Sepsis Guidelines: SSC 2026 (Updated)

Breaking: The Surviving Sepsis Campaign (SSC) 2026 Guidelines - for both adults (129 recommendations) and children (61 recommendations) - were published in April 2026 in Critical Care Medicine / Intensive Care Medicine and formally announced at SCCM2026 in Chicago, endorsed by 24 (adult) and 14 (pediatric) professional organisations. These supersede SSC 2021.

Definition (Sepsis-3, still current)

• Sepsis: Life-threatening organ dysfunction caused by a dysregulated host response to infection. Operationalized as SOFA score ≥ 2 above baseline.
• Septic shock: A subset of sepsis with circulatory and cellular/metabolic dysfunction; requires vasopressors to maintain MAP ≥ 65 mmHg AND serum lactate > 2 mmol/L despite adequate volume resuscitation. Hospital mortality > 40%.

SSC 2026: Adult Recommendations

1. Screening & Recognition

• Performance improvement programs: Hospitals should use sepsis performance improvement protocols (strong recommendation).
• Screening tools: Use validated tools (e.g., NEWS, qSOFA) to screen for sepsis in at-risk patients, including prehospital settings (conditional).
• Biomarkers: Procalcitonin (PCT) and CRP can support diagnosis; lactate ≥ 2 mmol/L identifies higher-risk patients.
• Blood cultures: Obtain ≥ 2 sets before antibiotics whenever feasible without meaningfully delaying therapy.
• Lactate: Measure serum lactate; repeat if initial > 2 mmol/L to guide resuscitation.

2. Initial Resuscitation

• Fluids: Begin IV crystalloid resuscitation promptly. The SSC 2026 moves away from a rigid 30 mL/kg protocol - use dynamic hemodynamic assessment (passive leg raise, pulse pressure variation, echocardiography) to guide fluid administration. For obese patients, calculate on adjusted body weight (not actual).
• Fluid type: Use balanced crystalloids (lactated Ringer's, Plasma-Lyte) over normal saline - reduces hyperchloremic acidosis risk.
• ROSE Framework (Resuscitation - Optimization - Stabilization - Evacuation): Give fluids early during shock; reassess dynamically; stop once shock resolves; actively de-resuscitate when congestion appears.

3. Vasopressors

• Timing (new 2026): Initial IV crystalloid fluid bolus first, then vasopressors if hypotension persists - but in unstable septic shock (mottled skin, altered mentation, profound hypotension), concurrent administration is appropriate. (Conditional, very low certainty - new recommendation)
• Route (new 2026): Start vasopressors peripherally rather than delaying until central venous access is secured. (Conditional, very low certainty)
• First-line agent: Norepinephrine remains first-line.
• Second-line: Vasopressin (to reduce norepinephrine dose or when norepinephrine alone is insufficient); epinephrine as an alternative.
• MAP target: ≥ 65 mmHg. New for 2026: In adults ≥ 65 years, an initial MAP target of 60-65 mmHg is conditionally recommended (lower target acceptable; no evidence for benefit of higher target in elderly).

4. Antimicrobial Therapy

• Timing: Administer IV antibiotics within 1 hour of septic shock recognition; within 3 hours for sepsis without shock.
• Empiric therapy: Broad-spectrum coverage appropriate to likely source, local resistance patterns, and patient risk factors (MRSA, Pseudomonas, fungi).
• De-escalation: Narrow antibiotics once culture/sensitivity results available - reduces resistance and adverse effects.
• Duration: Minimum effective course; procalcitonin-guided de-escalation/discontinuation is recommended to shorten duration.
• Source control: Identify and control the infectious source (drainage, debridement, device removal) as soon as medically and logistically feasible.

