Approach to the patient with electrolyte disorders Hypo natremia -Hypernatremia

1. Approach to the patient with electrolyte disordersHyponatremia-Hypernatremia Zehra Eren, M.D.

2. LEARNING OBJECTIVES • recallbody waterandfluiddistribution • recallserum osmolality • recalletiology of hyponatremiaandhypernatremia • describesingandsymptomsof hyponatremiaandhypernatremia • describelaboratoryfindingsof hyponatremiaandhypernatremia • explanetreatment of hyponatremiaandhypernatremia

4. Solute Composition of Body Water • Predominant solutes in ECF: Sodium (Na+) Chloride (Cl−) Bicarbonate (HCO3−) • Predominant solutes in ICF: Potassium (K+) Protein− Phosphate−

5. Osmolality • Posm=2×plasma Na++ Glucose/18 + BUN/2.8

6. Osmolality • Normal ECF osmolality: 280-290mOsm/kgH2O • ECF and ICF are in osmotic equilibrium, at steady state • Vasopressin (antidiuretichormone (ADH) -osmoticstumuli -nonosmoticstumuli: HF, Cirrhosis, vomiting, postoperativepain, pregnancy

8. Hyponatremia • Serum Na<135 mEq/L

9. European Society of Intensive Care Medicine (ESICM) European Society of Endocrinology(ESE) European Renal Association – European Dialysis and Transplant Association (ERA–EDTA)

10. Hyponatremia • Serum Na<135 mEq/L

12. Hyponatremia is a disorder of water balance

13. Dısorders of water and sodium balance • Hyponatremia (too much water) • Hypernatremia (too little water) • Hypovolemia (too little sodium, the main extracellular solute) • Edema (too much sodium with associated water retention)

15. Hyponatremia • almost always due to the oral or intravenous intake of water that cannot be completely excreted • impaired water excretion that is most often due to an inability to suppress the release of antidiuretic hormone (ADH) or to advanced renal failure

16. Diagnosis • Volume statusandserum osmolalityareessentialtodetermineetiology • Hyponatremiausuallyreflectsexcesswaterretentionrelativetosodiumratherthansodiumdeficiency, thesodiumconcentration is not a measure of total body sodium • Hypotonicfluidscommonlycausehyponatremia in hospitalizedpatients

24. Differences between SIADH and cerebral salt wasting Sherlock M, O’Sullivan E, et all. The incidence and pathophysiology of hyponatraemia after subarachnoid haemorrhage. Clinical Endocrinology; 2006, 64: 250–254

25. 6.3. Which parameters to be used for differentiatingcauses of hypotonic hyponatraemia? Clinical practice guideline on diagnosis and treatment of hyponatraemia; NephrolDialTransplant (2014) 0: 1–39

27. SymptomsandSing of Hyponatremia • symptomsdepends on severity and acuityhyponatremia • thesymptomsreflectneurologicdysfunctioninducedbycerebraledemaandpossibleadaptiveresponses of braincelstoosmoticswelling • Nausea, malaise, headache, lethargy, seizures, coma, respiratoryarrest • thephysical examination should help categorize the patient's volume status into hypovolemia, euvolemia, or hypervolemia.

28. Classification of symptoms of hyponatraemia Clinical practice guideline on diagnosis and treatment of hyponatraemia;Nephrol Dial Transplant (2014) 0: 1–39

29. Adaptation of the brain to hypotonicity Adrogue HJ & Madias NE. Hyponatremia. NEJM; 2000 342 1581–1589

30. Complications of hyponatraemia

32. Hyponatraemia with severe symptoms

35. 7.2. Hyponatraemia with moderately severe symptoms

36. 7.3. Acute hyponatraemia without severe or moderatelysevere symptoms

37. 7.4. Chronic hyponatraemia without severe ormoderately severe symptoms

38. 7.4. Chronic hyponatraemia without severe ormoderately severe symptoms

39. 7.4. Chronic hyponatraemia without severe ormoderately severe symptoms

40. Na+ deficit ≈ body weight X0.6 X (desired plasma Na+ concentration – plasma Na+concentration) 1mg/dl/ h 10-12mg/dl /24h

41. Hypernatremia • Serum Na>145 mEq/L

45. SymptomsandSings of Hypernatremia • Dehydratedpatient→ orthostatichypotensionandoliguria • Rise in plasmaNaandosmolality →watermovementout of thebrain →rupture of thecerebralveins →focalintracerebralandsubarachnoidalhemorrages→possibleireversibleneurologicdamage • Lethargy, weaknees, irritability, twitching, seuzures, coma • Osmoticdemyelination (uncommon)

47. Laboratory Findings • Urineosmolality > 400 mosm/kg→ renalwater-conserving ability is functioning (hypotonic fluid losses from excessive sweating, the respiratory tract, or bowel movements andlactulose) • Urineosmolality < 250 mosm/kg→ characteristicof DI -Central DI: inadequateADH release -Nephrogenic DI: renalinsensitivitytoADH (lithium, demeclocycline, relief of urinaryobstruction, interstitialnephritis, hypercalcemia, andhypokalemia)

48. Water deficit ≈ body weight X0.6 X (plasma Na concentration/ desired plasma Na concentration) - 1

50. Case 1 • A 72-year-old woman from a nursing home presents to the emergency department with a change in her mental state over the past few hours. She has a medical history of coronary artery disease and hypertension. • Her medications include hydrochlorothiazide: 25 mg a day, and aspirin, 80 mg a day. • On physical examination, she has decreased skin turgor, orthostatic hypotension, and disorientation to time, place, and person without focal neurologic deficits. • Initial laboratory tests show a serum sodium level of 110 mmol/L;blood urea nitrogen 65 mg/dL; creatinine 3.6mg/dL and plasma osmolality, 278 mOsm/kg of water. • Her serum sodium level 2 months before admission was 135 mmol/L, and her urine output was 400 mL a day.