The document discusses electrolyte imbalances and their neurology. It covers sodium, potassium, calcium and magnesium disorders. For sodium, it describes hyponatremia and hypernatremia in detail. Hyponatremia can be hypovolaemic, hypervolaemic or euvoleamic. Causes, clinical features and treatment approaches are provided. For potassium, it discusses hypokalemia and its neuromuscular and cardiac manifestations. Causes of hypokalemia include reduced intake, renal and non-renal losses, and intracellular shifting. ECG changes are also outlined.

1. NEUROLOGY OF ELECTROLYTE
IMBALANCE
DR. PIYUSH OJHA
DM RESIDENT
DEPARTMENT OF NEUROLOGY
GOVT MEDICAL COLLEGE, KOTA

2. • SODIUM - Hyponatremia
- Hypernatremia
• POTASSIUM - Hypokalemia
- Hyperkalemia
• CALCIUM - Hypercalcemia
- Hypocalcemia
• MAGNESIUM - Hypomagnesemia
- Hypermagnesemia

3. SODIUM
• Major ECF cation (140mEq/L ECF vs 25 mEq/L ICF)
• Total body sodium ~ 5,000 mEq in a normal adult
• 85-90% is extracellular.
• Responsible for > 90% of total osmolality of ECF.
• Daily requirement = 100 mEq or 6 gm of NaCl.

4. Sodium Disorders
• Abnormalities in water homeostasis that lead to changes
in the relative ratio of Na+ to body water
• Water intake and circulating AVP
• AVP secretion is stimulated as systemic osmolality
increases above a threshold level of 285 mosmol/kg
• Thirst and water ingestion also are activated at 285
mosmol/kg.

5. Hyponatremia

6. Hyponatremia
• Defined as plasma Na+ concentration < 135 mEq/L
• Occurs in approx 2.2% of hospitalised patients.
• Acute severe hyponatremia has a high morbidity and
mortality. ( Na level < 105 has >50% mortality)
• Mostly a result of an increase in circulating AVP and/or
increased sensitivity to AVP, combined with any intake of free
water.(EXCEPTION – hyponatremia due to low solute intake)
• MILD – 130 -135 mEq/L
• MODERATE – 125-129 mEq/L
• PROFOUND - <125
• ACUTE - <48 HRS . CHRONIC > 48 HRS

7. Hyponatremia
• Depending on Osmolality, hyponatremia is divided into
Pseudo hyponatremia and Hypoosmolar (True )
Hyponatremia.
• Depending on clinical history and volume status,
Hypoosmolar hyponatremia (TRUE hyponatremia ) is
subdivided into –
– Hypovolemic
– Euvolemic
– Hypervolemic.

8. Hypovolemic Hyponatremia
• Hypovolemia causes a marked neurohumoral activation -
increasing circulating levels of AVP.
• increase in circulating AVP helps preserve blood
pressure via vascular and baroreceptor V1A receptors
and increases water reabsorption via renal V2 receptors
• Nonrenal causes –
 gastrointestinal (GI) loss (vomiting, diarrhoea, tube
drainage, etc.) and insensible loss (sweating, burns) of
Na+Cl– and water.
 urine Na+ concentration is typically <20 mEq/L.

9. • Renal causes –
 Urinary Na concentration is typically > 20 mEq/L.
 Deficiency in circulating aldosterone and/or its renal
effects.
 Salt-losing nephropathies including reflux nephropathy,
interstitial nephropathies, post-obstructive uropathy,
medullary cystic disease, recovering ATN
 Thiazide diuretics
 Cerebral salt wasting syndrome – volume depleted state
(as in SAH, traumatic brain injury, encephalitis,
meningitis, craniotomy)
Hypovolemic Hyponatremia

10. Hypervolemic Hyponatremia
• Proportionately greater increase in total body water
compared to that of Na+, leading to a reduced plasma
Na+ concentration
• Congestive heart failure (CHF), cirrhosis, and nephrotic
syndrome (urinary Na < 20 mEq/L)
• Renal failure (urinary Na > 20 mEq/L)