5. ICU Admission

• Admit patients requiring ICU-level care within 6 hours. (Conditional, low certainty - carried forward from 2021)

6. Corticosteroids

• In patients with septic shock who remain on vasopressors despite adequate resuscitation: hydrocortisone 200 mg/day (continuous infusion) or 50 mg IV every 6 hours.
• Steroids achieve faster shock reversal but have not demonstrated consistent mortality benefit across trials (ADRENAL, APROCCHSS). Monitor for hyperglycemia.

7. Ventilation (if intubated)

• Lung-protective ventilation: TV 6 mL/kg predicted body weight, Pplat ≤ 30 cmH₂O for ARDS.
• Prone positioning: ≥ 12-16 hours/day in moderate-severe ARDS (P/F < 150).
• Avoid routine use of high-frequency oscillatory ventilation (HFOV).

8. Other Adjuncts

• Glucose control: Target blood glucose 7.8-10 mmol/L (140-180 mg/dL); avoid hypoglycemia.
• DVT prophylaxis: Pharmacologic (LMWH preferred) unless contraindicated.
• Stress ulcer prophylaxis: In patients with risk factors for GI bleeding.
• Renal replacement therapy: No benefit to early initiation in AKI without other indications.
• IV immunoglobulin: Not routinely recommended.

Pediatric SSC 2026 (New)

• 5 strong recommendations
• 24 conditional recommendations
• 10 good practice statements
• 20 recommendations are new (compared to 2020)

Bundle Compliance (SEP-1 / Hour-1)

1. Measure lactate (repeat if > 2 mmol/L)
2. Obtain blood cultures before antibiotics
3. Administer broad-spectrum antibiotics
4. Begin rapid IV crystalloid (30 mL/kg) for hypotension or lactate ≥ 4 mmol/L
5. Apply vasopressors if patient is hypotensive during/after fluid resuscitation

What Changed from SSC 2021

Key Sources

• SSC 2026 Adult Guidelines: Prescott HC et al., Critical Care Medicine 2026. DOI: 10.1097/CCM.0000000000007075 (PMID: 41869847)
• SSC 2026 Pediatric Guidelines: Weiss SL et al., Pediatric Critical Care Medicine 2026. PMID: 41869844
• ESICM resource hub: survivingsepsis.org via ESICM
• Goldman-Cecil Medicine, 26e - Circulatory Therapy/Vasopressors sections
• Harrison's Principles of Internal Medicine 22e, Cardiovascular Dysfunction in Sepsis

Note from EM News (June 2026): A viewpoint critiques the 2026 SSC guidelines for favouring protocolized care despite evidence pointing toward individualized resuscitation. The debate between fixed bundle targets vs. adaptive strategies is ongoing.

Inotropes: Complete Notes

What Is Inotropy?

• Action potential → L-type Ca²⁺ channel opens → Ca²⁺ influx triggers Ca²⁺-induced Ca²⁺ release from the SR (CICR)
• [Ca²⁺]i rises → binds troponin C → actin-myosin crossbridge cycling → contraction
• Ca²⁺ is pumped back into SR (SERCA) or extruded via NCX → relaxation

Classification of Inotropes

1. Cardiac Glycosides - Digoxin

Mechanism of Action

1. Inhibits Na⁺/K⁺-ATPase on the cardiac myocyte membrane
2. → Intracellular Na⁺ accumulates
3. → Reduced driving force for NCX (Na⁺/Ca²⁺ exchanger), which normally extrudes Ca²⁺
4. → More Ca²⁺ stored in SR → greater Ca²⁺ release on depolarization → positive inotropy

Pharmacokinetics

• Oral bioavailability ~60-80%
• Half-life ~36-48 hours (renally cleared - adjust in renal failure)
• Narrow therapeutic index: serum level 0.5-0.9 ng/mL (HF); toxic >2 ng/mL
• Volume of distribution large - loading dose often needed

Indications

• Chronic HF with reduced EF (HFrEF) - reduces hospitalizations, no mortality benefit (DIG trial)
• Rate control in atrial fibrillation (especially in HF patients)
• Not for acute decompensated heart failure

