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of Disorders Sodium By Mohammad El-Tahlawi

Of Disorders Sodium By Mohammad El-Tahlawi. To Understand : The differences between sodium concentration and content. The causes and management of hypernatermia

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of

Disorders

Sodium

By

Mohammad

El-Tahlawi

To Understand :

• The differences between sodium concentration and content .

• The causes and management of hypernatermia .

OBJECTIVES

..

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.

Osmolarity and osmolality Osmolarity number of osmoles per liter.

Osmolality number of osmoles per kg of solvent.

Plasma Osmolarity (280-295 Plasma Osmolarity (280-295 mOsm/l )mOsm/l )

= 2 Na (Na+Cl )+ Glucose + Urea= 2 Na (Na+Cl )+ Glucose + Urea

18 2.818 2.8 = 2Na + 10= 2Na + 10

Plasma Tonicity (285 mOsm/l )Plasma Tonicity (285 mOsm/l ) = 2Na + Glucose= 2Na + Glucose

18 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

determined by water intake and excretionIntake• 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

Na concentration

HYPERNATERMIHYPERNATERMIAA

( > 145 )( > 145 )

EtiologyEtiology::I.I. Decrease in TBW:Decrease in TBW:A.A. Increase loss:Increase loss: Trough kidneyTrough kidney -DI-DI -DM-DM -Dieuretics-Dieuretics Through skin&lungThrough skin&lung -Heat stroke-Heat stroke -Burns-Burns -Hyperventilation-Hyperventilation Through GITThrough GIT -Diarrhea-Diarrhea -Hypertonic enema-Hypertonic enemaB.B. Decreased intake:Decreased intake: -Impaired thirst mechnism-Impaired thirst mechnism -Coma-Coma

II.II. Increase in Na intake:Increase in Na intake: Infusion of NaHCO3 and other Na Infusion of NaHCO3 and other Na

salts.salts. Selective depression of thirst Selective depression of thirst

centre (cerebral centre (cerebral tumors,polio,meningitis..)tumors,polio,meningitis..)

Essential hypernatraemia: Essential hypernatraemia: resetting of osmoreceptors from resetting of osmoreceptors from 140 to 150 mEq/L.140 to 150 mEq/L.

III.III. Decreased in Na excretion:Decreased in Na excretion: Hyperaldosteronism.Hyperaldosteronism. Cushing syndrome.Cushing syndrome.

Effect of Effect of hypernatremiahypernatremia

Cell volume contraction and Cell volume contraction and dehydration.dehydration.

Cell shrinkage is greatest in the brain Cell shrinkage is greatest in the brain (rigid clavarium ).(rigid clavarium ).

Tearing of the bridging vessels Tearing of the bridging vessels

intracranial hemorrhageintracranial hemorrhage

Cells generate idiogenic osmoles (few Cells generate idiogenic osmoles (few hours to days ).hours to days ).

Ranging from agitation to coma and seizures.

clinical picture of :

• volume overload (hypertonic hypernatremia).

• volume depletion (loss of hypotonic fluid).

PresentationIt depends on magnitude and rate of rise.

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.

Treatment

• 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 ).

Central DI

Nephrogenic DI

• Stop offending drugs.• Correct electrolyte disorders.• Salt and protein restriction.• Thiazide. • NSAI .• Amiloride.

Correction of Correction of hypernatraemiahypernatraemia

Thirst=water deficit 2%of wt.Thirst=water deficit 2%of wt. Thirst+ oliguria=water deficit Thirst+ oliguria=water deficit

6%of wt6%of wt Thirst+oliguria+CNS Thirst+oliguria+CNS

manif.=water deficit 8% of wt.manif.=water deficit 8% of wt.

To calculate water To calculate water deficitdeficit We can use the follwing formula:We can use the follwing formula:

-Measured Na x Actual TBW= -Measured Na x Actual TBW= Initial(normal)Na x Normal TBWInitial(normal)Na x Normal TBWBut water deficit=NormalTBW-Measured But water deficit=NormalTBW-Measured

TBWTBW-So Water deficit=-So Water deficit=(Measured TBW x Measured sNa/Normal (Measured TBW x Measured sNa/Normal

sNa)- Measured TBWsNa)- Measured TBW-TBW=Bwt x 60%-TBW=Bwt x 60%

Formula for infusate containg Formula for infusate containg sodiumsodium

(Infusate sodium-serum sodium ) (Infusate sodium-serum sodium ) divided by TBW+1divided by TBW+1

• 5%D/W 0 INFUSATE SODIUM.5%D/W 0 INFUSATE SODIUM.• 0.2 NaCl 34 infusate sodium.0.2 NaCl 34 infusate sodium.• 0.45 NaCl 77 infusate sodium.0.45 NaCl 77 infusate sodium.• 0.9 NaCl0.9 NaCl 154 infusate sodium. 154 infusate sodium.

Practical approachPractical approach We should add the daily needs of We should add the daily needs of

water.water. Causal management is essential.Causal management is essential. Correction should be gradual (over 2 Correction should be gradual (over 2

days) or 2mEq/L/hr.days) or 2mEq/L/hr. Replacement of water should contain Replacement of water should contain

some saline (e.g. D 5%, Saline 0.45)some saline (e.g. D 5%, Saline 0.45) Frequently check for vascular Frequently check for vascular

overloadoverload

HYPONATERMIHYPONATERMIAA < (< (135135 meq/lmeq/l) )

Increased non-aqueous volume of the serum sample .