11. Euvolemic Hyponatremia
• Moderate to severe hypothyroidism - after the
achievement of a euthyroid state
• Psychogenic Polydipsia
• secondary adrenal insufficiency due to pituitary disease
• Syndrome of inappropriate antidiuretic hormone (most
common cause)
• SIADH is characterised by high urinary sodium,
osmolality and specific gravity, inspite of low serum
sodium and hypoosmolality.
• erratic AVP secretion is seen in about a third of patients

12. Pseudohyponatremia and
Translocational hyponatremia
• Pseudohyponatremia -high concentrations of lipids
or proteins in the blood interfere with the accurate
measurement of sodium
• Normal osmolality- hyperlipdemia, hyperprotenemia
• High osmolality – hyperglycemia, Mannitol

13. • Low Solute Intake and Hyponatremia –
 Very low intake of dietary solutes
 Alcoholics –beer potomania
 Very low urine osmolality < 100-200 mosmol/kg with a urine
Na+ concentration <10-20mM.

14. Clinical features of Hyponatremia
• The severity of symptoms depend on severity of
Hyponatremia and rate at which Na concentration is
lowered.
• So acute and severe hyponatremia is symptomatic while
chronic and mild hyponatremia is well tolerated.

15. Mild Moderate Severe
Anorexia
Headache
Nausea
Vomiting
Lethargy
Personality changes
Muscle cramps
Muscular weakness
Confusion
Ataxia
Drowsiness
Diminished reflexes
Convulsions
Coma
death
Clinical features of Hyponatremia

17. Diagnosis of Hyponatremia
• History and physical examination is often helpful in
identifying hypovolemic hyponatremia. (diarrhoea,
vomiting, burns, diuretics etc.)
• Severity of hyponatremia often correlates with severity of
underlying condition and is an important prognostic factor.
• Three important diagnostic tests are :-
1. plasma osmolality
2. urinary osmolality
3. urinary Na concentration
• Levels can be repeated to rule out any lab error.
• Blood should always be drawn from a vein that does
not have IV fluids flowing through it.

18. • MEASURE PLASMA OSMOLARITY –
= 2 X Na + [Glucose(mg/dl)/18] + [BUN(mg/dl)/2.8]
• Hyponatremia is usually associated with low plasma
osmolality. But if it is normal or high, exclude
pseudohyponatremia
• Pseudohyponatremia does not cause brain edema.
Diagnosis of Hyponatremia

19. • Hyponatremia in edematous patient – consider CHF,
cirrhosis, nephrotic disease or other renal disease.
• In hypovolemic patients, rule out renal or extrarenal
causes.
• Associated hyperkalemia- suggests renal insufficiency or
adrenal insufficiency with hypoaldosteronism.
• Associated hypokalemia and metabolic alkalosis –
suggests vomiting or diurteic therapy.
• Diuretic induced hyponatremia is almost always due
to thiazide diuretics and rare with loop diuertics.

20. Steps in initial Evaluation of Hyponatremia
• Measure Plasma osmolality
• Low – True Hyponatremia
• Normal or elevated – Pseudohyponatremia
• Measure Urinary Osmolality
• <100 mOsm/kg or sp gravity < 1.003, dilute urine suggest
primary polydipsia with normal water excretion.
• > 100 mOsm/kg, other causes in which water excretion is
impaired
• Urine Na Concentration
• < 15 mEq/L – effective volume depletion eg diarrhoea,
vomiting
• > 20 mEq/L – SIADH or renal salt wasting.

21. Confirm diagnosis of
Hyponatremia
Rule out Pseudohyponatremia
Normal or High Osmolality
Hypoosmolality
Assess Renal status Primary renal disease
Impaired
renal function
Assess Volume status
Normal
OEDEMA – CHF, Cirrhosis,
Nephrotic Syndrome
VOLUME DEPLETION
Urinary Na excretion (mEq/L)
Urinary Na < 15
Diarrhoea, vomiting,
burns, pancreatitis
Urinary Na > 20
Diuretics, salt losing
nephropathy
Normovolemic

22. Normovolemic
Assess Adrenal &
Thyroid function
Adrenal or thyroid insufficiency
Normal
Able to dilute urine in
response to water load
SIADH
Dilute Urine
No
Yes
Psychogenic Polydypsia

