![ Osmolality of body fluids 280 – 295 mosm/l
Posm = 2[ Na+ ] + BUN(mg/dl) + glucose(mg/dl)
2.8 18
e.g. serum Na + 92,BUN-28,blood glucose-90
Posm = 2[ Na+ ] + BUN(mg/dl) + glucose(mg/dl)
2.8 18
Posm = 2[ 92 ] + 28(mg/dl) + 90(mg/dl)
2.8 18
This is true hyponatremia
=199](https://image.slidesharecdn.com/hyponatremia1-210129145234/85/Hyponatremia-1-20-320.jpg)
Hyponatremia (1)
- 1. HYPONATREMIA PRESENTED BY PRAVEEN JR2 MEDICINE DEPARTMENT G.S.V.M. MEDICAL COLLEGE KANPUR
- 2. HYPONATREMIA ● Definition: Plasma Na+ concentration <135 mM. ● It is a very common disorder, occurring in up to 22% of hospitalized patients. ●Result of an increase in circulating ADH and/or increased renal Sensitivity to ADH, combined with any intake of free water. HYPONATREMIA USUALLY MEANS WATER RETENTION
- 3. Hyponatremia is subdivided in three groups on basis of clinical history and volume status :- 1-Hypovolemic Hyponatremia 2-Euvolemic Hyponatremia 3-Hypervolemic Hyponatremia
- 4. Hypovolemic hyponatremia Reduction in total body sodium >reduction in total body water. ECF volume depletion Patient dehydrated; Hypovolemia causes a marked neurohumoral activation increase circulating level of AVP Increase water reabsorption Hyponatremia
- 5. Nonrenal Cause of hypovolemic hyponatremia GI Loss:-vomiting ,diarrhea, Insensible loss of Na+Cl-:-sweating ,burn Pancreatitis Third spacing of fluid Urinary Sodium excretion < 20 mM
- 6. Renal Cause of hypovolemic hyponatremia Inappropriate loss of Na+-Cl– in the urine lead to volume depletion and an increase in circulatingADH. Urine Na+ concentration is typically > 20 mM Cause;- Primary Adrenal Insufficiency-decrease aldosterone lead to hyponatremia Salt –losing nephropathy-lead to hyponatremia Typical causes-reflux nephropathy, post obstructive uropathy, recovery phase of ATN
- 7. Thiazide diuretic Glycosuria ,ketonuria ( in starvation or in diabetic or alcoholic ketoacidosis) Bicarbonaturia (in renal tubular acidosis or metabolic alkalosis ) Cerebral salt wasting syndrome
- 8. Cerebral Salt Wasting Syndrome(CWS) Development of extracellular volume depletion due to renal Na+ transport abnormality in patient with intracranial disease ; associated disorders include subarachnoid hemorrhage, traumatic brain injury ,craniotomy, encephalitis and meningitis. Mechanism:- injured brain cell lead to release of natriuretic protein lead to natriuresis Hyponatremia
- 9. Clinical feature of CSW Syndrome Severe hypovolemic hyponatremia Urine output:-often high Polyuria+ Dehydration Present after 1-2 week of head injury Treatment-fluids(hydration)
- 10. Euvolemic Hyponatremia Patient has a normal store of sodium but excess 0f total body water. Can occur in moderate to severe hypothyroidism(decrease cardiac output GFR ↓ ↑ Vasopressin hyponatremia Secondary adrenal failure (predominant Glucocorticoid deficiency) is associated with euvolemic hyponatremia. Psychogenic polydypsia The syndrome of inappropriate antidiuresis(SIAD)
- 11. SIADH Most common cause of euvolemic hyponatremia. The secretion of ADH is not inhibited by either low serum osmolality or expanded intravascular volume. Patient with SIADH is unable to excrete water. This results in dilution of the serum sodium lead to hyponatremia. Kidney increases sodium excretion in an effort to decrease intravascular volume to normal; thus, the patient has a mild decrease in body sodium.
- 13. Diagnostic Criteria for SIADH 1-Normovolemic ,(absence of hypotension/dehydration). 2-Hyponatremia with hypoosmolality (serum sodium <135 mEq/L and Serum osmolality <280 mOsm/kg ) 3-Urine osmolality >100 mOsm/kg (usually > plasma) 4-Urine sodium >30 mEq/L 5-Rule out hypothyroidism ,hypoaldosteronism, renal failure or diuretic therapy before diagnosing SIADH 6-Low serum uric acid (<4 mg /dl) and BUN are commonly associated finding.
