electrolytes imbalance :Sodium Potassium and their correction

1. FLUID AND
ELECTROLYTE
IMBALANCE
(Na, K)

2. Intravascular
9%
Interstitial fluid
24%
Intracellular fluid 67%
TBW is 60 % of body
weight.

3. • A healthy person consumes an average of 2000 mL of
water per day, approximately 75% from oral intake
and the rest extracted from solid foods.

4. Daily water losses include:
• 800 to 1200 mL in urine
• 250 mL in stool
• 600 mL insensible losses
Insensible losses of water occur through
skin (75%)
lungs (25%)
increased by such factors
fever (100-150 ml/day for each degree rise over 37 c)
hyperventilation.

5. Sensible water losses such as sweating or pathologic
loss of gastrointestinal (GI) fluids vary widely, but
these include the loss of electrolytes as well as
water.

6. Signs and symptoms of volume disturbances
SYSTEM VOLUME DEFICIT VOLUME EXCESS
Generalized Weight loss
Decreased skin turgor
Dry mucous membrane
Weight gain
Peripheral edema
Cardiac Tachycardia
Hypotension
Collapsed neck veins
Increased cardiac output
Increased central venous
pressure
Distended neck veins
Murmur
Renal Oliguria
Azotemia
GI Ileus Bowel edema
Pulmonary ------------- Pulmonary edema

7. Principles of Fluid Therapy
• Which fluid
• How much
• How fast

8. IMPORTANT ELECTROLYTES IN BODY
Cations:
• Sodium Na, Potassium K, Calcium Ca, Magnesium Mg.
Anions:
• Bicarbonate HCO3, Phosphate PO4, Chloride Cl.

9. Sodium

10. Sodium Na
• Most abundant cation in extracellular fluid
• Normal range:135 to 145 mEq/L
• Daily requirement 1-2 mmol/kg/day
• 600ml-1000ml of normal saline is sufficient to provide daily requirement
• Maintains balance of extracellular fluid
• Transmission of nerve impulse
• Neuromuscular and myocardial nerve impulse

11. Sodium (Na) regulation
• Aldosterone
• Urine output
• Salt intake
Note : To a large extent, extracellular fluid sodium
concentration and osmolarity are regulated by the amount
of extracellular water. The body water in turn is controlled
by
(1) fluid intake, which is regulated by factors that determine
thirst, and
(2) renal excretion of water.

12. Hyponatremia
• defined as a serum [Na+] <135 mmol/L
• one of the most common electrolyte abnormalities encountered
in hospitalized pts
• Symptoms include nausea, vomiting, confusion, lethargy, and
disorientation
• if severe (<120 mmol/L) and/or abrupt, seizures, central
herniation, coma, or death may result
• Clinical manifestations primarily have a central nervous system
origin and are related to cellular water intoxication and
associated increases in intracranial pressure

13. Causes of hyponatremia with decreased extracellular volume
(hypovolemia)
Extra Renal :
• Vomiting ,Diarrhea ,Hemorrhage, Burns, Pancreatitis
Renal: high urine sodium levels (>20 mEq/L)
• Osmotic diuresis (e.g. hyperglycemia, severe
uremia)
• Diuretics
• Adrenocortical insufficiency
• Tubulo-interstitial renal disease
• Unilateral renal arterystenosis
• Recovery phase of acute tubular necrosis

14. Causes of hyponatremia with normal extracellular volume
(euvolemic)
• Abnormal ADH release
• Vagal neuropathy (failureof inhibition of ADH release)
• Deficiency of adreno corticotrophic hormone (ACTH) or
glucocorticoids (Addison’s disease)
• Hypothyroidism
• Severe potassium depletion
• Syndrome of inappropriate antidiuretic hormone
• Major psychiatric illness ‘Psychogenic polydipsia’
• Anti-depressant therapy
• Increased sensitivity to ADH : Chlorpropamide ,Tolbutamide
• ADH-like substances : Oxytocin , Desmopressin

15. Causes of hyponatremia with normal extracellular volume (euvolemic) contd.
• Unmeasured osmotically active substances stimulating osmotic ADH
release
• Glucose
When hyponatremia in the presence of hyperglycemia is being evaluated, the corrected sodium
concentration should be calculated as follows:
For every 100-mg/dL increment in plasma glucose above normal, the plasma sodium should
decrease by 1.6 mEq/L
• Chronic alcohol abuse
• Mannitol
• Sick-cell syndrome (leakage of intracellular ions)

16. Causes of hyponatremia with increased extracellular volume
(hypervolemia)
• Heart failure
• Liver failure
• Oliguric renal failure
• Hypoalbuminemia

17. High
• Increased intake
• Postoperative ADH
secretion
• Drugs
Normal
• Hyperglycemia
• ↑Plasma Lipids/proteins
• SIADH
• Water intoxication
• Diuretics
Low
• Decreased sodium intake
• GI losses
• Renal losses
• Diuretics
• Primary renal disease
HYPONATREMIA
VOLUME STATUS