23. • Must be individualized considering etiology, rate of
development, severity and clinical signs and symptoms.
• In short,
Treatment of Hyponatremia
HYPONATREMIA
NORMOVOLEMIAOEDEMAHYPOVOLEMIA
salt & water
supplementation
No salt
Fluid restriction
Loop diuretics
Fluid
restriction

24. • Specific treatment :-
– Treatment of the underlying disease like adrenal
insufficiency, hypothyroidism, nephrotic syndrome,
CHF, DM
– Removal of the offending drug like Thiazide diuretics,
chlorpropamide or IV cyclophosphamide

25. General guidelines for sodium correction
• Chronic Asymptomatic Hyponatremia :-
– The target rate of plasma sodium correction should
be < 10-12 mEq/L on the first day and < 18 mEq/L
over first 2 days.
– As per recent recommendations, the correction rate
should not exceed 8 mEq/L on any day of treatment.
– If the rate of correction is faster or rise in serum Na is
> 25 mEq/48 hrs, there is a high risk of central
pontine myelinosis.

26. General guidelines for sodium correction
• Acute Hyponatremia with severe Neurological
symptoms :-
– Require rapid correction with hypertonic saline 3% or
1.6% .
– The initial rate of rise of plasma sodium correction
should be < 1.5-2 mEq/L/hr for the first 3 to 4 hours or
until severe neurological symptoms improve
– Besides this initial rapid correction, rise in the plasma
Na concentration should not exceed 10-12 mEq in
first 24 hours.

27. General guidelines for sodium correction
• Chronic Hyponatremia
• Vassopressin-2 receptor antagonists
• Conivaptan and tolvaptan - FDA approved indicated for
hypervolemic and euvolemic hyponatremia (ie, serum Na
level < 125 mEq/L )
• Demeclocycline - a 2–3 day delay in onset .Nephrotoxic

28. HYPERNATREMIA

29. HYPERNATREMIA
• Defined as plasma Na concentration > 145mEq/L.
• A less frequent diorder.
• Mortality rates 40-60%
• Mostly due to combined losses of water and electrolytes with
losses of H2O in excess of those of Na+.
• Less frequently due to ingestion or iatrogenic administration
of excess Na+

30. ETIOLOGY OF HYPERNATREMIA
1. Excess water loss
a. Insensible loss :
Dermal : heat exposure, severe burns, severe exercise
Respiratory : mechanical ventilation
b. Renal loss : Diabetes inspidus (central or nephrogenic),
excessive diuretics, uncontrolled DM
c. GI losses : Osmotic diarrhoea
2. Water defecit due to imapaired thirst.
Primary hypodypsia, confused or comatose conditions
3. Sodium retention.
excesive IV hypertonic NaCl or NaHCO3

31. ETIOLOGY
• Elderly individuals with reduced thirst and/or diminshed
access to fluids are at highest risk.
• renal water loss including osmotic diuresis secondary to
hyperglycemia, excess urea, postobstructive diuresis, and
mannitol
• Insensible losses of water may increase in the setting of
fever, exercise, heat exposure, severe burns or mechanical
• Diarrhea is the most common gastrointestinal cause of
hypernatremia
• Nephrogenic DI (NDI) characterized by renal resistance to
AVP (Hypercalcemia & Hypokalemia and drugs like
Li,Ifosfamide may also lead to NDI)
• Central DI

32. Clinical Features of Hypernatremia
• Hypernatremia leads to increased osmolality of ECF –
osmotic gradient btwn ECF and ICF – efflux of
intracellular water – cellular shrinkage.
• Symptoms are predominantly Neurologic.
• Altered mental status is the most common manifestation,
ranging from mild confusion and lethargy to deep coma
• Sudden shrinkage of brain cells may lead to
parenchymal or subarachnoid hemorrhages and/or
subdural hematomas – predominantly in children.

33. Clinical Features of Hypernatremia
• Other features include nausea, muscular weakness,
focal neurological defecit, seizures.
• Osmotic damage to muscle membranes also can lead to
Hypernatremic rhabdomyolysis.
• Chronic hypernatremia are less likely to develop severe
neurologic compromise because of cerebral adaptations.