- 15. CAUSES OF SIADH Ectopic Vasopressin:-most commonly with small –cell lung carcinoma Pulmonary disorder:-pneumonia, tuberculosis, pleural effusion CNS Disorder:-tumor ,SAH, meningitis Drugs:-most common with SSRI
- 16. SIADH CSW Syndrome Volume and serum Na+ Euvolemic hyponatremia Hypovolemic hyponatremia Urine Na+ Increased Increased Mechanism Water retention due to elevated ADH Excessive secretion of Na+ and water Present immediately after head injury Present after 1-2 week of head injury Uric acid level Decreased uric acid level Normal uric acid levels Urine output Polyuria absent Polyuria+ Treatment >48 water restriction Treatment- fluids(hydration
- 17. Hypervolemic Hyponatremia Increase in total body water > increase in total body sodium. Patients are oedematous. RENAL CAUSES(urinary sodium > 20mEq/L): Acute or Chronic renal failure. NON RENAL CAUSES(urinary sodium < 20mEq/L): CHF, Cirrhosis, Nephrotic syndrome.
- 19. Psuedo hyponatremia Pseudohyponatremia is defined as coexistence of hyponatremia with a normal or increased plasma tonicity A-NORMAL OSMOLALITY- mannitol, Hyperglycemia B-HIGH OSMOLALITY-hyperlipidemia hyperproteinemia. Plasma Na+ concentration falls by 1.6-2.4 mM for every 100 mg /dl increase in glucose due to glucose –induced water efflux from cell.
- 20. Osmolality of body fluids 280 – 295 mosm/l Posm = 2[ Na+ ] + BUN(mg/dl) + glucose(mg/dl) 2.8 18 e.g. serum Na + 92,BUN-28,blood glucose-90 Posm = 2[ Na+ ] + BUN(mg/dl) + glucose(mg/dl) 2.8 18 Posm = 2[ 92 ] + 28(mg/dl) + 90(mg/dl) 2.8 18 This is true hyponatremia =199
- 21. MILD HYPONATREMIA MODERATE HYPONATREMIA SEVERE HYPONATREMIA 130-135 mEq/L 125-130 mEq/L <125 mEq/L Headache Muscle cramps Diminished reflexes Nausea Muscular weakness Convulsion Vomiting confusion Coma Lethargy ataxia Death Anorexia Personality changes Drowsiness CLINICAL FEATURES
- 22. Severity of symptoms depends upon :- The severity of hyponatremia and The rate at which the sodium concentration is lowered. Acute Hyponatremia: develops in 48 hours or less. Subjected to more severe degrees of cerebral edema. Acute symptomatic hyponatremia is a medical emergency.
- 23. Hyponatremia induces cellular swelling ,consequence of water movement from hypotonic ECF to ICF. Symptoms of hyponatremia are primarily neurologic, reflecting development of cerebral edema. Early symptoms can be nausea ,headache ,vomiting Severe complication can seizure activity, brainstem herniation, coma and death
- 24. Chronic hyponatremia Develops over 48 hours and brain edema is less and is well tolerated. The signs and symptoms are due to increase in volume of ICF and increase in volume of brain cells rather than decrease in serum sodium Clinical feature - nausea ,vomiting, confusion, seizure, usually at plasma Na < 125 mM . cognitive defect Increase risk of bony fracture.
- 25. DIAGNOSIS History and physical examination- to identify hypovolemic hyponatremia (diarrhoea, vomiting, burns). Radiologic imaging - to assess whether patient has a pulmonary or CNS cause for hyponatremia
- 26. Laboratory tests- Provide important initial clue in the differential diagnosis 1. Plasma Osmolality 2. Urine Osmolality 3. Urine Sodium concentration 4. Uric acid level 5. Serum potassium 6. Serum glucose
- 27. Steps in evaluation of hyponatremia 1-Plasma osmolality Low- true hyponatremia Normal or elevated-pseudohyponatremia 2- Urine osmolality- < 100 mosm/kg – primary polydipsia with normal water excretion >100 mosm/kg –other causes of hyponatremia in which water excretion is impaired 3-Urine sodium concentration
- 29. TREATMENT • Hyponatremia which developed quickly needs to be treated fast • whereas slow developing hyponatremia should be corrected slowly. GOALS of THERAPY: 1.To raise the plasma sodium concentration at a slow rate. 2.To replace sodium or potassium deficit or both. 3.To correct underlying etiology.
- 30. BASIC PRINCIPLES OF CORRECTION: Rapid correction is indicated in :- acute (<48hours) symptomatic or severe hyponatremia.(serum Na <120 mEq/L). In chronic cases patients are at little risk, however rapid correction can lead to demyelination.
