Simple way to understand Sodium imbalance in hospital setting and its management in a nutshell

1. APPROACH TO PATIENT OF
SODIUM IMBALANCE
Presented by:
Dr. Md. Toufiq
Hasan
Intern Doctor
Medicine unit-III

2. WHAT IS ELECTROLYTES?
“A Substance that dissociates into ions in solution acquires
the capacity to conduct electricity”
- Wikipedia
Mostly two types
• Cations
•Anions
Integral part of metabolic and cellular processes

3. COMPOSITION OF ELECTROLYTES

4. POSITIVE OR NEGATIVE?
Cations (+)
Sodium
Potassium
Calcium
Magnesium
Anions (-)
Chloride
Bicarbonate
Phosphate
Sulfate

5. DISTRIBUTION OF ELECTROLYTES
IN BODY FLUID

6. MAJOR CATIONS
EXTRACELLULAR
SODIUM (Na+)
INTRACELLULAR
POTASSIUM (K+)

8. DAILY REQUIREMENT

9. ELECTROLYTE IMBALANCES
oHyponatremia/ hypernatremia
oHypokalemia/ Hyperkalemia
oHypomagnesemia/ Hypermagnesemia
oHypocalcemia/ Hypercalcemia
oHypophosphatemia/ Hyperphosphatemia
oHypochloremia/ Hyperchloremia

10. SODIUM
oMajor extracellular cation
oAttracts fluid and helps preserve fluid volume
oCombines with chloride and bicarbonate to help regulate acid-base
balance
oNormal range of serum sodium 135 - 145 mEq/L

11. SODIUM AND FLUID
If sodium intake suddenly increases, extracellular fluid
concentration also rises.
Increased serum Na+ increases thirst and the release of ADH,
which triggers kidneys to retain water.
Aldosterone also has a function in water and sodium
conservation when serum Na+ levels are low.

12. SODIUM-POTASSIUM PUMP
•Sodium (abundant outside cells)tries
to get into cells
•Potassium (abundant inside cells) tries
to get out of cells
•Sodium-potassium pump maintains
normal concentrations
•Pump uses ATP, magnesium and an enzyme
to maintain sodium-potassium concentrations
•Pump prevents cell swelling and creates
an electrical charge allowing neuromuscular impulse transmission

14. HYPONATREMIA
Serum Na+ level < 135 mEq/L
Deficiency in Na+ related to amount of body fluid
Several types
Hypovolemic - Na+ loss is greater than water loss; can be renal
(diuretic use) or non-renal (vomiting)
Hypervolaemic - water gain is greater than Na+ gain; edema
occurs
Euvolaemic - normal Na+ level, too much fluid.
Dilutional - results from Na+ loss, water gain.
Depletional - insufficient Na+ intake

16. CAUSES

17. CLINICAL PICTURE
• Patient may often asymptomatic to profound disturbance of cerebral
function manifest as headache, nausea and vomiting, muscle twitching,
altered mental status, stupor, seizures & coma.
• Other features according to the cause like--
Hypovolaemia – Thirst, Dizziness on standing, Weakness, Low JVP,
Postural hypotension, Tachycardia,Dry mouth ,Reduced skin turgor,
Reduced urine output, Weight loss,Confusion, stupor.
Hypervolaemia - Ankle swelling, Abdominal swelling, Breathlessness,
Peripheral oedema, Raised JVP, Pulmonary crepitations, Ascites,Pleural
effusion, hypertension, weight gain.

20. RELATIONSHIP OF HYPONATREMIA
WITH BRAIN

21. INVESTIGATIONS
 plasma electrolytes and osmolarity
Urine electrolytes and osmolarity
Plasma renin activity ( when doubt about clinical signs of ECF
volume)

22. MANAGEMENT
oCritically dependent on its rate of development, severity and
underlying cause.
o If hyponatraemia develops rapidly (over hours to days) and there
are signs of cerebral oedema, sodium levels should be restored to
normal rapidly by infusion of hypertonic (3%) sodium chloride.
oA common approach is to give an initial bolus of 100 mL, which
may be repeated once or twice over the initial hours of
observation, depending on the neurological response and rise in
plasma sodium.