34. APPROACH TO HYPERNATREMIA
• Detailed history with focus on thirst, polyuria and/or
extrarenal water loss.
• Detailed neurological examination.
• Assessment of ECFV.
• Accurate I/O charting.
• Lab investigations – serum and urine osmolality and
urinary electrolytes.

35. APPROACH TO HYPERNATREMIA

36. Treatment of Hypernatremia
• Correction of underlying cause.
• To replace the calculated free-water deficit over
48-72 hrs to avoid cerebral edema.(ongoing loss and
insensible loss are to be considered seperately)
Water Defecit = [(plasma Na -140)/140] x 0.6 x body wt (kg)
• No more than 10 mEq/L/day or
• A rare exception is acute hypernatremia (<48hrs)
due to sodium loading.
(can be corrected at rate of 1mM/hr).

37. Treatment of Hypernatremia
• Goal of treatment is to reduce Na to 145mEq/L.
• Free water orally or through RT.
• Acute hypernatremia is treated vigorously by D-5%
infusion.
• Hypotonic saline solutions (0.45% NS)
•
• Patients with central DI - DDAVP
• NDI due to lithium may reduce their polyuria with
amiloride (2.5–10 mg/d).

38. POTASSIUM

39. POTASSIUM
• Major intracellular cation.
• Total body potassium ~ 3,500 mEq (98% intracellular &
2% extracellular )
• Normal serum potassium concentration = 3.5 – 5 mEq/ L
( vs intracellular 150 mEq/L)
• Normal daily potassium requirement = 50-80 mEq/day

40. HYPOKALEMIA
• Potassium levels below 3.5 mEq/L.
• Causes of Hypokalemia :-
1.Poor intake – low dietary intake or potassium free fluids.
2. Non-renal loss (Urinary K excretion <20mEq/day)
vomiting, diarrhoea, excessive sweating, large
nasogastric aspiration
3. Renal loss – (Urinary K excretion >30mEq/day)
diuretics, salt wasting nephropathies, mineralocorticoid
excess, cushing’s syndrome, steroid therapy,
Magnesium deficiency, amhotericin B therapy
4. Redistribution (shift of K into cells)
metabolic alkalosis, insulin, adrenergic agonist
(eg Salbutamol)

41. CLINICAL FEATURES OF HYPOKALEMIA
• Manifestations are mainly neuromuscular and cardiac.
• Fatigue, myalgias and muscular weakness.
• Smooth muscle weakness- constipation,ileus or urinary
retention.
• Acute onset quadriparesis with preserved consciousness
• Respiratory and Bulbar involvement – not common
• Attacks of periodic paralyses
• Examination- Proximal > distal muscle weakness , Legs
more than arms , hypotonia, hyporeflexia
• In between attacks examination is normal.
• Progressive Proximal Myopathy develops usually at the
age of 50 years

42. ECG CHANGES IN HYPOKALEMIA
• Early changes :
– Flattening or inversion of T waves
– Prominent U waves
– ST segment depresion
– Prolonged QT interval
• Severe potassium depletion :
– Prolonged PR interval
– Decreased voltage
– Widening of QRS complex
– Ventricular arrhythmia

44. DIAGNOSIS OF ETIOLOGY OF HYPOKALEMIA
A. History – poor dietary intake, abnormal losses,
diuretics, drugs causing transcellular shift
B. Urinary K excretion –
1. Hypokalemia with low renal K excretion (<25 m
Eq/day)
suggests poor oral intake, diarrhoea, excessive
sweating, vomiting or diuretics.

45. 2. Hypokalemia with high urinary K excretion :
a. K wasting with metabolic acidosis with no
hypertension : DKA, proximal and distal RTA,
amphotericin B
b. K wasting with variable pH : renal salt wasting :
recovering ATN, postobstructive diuresis
c. K wasting with metabolic alkalosis with no
hypertension :
- low urinary chloride (<20 mEq/day) : vomiting
- High urinary chloride : Diuretics, Bartter syndrome
d. K wasting with metabolic alkalosis with
hypertension.
Primary and secondary aldosteronism, cushing’s syndrome,
renovascular hypertension, Liddle’s syndrome
DIAGNOSIS OF ETIOLOGY OF HYPOKALEMIA

46. TREATMENT OF HYPOKALEMIA
• Therapeutic goals :-
1. Prevention of hypokalemia
2. To prevent life threatening complications
(arrhythmia & respiratory failure)
3. To correct K deficeit
4. To minimize ongoing losses
5. To treat underlying etiology

47. TREATMENT OF HYPOKALEMIA
• Normal potassium intake of 60 mEq/day is sufficient to
prevent hypokalemia .
• Patients at risk like on digitalis therapy, DM, cirrhosis
should be given adequate supplementation.
• Roughly 1mEq/L fall in serum potassium = 200-400 mEq
total body potassium.

