of

1
Disorders
By Mohammad El-Tahlawi
of
Sodium
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OBJECTIVES

• To Understand
• The differences between sodium concentration and
  content .
• The causes and management of hypernatermia .

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Osmolarity and 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.

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Plasma Osmolarity (280-295 mOsm/l )

• 2 Na (NaCl ) Glucose Urea
• 18 2.8
• 2Na 10
• Plasma Tonicity (285 mOsm/l )
• 2Na Glucose
• 18

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• Na content (hemostasis)
• determines ECF volume.
• balance between Na intake and excretion.
• -Intake lt Excretion ? -ve balance ? ECF
  shrinks.
• -Intake gt 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
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Na concentration

• 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

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HYPERNATERMIA
( gt 145 )
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Etiology

• Decrease in TBW
• Increase loss
• Trough kidney
• -DI
• -DM
• -Dieuretics
• Through skinlung
• -Heat stroke
• -Burns
• -Hyperventilation
• Through GIT
• -Diarrhea
• -Hypertonic enema
• Decreased intake
• -Impaired thirst mechnism
• -Coma

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• 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.

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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 ).

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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).

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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.

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• Central DI

• Fluid replacement.
• If urine output gt 300 ml/hr
• - Aqueous vasopressin (5 U Sc/4 hr).
• - Vasopressin in oil ( 0.3 ml IM/day ).
• - Desmopressin ( 5-10 U/day ).

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

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Correction of hypernatraemia

• Thirstwater deficit 2of wt.
• Thirst oliguriawater deficit 6of wt
• ThirstoliguriaCNS manif.water deficit 8 of
  wt.

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To calculate water deficit

• We can use the follwing formula
• -Measured Na x Actual TBW
• Initial(normal)Na x Normal TBW
• But water deficitNormalTBW-Measured TBW
• -So Water deficit
• (Measured TBW x Measured sNa/Normal sNa)-
  Measured TBW
• -TBWBwt x 60

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Formula for infusate containg sodium

• (Infusate sodium-serum sodium ) divided by TBW1
• 5D/W 0 INFUSATE SODIUM.
• 0.2 NaCl 34 infusate sodium.
• 0.45 NaCl 77 infusate sodium.
• 0.9 NaCl 154 infusate sodium.
  

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Practical approach

• 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

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HYPONATERMIA
( lt135 meq/l )
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• Isotonic hyponatremia

(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 .

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Etiology

• Increase in TBW(Dilutional hyponatraemia)
• Increased intakee.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, Addisons 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.

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SIAD H

• Definition
• Persistent unregulated secretion of ADH.
• Diagnosis
• Hyponatremia
• Hypotonicity
• Euvolemia
• Urine osm. (gt 100 mosm/kg).
• Water loading test (unnecessary).
• Absence of endocrinal and diuretic causes.

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• 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).

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Clinical presentation

• lt 110 (seizures, coma and respiratory arrest).
• lt 125 (anorexia, nausea and malaise).
• lt 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.

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• 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.

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Mortality and Morbidity

• Magnitude of rate of development .
• Age and gender.
• Nature and severity of underlying diseases.

• influenced by

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Assessment of hyponatraemia

1. Exclude lab. error (dilution of blood sample by
   running IV fluid).
2. Exclude pseudohyponatraemia (in cases of
   hyperglycaemia and hyperlipidaemia) .
3. Exclude redistribution (hyponatraemia due to
   hyperglycaemia or mannitol infusion K
   deficiency.
4. Assess ECF volume.
5. Assess renal function and urine analysis for
   osmolarity and electrolytes.

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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 .

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• 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 .

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Symptomatic Hyponatermia

• Acute lt 48 h.
• - Hypertonic Saline 3
• 1-2 ml/kg/hr.
• - Frusemide.
• Chronic gt 48 h. or Unknown
• - Hypertonic Saline
• 1-2ml/kg/hr.
• - Frusemide.
• - Change to water restriction.
• - Frequent assessment
• - Not exceed 12 meq/l/day.

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Practical approach

• Treatment of the cause
• Aim of correction is to get a Na level of 120
  mEq/L.
• Rate of correction
• in acute cases20 mEq/L/day
• in chronic cases12 mEq/L/day

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• Dilutional hyponatraemia
• mild/moderate cases fluid restriction by
  600ml/h till clinical improvement or Na level gt
  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

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• E.g 80 Kg woman with sNa118mmol/L.
• -Na deficit80 x 0.5 x (130-118)480mmol
• -Normal isotonic saline contains 154mmol/L of Na
• -so patient should receive 480/1543.12L of
  normal saline in a rate of 0.5 mmol/L/hr
• -So it needs 24h i.e 130ml/hr