HyperNa ( >145)


THE CALL

Overview

Pathophysiology

  • Mechanism
    • Usually a disorder of water balance, due to decreased intake or increased loss, rather than actual disruption of Na+ balance
      • Can also be due to intake of salt in excess of water
    • Hypovolemic Hypernatremia: salt and water loss, decreased Extracellular fluid (ECF) volume
      • H20 depletion >> Na+ depletion
      • Loss of free water from ECF and Intracellular fluid (ICF)
      • Loss of fluid that is isosmotic to plasma (GI loss of Na+ and K+, urinary osmotic diuresis)
        • Raises the plasma [Na+] because water loss >> Na+ and K+ depletion
      • Dehydration with normal total body Na+ and decreased total body water (TBW) due to increased sensible or renal loss (eg., diarrhea, DI)
    • Euvolemic Hypernatremia: loss of free water (ICF >> ECF)
      • TBW decreased, total body Na+ unchanged, increase in serum [Na+]
      • High plasma osmolarity with low urine concentration
      • Diabetes insipidus, physical or mental inability to access water, insensible losses
    • Hypervolemic Hypernatremia: gain of Na+ and water to ECF
      • Gain of hypertonic solution
      • TBW increase << total body Na+ increase, serum [Na+] increases
      • Increase serum Na+ leads to reduced ICF
      • Rare
         
  • Etiology/Risk Factors
    • The Na+ plus K+ concentration in fluid lost or gained determines the effect on serum Na+, not osmolality
    • Primarily occurs in patients who can't experience or respond to thirst normally
      • Elderly, critically ill, children
    • Hypovolemic Hypernatremia: unreplaced electrolyte-free water loss
      • Almost all emergency dept (ED) cases will be due to volume loss, usually severe
      • Elderly, bed-ridden, mentally impaired, osmotic diuretics, increased water loss (eg., heat, GI), glycosuria
      • Renal Loss: Inability to concentrate urine
        • Osmotic diuresis (eg., mannitol, glucose, urea), loop/thiazide diuretics, post-obstructive diuresis, ATN diuresis
      • Osmotic diuresis: non-reabsorbed solutes (eg., glucose, mannitol, urea), increased urine output
        • DKA, nonketotic hyperglycemia: glycosuria-induced diuresis
        • Mannitol raises serum Na+ due to both removal of mannitol from plasma, pulling water back into cells, and water loss due to diuresis
        • During resolution of azotemia, excretion of urea in urine causes water loss
      • Skin loss: Burns, sweat
        • Sweat losses increased dramatically with fever, exercise, hyperthermia
        • Sweat hypotonic to plasma, promoting free water loss
      • Vomiting, NG suctioning
        • Patients receive isotonic saline to replace fluid losses
      • Osmotic diarrheas (eg., viral, bacterial, lactulose, charcoal-sorbitol)
    • Euvolemic Hypernatremia: no change in ECF
      • Diabetes Insipidus (DI): free water loss in urine
        • Decreased release of ADH (central) or renal resistance to it (nephrogenic) leads to excretion of dilute urine
        • Most significant in patients with
          • Central lesions that impair ADH release and thirst
          • Who cannot access water
          • Post-op patients with unrecognized DI
          • Elderly patients with DI due to lithium therapy
      • Hypodipsia: thalamic lesion, congenital, MR, tumor, traumatic brain lesion
      • Increased sensible losses: fever, hyperventilation, mechanical ventilation
      • Increased Ca2+, decreased K+, EtOH, lithium, starvation
    • Hypervolemic Hypernatremia: primary gain of Na+
      • Increase aldosterone, Cushing's
      • Often iatrogenic: replacement of hypotonic fluid losses with isotonic saline
      • Osmotic diuresis in diabetes mellitus or recovering azotemia patients, nasogastric suctioning, etc.
      • Edematous, critically ill patients who receive large volumes of saline and then loop diuretic treatment, impairs renal concentrating ability leading to water loss
      • Administration of:
        • Excessive 3% NaCl (traumatic head injury)
        • Sodium bicarbonate (during ACLS or overcorrection of acidosis)
        • Salt tablets, tube feeds
        • Hypertonic dialysate error
        • Antibiotic containing Na+
        • Massive salt ingestion
           
  • Epidemiology
    • Incidence/Prevalence
      • Chronic hypernatremia more common than acute
      • Hypovolemic hypernatremia most common in ED
    • Mortality/Morbidity
      • Mortality rate 20-60% depending on co-morbidities, associated illness
      • Under and over correction also associated with increased mortality
      • Paucity of literature for hypernatremic patients in the ED, suggests approximately 2% of pts have hypernatremia on admission

 

  • Deficit in free water
  • Renal losses: diuretics, osmotic diuresis, diabetes insipidus
  • Extrarenal losses: GI (vomiting/NG, diarrhea, fistula), insensible losses (cutaneous, respiratory)
  • Rarely: salt intake (hypertonic IV fluids: bicarbs), hypertonic dialysis, primary hyperaldosteronism

