Overview

Hypernatraemia

Quick Reference

Critical Alerts

Hypernatraemia indicates water deficit, not sodium excess
Correct slowly - aim for Na decrease 10-12 mEq/L per 24 hours
Rapid correction causes cerebral edema - potentially fatal
Acute hypernatraemia (<48h) can be corrected faster
Treat underlying cause while correcting sodium

Key Diagnostics

Serum sodium (confirm hypernatraemia >145 mEq/L)
Serum osmolality (elevated)
Urine osmolality and sodium (determine cause)
BUN/creatinine (assess volume status)
Glucose (exclude osmotic diuresis)

Emergency Treatments

Calculate water deficit: 0.6 × weight × (Na/140 - 1)
IV D5W or 0.45% saline: Replace free water
Rate of correction: Max 10-12 mEq/L per 24 hours
Desmopressin (DDAVP): For central diabetes insipidus
Address underlying cause: Infection, GI losses, medications

Definition

Hypernatraemia is defined as a serum sodium concentration >145 mEq/L. It represents a deficit of water relative to sodium and indicates hyperosmolality. Hypernatraemia always causes cellular dehydration and, if severe or rapidly developing, can cause significant neurological dysfunction.

Classification by Severity

Severity	Sodium Level	Clinical Significance
Mild	146-150 mEq/L	Often asymptomatic
Moderate	151-159 mEq/L	Symptomatic
Severe	≥160 mEq/L	High mortality risk

Classification by Onset

Type	Timeframe	Correction Rate
Acute	<48 hours	Can correct more rapidly (1 mEq/L/hr)
Chronic	>8 hours	Slow correction (0.5 mEq/L/hr; max 10-12/day)
Unknown	Assume chronic	Slow correction

Epidemiology

Hospital prevalence: 1-3% of hospitalized patients
ICU prevalence: Up to 9%
Hospital-acquired: More common than community-acquired
Mortality: 30-70% (often reflects underlying disease)

Pathophysiology

Normal Water Homeostasis

Thirst Mechanism

Osmoreceptors in hypothalamus detect increased osmolality
Triggers thirst when plasma osmolality >295 mOsm/kg
Drives water intake to correct hyperosmolality

ADH (Vasopressin) Secretion

Released from posterior pituitary when osmolality increases
Signals kidneys to concentrate urine and retain water
Deficiency or resistance causes diabetes insipidus

Mechanisms of Hypernatraemia

Mechanism	Examples
Water loss > Sodium loss	GI losses (diarrhea, vomiting), insensible losses (fever, burns)
Pure water loss	Diabetes insipidus, inadequate water intake
Sodium gain (rare)	Hypertonic saline, sodium bicarbonate, seawater ingestion

Causes by Volume Status

Volume Status	Causes
Hypovolemic (most common)	GI losses, diuretics, burns, osmotic diuresis
Euvolemic	Diabetes insipidus, insensible losses, hypodipsia
Hypervolemic (least common)	Hypertonic saline, sodium bicarbonate, mineralocorticoid excess

Diabetes Insipidus Types

Type	Cause	Urine Osm	Response to DDAVP
Central DI	Lack of ADH (pituitary)	Low (<300)	Increases >0%
Nephrogenic DI	Kidney resistance to ADH	Low (<300)	No response
Gestational DI	Vasopressinase in pregnancy	Low	Variable

Clinical Presentation

Symptoms

Neurological (Most Important)

Symptom	Severity
Lethargy	Mild-moderate
Irritability	Mild-moderate
Confusion	Moderate
Weakness	Moderate
Seizures	Severe
Coma	Severe

Other

Physical Examination

Volume Assessment

Finding	Suggests
Dry mucous membranes	Hypovolemia
Decreased skin turgor	Hypovolemia
Tachycardia	Hypovolemia
Hypotension	Severe hypovolemia
Normal volume	Diabetes insipidus, pure water loss
Edema	Hypervolemic hypernatraemia

Neurological

Brain Adaptation

Why Rapid Correction is Dangerous

Chronic hypernatraemia:
1. Brain cells become hyperosmolar
2. Generate idiogenic osmoles (organic solutes)
3. This prevents brain cell shrinkage

If sodium corrected too rapidly:
1. Water moves into brain cells
2. Cells swell
3. Cerebral edema develops
4. Herniation possible

Thirst (if conscious and able to sense)

Common presentation.

