Hyponatremia clinical features , diagnosis, treatment.pptx

Hyponatremia, clinical features, diagnosis treatment

1. HYPONATREMIA Dr azmeera gouthami

2. Disorder of sodium concentration are ca used by abnormalities in water homeostasis, leading to changes in the relative ratio of Na+ to body water Water intake and circulating AVP constitute the two key effector in the serum osmolality. Defects in one or both of these two defense mechanisms most causes of hyponatremia or hypernatremia .

3. DEFINITION OF HYPONATREMIA Based on sodium concentration Mild: NA 130 - 135meq/L Moderate: 125 to 130 meq/L Severe: <125 meq/L Rate of development Acute hyponatremia :exist For <48 hrs Chronic hyponatremia:> 48hrs

4. S. osmolarity=(2×Na)+ Glucose/18+ BUN/2.8 Normal osmolarity =280 to 295 mosm/L Corrected sodium formula =Measured Na+{1.6×(glucose-100)/100} if sugar <400 =Measured Na+{2.4× (glucose-100)/100} if sugar> 400

5. SYMPTOMS Mild :headache, irritability, altered mood, depression, difficulty in concentration Moderate :nausea, confusion, disorientation, altered mental status, unstable gait Severe: seizures, respiratory distress, coma

6. Diagnosis of hyponatremia Sequential assesment of Serum osmolality Urine osmolality Volume status Urinary sodium

7. Goal of therapy 1. To raise the plasma sodium concentration at a safe rate. 2. To correct underlying etiology. In general hyponatremia is corrected acutely by giving sodium to patients who are volume depleted and by restricting water intake in patients who are normovolemic or oedematous.

8. Correction Change in serum sodium concentration = Infusate Na/L - Serum Na / Total body water +1 Total Body Water= 0.6× Body weight in children and young men 0.5× Body weight in women and elderly men

9. • Removal of the drugs responsible for hyponatremia · Diuretics, Chlorpropamide or l.V. Cyclophosphamide. • Management of physical stress, postoperative pain. • Specific treatment for adrenal insufficiency hypothyroidism ,nephrotic syndrome, CHF, uncontrolled diabetes or ketoacrdosrs, salt losing nephropathy etc.

10. General guidelines for treatment are : i. Chronic asymptomatic hyponatremia : Correction rate 0.5 to 1 .0 mEq/L/hour . ii. Raise the plasma sodium by Iess than 8 meq/L on the first day and less than 18 mEq/L over the first two days. If the correction >25meq/L / 48 hrs or correction made until 140 meq/L risk of ODS very high

11. 2. Acute hyponatremia with severe neurological symptoms : These patients require rapid correction of plasma Na with hypertonic saline. Initial rate of rise of Na concentration should be 1.5-2 mEq/L/hr for the first 3 to 4 hours or until the severe neurological symptoms improve. Besides this initial rapid correction rise in the plasma sodium concentration should not exceed 10-12 mEq in first 24 hours. Patient with seizures also require immediate anticonvulsant drug therapy and adequate ventilation

12. Asymptomatic hyponatremia Hypovolumic hyponatremia:isotonic saline can be used to restore the intravascular volume Restoration of a euvolemic state corrects the hyponatremia Hypert onic hyponatremia CHF,cirrhosis often reflects the severity of underlying disease Restriction of fluid and water diuretics help to attenuate degree of hyponatremia

13. Siadh should be disti nguished from the previously listed conditions that stimulate vasopressin secretions Standard first line therapy is water restriction and correction of any contributing factors (nausea,vomiting, drugs,pneumonia)

14. Diagnostic criteria for SIADH ESSENTIAL CRITERIA Hypoosmotic hyponatremia serum osm <275mosm/L Urine osmolality >100mosm /L Euvolemia Urine sodium >30 mmol/L with normal salt and water intake No recent use of diuretics Absence of conditions that stimulate ADH secretions

15. SUPPLEMENTARY CRITERIA Serum uric acid <4mg/dl Serum urea<21.6 mg/dl Fractional urea excretion >55% Fractional uric acid ex cretion >12%

16. Frusemide 20mg Bd and salt tablets Demeclocycline or lith ium _ inhibitors of p cell used when hyponatremia not corrected after use of diuretics and salt tablets Demeclocycline contraindicated in cirrhosis ,risk of nephrotoxicity high AVP antagonist (vaptans) Highly effective in SIADH and hypertonic hyponatremia due to CHF,cirrhosis LFT have to monitor in tolvaptan therapy Treatment for 1 to 2months

17. WHEN TO STOP CORRECTION once any of the three end points is reached. 1. Patient's symptoms are abolished. 2. A safe plasma sodium (generally 120-125 mEq/L) is achieved or 3. A total magnitude of correction of 20 mEq/L is achieved. It is necessary to correct hyponatremia accurately to a safer range, rather than correcting completely to normonatremia.

