Hypernatremia and Fluid
Resuscitation
Staci Smith, DO
Hypernatremia
• serum sodium level >145 mEq/L
• hypertonic by definition
• usually due to loss of hypotonic fluid
– occasionally infusion of hypertonic fluid
• due to too little water, too much salt, or a combination
– typically due to water deficit plus restricted access to free
water
• approximately 1-4% of hospitalized patients
• tends to be at the extremes of age
Mortality Eye Opener
• mortality rate across all age groups is
approximately 45%.
• mortality rate in the geriatric age group is as
high as 79%
Hypernatremia
• sodium levels are tightly controlled
– by regulation of urine concentration
– production and regulation of the thirst response
• normally water intake and losses are matched
• to maintain salt homeostasis, the kidneys adjust urine
concentration to match salt intake and loss
• kidneys' normal response
– is excretion of a minimal amount of maximally concentrated
urine
Hypernatremia
• normal plasma osmolality (Posm )
– 275 to 290 mosmol/kg
• Na is the primary determinant of serum osmolarity
•number of solute particles in the solution
• mechanisms to return the Posm to normal
– sensed by receptor cells in the hypothalamus
•affect water intake via thirst
– water excretion via ADH
•increases water reabsorption in the collecting
tubules
ADH
ADH Mechanism of Action
Protection Mechanism
• major protection against the development of
hypernatremia
– is increased water intake
– initial rise in the plasma sodium concentration
stimulates thirst
•via the hypothalamic osmoreceptors
Hypernatremia
• usually occurs in infants or adults
– particularly the elderly
– impaired mental status
•may have an intact thirst mechanism but are unable to
ask for water
– increasing age is also associated with diminished
osmotic stimulation of thirst
•unknown mechanism
Hypernatremia
• cells become dehydrated
• sodium acts to extract water from the cells
– primarily an extracellular ion
– is actively pumped out of most cells
• dehydrated cells shrink from water extraction
• effects seen principally in the CNS
Protective Mechanism
• cells respond to combat this shrinkage
– by transporting electrolytes across the cell
membrane
– altering rest potentials of electrically active
membranes
• intracellular organic solutes
– generated in an effort to restore cell volume and
avoid structural damage
Risk factors for hypernatremia
– Age older than 65 years
– Mental or physical disability
– Hospitalization (intubation, impaired cognitive
function)
– Residence in nursing home
– Inadequate nursing care
– Urine concentrating defect (diabetes insipidus)
– Solute diuresis (diabetes mellitus)
– Diuretic therapy
Assessment
• Two important questions:
– What is the patient's volume status?
– Is the problem acute or chronic?
• Does the patient complain of polyuria or
polydipsia ?
– Central vs Nephrogenic DI
– often crave ice-cold water
Clinical Manifestations
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•
•
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lethargy
general weakness
irritability
weight loss
diarrhea
twitching
seizures
coma
• orthostatic hypotension
• tachycardia
• oliguria
• prerenal :High BUN-tocreatinine ratio
• dry axillae/ dry MMM
• hyperthermia
• poor skin turgor
• nystagmus
• myoclonic jerks
Work-up : Sodium levels
– more than 170 mEq/L usually indicates longterm salt ingestion
– 50-170 mEq/L usually indicates dehydration
– chronicity typically has fewer neurologic
symptoms
Lab Work-up : Sodium levels
• order urine osmolality and sodium levels
• glucose level to ensure that osmotic diuresis has
not occurred
• CT or MRI head
• water deprivation test
• ADH stimulation
Hypernatremia Work -Up
• Head CT scan or MRI is
suggested in all patients
• Traction on dural bridging
veins and sinuses
• Leads to intracranial
hemorrhage
– most often in the subdural
space
Intracranial Hemorrhage
Intracranial Hemorrhage
