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Disorders
By
of
Sodium
Mohammad
El-Tahlawi
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.
 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
= 2Na + 10
18
Plasma Tonicity (285 mOsm/l )
 = 2Na + Glucose
18
2.8
Na content and concentration
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 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
HYPERNATERMIA
( > 145 )
Etiology:
I.
A.



B.
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
II.



III.


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
• 0.2 NaCl
• 0.45 NaCl
• 0.9 NaCl
0 INFUSATE SODIUM.
34 infusate sodium.
77 infusate sodium.
154 infusate sodium.
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
HYPONATERMIA
( <135 meq/l )
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 .
Etiology

1.
2.

1.
2.

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
influenced by:
• Magnitude of rate of development .
• Age and gender.
• Nature and severity of underlying diseases.
Assessment of hyponatraemia
1.
2.
3.
4.
5.
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 .
Symptomatic Hyponatermia
 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
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1.
2.
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:
1. mild/moderate cases: fluid restriction by
600ml/h till clinical improvement or Na level
> 130
2. Severe cases: -Lasix
-Hypertonic saline
3. 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