18. Treatment
• This is directed at the primary cause whenever
possible.
In a healthy patient:
• give oral electrolyte–glucose mixtures; ORS
• increase salt intake ; 60–80 mmol/day.
• In a patient with vomiting or severe volume depletion:
■ give intravenous fluid with potassium supplements, i.e. 1.5–2
L 5% Dextrose (with 20 mmol K+) and 1 L 0.9%
saline over 24 hours PLUS measurable losses
■ correction of acid–base abnormalities is usually not
required
 Euvolemic hyponatremia is managed by restriction of water
intake (to 1000 or even 500mL per day) with review of
diuretic therapy. Magnesium and potassium deficiency must
be corrected. In mild sodium deficiency, 0.9% saline given
slowly (1 L over 12 hours) is sufficient.

19. The aim of treatment should be to correct the serum sodium
concentration at a rate no faster than 1mmol/L/hour or
25mmol/L/day.
In asymptomatic patient 0.5mmol/L/hr is acceptable.
• Those who have profound hyponatremia ; <120mEq/L and/or
neurological symptoms
Hypertonic saline 3%: 100 to 200 ml over 30 min.

20. HYPERNATRAEMIA
• This is much rarer than hyponatremia and nearly alwaysindicates a
water deficit.
• impaired thirst or impaired conscious state
• pituitary diabetes insipidus (failure of ADH
secretion)
• nephrogenic diabetes insipidus (failure of response to
ADH)
• osmotic diuresis, e.g. hyperglycemic, hyperosmolar
state
• excessive loss of water through the skin or lungs.
• Excessive administration of sodium may also contribute,
for example: excessive reliance on 0.9% (150 mmol/L)
saline for volume replacement
• administration of drugs with a high sodium content
(e.g. piperacillin)
• use of 8.4% sodium bicarbonate after cardiac arrest

21. note that…..
• Hypernatremia is always associated with increased plasma
osmolality, which is a potent stimulus to thirst. None
of the above cause hypernatremia unlessthirst sensation
is abnormal or access to water limited. For
instance, a patient with diabetes insipidus will
maintain a normal serum sodium concentrationby
maintaining a high water intake until an intercurrent
illness prevents this. Thirst is frequently deficient in
elderlypeople, making them more prone to water
depletion. Hypernatremia may occur in the presence
of normal, reduced or expanded extracellular
volume, and does not necessarily imply that total body
sodium is increased.

22. High
• Iatrogenic sodium
administration
• Mineralocorticoid
excess
• Aldosteronism
• Cushing’s disease
• Congenital adrenal
hyperplasia
Normal
• Nonrenal water loss
• Skin
• GI
• Renal water loss
• Renal disease
• Diuretics
• Diabetes insipidus
Low
• Nonrenal water loss
• Skin
• GI
• Renal water loss
• Renal (tubular)
disease
• Osmotic diuretics
• Diabetes insipidus
• Adrenal failure
Hypernatremia
Volume status

23. Clinical features of Hypernatremia
• Symptoms of hypernatraemia are non-specific.
• Nausea, vomiting,
• fever
• confusion
• A history of longstanding polyuria, polydipsia
and thirst suggests diabetes insipidus.

24. Treatment
The aim of treatment should be to correct the serum sodium concentration at a rate no faster
than 1mmol/L/hour or 25mmol/L/day.
In asymptomatic patient 0.5mmol/L/hr is acceptable
• Treatment is that of the underlying cause for
example:
 in ADH deficiency, replace ADH in the form of
desmopressin, a stablenon-pressor analogue of
ADH.
• remember to withdraw nephrogenicdrugs wherepossible
and replace watereitherorally or, if necessary,
intravenously.

25. Treatment contd.
In severe (> 170 mmol/L) hypernatraemia:
• 0.9% saline (150 mmol/L) should be used initially.
• Avoid too rapid drop in serumsodium concentration;
• the aim is correction over 48 hours
• as over-rapid correction may lead to cerebral edema.
In less severe (e.g. > 150 mmol/L) hypernatraemia :
• the treatment is 5% dextrose or 0.45%saline; the
latter is obviously preferable in hyperosmolar diabetic
coma.Very large volumes –upto 5 L a day or
more – may need to be given in diabetes insipidus.

26. .

27. Potassium
• Main intracellular cation
• Normal conc. : 3.5-5.0 mEq/L
• Daily requirement 0.5-1 mEq/L
• The average dietary intake of potassium is approximately 50 to
100 mEq/day
• Regulates neuromuscular excitability and muscle contraction
• Role in glycogen formation and protein synthesis
• Role in acid base balance

28. Potassium regulation
• The kidney plays a dominant role in K+ regulation.
• aldosterone
• Insulin, β2-adrenergic agonists, and alkalosis tend to promote
K+ uptake by cells
• acidosis, insulinopenia, major surgery or acute
hyperosmolality (e.g., after treatment with mannitol)
promote the efflux or reduced uptake of K+.

