Hypernatremia and Fluid Resuscitation

1. Hypernatremia and Fluid Resuscitation Staci Smith, DO

2. 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

3. Mortality Eye Opener • mortality rate across all age groups is approximately 45%. • mortality rate in the geriatric age group is as high as 79%

4. 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

5. 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

6. ADH

7. ADH Mechanism of Action

8. 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

9. 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

10. 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

11. 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

12. 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

13. 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

14. 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 Clinical Manifestations

15. 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

16. 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

17. 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

18. Intracranial Hemorrhage

19. Intracranial Hemorrhage

20. 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

21. 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

22. 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

23. 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

24. Common Na Contents

25. 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

26. Hypervolemic Hypernatremia • Treatment • D5 W plus loop diuretic such as Lasix • may require dialysis for correction

27. 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

28. 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

29. 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 Diabetes Insipidus: Euvolemic Hypernatremia

30. Euvolemic Hypernatremia • Seizures where osmoles are generated that cause water shifts • transient increase in Na • Increased insensible losses (hyperventilation)

31. Hypovolemia Hypernatremia • Combo of volume deficit plus hypernatremia • intravascular volume should be restored with isotonic sodium chloride (.9 NS) beforefree water administration

32. 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 ?

33. 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

34. References • Harrison’s Internal Medicine • E-medicine • http://www.mdcalc.com/bicarbdeficit.php