Treatment
• Replace free water deficit
– IVF
– TPN / tube feeds
• Rapid correction of extracellular hypertonicity
– passive movement of water molecules into the
relatively hypertonic intracellular space
– causes cellular swelling, damage and ultimate death
Treatment
• First, estimate TBW (Total Body Water)
– TBW= .60 x IBW x 0.85 if female & 0.85 if elderly
•IBW for women= 100 lbs for the first 5 feet and 5lbs for
each additional inch
•IBW men= 110 lbs for the first 5 feet and 5 lbs for each
additional inch
•Our pt IBW= 120 (5 ft , 4’’)
•TBW= 52.0
– = .60 x 120 x 0.85. 0.85
General Treatment
• Next, calculate the free water deficit
• Free water deficit= TBW x (serum Na 140/140)
• Our Pt’s FWD= 52 x (154-140/140)
– = 52 x 0.1
– = 5.2 L free water deficit
Avoiding Complications: Cerebral Edema
• Acute hypernatremia
– occurring in a period of less than 48 hours
– can be corrected rapidly (1-2 mmol/L/h)
• Chronic hypernatremia
– rate not to exceed 0.5 mmol/L/h or a total of 10
mmol/d
– Change in conc of Na per 1L of infusate = conc of
Na in serum- conc of Na in infusate / TBW + 1
Common Na Contents
5% dextrose in water
(D5W)
0 mEq Na
0.2% sodium chloride in 34 mmol/L
5% dextrose in water
(D5 1/4 NS)
0.9 NS
154 mmol/L
0.45NS
77 mmol/L
Lactated Ringer’s
130 mmol/L
Hypervolemic Hypernatremia
• Hypertonic saline
• Sodium bicarbonate administration
• Accidental salt ingestion
• Mineralocorticoid excess (Cushing’s syndrome)
– ectopic ACTH
• small cell lung ca, carcinoid, pheo, MTC (MEN II)
–
–
–
–
pituitary adenoma
pituitary hyperplasia
adrenal tumor
Dx: Dexamethasone suppression test
Hypervolemic Hypernatremia
• Treatment
– D5 W plus loop diuretic such as Lasix
– may require dialysis for correction
Hypovolemia Hypernatremia
• water deficit >sodium deficit
– Extrarenal losses
•diarrhea, vomiting, fistulas, significant burns
•Urine Na less than 20 and U Osm >600
– Renal losses
•urine Na >20 with U Osm 300-600
•osmotic diuretics, diuretics, postobstructive diuresis,
intrinsic renal disease
•DM / DKA
– increased solute clearance per nephron, increasing free water
loss
Euvolemic Hypernatremia
• Diabetes Insipidus
– Typically mild hypernatremia with severe polyuria
– Central DI = ADH deficiency
•Sx, hemorrhage, infxn, ca/tumor, trauma, anorexics,
hypoxia, granulomatous dz (Wegener’s, sarcoidosis, TB),
Sheehan’s
•U Osm less than 300
•Tx is DDAVP
Diabetes Insipidus: Euvolemic Hypernatremia
• Nephrogenic DI = ADH
resistance
• Congenital
• Meds – Lithium, ampho B,
demeclocycline,foscarnet
• Obstructive uropathy
• Hypercalcemia, severe
hypokalemia
• Chronic tubulointerstitial diseases
- Analgesic abuse nephropathy,
polycystic kidney disease,
medullary cystic disease
• Pregnancy
• Sarcoidosis
• Sjogren’s synd
• Sickle Cell Anemia
– U osm 300-600
– Tx: salt restriction plus
thiazide
– Tx underlying cause
Euvolemic Hypernatremia
• Seizures where osmoles are generated that
cause water shifts
– transient increase in Na
• Increased insensible losses (hyperventilation)
Hypovolemia Hypernatremia
• Combo of volume deficit plus hypernatremia
– intravascular volume should be restored with
isotonic sodium chloride (.9 NS) before free water
administration
Summary
• Dehydration is NOT synonomous with hypovolemia
• Hypernatremia due to water loss is called dehydration.
• Hypovolemia is where both salt and water are lost.
• Two important questions:
– What is the patient's volume status?
– Is the problem acute or chronic?
• Does the patient complain of polyuria or polydipsia ?
Summary
• Divide causes of hypernatremia into hyper, hypo, and
euvolemic.
• Estimate TBW (Total Body Water)
– TBW= .60 x IBW x 0.85 if female & 0.85 if elderly
• Free water deficit= TBW x (serum Na -140/140)
• Check electrolytes frequently not to replace Na more
than 0.5 mmol/L/h or a total of 10 mmol/d
• Avoid cerebral edema
References
• Harrison’s Internal
Medicine
• E-medicine
• http://www.mdcalc.co
m/bicarbdeficit.php