23. CONT. : MANAGEMENT
Rapid correction of hyponatraemia that has developed slowly (over
weeks to months) can be hazardous, since brain cells adapt to slowly
developing hypo-osmolality by reducing the intracellular osmolality, thus
maintaining normal cell volume.
An abrupt increase in extracellular osmolality can lead to water shifting
out of neurons, abruptly reducing their volume and causing them to
detach from their myelin sheaths. The resulting ‘myelinolysis’ can
produce permanent structural and functional damage to mid-brain
structures, and is generally fatal.
The rate of correction of the plasma Na concentration in chronic
asymptomatic hyponatraemia should not exceed 10 mmol/L/day and an
even slower rate is generally safer.

24. CONT. :MANAGEMENT
Firstly, we see hyponatraemia is
Acute - need immediate treatment
or
Chronic –should be cautious before treatment

25. CONT. :MANAGEMENT
Dilutional hyponatremia – Fluid restriction (600-1000mL/day) with
withdrawal of precipitating stimulus
Hypovolaemic hyponatremia – Treatment of underlying cause
accompanied by cautions use of diuretics with strict fluid restriction.
Persistant hyponatremia due to prolonged SIADH- Oral urea
therapy (30-45 g/day), Tolvaptan (Oral vasopressin receptor antagonist)

26. MANAGEMENT ACCORDING TO
SEVERITY
Classification
Mild - 135 to 125 mmol/L
Moderate - 124 to 115 mmol/L
Severe - < 115 mmol/L
IT IS BETTER TO UNDER CORRECTION THEN OVER
CORRECTION.

27. CONT.
IN MILD – (135-125 mmol/L)
Oral correction with Table salt and ORS only
Inj. Normal saline (0.9%NaCl) may given
MODERATE –(124 to 115 mmol/L)
Oral + Inj. Normal saline
SEVERE -- < 115 mmol/L
Oral+ 3% NaCl with caution

28. LIMITATIONS OF 3% NACL
Always needs senior consultation.
Less availability.
Should be correct slowly with micro burette set
Never be given in hypovolaemic patient.
No need to give if the patient is conscious and well oriented
(chronic hyponatraemia )

29. WORKING FORMULA
Calculation of sodium deficit= 0.6×(weight in Kg)×(desired
sodium-Actual Sodium)
Daily correction is not more than 10 mmol/kg body weight per
day.
1 litre of 3% NaCl Will correct 513 mmol
1 litre of 0.9% NaCl Will correct 154 mmol
1 spoon table salt Will correct 85 mmol

30. FLOW CHART:
HYPONATREMIA

31. Excess Na+ relative to body water (>148 mmol/L)
Occurs less often than hyponatremia
Thirst is the body’s main defense
When hypernatremia occurs, fluid shifts outside the cells
May be caused by water deficit or over-ingestion of Na+
Also may result from diabetes insipidus
HYPERNATREMIA

32. Failure to generate an adequate medullary concentration gradient
(low GFR states, loop diuretic therapy) causes inadequate
concentration of the urine in the face of restricted water intake.
But more commonly, it is due to failure of the ADH system or
because the collecting duct cells are unable to respond to circulating
ADH.
Patients with hypernatraemia generally have reduced cerebral
function which results in dehydration of neurons and brain shrinkage.

33. Presence of an intact thirst mechanism and preserved capacity to
obtain and ingest water, hypernatraemia may not progress very far.
Hypernatraemia may be iatrogenic
Whatever the underlying cause, sustained or severe hypernatraemia
generally reflects an impaired thirst mechanism or responsiveness to
thirst.

35. CAUSES

36. CLINICAL PICTURE
Think S-A-L-T
Skin flushed
Agitation
Low grade fever
Thirst
Neurological symptoms- dizziness, confusion, weakness
and ultimately coma and death
Signs of hypovolemia

38. INVESTIGATION
 plasma electrolytes and osmolarity
Urine electrolytes and osmolarity

39. MANAGEMENT : TOP NOTE
•Treatment of hypernatraemia depends on both the rate of
development and the underlying cause.
•If the condition has developed rapidly, neuronal shrinkage may be
acute and relatively rapid correction may be attempted. This can
be achieved by infusing an appropriate volume of intravenous
fluid(isotonic 5% dextrose or hypotonic 0.45% saline) at an initial
rate of 50–70 mL/hour.
•In older, institutionalized patients it is more likely that the disorder
has developed slowly and extreme caution should be exercised in
lowering plasma sodium to avoid the risk of cerebral oedema.

40. MANAGEMENT
Correct underlying disorder
Gradual fluid replacement
Monitor for s/s of cerebral edema
Monitor serum Na+ level
Seizure precautions

41. FLOW CHART:

42. THE POWER OF SALT