48. TREATMENT OF HYPOKALEMIA
• WHEN TO TREAT :-
– 3.5 – 4 mEq/L : no potassium supplementation,
increased oral intake of K rich foods, add K sparing
diuretic or decrease dose of diuretic
– 3 – 3.5 mEq/L : treatment in selected high risk
patients (risk of arrhythmia eg. CHF, digitalis therapy,
IHD)
– < 3 mEq/L : needs definitive therapy

49. TREATMENT OF HYPOKALEMIA
• In oliguria / anuria, avoid or supplement K cautiously.
• Failure to increase serum K after sufficient doses and
duration of potassium supplement should raise
possibility of associated Magnesium deficiency.

50. TREATMENT OF HYPOKALEMIA
• Potassium chloride (KCl) is usually the preparationof
choice and will promote correction of hypokalemia as
well as of metabolic alkalosis.
• KCl is available in market as solution containing 20 mEq
potassium per 15 ml solution (1 gm KCl= 13.4 mEq of K).
• KCl tablets are also available as 8 mEq potassium per
tablet.

52. TREATMENT OF HYPOKALEMIA
• Potassium bicarbonate and citrate tend to alkalinize the
patient and would be more appropriate for hypokalemia
associated with chronic diarrhoea or distal RTA.
• Oral potassium preparation may frequently cause GI
irritation so patient is adviced to take KCl solution with
proper dilution in a glass of water, after food.
• Oral potassium supplementation is safer than IV route as
there is minimal risk of hyperkalemia.

53. TREATMENT OF HYPOKALEMIA
• In mild to moderate Hypokalemia (3-3.5 mEq/L), average
dose of KCl is 60-80 mEq/day (20mEq, 3-4 times) along
with treatment of underlying disorder.
• In severe (<2mEq/L) or symptomatic hypkalemia, more
rapid replacement is needed and dose can be increased
to 40 mEq 6 hourly under close ECG monitoring.

54. TREATMENT OF HYPOKALEMIA
• IV potassium supplementation should be reserved for
severe symptomatic hypokalemia (<3mEq/L) or those
cannot ingest oral potassium.
• Continuous ECG monitoring and frequent K level
monitoring is recommended.
• Avoid IV potassium, till urine output is established.
• Don’t give > 10-20 mEq/ hour or > 40 mEq/litre or >240
mEq/day.
• Injection KCl available as : Inj KCl 15%, 10 ml ampoule
• 10 ml of 15 % KCl = 20 mEq of potassium = 1.5 gm KCl

56. TREATMENT OF HYPOKALEMIA
• IV KCl bolus injection are contraindicated as it may lead
to sudden hyperkalemia and cardiac arrest.
• KCl should be mixed with isotonic saline while
administration.
• As soon as cardiac rhythm stabilises or respiratory
muscle strength is restored to normal, IV potassium is
discontinued and oral KCl is initiated.
• Potassium rich food : fruit juice, coconut water, banana,
dry fruits, chocolate, coffee, salt substitute eg Lona salt.

57. HYPERKALEMIA

58. HYPERKALEMIA
• Serum potassium level > 5.5 mEq/L.
• Often asymptomatic until K level is 6.5-7.0 mEq/L.
• Vague muscular weakness is usually the first symptom
of hyperkalemia.
• Muscular weakness with preserved consciousness may
be present beside cardiac manifestation

59. CAUSES OF HYPERKALEMIA
• Increased intake
• Tissue breakdown – bleeding into soft tissues,
hemolysis, catabolic state
• Shift of potassium out of cell – tissue damage
(ischemia), severe exercise, metabolic acidosis,
uncontrolled DM, aldosterone deficiency, succinyl
choline
• Impaired excretion – ARF/CRF, potassium sparing
diuretics, ACE inhibitors, heparin, reduced tubular
excretion as in Addison disease
• Pseudohyperkalemia – traumatic hemolysis in blood
drawing, marked leucocytosis