Adverse Effects / Toxicity

• GI: nausea, vomiting, anorexia (early signs)
• CNS: confusion, visual disturbances (yellow-green halos, xanthopsia)
• Cardiac: virtually any arrhythmia - PAT with block (classic), PVCs, bidirectional VT, AV block
• Toxicity worsened by: hypokalemia (most important), hypomagnesemia, hypoxia, hypothyroidism, renal failure
• Treatment of toxicity: digoxin-specific antibody fragments (Fab/Digibind)

Contraindications

• Wolff-Parkinson-White syndrome (can enhance accessory pathway conduction)
• Hypertrophic obstructive cardiomyopathy
• Ventricular arrhythmias

2. Dobutamine

Mechanism of Action

• Synthetic catecholamine; racemic mixture of two enantiomers:
  • (−) enantiomer: α₁ agonist + weak β agonist
  • (+) enantiomer: potent β₁ and β₂ agonist
• Net clinical effect: predominantly β₁ agonism in the myocardium
  • β₁ → Gs → ↑adenylyl cyclase → ↑cAMP → ↑PKA → phosphorylates L-type Ca²⁺ channels, phospholamban (speeds Ca²⁺ re-uptake by SR), and troponin I → ↑contractility + faster relaxation (lusitropic effect)
• Vascular: α₁ vasoconstriction offset by β₂ vasodilation → net modest ↓SVR (afterload reduction)
• No dopamine receptor activity

Hemodynamic Effects

Dosing

• IV infusion: start 2-3 μg/kg/min, uptitrate to 5-20 μg/kg/min
• Tachyphylaxis occurs after 24-48 hours (receptor desensitization)
• Patients on beta-blockers require higher doses (10-20 μg/kg/min) - carvedilol most resistant

Indications

• Cardiogenic shock (hypoperfusion despite adequate filling)
• Acute decompensated HFrEF with low output/organ hypoperfusion
• Stress echocardiography (dobutamine stress echo)
• Bridge to mechanical support or transplant

Adverse Effects

• Tachycardia, palpitations
• Atrial and ventricular arrhythmias
• Myocardial ischemia (↑O₂ demand)
• Hypotension (due to β₂-mediated vasodilation at moderate doses)
• Possible myocyte necrosis/apoptosis with prolonged use
• Increased mortality with prolonged/chronic use

Caution

• Inadequate if profound hypotension (need vasopressor + inotrope or switch to dopamine/epinephrine)
• Preferred over milrinone when renal dysfunction present (milrinone renally cleared)

3. Dopamine

Mechanism of Action

⚠️ Important caveat: The "renal dose dopamine" concept (low-dose for renal protection) has not been validated in clinical trials and is no longer recommended. There is significant interpatient variability in dose-receptor response.

Pharmacokinetics

• Half-life 2-3 minutes
• Metabolized by MAO and COMT
• If on MAO inhibitors: reduce dose to 1/10th of usual

Indications

• Cardiogenic shock (when both inotropy and vasoconstriction needed at high doses)
• Septic shock - second-line to norepinephrine (higher arrhythmia risk)
• Historically used for "renal protection" - no longer supported

Adverse Effects

• Tachyarrhythmias (more than norepinephrine - randomized trial confirmed this)
• Increased myocardial oxygen demand
• At high doses: excessive vasoconstriction, digital/limb ischemia
• Higher mortality than norepinephrine in cardiogenic shock subgroup

Contraindications

• Ventricular arrhythmias
• Suspected pheochromocytoma
• Avoid as first-line in cardiogenic shock complicating MI (SSC and ESC guidelines prefer norepinephrine)

4. Epinephrine (Adrenaline)

Mechanism of Action

• Endogenous catecholamine from adrenal medulla
• Balanced α₁, β₁, β₂ agonist - dose-dependent:
  • Low doses (≤0.05 μg/kg/min): β predominant → ↑CO, slight ↓SVR
  • High doses (>0.05 μg/kg/min): α predominant → vasoconstriction, ↑SVR