Muscle twitching

Common presentation.

Oliguria or polyuria (depending on cause)

Common presentation.

Red Flags (Life-Threatening)

Critical Findings

Red Flag	Concern	Action
Sodium >60 mEq/L	Severe hypernatraemia	ICU admission
Seizures	Severe neurological dysfunction	Emergent correction if acute
Coma	Severe hypernatraemia or complication	ICU, slow correction
Signs of herniation	Cerebral edema from overcorrection	Mannitol, hypertonic saline
Hemodynamic instability	Severe hypovolemia	Fluid resuscitation (isotonic first)
Acute onset <48h	Can correct faster	But still carefully

Complications of Overcorrection

Cerebral edema
Seizures
Permanent neurological damage
Death

Target: Decrease Na no more than 10-12 mEq/L in first 24 hours

Differential Diagnosis

Causes of Hypernatraemia

Water Loss

Category	Causes
GI losses	Diarrhea (especially osmotic), vomiting, NG suction
Renal losses	Diabetes insipidus, osmotic diuresis (glucose, mannitol)
Skin losses	Burns, excessive sweating, fever
Respiratory	Mechanical ventilation without humidification

Decreased Water Intake

Impaired thirst (hypodipsia - elderly, dementia)
Unable to access water (nursing home residents, infants)
Altered mental status

Sodium Gain

Hypertonic saline administration
Sodium bicarbonate
Hypertonic dialysis
Salt poisoning

Other Causes of Altered Mental Status

Stroke
Intracranial hemorrhage
Infection/sepsis
Medication effects
Metabolic encephalopathy (uremia, hepatic)

Diagnostic Approach

Initial Assessment

Key History

Fluid intake (access to water?)
GI losses (diarrhea, vomiting)
Urine output (polyuria in DI)
Medications (lithium, diuretics)
Recent illness (fever, infection)
Underlying conditions (dementia, nephrogenic DI cause)

Laboratory Studies

Test	Purpose	Expected Finding
Serum sodium	Diagnosis	>45 mEq/L
Serum osmolality	Confirm hyperosmolality	>95 mOsm/kg
Urine osmolality	Determine renal response	See below
Urine sodium	Volume status	Variable
BUN/Creatinine	Assess volume, renal function	Elevated BUN/Cr ratio if hypovolemic
Glucose	Exclude osmotic diuresis	Elevated = diabetic cause

Urine Osmolality Interpretation

Urine Osm	Interpretation
>00 mOsm/kg	Appropriate renal response; extrarenal water loss
300-800	Partial DI or osmotic diuresis
<300	Complete DI; kidneys not concentrating

Water Deprivation Test (Not in ED)

Used to diagnose and differentiate diabetes insipidus types (performed in controlled setting).

ADH (Vasopressin) Level

Low = Central DI
Normal/High with dilute urine = Nephrogenic DI

Treatment

Principles of Correction

Key Principle: Replace free water deficit SLOWLY

Rate of Correction:
- Chronic (&gt;48h or unknown): Max 10-12 mEq/L per 24 hours
- Acute (&lt;48h): Can correct 1-2 mEq/L per hour
- Monitor sodium every 2-4 hours during correction

Calculate Water Deficit:
Water Deficit (L) = TBW × [(Serum Na / 140) - 1]
Where TBW = 0.6 × weight (kg) for men; 0.5 for women

Choice of Fluid

Fluid	Free Water Content	Use
D5W	100% free water	Pure water replacement
0.45% NaCl	50% free water	Hypovolemic hypernatraemia
0.9% NaCl	0% free water	Initial volume resuscitation only

Treatment by Volume Status

Hypovolemic Hypernatraemia

1. Volume resuscitation first (if hypotensive)
   - 0.9% NaCl until hemodynamically stable
   
2. Then replace water deficit
   - Switch to 0.45% NaCl or D5W
   - Calculate deficit and ongoing losses
   
3. Add ongoing losses to replacement

Euvolemic Hypernatraemia (DI)

Central DI:
- Desmopressin (DDAVP) 1-2 mcg IV/SC or 10-20 mcg intranasal
- Free water replacement

Nephrogenic DI:
- Treat underlying cause if possible
- Thiazide diuretics (paradoxically help)
- Low sodium diet
- NSAIDs may help
- Free water replacement

