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Disorders. By Mohammad El-Tahlawi. of. Sodium. OBJECTIVES. To Understand : The differences between sodium concentration and content . The causes and management of hypernatermia. Osmolarity and osmolality. Osmolarity number of osmoles per liter.
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Disorders By Mohammad El-Tahlawi of Sodium
OBJECTIVES • To Understand : • The differences between sodium concentration and content . • The causes and management of hypernatermia .
Osmolarityand osmolality • Osmolarity number of osmoles per liter. • Osmolality number of osmoles per kg of solvent. • . • . • Effective and ineffective osmoles • Effective osmoles • NaCl, glucose, mannitol (ECF) • Kcl (ICF) • contribute to tonicity . • Ineffective osmoles • urea and ethanol • with effective osmoles, contribute to osmolarity.
Plasma Osmolarity (280-295 mOsm/l ) • = 2 Na (Na+Cl )+ Glucose + Urea 18 2.8 • = 2Na + 10 Plasma Tonicity (285 mOsm/l ) • = 2Na + Glucose 18
Na content (hemostasis): • determines ECF volume. • balance between Na intake and excretion. • -Intake < Excretion → -ve balance → ECF shrinks. • -Intake > Excretion → +ve balance → ECF expands. • Intake : • enteral or parenteral.(normally 50-300mEq Na/day) • Excretion • renal (mainly).(normally 100-70 mEq/day). • skin, GIT, burn and diarrhea (less). Na content and concentration
Naconcentration • determined by water intake and excretion • Intake • oral or IV fluids (hospitalized patient) • 2500 ml/day. • physiologic stimulus is thirst. • Excretion • 2500 ml . • determinants of excretion : • EABV • - Absolute blood volume. • - COP. • - SVR. • ADH
HYPERNATERMIA ( > 145 )
Etiology: • Decrease in TBW: • Increase loss: • Trough kidney -DI -DM -Dieuretics • Through skin&lung -Heat stroke -Burns -Hyperventilation • Through GIT -Diarrhea -Hypertonic enema • Decreased intake: -Impaired thirst mechnism -Coma
Increase in Na intake: • Infusion of NaHCO3 and other Na salts. • Selective depression of thirst centre (cerebral tumors,polio,meningitis..) • Essential hypernatraemia: resetting of osmoreceptors from 140 to 150 mEq/L. • Decreased in Na excretion: • Hyperaldosteronism. • Cushing syndrome.
Effect of hypernatremia • Cell volume contraction and dehydration. • Cell shrinkage is greatest in the brain (rigid clavarium ). • Tearing of the bridging vessels intracranial hemorrhage • Cells generate idiogenic osmoles (few hours to days ).
Presentation • It depends on magnitude and rate of rise. • Ranging from agitation to coma and seizures. • clinical picture of: • volume overload (hypertonic hypernatremia). • volume depletion (loss of hypotonic fluid).
Treatment • Hypervolemic hypernatremia: • Loop diuretics. • Replace water deficit. • Hypovolemic hypernatremia • Restoring vascular volume quickly. • Replace water deficit. • Isovolemic hypernatremia • Replacing water deficit over 48 -72 hours . • Rate of decrease ≤ 0.5 meq/l per hr. • Half of free water in the first 24 hours. • Remaining half over 24-48 hours.
Central DI • Fluid replacement. • If urine output > 300 ml/hr : • - Aqueous vasopressin (5 U Sc/4 hr). • - Vasopressin in oil ( 0.3 ml IM/day ). • - Desmopressin ( 5-10 U/day ).
Nephrogenic DI • Stop offending drugs. • Correct electrolyte disorders. • Salt and protein restriction. • Thiazide. • NSAI . • Amiloride.
Correction of hypernatraemia • Thirst=water deficit 2%of wt. • Thirst+ oliguria=water deficit 6%of wt • Thirst+oliguria+CNS manif.=water deficit 8% of wt.
To calculate water deficit • We can use the follwing formula: -Measured Na x Actual TBW= Initial(normal)Na x Normal TBW But water deficit=NormalTBW-Measured TBW -So Water deficit= (Measured TBW x Measured sNa/Normal sNa)- Measured TBW -TBW=Bwt x 60%
Formula for infusate containg sodium • (Infusate sodium-serum sodium ) divided by TBW+1 • 5%D/W 0 INFUSATE SODIUM. • 0.2 NaCl 34 infusate sodium. • 0.45 NaCl 77 infusate sodium. • 0.9 NaCl 154 infusate sodium.