Hemodynamic Effects

• ↑↑ HR (more tachycardic than dobutamine)
• ↑↑ Contractility
• ↑ SVR at high doses
• ↑ Cardiac output
• Raises serum lactate (non-ischemic - via β₂-mediated glycogenolysis/gluconeogenesis)

Indications

• Anaphylactic shock (first-line, IM)
• Cardiac arrest (IV/IO)
• Refractory cardiogenic shock (when dobutamine insufficient)
• Bradycardia/heart block (second-line)
• Anesthesia: added to local anesthetics for vasoconstriction

Adverse Effects

• Significant tachycardia and arrhythmias
• Hypertension (dose-dependent)
• Myocardial ischemia
• Metabolic: hyperglycemia, hyperlactatemia, hypokalemia
• Mesenteric ischemia at high doses

5. Milrinone (and Enoximone)

Mechanism of Action

• Selective phosphodiesterase type 3 (PDE-3) inhibitor
• PDE-3 normally degrades cAMP in cardiac and vascular smooth muscle
• Inhibition → ↑cAMP → activates PKA pathway (same downstream as β-agonists)
• In myocardium: ↑Ca²⁺ → positive inotropy
• In smooth muscle (arterial + venous + pulmonary): ↑cAMP → relaxation → vasodilation
• Hence "inodilator" - inotrope + vasodilator combined
• Mechanism is independent of β-receptors - works even in patients on beta-blockers or with downregulated β-receptors (chronic HF)

Hemodynamic Effects

Dosing

• IV infusion: 0.125-0.75 μg/kg/min (loading dose 50 μg/kg over 10 min often omitted to avoid hypotension)
• Renally cleared - reduce dose in renal impairment
• Half-life ~2.3 hours (much longer than dobutamine)

Indications

• Acute decompensated HFrEF with low output
• Right heart failure / RV failure (pulmonary vasodilatory effect is advantageous)
• Post-cardiac surgery low output syndrome
• Pulmonary arterial hypertension (reduces PVR)
• Patients on beta-blockers where dobutamine response is blunted (milrinone bypasses β-receptor)
• Bridge to transplant/mechanical support

Adverse Effects

• Hypotension (most common - especially with loading dose and in hypovolemic patients)
• Ventricular arrhythmias
• Thrombocytopenia (amrinone > milrinone)
• Increased mortality with chronic oral use (PROMISE trial - oral milrinone increased mortality in chronic HF)

Note: Despite short-term hemodynamic benefit, IV milrinone showed no survival advantage vs. dobutamine (OPTIME-CHF trial).

6. Levosimendan

Mechanism of Action - Unique, Two-Component

• Binds to cardiac troponin C (TnC) in a Ca²⁺-dependent manner
• Stabilizes the TnC-Ca²⁺ complex during systole → prolongs actin-myosin crossbridge coupling
• Increases contractile force WITHOUT increasing [Ca²⁺]i
• Key advantage: does not increase myocardial oxygen consumption (no extra ATP to pump extra Ca²⁺)
• Does not impair diastolic relaxation (dissociates from TnC as [Ca²⁺]i falls in diastole)

• Opens ATP-sensitive K⁺ channels in vascular smooth muscle → hyperpolarization → vasodilation
• Lowers SVR and PVR (afterload reduction)
• Also has PDE-3 inhibitory properties at higher concentrations

Pharmacokinetics

• IV infusion: 0.05-0.2 μg/kg/min over 24 hours (optional loading dose 6-12 μg/kg)
• Parent drug half-life ~1 hour, but active metabolites (OR-1896) have half-life ~80 hours
• This explains prolonged hemodynamic effect lasting 7-9 days after a single infusion