Hypervolemic Hypernatraemia

- Stop sodium-containing fluids
- D5W for free water
- Diuretics (furosemide) to remove excess sodium
- Dialysis if severe or renal failure

Monitoring

Parameter	Frequency
Serum sodium	Every 2-4 hours during acute correction
Urine output	Hourly
Neurological status	Hourly
Glucose (if D5W)	Every 4-6 hours

Adjusting Therapy

If Na dropping too fast → slow infusion
If Na not improving → increase rate or check for ongoing losses
Watch for hyperglycemia with D5W
Consider adding DDAVP to slow overcorrection

Disposition

ICU Admission Criteria

Severe hypernatraemia (Na >160 mEq/L)
Neurological symptoms (seizures, altered mental status)
Hemodynamic instability
Need for frequent sodium monitoring
Complex underlying condition

Floor Admission

Moderate hypernatraemia (151-159 mEq/L)
Mild symptoms
Stable vital signs
Clear etiology
Able to monitor every 4-6 hours

Discharge Considerations

Rare for significant hypernatraemia
Mild, chronic, asymptomatic may be managed outpatient
Must address underlying cause
Ensure adequate water access

Patient Education

Understanding Hypernatraemia

Hypernatraemia means too little water in your body
Your body needs enough water to keep cells working properly
Treatment involves slowly giving fluids to restore balance

Prevention

Drink adequate water daily
Increase intake during hot weather or exercise
Caregivers should ensure elderly/dependent patients have water access
Take medications as prescribed (if on diuretics, etc.)

Warning Signs

Seek care if you experience:

Confusion or unusual behavior
Extreme thirst
Decreased urination
Muscle weakness or twitching

Special Populations

Elderly Patients

Impaired thirst mechanism
Often institutionalized with limited water access
Multiple medications (diuretics)
Higher mortality
More likely to have chronic hypernatraemia

Neonates/Infants

Cannot express thirst or obtain water
Immature kidneys
Breastfeeding insufficient supply
Hypernatraemia can cause severe brain injury

Diabetes Insipidus Patients

Central DI

Post-neurosurgery, pituitary tumors, trauma
Triphasic response after pituitary surgery
Treat with DDAVP

Nephrogenic DI

Lithium (most common medication cause)
Hypercalcemia, hypokalemia
Chronic kidney disease
Sickle cell disease
Pregnancy

ICU Patients

High incidence of hospital-acquired hypernatraemia
Often due to hypertonic saline, inadequate free water
Fever, mechanical ventilation increase insensible losses
Monitor sodium regularly

Quality Metrics

Performance Indicators

Metric	Target
Sodium checked in altered mental status	100%
Rate of correction within guidelines	<10-12 mEq/L per 24h for chronic
Serial sodium monitoring during treatment	Every 2-4 hours
Underlying cause identified	>0%
Fluid administration rate documented	100%

Documentation Requirements

Initial sodium and osmolality
Volume status assessment
Water deficit calculation
Fluid type and rate ordered
Target correction rate
Serial sodium levels with times
Neurological status
Response to treatment

Key Clinical Pearls

Diagnostic Pearls

Hypernatraemia = water deficit, not sodium excess
Check urine osmolality - low suggests DI
Assume chronic if onset unknown - correct slowly
Elderly with altered mental status - check sodium
Hospital-acquired is common - review IV fluids

Treatment Pearls

Slow correction - max 10-12 mEq/L per 24 hours for chronic
Volume resuscitation first if hypovolemic and hypotensive
D5W or 0.45% NaCl for water replacement
DDAVP for central DI - corrects immediately
Monitor sodium frequently - adjust fluids accordingly

Disposition Pearls

ICU for severe (>160) or symptomatic
Frequent monitoring essential - every 2-4 hours
Address underlying cause - or will recur
Ensure follow-up to confirm normalization
Patient/caregiver education for prevention

References

Sterns RH. Disorders of plasma sodium — causes, consequences, and correction. N Engl J Med. 2015;372(1):55-65.
Hoorn EJ, Zietse R. Diagnosis and treatment of hyponatremia: compilation of the guidelines. J Am Soc Nephrol. 2017;28(5):1340-1349.
Verbalis JG, et al. Diagnosis, evaluation, and treatment of hyponatremia: expert panel recommendations. Am J Med. 2013;126(10 Suppl 1):S1-42.
Muhsin SA, Mount DB. Diagnosis and treatment of hypernatremia. Best Pract Res Clin Endocrinol Metab. 2016;30(2):189-203.
Adrogué HJ, Madias NE. Hypernatremia. N Engl J Med. 2000;342(20):1493-1499.
Liamis G, et al. Clinical and laboratory characteristics of hypernatraemia in an internal medicine clinic. Nephrol Dial Transplant. 2008;23(1):136-143.

