6 in high-risk patients).

What are the most dangerous medications that cause SIADH?

SSRIs are the #1 drug cause of SIADH (sertraline, fluoxetine, paroxetine -onset typically 1-4 weeks). Other common offenders: carbamazepine/oxcarbazepine (direct ADH-like effect on collecting duct), cyclophosphamide (especially with high-volume hydration), vincristine (neuropathic ADH release), opioids, PPIs, NSAIDs, ecstasy/MDMA (causes acute hyponatremia from both ADH release and excessive water intake → can be fatal).

Clinical Examples

📋 Case 1, SIADH from SSRI with Overcorrection Risk

Patient: 72 y/o F on sertraline x3 weeks, presents with confusion. Na⁺ 112 (was 128 two weeks ago).

Key findings: Serum osm 238, urine osm 480, UNa 52, euvolemic. TSH and cortisol normal. SIADH from sertraline.

Management:

Stop sertraline, removing the SIADH stimulus may cause rapid free water excretion
Fluid restriction < 1L/day + salt tabs 1g TID
Na rose 10 mEq in 18h (overcorrection), start ODS rescue: D5W + DDAVP 2 mcg IV q8h
Re-lower Na back to safe correction rate (≤ 8 mEq/24h); recheck Na q2h

Teaching point: When the SIADH stimulus is removed, ADH drops and free water is excreted rapidly, causing overcorrection. ODS is devastating and irreversible. High-risk patients need proactive DDAVP clamping.

📋 Case 2, Severe Symptomatic Hyponatremia with Seizures

Patient: 55 y/o M with SCLC, found seizing at home. Na⁺ 104, obtunded.

Key findings: Serum osm 218, urine osm 640, UNa 68, GCS 8. Euvolemic. Ectopic ADH from SCLC.

Management:

3% NaCl 100-150 mL bolus over 10 min, repeat x1 if still seizing
Target 4-6 mEq/L acute rise to stop seizures, then ≤ 8 mEq/24h total
Check Na q2h during correction; DDAVP 2 mcg IV q8h proactively to prevent overcorrection
ICU admission, oncology for underlying SCLC treatment

Teaching point: Seizures from hyponatremia require emergent 3% NaCl, the one scenario where rapid correction is indicated. Target only enough rise to stop symptoms, then strictly limit total correction.

📋 Case 3, Beer Potomania (Low Solute Hyponatremia)

Patient: 48 y/o M, chronic alcohol use, Na⁺ 118. Drinks 12+ beers daily, minimal food intake.

Key findings: Serum osm 248, urine osm 52 (maximally dilute, ADH suppressed), UNa 8. Malnourished.

Management:

Urine osm 52 = ADH appropriately suppressed, this is NOT SIADH
Low solute intake → low obligate urine output → cannot excrete enough free water
Treatment: normal diet (increase solute) + fluid restriction
HIGH overcorrection risk when diet resumes, use prophylactic DDAVP

Teaching point: Urine osm < 100 rules out SIADH. Beer potomania corrects rapidly when normal diet resumes, proactive DDAVP is essential to prevent ODS. SALT-1/2, 2006 showed tolvaptan is effective for SIADH but is NOT appropriate for low-solute states.

📣 Sample Presentation

One-Liner

"Mrs. Lee is a 68-year-old with SCLC presenting with Na⁺ 118, serum osm 252, urine osm 520, urine Na 45, euvolemic on exam. Consistent with SIADH from malignancy."

Key Points to Cover on Rounds

Euvolemic hypoosmolar hyponatremia. Urine osm 520 (inappropriately concentrated), UNa 45 (>40). TSH and cortisol normal. Etiology: SIADH from SCLC. Asymptomatic (no seizure, no AMS). Treatment: fluid restriction <1L/day. Na trending 118→120→122 over 24h (rate 4 mEq/24h -safe). Salt tabs 1g TID added. If refractory → tolvaptan 15 mg daily SALT-1/2, 2006 (monitor in-hospital, check Na q6h). Goal: ≤8 mEq/L correction per 24h to avoid ODS. Plan: treat underlying malignancy, continue fluid restriction.