Indications

• Acute decompensated HFrEF with low output refractory to standard therapy
• Cardiogenic shock (especially in patients on beta-blockers)
• RV failure / pulmonary hypertension
• Weaning from cardiopulmonary bypass (perioperative low output syndrome)
• Particularly useful when dobutamine is ineffective (chronic beta-blocker use, downregulated receptors)
• Some use as "pulsed" therapy in ambulatory chronic HF

Adverse Effects

• Hypotension (most significant limiting factor - especially with loading dose)
• Tachycardia
• Headache
• Hypokalemia
• Arrhythmias (less than catecholamines)

Key Trials

• REVIVE-II: levosimendan vs. placebo in AHF → improved symptoms but no mortality benefit, more hypotension
• SURVIVE: levosimendan vs. dobutamine → no mortality difference at 6 months
• LIDO: levosimendan superior to dobutamine in hemodynamic parameters

7. Norepinephrine (Noradrenaline)

• α₁ dominant: potent vasoconstriction → ↑SVR → ↑MAP
• β₁: ↑contractility and mild ↑HR
• First-line vasopressor in septic shock (SSC 2026)
• Used in cardiogenic shock when hypotension is profound and vasopressor effect needed alongside inotropy

Quick Reference: Receptor Pharmacology Table

Key Principles for Clinical Use

When to use inotropes

• Cardiogenic shock: SBP ≤ 90 mmHg with signs of hypoperfusion (oliguria, altered consciousness, cold peripheries, high lactate) despite adequate volume resuscitation
• Acute decompensated HF with low cardiac output and organ dysfunction
• Bridge to mechanical circulatory support (IABP, Impella, LVAD) or transplant
• Perioperative low cardiac output after cardiac surgery

Cardinal rule (Braunwald's, Goodman & Gilman)

Inotropes increase cardiac energy expenditure (greater Ca²⁺ cycling → more ATP consumption → ↑O₂ demand). In the already-ischemic failing heart, this risks diffuse myocyte necrosis and arrhythmias. Use at the lowest effective dose for the shortest possible duration, with continuous hemodynamic and ECG monitoring. Stop as soon as adequate organ perfusion is restored.

Choosing the right inotrope

Negative Inotropes (for contrast)

• Ca²⁺ channel blockers (verapamil, diltiazem, nifedipine)
• Beta-blockers (negative inotropy + chronotropy)
• Antiarrhythmics: disopyramide (significant), flecainide
• Volatile anesthetics (dose-dependent)

Sources

• Goodman & Gilman's Pharmacological Basis of Therapeutics, Ch. 33 - Inotropic Agents and Cardiac Contractility
• Braunwald's Heart Disease 12e - Inotropes and Inodilators (Table 49.7)
• Harrison's Principles of Internal Medicine 22e (2025) - Vasopressors and Inotropes
• Medical Physiology (Boron & Boulpaep) - Ca²⁺ and Positive Inotropic Agents
• Washington Manual of Medical Therapeutics - Vasoconstrective and Inotropic Agents
• Lippincott Illustrated Reviews: Pharmacology - Inotropic Agents
• Goldman-Cecil Medicine 26e - Vasopressors and Inotropes
• Fuster's The Heart 15e - Inodilators

Bilastine + Montelukast in Liver Cirrhosis for Itching - Clinical Assessment

1. Bilastine in Liver Cirrhosis

Pharmacokinetics

• Bilastine is a 2nd-generation non-sedating antihistamine (H1 receptor antagonist)
• Key fact: Bilastine is NOT metabolized in the liver - it is excreted virtually unchanged, predominantly via the kidneys (renal clearance is the major elimination route)
• Biliary excretion is only marginally involved
• The official SmPC (MHRA) and product monograph (Sandoz) both state:

"Since bilastine is not metabolized and renal clearance is its major elimination route, hepatic impairment is not expected to increase systemic exposure above the safety margin. Therefore, no dosage adjustment is required in patients with hepatic impairment."