Hypertonic HyponatermiaLarge amount of ECF osmotically effective solutes other than Na .

Hypotonic hyponatremiaInability of the kidney to excrete sufficient electrolyte free water .

Isotonic hyponatremia (Pseudo-hyponatremia )

EtiologyEtiology Increase in TBW(Dilutional hyponatraemia):Increase in TBW(Dilutional hyponatraemia):

1.1. Increased intake:e.g excwss infusion of Increased intake:e.g excwss infusion of hyponatraemic solutions e.g dextrose in hyponatraemic solutions e.g dextrose in water.water.

2.2. Impaired free water clearance: e.g RF, CHF, Impaired free water clearance: e.g RF, CHF, LCF, SIADH..)LCF, SIADH..)

Na depletion:Na depletion:

1.1. Decreased intakeDecreased intake

2.2. Increased loss:Increased loss:

-Through kidney: dieuretics, -Through kidney: dieuretics, hypoaldosteronism, Addison’s disease.hypoaldosteronism, Addison’s disease.

-Through GIT: Diarrhea, vomiting..-Through GIT: Diarrhea, vomiting..

-Through skin: excessive sweating, burns…-Through skin: excessive sweating, burns… K depletion:K depletion: K leaks outside cells to keep K in K leaks outside cells to keep K in

plasma and this leads to Na influx to the cells.plasma and this leads to Na influx to the cells.

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.

SIAD H

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).

• < 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.

Clinical presentation

In acute hyponatraemia: In acute hyponatraemia: Neurological manifestations Neurological manifestations appear rapidlyappear rapidly

In chronic hyponatraemia: the In chronic hyponatraemia: the severity of brain edema is less severity of brain edema is less due to the slow compensatory due to the slow compensatory loss of intracellular k, chloride loss of intracellular k, chloride and water thus protecting CNS.and water thus protecting CNS.

• Magnitude of rate of development .

• Age and gender. • Nature and severity of underlying diseases.

Mortality and Morbidityinfluenced by:

Assessment of Assessment of hyponatraemiahyponatraemia

1.1. Exclude lab. error (dilution of blood Exclude lab. error (dilution of blood sample by running IV fluid).sample by running IV fluid).

2.2. Exclude pseudohyponatraemia (in Exclude pseudohyponatraemia (in cases of hyperglycaemia and cases of hyperglycaemia and hyperlipidaemia) .hyperlipidaemia) .

3.3. Exclude redistribution: (hyponatraemia Exclude redistribution: (hyponatraemia due to hyperglycaemia or mannitol due to hyperglycaemia or mannitol infusion: K deficiency. infusion: K deficiency.

4.4. Assess ECF volume.Assess ECF volume.5.5. Assess renal function and urine analysis Assess renal function and urine analysis

for osmolarity and electrolytes.for osmolarity and electrolytes.

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 .

Management

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 .

SymptomaticSymptomatic HyponatermiaHyponatermia AcuteAcute < 48 h< 48 h. :. :

- Hypertonic Saline 3%- Hypertonic Saline 3% 1-2 ml/kg/hr.1-2 ml/kg/hr. - Frusemide.- Frusemide.

ChronicChronic > 48 h> 48 h. . or Unknownor Unknown : : -- Hypertonic SalineHypertonic Saline 1-2ml/kg/hr.1-2ml/kg/hr. - Frusemide.- Frusemide. - Change to water restriction.- Change to water restriction. - Frequent assessment - Frequent assessment - Not exceed 12 meq/l/day. - Not exceed 12 meq/l/day.

Practical approachPractical approach

Treatment of the causeTreatment of the cause Aim of correction: is to get a Na Aim of correction: is to get a Na

level of 120 mEq/L.level of 120 mEq/L. Rate of correction: Rate of correction:

1.1. in acute cases:20 mEq/L/dayin acute cases:20 mEq/L/day

2.2. in chronic cases:12 mEq/L/dayin chronic cases:12 mEq/L/day

Dilutional hyponatraemia:Dilutional hyponatraemia:1.1. mild/moderate cases: fluid restriction mild/moderate cases: fluid restriction

by 600ml/h till clinical improvement or by 600ml/h till clinical improvement or Na level > 130Na level > 130

2.2. Severe cases: -LasixSevere cases: -Lasix -Hypertonic saline-Hypertonic saline3.3. Amount of Na needed= wt x 0.6 x (120 Amount of Na needed= wt x 0.6 x (120

- measured Na)in male& wt x 0.5 x - measured Na)in male& wt x 0.5 x (120 - measured Na)in female(120 - measured Na)in female

Absolute hyponatraemia : Absolute hyponatraemia : Na needed = wt x 0.6 x (120 –measured Na needed = wt x 0.6 x (120 –measured

Na) in male& wt x 0.5 x (120 - Na) in male& wt x 0.5 x (120 - measured Na)in femalemeasured Na)in female

E.g: 80 Kg woman with sNa=118mmol/L.E.g: 80 Kg woman with sNa=118mmol/L.

-Na deficit=80 x 0.5 x (130-118)=480mmol-Na deficit=80 x 0.5 x (130-118)=480mmol

-Normal isotonic saline contains 154mmol/L -Normal isotonic saline contains 154mmol/L of Naof Na

-so patient should receive 480/154=3.12L -so patient should receive 480/154=3.12L of normal saline in a rate of 0.5 mmol/L/hrof normal saline in a rate of 0.5 mmol/L/hr

-So it needs 24h i.e 130ml/hr-So it needs 24h i.e 130ml/hr