Version History

Version	Date	Changes
1.0	2025-01-15	Initial comprehensive version with 14-section template

Severity

Sodium Level

Clinical Significance

Mild

146-150 mEq/L

Often asymptomatic

Moderate

151-159 mEq/L

Symptomatic

Severe

≥160 mEq/L

High mortality risk

Type

Timeframe

Correction Rate

Acute

<48 hours

Can correct more rapidly (1 mEq/L/hr)

Chronic

>8 hours

Slow correction (0.5 mEq/L/hr; max 10-12/day)

Unknown

Assume chronic

Slow correction

Mechanism

Examples

Water loss > Sodium loss

GI losses (diarrhea, vomiting), insensible losses (fever, burns)

Pure water loss

Diabetes insipidus, inadequate water intake

Sodium gain (rare)

Hypertonic saline, sodium bicarbonate, seawater ingestion

Volume Status

Causes

Hypovolemic (most common)

GI losses, diuretics, burns, osmotic diuresis

Euvolemic

Diabetes insipidus, insensible losses, hypodipsia

Hypervolemic (least common)

Hypertonic saline, sodium bicarbonate, mineralocorticoid excess

Type

Cause

Urine Osm

Response to DDAVP

Central DI

Lack of ADH (pituitary)

Low (<300)

Increases >0%

Nephrogenic DI

Kidney resistance to ADH

Low (<300)

No response

Gestational DI

Vasopressinase in pregnancy

Low

Variable

Symptom

Severity

Lethargy

Mild-moderate

Irritability

Mild-moderate

Confusion

Moderate

Weakness

Moderate

Seizures

Severe

Coma

Severe

Finding

Suggests

Dry mucous membranes

Hypovolemia

Decreased skin turgor

Hypovolemia

Tachycardia

Hypovolemia

Hypotension

Severe hypovolemia

Normal volume

Diabetes insipidus, pure water loss

Edema

Hypervolemic hypernatraemia

Chronic hypernatraemia: 1. Brain cells become hyperosmolar 2. Generate idiogenic osmoles (organic solutes) 3. This prevents brain cell shrinkage If sodium corrected too rapidly: 1. Water moves into brain cells 2. Cells swell 3. Cerebral edema develops 4. Herniation possible

Red Flag

Concern

Action

Sodium >60 mEq/L

Severe hypernatraemia

ICU admission

Seizures

Severe neurological dysfunction

Emergent correction if acute

Coma

Severe hypernatraemia or complication

ICU, slow correction

Signs of herniation

Cerebral edema from overcorrection

Mannitol, hypertonic saline

Hemodynamic instability

Severe hypovolemia

Fluid resuscitation (isotonic first)

Acute onset <48h

Can correct faster

But still carefully

Elderly Patients

Impaired thirst mechanism
Often institutionalized with limited water access
Multiple medications (diuretics)
Higher mortality
More likely to have chronic hypernatraemia

Neonates/Infants

Cannot express thirst or obtain water
Immature kidneys
Breastfeeding insufficient supply
Hypernatraemia can cause severe brain injury

Diabetes Insipidus Patients

Central DI

Post-neurosurgery, pituitary tumors, trauma
Triphasic response after pituitary surgery
Treat with DDAVP

Nephrogenic DI

Lithium (most common medication cause)
Hypercalcemia, hypokalemia
Chronic kidney disease
Sickle cell disease
Pregnancy

ICU Patients

High incidence of hospital-acquired hypernatraemia
Often due to hypertonic saline, inadequate free water
Fever, mechanical ventilation increase insensible losses
Monitor sodium regularly

Metric

Target

Sodium checked in altered mental status

100%

Rate of correction within guidelines

<10-12 mEq/L per 24h for chronic

Serial sodium monitoring during treatment

Every 2-4 hours

Underlying cause identified

>0%

Fluid administration rate documented

100%

Version

Date

Changes

1.0

2025-01-15

Initial comprehensive version with 14-section template