• Population pharmacokinetic analyses found no clinically relevant influence of liver transaminases, alkaline phosphatase, or bilirubin on bilastine pharmacokinetics

Verdict on Bilastine

2. Montelukast in Liver Cirrhosis

Pharmacokinetics - Caution Needed

• Montelukast is extensively metabolized by the liver via CYP2C8, CYP3A4, and CYP2C9
• Metabolites undergo biliary excretion (hepatic route is primary)
• In patients with hepatic impairment (Child-Pugh B), AUC increases significantly (reduced first-pass metabolism + reduced biliary clearance)
• No data in Child-Pugh C (severe cirrhosis)

Hepatotoxicity Risk

• Cholestatic hepatitis (jaundice, elevated bilirubin) developing after weeks-months of montelukast use
• Drug-induced intrahepatic cholestasis on liver biopsy
• Mechanism: possibly toxic/immunogenic metabolite formation via CYP450

1. Accumulation of drug (reduced metabolism in cirrhosis)
2. Adding drug-induced hepatotoxicity on top of pre-existing liver disease
3. Worsening cholestasis

Verdict on Montelukast

3. The Bigger Problem: Wrong Drug for This Type of Itch

Why antihistamines and leukotriene antagonists don't work well here

• Lysophosphatidic acid (LPA) produced by autotaxin (ATX) - a neuronal activator; ATX levels correlate directly with itch intensity
• Bile acid accumulation activating MRGPRX4 receptors on sensory neurons
• Increased central opioidergic neurotransmission
• Serotonergic pathways

4. Evidence-Based Treatment of Cholestatic Pruritus in Cirrhosis

Summary

Hyponatremia: Treatment & Correction Limits

Step 1: Classify Before You Treat

A) Acute or Chronic?

B) Symptomatic Severity?

C) Volume Status? (Essential for choosing fluid type)

Step 2: Correction Rate Targets - The Most Important Numbers

The Core Rule

Chronic hyponatremia (>48 hrs or unknown duration): the rate of correction must NEVER exceed 10-12 mmol/L in any 24-hour period - and should be much slower in high-risk patients.

Target Correction Rates

High-Risk Patients for ODS (more conservative targets apply)

• Serum Na⁺ < 105 mmol/L (severe hyponatremia)
• Chronic alcoholism / alcohol use disorder
• Severe malnutrition (including anorexia nervosa)
• Advanced liver disease / cirrhosis
• Severe hypokalemia
• Duration > 48 hours (i.e., all chronic hyponatremia)

Step 3: Treatment by Scenario

Scenario 1 - Severe Symptoms (Seizures, Coma, Respiratory Arrest)

1. Bolus method (preferred): 100 mL of 3% NaCl IV over 10 minutes, repeated up to 3 times if no clinical improvement, checking Na⁺ after each bolus
2. Infusion method: 1-2 mL/kg/hr of 3% NaCl (or 4-6 mL/kg/hr in severe cases)

Scenario 2 - Moderate Symptoms (Confusion, Nausea, Falls)

• Begin 3% NaCl at a lower rate (0.5-1 mL/kg/hr) OR isotonic saline if hypovolemic
• Target: raise Na⁺ by 4-6 mmol/L over 6-12 hours, then slow/reassess
• Stay within the 24-hour limit (≤ 10-12 mmol/L, or ≤ 8 mmol/L if high-risk)
• Switch to fluid restriction or oral therapy once symptoms improve

Scenario 3 - Mild/Asymptomatic Chronic Hyponatremia

1. Fluid restriction - first-line; restrict to 800-1000 mL/day (or less than urine output)
2. Salt tablets + loop diuretic (furosemide) - increases free water excretion
3. Urea 15-60 g/day orally - safe, cheap, effective in SIADH (particularly in Europe)
4. Demeclocycline 600-1200 mg/day - causes nephrogenic DI; slow onset (days); avoid in liver/renal disease
5. Vaptans (see below)