- 31. Osmotic demyelination syndrome(ODS) Patient with chronic hyponatremia are at risk for ODS. Overly rapid correction of hyponatremia (>8-10 mM in 24 hr or > 18 mM in 48 hr) is associated with disruption in BBB, allowing entry of immune mediators that may contribute to demyelination. ODS embraces central pontine myelinosis and extrapontine myelinosis Patient can present with paraparesis or quadriparesis, loss of consciousness, dysarthria, diplopia
- 32. Treatment of Hypovolemic Hyponatremia will respond to intravenous hydration with isotonic normal saline, with a rapid reduction in circulating ADH and a brisk water diuresis. Diuretics induced hyponatremia is treated with saline and potassium supplementation.
- 33. Increase Na+ = 𝒊𝒏𝒇𝒖𝒔𝒆𝒅 𝑵𝒂−𝒔𝒆𝒓𝒖𝒎 𝑵𝒂 𝑻𝑩𝑾+𝟏 TBW= .60 X BODY WEIGHT IN MALE .50 X BODY WEIGHT IN FEMALE Eg-if a male serum Na=100, Body weight-60 kg 1 Lt of NS FLUID= 154−100 6𝑂% 𝑋60 +1 =1.5 meq/Lt 5Lt of NS per day required
- 34. Treatment of Hypervolemic hyponatremia Manage the etiology. Responds to salt, water restriction(intake < urine output), and loop diuretics . 𝒖𝒓𝒊𝒏𝒆(𝑵𝒂)+(𝑲) 𝑷𝒍𝒂𝒔𝒎𝒂 𝑵𝒂+ urine to plasma electrolyte ratio is useful to predict the response to fluid restriction. If ratio >1 then should be fluid restriction< 500 ml/D Ratio is 1 then fluid restriction to 500-700 ml/D Ratio is <1 then fluid restriction to <1 L/D Vaptans are effective in hypervolemic hyponatremia.
- 35. Treatment of Euvolemic hyponatremia Will respond to successful treatment of the underlying cause, Euvolemic hyponatremia in severe hypothyroidism will correct after achieving a euthyroid state. Vasopressin antagonists (vaptans)- highly effective in treating SIADH
- 36. 0.9% NS is not used to correct hyponatremia in SIADH 3% NS and furosemide can be use. Many patient with SIADH respond to combined therapy oral furosemide and oral salt tablet if Na + level not increased then Demeclocycline can be used. Oral urea can be used to manage SIADH.
- 37. Acute symptomatic Hyponatremia treatment Fluid of choice-3% NS(513 Mm) Increase plasma Na+ concentration by 1-2 mM/ h to a total of 4-6 mM Total body sodium deficit is approximated as : Na+ deficit(meq/lit)=(target Na+ conc - serum Na+) x 0.6 x BW(kg)
- 38. eg -60kg weighted male patient presented altered sensorium for 1 day with S.Na+=110 meq/Lt,S.osmolality-230 mosm/kg and urine osmolality-480 mOsm/kg. Diagnosis- Acute hypotonic hyponatremia Treatment plan –infusion of 3% NS Sodium deficeit = .6 x 60 x(135-110)=1000 mEq Expected Increase Na+ = 𝐢𝐧𝐟𝐮𝐬𝐞𝐝 𝐍𝐚−𝐬𝐞𝐫𝐮𝐦 𝐍𝐚 𝐓𝐁𝐖+𝟏 = 513−110 .6𝑋60+1 =10.9 mEq/L To raise 10.9 mEq/L of Na ,1000 ml of 3% NS required
- 39. Treatment option 1- Bolus therapy Approach-100 ml bolus of 3% saline over 10 minutes followed if symptom persist with up to 2 additional 100 ml doses. 2-Round the clock approach- if we want to correct 8 meq/L/day( maximum target correction) To raise 10.9 mEq/L of Na ,1000 ml of 3% NS required so to raised 8 mEq of Na, amount of 3% NS required = 700 ml approx 3% NS will require to raise 8 meq 7 bottles of 100 ml 3% NS over 24 hours. give 1 bottle over every 3-4 hrs
- 40. Asymptomatic or Chronic Hyponatremia Rate of correction should be comparatively slow . <8–10 mM in the first 24 h and <18 mM in the first 48 h Target rate of plasma sodium should not be >.5-1 mEq/L/Hour. TOC- Fluid restriction DOC-Vaptans Fluid -3% NS
- 41. Infusion rate of hypertonic saline= BW X Desired rate of increase in plasma Na+ eg- 70 kg weight of pt ,desired rate of rise in Na is .5 mEq/l Then infusion rate of 3% NS=70 X .5=35 ML/Hr.
- 42. SPECIFIC THERAPY: 1. Removal of responsible drugs- diuretics, chlorpropamide etc 2-Specific treatment of underlying cause. 3-Vasopressin antagonists (vaptans)- highly effective in treating SIADH and hypervolemic hyponatremia Tolvaptan is only oral V2 antagonist Conivaptan is only intravenous vaptan
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