18. Aim of fluid infusion is to raise Na by correcting Na deficit. So the infused fluid should contain higher Na concentration than desired or normal serum sodium concentration . higher Na concentration However, for the treatment of hyponatremia due to SlADH, infusion of 0.9°/o NaCl is ·inappropriate. When hyponatremia is associated with hypovolemia or in absence of ,fluid retention or oedema, 0.9%saline is the preferred fluid. But when patient needs salt supplementation along with fluid restriction hypertonic saline is the preferred fluid (e.g. severe form of SIADH).

19. Increase in serum sodium of 4–5 mEq/L is sufficient to promptly reverse severe neurologic symptoms and decrease intracranial pressure. This can be accomplished most effectively by using boluses of 100 mL of 3% NaCl over 10 minutes, which can be repeated twice if needed. Each bolus might be predicted to raise the serum sodium by 1–2 mEq/L. In patients with less severe symptoms, an intravenous infusion of 3% NaCl (0.5–2 mL/kg/h) may be used.

20. Osmotic demyelination syndrome Central pontine myelinolysis (CPM) is a component of osmotic demyelination syndrome (ODS). It is characterized by damage to regions of the brain, most commonly pontine white matter tracts, after rapid correction of metabolic disturbances such as hyponatremia The incidence of CPM is not well-known due to under-diagnosis. A retrospective study from 2015 shows the incidence of osmotic demyelination syndrome is 2.5% among intensive care unit (ICU) admissions. Studies have reported neurologic complications in 25% of severely hyponatremic patients after rapid sodium correction.

21. Adaptation to decreased serum tonicity Displacement of water from the cells into the cerebrospinal fluid The removal of intracellular solutes and water via ion channels to reduce brain swelling and normalize brain volume With chronic hyponatremia (greater than 48 hours in duration), other adaptive mechanisms include the efflux of organic osmolytes (glutamate, taurine, and glycine) with water, which also reduces cellular swelling

22. More susceptible patients Malnutrition Alcohol use disorder Chronic liver disease Hyperemesis gravidarum

23. Presentation Dysphagia, dysarthria, spastic quadriparesis, pseudobulbar paralysis, ataxia, lethargy, tremors, dizziness, catatonia, and in the most severe cases, locked-in-syndrome and coma

24. Treatment Treatment is primarily aimed at prevention . In patients with hyponatremia lasting 48 hours or of unknown duration , the rate of serum sodium correction should not exceed 6-8 mEq/L per 24 hours. During the infusion of fluids, it is essential to monitor serum sodium levels every 4-6 hours A proactive strategy of desmopressin administration with hypertonic saline was associated with a lower incidence of sodium overcorrection. Desmopressin 1 to 2 mcg is administered intravenously or subcutaneously, every 6-8 hours for 24 hours. Patients are simultaneously given intravenous hypertonic saline at 15 to 30 ml/hr

25. Reintroduction of Hyponatremia for overcorrection to prevent ODS 5% dextrose (D5W) and desmopressin can be utilized with the goal of reintroducing hyponatremia to ensure that the rate of correction will be 8-12 mEq/L when the rate of sodium correction has been too rapidly corrected Desmopressin binds to V2 receptors of the renal collecting duct, which translocates aquaporin channels to the apical lumen of the collecting duct and increases water reabsorption. It can be given at a dose of 2 to 4 mcg intravenously or subcutaneously. D5W at 6 mL/kg of lean body weight can be infused over 1 to 2 hours and should decrease serum sodium by 2 mEq/L. Infusion of D5W is continued until goal serum sodium is reached

26. Sodium concentration in fluids . Infusates Na (mEq/L) 3%NaCl 513 0.9%NaCl 154 Ringers lactate 130 O.45% NaCl 77 5%Dextrose DNS 154

27. Take home messages When hyponatremia is associated with hypovolemia or in absence of fluid retention or edema, 0.9%Saline is the preferred fluid In severe hyponatremia, sodium should be monitored every 4 to 6 hours Desmopressin can be given to prevent overcorrection of hyponatremia

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