• Fluid restriction + treat underlying cause
• Loop diuretics to remove excess water > sodium
• Vaptans (see below) - avoid tolvaptan in cirrhosis (hepatotoxicity risk)

Step 4: Specific Drug Treatments

Vaptans (Vasopressin V2-Receptor Antagonists)

Step 5: Overcorrection - What To Do

1. Stop all hypertonic saline or agents driving up Na⁺
2. Desmopressin (DDAVP) 2-4 mcg IV/SC every 8 hours → restores ADH effect, slows free water loss
3. 5% Dextrose in Water (D5W) IV at 3 mL/kg/hour → dilutes Na⁺ back down
4. Recheck Na⁺ hourly until within goal
5. Consider dexamethasone 4 mg IV every 6 hours for 24-48 hours if severe overcorrection has already occurred

Re-lowering is most critical when starting Na⁺ < 120 mmol/L - this is where ODS risk is highest if limits are exceeded.

Step 6: Osmotic Demyelination Syndrome (ODS) - Know the Enemy

Pathophysiology

Symptoms (appear 2-7 days AFTER overcorrection)

• Initial: dysarthria, dysphagia, confusion
• Progression: locked-in syndrome (quadriplegia, inability to speak, preserved vertical eye movements)
• Pseudobulbar palsy, spastic paresis, behavioral changes
• MRI: hyperintense signal in pons/basal ganglia on T2/FLAIR

Meta-analysis data (2024-2025 - PMID 39967825)

• ODS incidence: 0.23% overall in hospitalized hyponatremia patients
• With rapid correction (> 8 mmol/L/24h): 0.73%
• Without rapid correction: 0.10%
• Odds ratio for ODS with rapid correction: 3.16 (95% CI 1.54-6.49)

Risk thresholds (from meta-analysis)

• Risk begins at > 8 mmol/L/24h
• American guidelines: ≤ 10-12 mmol/L/24h (normal risk), ≤ 8 mmol/L/24h (high risk)
• European guidelines: ≤ 10 mmol/L/24h

Quick Reference: The Numbers to Remember

Practical memory aid: For chronic hyponatremia, aim for no more than 8-10 mEq/L per day in most patients, and no more than 6-8 mEq/L per day in high-risk patients. If in doubt, go slower.

Formulas (When You Need to Calculate)

Adrogue-Madias Formula (Infusate Effect on Na⁺)

• Total Body Water = 0.6 × weight (men), 0.5 × weight (women), 0.45 (elderly)
• Use this to estimate the infusion rate needed to achieve the desired correction rate

Sodium content of common IV fluids (per liter):

Summary Algorithm

Hyponatremia detected
        ↓
Severe symptoms? (seizures, coma, respiratory arrest)
        YES → 3% NaCl 100 mL bolus IV × up to 3 doses
               Target: +4-6 mmol/L in 1-2 hrs
               Check Na⁺ every 1-2 hrs
               STOP at limits (see above)
        ↓ NO
Acute (<48h) or Chronic (>48h / unknown)?
        ↓
Volume status: Hypovolemic / Euvolemic / Hypervolemic?
        ↓
Hypovolemic → 0.9% NaCl
Euvolemic (SIADH) → Fluid restriction ± urea ± tolvaptan
Hypervolemic (HF, cirrhosis) → Fluid restriction + furosemide ± tolvaptan (not in cirrhosis)
        ↓
Monitor Na⁺ every 4-6 hrs
Stay within correction limits
If overcorrected → DDAVP + D5W to re-lower

• Brenner & Rector's The Kidney (Hyponatremia Treatment Guidelines)
• Comprehensive Clinical Nephrology 7e
• NKF Primer on Kidney Diseases 8e
• Goldman-Cecil Medicine 26e
• Systematic review & meta-analysis: Suppadungsuk et al., Kidney Medicine 2025 (PMID 39967825)