History/Symptoms

  • Cause usually evident from history
    • Ask about fluid intake, loss, medications
  • Severity of symptoms determined by both speed and magnitude of Na+ change
  • Acute symptoms usually seen once Na+ > 158 mEq/L
    • Rise in serum Na+ and serum Osm cause water movement out of brain
  • Thirst, confusion, decreased mental status, ataxia, seizure, coma, weakness, irritability, focal neuro deficits
  • Acute hypernatremia (eg., hypertonic NaCl administration, ingestion)
    • Rapid decrease in brain volume can cause rupture of cerebral veins leading to
      • Intracranial Hemorrhage (ICH)
      • Subarachnoid Hemorrhage (SAH)
      • Demyelinating lesions
  • Chronic hypernatremia
    • Elevation of Na+ for > 24 hours
    • Less likely to have neurological symptoms
       

Physical Exam/Signs

  • General appearance, vitals
    • Hypovolemic: orthostasis, signs/symptoms hypovolemia, hypotension, tachycardia
    • Hypervolemic: edematous, anasarca, BP may vary
    • Euvolemic: normal vitals and appearance
  • HEENT
    • Hypovolemic: dry mucous membranes
  • Cardiovascular
    • Hypovolemic: tachycardic, decreased capillary refill and peripheral perfusion
    • Hypervolemic: volume overload, cardiomegaly
  • Pulmonary/Chest
    • Hypovolemic: signs/symptoms consistent with respiratory infection such as pneumonia, sepsis, leading to increased losses
    • Hypervolemic: rales, volume overload
  • Abd/GI/GU
    • Hypovolemic: nausea, vomiting, and/or diarrhea
  • Musculoskeletal/Nervous System
    • Somnolence, confusion, disorientation
    • Increased muscle tone, spasticity
    • Lethargy, weakness, irritability, twitching, seizures, coma
    • Cerebral adaptation
      • Starts on first day
      • Reduction of brain volume reversed by water movement from CSF into brain
      • Uptake of solutes by cells to restore interstitial and cell volume
  • Skin/Extremities
    • Hypovolemic: signs consistent with dehydration (eg., decreased skin turgor)
    • Hypervolemic: peripheral edema
       

Diagnosis

  • Labs/Tests
    • CMP, LFTs
    • Urine electrolytes: urine Na+, urine K+, fractional excretion of Na+
      • Urine Na+ < 25 meq/L if volume depleted
      • Urine Na+ > 100 meq/L common after large salt ingestion or hypertonic saline administration
    • Renal function tests: BUN/Cr usually elevated
    • Serum osmolarity
      • 350-375: restless, irritability
      • 375-400: tremulousness, ataxia
      • 400-430: hyperreflexia, twitching, spasticity
      • > 430: seizures and death
    • Urine osmolarity (Uosm)
      • Can be used to determine cause when etiology unclear (not usually in ED, part of inpatient workup)
      • Uosm should be > 600 mosmol/kg if hypothalamic and renal fxn intact in presence of hypernatremia
      • Uosm Low: central or nephrogenic DI
      • Uosm Intermediate: (300-600) osmostic diuresis or DI
      • Uosm High: (> 600) ADH function intact (eg., unreplaced losses, Na+ overload, thirst defect)
    • Urinalysis (obtain urine chemistry prior to administration of diuretics)
       
  • Imaging
    • CT brain
      • Most will have neurological symptoms or decreased level of consciousness
      • Consider ICH, SAH in acute hypernatremia
    • Chest X-ray
      • CHF, volume overload, malignancy
         

Differential Diagnosis

  • Neurological
    • CVA, TIA
    • ICH, SAH
    • Intracranial mass
  • Malignancy
  • Renal failure
  • Sepsis