29. HYPOKALEMIA
much more common than hyperkalemia in the surgical patient.
Clinical features
• usually asymptomatic
• severe hypokalemia (< 2.5 mmol)
causes muscle weakness.
• Paralytic ileus, constipation
• symptomatic hyponatremia
• increased frequency of atrial and
ventricular ectopic beats ,cardiac arrest.
• diminished tendon reflexes, paralysis.

30. ECG changes suggestive of hypokalemia
• U waves
• T-wave flattening
• ST-segment changes
• arrhythmias

31. Causes of HYPOKALEMIA
 Vomiting
 Severe diarrhea
 Purgative abuse
 Villous adenoma
 Ileostomy
 Fistulae
 high nasogastric output

32. Causes of HYPOKALEMIA contd.
• Increased renal excretion (urinary K+> 20 mmol/day) Diuretics:
Thiazides Loop diuretics
• Increased aldosterone secretion
Liver failure
 Heart failure
Nephrotic syndrome
Cushing’s syndrome
Conn’s syndrome
ACTH-producing tumors

33. Causes of hypokalemia contd.
• Exogenous mineralocorticoid
 Corticosteroids
 Carbenoxolone
 Liquorice (potentiates renal actionsof cortisol)
• Renal disease
 Renal tubularacidosis Types 1 and 2
 Renal tubulardamage (diuretic phase)
 Acute leukemia
 Nephrotoxicity ; Amphotericin, Aminoglycosides, Cytotoxic drugs,
 Release of urinarytract obstruction
 Bartter’s syndrome
 Liddle’s syndrome
 Gitelman’s syndrome

34. Causes of hypokalemia contd.
• Reduced intake of K+
 Intravenousfluids without K+
 Dietary deficiency
• Redistribution into cells
 β-Adrenergic stimulation
 Acute myocardial infarction
 Beta-agonists: e.g. fenoterol, salbutamol
 Insulin treatment, e.g. treatment of diabetic ketoacidosis
 Alkalosis

35. Management of Hypokalemia
• correction of the underlying disease process (e.g., diarrhea)
• or withdrawal of an offending medication (e.g., loop or thiazide diuretic),
• oral KCl supplementation
• Correction of Mg deficiency
• If hypokalemia is severe (<2.5 mmol/L) and/or if oral supplementation is not
feasible or tolerated, IV KCl can be administered through a central vein with
cardiac monitoring, at rates that should not exceed 10 mmol/ h.
• KCl should always be administered in saline solutions, rather than dextrose; the
dextrose-induced increase in insulin can acutely exacerbate hypokalemia.

36. HYPERKALEMIA
Clinical features
• Serum potassium greaterthan 7.0 mmol/L is an
emergency
• ECG changes ; high peaked T waves (early), widened QRS complex,
flattened P wave, prolonged PR interval (first-degree block), sine wave formation,
and ventricular fibrillation.
• Severe hyperkalemia may predispose to suddendeath from
arrhythmias , asystole & cardiac arrest.
• GI symptoms include nausea, vomiting, intestinal colic, and diarrhea
• Neuromuscular symptoms range from weakness to ascending paralysis to
respiratory failure.

37. Causes of Hyperkalemia
• Decreased excretion
 Renal failure
 Drugs: Amiloride, Triamterene, Spironolactone/eplerenone ,
ACE inhibitor ACE blockers ,NSAIDs
 Ciclosporin treatment
 Heparin treatment
 Aldosterone deficiency
 Hyporeninemic hypoaldosteronism (RTA type 4)
 Addison’s disease
 Acidosis
 Gordon’s syndrome

38. Causes of Hyperkalemia contd.
• Increased release from cells (decreased Na+/K+ATPase activity)
 Acidosis
 Diabetic ketoacidosis
 Rhabdomyolysis/major surgery/crush injury
 Tumor lysis
 Succinylcholine (amplified by muscledenervation)
 Digoxin poisoning
 Vigorous exercise (α adrenergic; transient)
• Transfusionof stored blood

39. Correction of severe Hyperkalemia
• IMMEDIATE
 ECG monitor
 i.v. access
 Protect myocardium
10 mL of 10% calcium gluconate i.v. over 5 min
,
Effect is temporary but dose can be repeated after
15 min

40. • Drive K+ into cells
• Insulin regular 20 units + 100 mL of 25%
glucose i.v. over 10–15min
• Nebs with salbutamol
• followed by regular checks of blood glucose
and plasma K+
• Repeat as necessary
• correction of severe acidosis (pH < 6.9)
– infuseNaHCO3 (1.26%) and/or salbutamol 0.5
mg in 100 mL of 5% glucose over 15
min (rarely used)

41. To be continued.
In next presentation
• Calcium
• Bicarbonate with (acid base balance)
• Magnesium

42. Thank you