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

• lethargy• general weakness• irritability• weight loss• diarrhea• twitching• seizures• coma

• orthostatic hypotension• tachycardia• oliguria

• prerenal :High BUN-to-creatinine ratio

• dry axillae/ dry MMM• hyperthermia• poor skin turgor• nystagmus

• myoclonic jerks

Work-up : Sodium levels

– more than 170 mEq/L usually indicates long-term 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 Contents5% dextrose in water (D5W)

0 mEq Na

0.2% sodium chloride in 5% dextrose in water (D5 1/4 NS)

34 mmol/L

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.com/bicarbdeficit.php