Management

  1. Change IV fluids to (at least) isotonic fluids.
     
  2. Initial/Prep/Goals
    • Most common goal in ED is volume repletion
      • First with NS or LR until tissue perfusion is restored
      • Then switch to hypotonic solution (1/2 NS, D5W, D5 1/2NS, etc.)
    • Each liter of water deficit raises serum Na+ approximately 3-5 meq/L
    • Estimate magnitude of water deficit
      • Calculate TBW
        • Young males: 0.6 x weight (kg)
        • Young women/elderly males: 0.5 x weight (kg)
        • Elderly women: 0.45 x weight (kg)
      • Water deficit = TBW x ([serum Na+/140] – 1)
      • Does not account for ongoing water losses or co-existing isosmotic fluid deficit (eg., diarrhea)
    • Determine rate of correction (determine acute vs chronic hypernatremia)
      • Overly rapid correction in chronic hypernatremia
        • Leads to additional osmotic water movement into brain cells
        • Resulting in cerebral edema, permanent neurological damage, death
      • Chronic: goal is lower Na+ by no more than 10 meq/L/day
      • Acute: lower rapidly, correcting Na+ in < 24 hours, lowering 1-2 meq/L/hr
    • Calculate initial fluid regimen to correct water deficit
      • Based on calculated water deficit and desired rate of correction
      • Acute: hourly infusion rate > water deficit mL/24 hrs
        • Monitor serum Na+ q1-2hrs until < 145 meq/L
        • Then reduce infusion until 140 meq/L
      • Chronic: desired water replacement in first day = 10 meq/L in 24 hrs
        • Change in Serum Sodium = ([Infused Na+] - [serum Na+] ) / (TBW + 1)
        • Hourly infusion rate = Change in Serum Sodium / 24 hours
          • Example: If sodium was 155 in 70 kg young male corrected with D5W
          • (0 - 155) / ([70 x 0.6] +1) = -3.6 mEq/L
          • Infusion rate of D5W at 250 cc/hr changes sodium at 0.9 mEq/hr
        • Monitor serum Na+ q4-6hrs, modify infusion rate as needed
    • Administration of dilute (hypotonic) fluids
      • D5W is isosmotic to plasma, but electrolyte free, so most effective
      • Many patients with hypernatremia also have reduced ECF and/or are K+ depleted, and will require ½ NS or ¼ NS
        • This will give a smaller reduction of Na+ than D5W
        • Even less if supplemental K+ is added to IVF
    • In the ED most appropriate to
      • Start treatment without accounting for ongoing losses
      • Monitor serum Na+
      • Increase rate of administration as needed
      • Limit further volume loss, replace additional electrolytes PRN (eg., K+)
      • Treat underlying cause
         
  3. Medical/Pharmaceutical
    • Hypovolemic
      • Correct water deficit as described above with hypotonic fluids (D5W or D5 ½ NS)
      • Severely volume-depleted patients may require normal saline boluses to restore hemodynamic stability
      • Avoid overly rapid correction due to potential for cerebral edema
      • Patient also likely K+ depleted, add to fluids as needed
        • Addition of extra electrolytes to IVF will decrease amount of free water available, will further slow rate of correction
    • Euvolemic
      • Diabetes Insipidus (DI): may need to account for ongoing urinary losses (more likely part of inpatient workup)
        • Central DI
          • Na+ restriction
          • May require vasopressin
        • Nephrogenic DI
          • Na+ restriction
          • May require dialysis
    • Hypervolemic
      • D5W plus diuretic (Furosemide), or dialysis
      • Stop exogenous administration of Na+
         
  4. Symptomatic
  5. (lethargy, coma)
    • Aim for a correction of max 1 mEq/L/h, max 12 mEq/day using D5W.
    • Monitor sodium q2 - 4h when replacing.
    • Monitor glucose.
       
  6. Complications
    • Too rapid correction: cerebral edema, demyelination, irreversible neurological damage, death
    • Too slow correction: increased morbidity/mortality
    • Hyperglycemia from dextrose containing IVF leads to osmotic diuresis, further water loss
       
  7. Prevention
    • Judicious fluid resuscitation in volume depleted patients to avoid iatrogenic sodium loading
    • Close monitoring of patients with inadequate thirst mechanisms or access to water
       
 

Disposition

  1. Admission criteria
    • Consider admitting Na+ > 150 mEq/L [> 150 mmol/L]
    • Depending on neuro status, initial [Na+], etiology, may need ICU
       
  2. Consults: nephrology
    • Dialysis, fluid regimen
       
  3. Discharge/Follow-up instructions
    • Depending on etiology and per primary care provider recommendations

ADMISSION ORDERS

1. Admit to:
2. Diagnosis: Hypernatremia
3. Condition:
4. Vital Signs: q2-8h. Call physician if BP >160/90, <70/50; P >140, <50; R>25, <10; T >38.5 C.
5. Activity: Bed rest; up in chair as tolerated.
6. Nursing: Inputs and outputs, daily weights.
7. Diet: No added salt. Push oral fluids.
8. Special Medications:
Hypernatremia with Hypovolemia:
If volume depleted, give 1-2 L NS IV over 1-3 hours until not orthostatic, then give D5W IV to replace half of body water deficit over first 24 hours (correct sodium at 1 mEq/L/h), then remaining deficit over next 1-2 days.

Body water deficit (L) = 0.6(weight kg)([Na serum]-140)
          140

Hypernatremia with ECF Volume Excess:
-Furosemide 40-80 mg IV or PO qd-bid.
-Salt poor albumin (25%) 50-100 mL.

Hypernatremia with Diabetes Insipidus:
-D5W to correct body water deficit.
-Pitressin 5-10 U IM/IV q6h or desmopressin (DDAVP) 4 mcg IV/SQ q12h; keep urine specific gravity >1.010.

9. Extras: CXR, ECG.
10. Labs: chem 7&12, serum osmolality, liver panel, ADH. UA, urine specific gravity. Urine osmolality, Na, 24h urine K, creatinine.