We should add the daily needs of water. Causal management is essential. Correction should be gradual (over 2 days) or 2mEq/L/hr. Replacement of water should contain some saline (e.g. D 5%, Saline 0.45) Frequently check for vascular overload Practical approach
HYPONATERMIA ( <135 meq/l )
Isotonichyponatremia (Pseudo-hyponatremia ) • Increased non-aqueous volume of the serum sample . • Hypertonic Hyponatermia • Large amount of ECF osmotically effective solutes other • than Na . • Hypotonic hyponatremia • Inability of the kidney to excrete sufficient electrolyte free • water .
Etiology • Increase in TBW(Dilutional hyponatraemia): • Increased intake:e.g excwss infusion of hyponatraemic solutions e.g dextrose in water. • Impaired free water clearance: e.g RF, CHF, LCF, SIADH..) • Na depletion: • Decreased intake • Increased loss: -Through kidney: dieuretics, hypoaldosteronism, Addison’s disease. -Through GIT: Diarrhea, vomiting.. -Through skin: excessive sweating, burns… • K depletion: K leaks outside cells to keep K in plasma and this leads to Na influx to the cells.
SIAD H • Definition: Persistent unregulated secretion of ADH. • Diagnosis: • Hyponatremia • Hypotonicity • Euvolemia • Urine osm. : (> 100 mosm/kg). • Water loading test (unnecessary). • Absence of endocrinal and diuretic causes.
Conditions Associated with SIAD H: • CNS (head trauma, stroke , tumour and meningitis ) • Pulmonary (TB, pneumonia and abscess). • Neoplastic (pancreatic and bronchogenic). • Drugs (Thiazide and NSAIDs).
Clinical presentation • < 110 (seizures, coma and respiratory arrest). • < 125 (anorexia, nausea and malaise). • < 110-120 (headache, lethargy, confusion and agitation). • Focal neurologic finding is unusual. • Oedema (overhydration) in dilutional hyponat. but dehydration in Na depletion causes And normal hydration in K depletion causes.
In acute hyponatraemia: Neurological manifestations appear rapidly • In chronic hyponatraemia: the severity of brain edema is less due to the slow compensatory loss of intracellular k, chloride and water thus protecting CNS.
Mortality and Morbidity • Magnitude of rate of development . • Age and gender. • Nature and severity of underlying diseases. • influenced by:
Assessment of hyponatraemia • Exclude lab. error (dilution of blood sample by running IV fluid). • Exclude pseudohyponatraemia (in cases of hyperglycaemia and hyperlipidaemia) . • Exclude redistribution: (hyponatraemia due to hyperglycaemia or mannitol infusion: K deficiency. • Assess ECF volume. • Assess renal function and urine analysis for osmolarity and electrolytes.
Management • Detect • osmolarity (serum and urine). • . Na (serum and urine). • Assess • ECF volume. • . Necessity of rapid treatment . • chronicity. • presence or abcence of symptoms . • degree of decrease .
Asymptomatic Hyponatermia (Chronic ) • Hypovolemic hyponatermia • Replace volume • Euvolemic hyponatermia • water restriction . • Hypervolemic hyponatermia • Salt and water restriction . • Treatment of the cause : • - Heart Failure . • - Nephrotic syndrome. • - Hepatic cirrhosis . • - Renal Failure .
SymptomaticHyponatermia • Acute< 48 h. : - Hypertonic Saline 3% 1-2 ml/kg/hr. - Frusemide. • Chronic> 48 h. or Unknown : -Hypertonic Saline 1-2ml/kg/hr. - Frusemide. - Change to water restriction. - Frequent assessment - Not exceed 12 meq/l/day.
Practical approach • Treatment of the cause • Aim of correction: is to get a Na level of 120 mEq/L. • Rate of correction: • in acute cases:20 mEq/L/day • in chronic cases:12 mEq/L/day
Dilutional hyponatraemia: • mild/moderate cases: fluid restriction by 600ml/h till clinical improvement or Na level > 130 • Severe cases: -Lasix -Hypertonic saline • Amount of Na needed= wt x 0.6 x (120 - measured Na)in male& wt x 0.5 x (120 - measured Na)in female • Absolute hyponatraemia : Na needed = wt x 0.6 x (120 –measured Na) in male& wt x 0.5 x (120 - measured Na)in female
E.g: 80 Kg woman with sNa=118mmol/L. -Na deficit=80 x 0.5 x (130-118)=480mmol -Normal isotonic saline contains 154mmol/L of Na -so patient should receive 480/154=3.12L of normal saline in a rate of 0.5 mmol/L/hr -So it needs 24h i.e 130ml/hr