Monitoring -Hyponatremia Correction

Parameter	Frequency	Target / Action
Serum sodium	q2h if on hypertonic saline; q4-6h during active correction; q6-8h once stable	Max correction ≤ 8 mEq/L in any 24h period (≤ 6 in high-risk: alcoholism, malnutrition, hypokalemia, liver disease, Na < 105). If overcorrecting → DDAVP + D5W rescue immediately.
Serum osmolality	At baseline, then q12-24h during correction	Should rise proportionally with Na. Guides assessment of correction adequacy.
Urine output	q1-2h during active treatment	Sudden brisk water diuresis (> 200 mL/hr of dilute urine) = danger sign for overcorrection. This happens when ADH stimulus is removed (e.g., volume resuscitation in hypovolemic hyponatremia). Start DDAVP preemptively if UOP surges.
Neurological status	q2-4h during active correction	Improving: resolution of confusion, seizures, lethargy = adequate correction. New dysarthria, dysphagia, quadriparesis 2-6 days after correction = ODS -MRI brain, neurology consult.
Potassium	With each Na check	K⁺ correction counts toward Na correction (K⁺ enters cells, Na⁺ comes out). If repleting K⁺ aggressively, account for this in your correction rate calculation.
I&Os	Strict q1h during active treatment	Track all free water intake (IV and PO). Ensure fluid restriction is enforced if indicated. Document urine osmolality if available (Uosm < 200 on tolvaptan = expected).

Overcorrection rescue protocol: If Na rises > 8-10 mEq/L in 24h → (1) Stop all hypertonic saline and salt tabs, (2) D5W at 3-6 mL/kg/hr, (3) DDAVP 2 mcg IV q8h, (4) Recheck Na q2h until back within safe range. Act immediately -ODS is irreversible.

⚡ Summary

Summary

Step 1

Serum osm: < 275 = true hypoosmolar hyponatremia. ≥ 275 = pseudohyponatremia (hyperglycemia, mannitol, IVIG).

Volume Status

Hypovolemic (FENa < 1): dehydration, diuretics. Euvolemic (UNa > 40): SIADH, hypothyroid, adrenal insuff. Hypervolemic: CHF, cirrhosis, nephrotic.

SIADH Treatment

Fluid restriction < 1L/day → salt tabs → tolvaptan (inpatient only, check Na q6h). Treat the cause.

Correction Rate

≤ 8 mEq/L per 24h (some say ≤ 6 in high-risk). Overcorrection → ODS (osmotic demyelination). Devastating and irreversible.

ODS Rescue

If overcorrecting: D5W + DDAVP 2 mcg IV q8h → re-lower sodium to safe rate. Act immediately.

Severe Symptoms

Seizures, AMS → hypertonic saline 3% NaCl 100-150 mL bolus over 10 min. Target 4-6 mEq/L rise acutely to stop seizures.

📄 One Pager

Nephrology · One Pager

Hyponatremia

Check serum osm → volume status → urine studies. Correct ≤ 8 mEq/24h. Overcorrection → ODS (devastating). Severe symptoms → 3% NaCl 100-150 mL bolus.

🧪 Approach

Step 1: Serum osm (< 275 = true). Step 2: Volume status (hypo/eu/hyper). Step 3: UNa + urine osm. Euvolemic + UNa > 40 + concentrated urine = SIADH.

🚨 Acute Severe Symptoms

Seizures or AMS → 3% NaCl 100-150 mL bolus over 10 min (can repeat ×1). Target 4-6 mEq rise to stop seizures. Then slow correction to ≤ 8/24h total.

⚠️ ODS Prevention

Correct ≤ 8 mEq/24h (≤ 6 if high-risk: Na < 105, chronic, alcoholism, malnutrition, liver disease). If overcorrecting: D5W + DDAVP 2 mcg IV q8h immediately.

💊 Key Drugs

3% NaCl100-150 mL bolus (severe)

DDAVP2 mcg IV q8h (ODS rescue)

Tolvaptan15 mg daily (SIADH, inpatient only)

Salt tabs1g TID (chronic SIADH)

⚠️ Pitfalls

Overcorrection → ODS (irreversible pontine demyelination)
Not checking TSH and cortisol (must exclude before diagnosing SIADH)
Free water restriction while on tolvaptan (dangerous combo)
IV NS for hypovolemic hyponatremia in SIADH (worsens it)