60. DIAGNOSIS OF HYPERKALEMIA
• Depends on clinical suspicion, serum K levels and
characteristic ECG changes.
• ECG changes are as follows :-
– 6-7 mEq/L – tall peaked T waves
– 7-8 mEq/L – loss of P waves and widening of QRS
complexes
– 8-10 mEq/L – QRS merges with T waves forming Sine
waves
– > 9 mEq/L – AV dissociation, VT or fibrillation and
cardiac standstill

61. DIAGNOSIS OF ETIOLOGY OF HYPERKALEMIA
• The urinary K excretion rate or transtubular potassium
gradient (TTKG) is widely used to differentiate renal
(hypoaldosteronism) and extrarenal causes of
hyperkalemia.
• Extrarenal Causes – urinary K excretion > 80 mEq/day
and TTKG >10
• Renal causes – urinary K excretion <20 mEq/day and
TTKG < 3
• Transtubular potassium gradient (TTKG) =
(Uk) / [Uosm/Posm]/Pk

62. TREATMENT OF HYPERKALEMIA
• Principles of treatment of Hyperkalemia : -
– Antagonism of membrane effects of hyperkalemia
: Ca Gluconate
– Potassium movement into cells : insulin & glucose,
Inj Sodium Bicarbonate, Beta2 agonist (salbutamol)
– Removal of potassium from the body : loop or
thiazide diuretics, cation exchange resin (Keyxalate),
peritoneal dialysis or hemodialysis

63. TREATMENT OF HYPERKALEMIA
• CALCIUM GLUCONATE : -
– Available as 10% solution in 10 ml ampoules.
– Usual dose is 10-20 ml infused over 5-10 mins.
– Rapid but short lived effect.
– Dose can be repeated if no change is seen in ECG
after 10 mins
– Prevents cardiotoxicity of hyperkalemia.
– NO EFFECT ON POTASSIUM LEVELS.

65. TREATMENT OF HYPERKALEMIA
• INSULIN & GLUCOSE: -
– Rapid way to lower K levels.
– 25 to 50 gms of glucose together with 10-20 units of
regular insulin is to be given.
– If effective, the plasma potassium concentration will
fall by by 0.5 to 1.5 mEq/L. this effect begins in 15
mins, peaks at 60 mins and may last for
approximately 4-6 hours.

66. TREATMENT OF HYPERKALEMIA
• SODIUM BICARBONATE INFUSION: -
– Shifts K into cells.
– NaHCO3 7.5%, 50-100 ml(45-90 mEq) is given as
bolus IV slowly over 10-20 mins followed by IV
NaHCO3 infusion.
– Onset of its effect is within 5-10 mins and effect lasts
for 1-2 hours.
– Most likely to be useful in severe hyperkalemia with
metabolic acidosis.

67. TREATMENT OF HYPERKALEMIA
• BETA ADRENERGIC AGONISTS: -
– Beta2 agonists such as Salbutamol promote cellular
uptake of potassium and thus decrese level.
– Dose 20 mg in 4 ml of saline by nasal inhalation over
10 minutes, or 0.5 mg by IV infusion.
– Generally becomes effective in 30-60 mins and its
effect persists for 2-4 hrs. it lowers K level by 0.5-
1.5mEq/L.

68. TREATMENT OF HYPERKALEMIA
– Calcium gluconate, glucose insulin , NaHCO3 and
Beta2 agonists are temporary measures. They donot
remove excess potassium from the body.
– Measures to remove potassium from body are
diuretics, cation exchange resins and dialysis.

69. TREATMENT OF HYPERKALEMIA
• CATION EXCHANGE RESINS: -
– Eg Sodium polystyrene sulphonate (Keyxalate) promote
exchange of sodium for potassium in GI tract.
– Each gram binds 1 mEq of potassium and releases 2-3 mEq of
sodium.
– When given orally, usual dose is 25-30 grams mixed with 100ml
20% sorbitol 3-4 times daily.(sorbitol prevents constiaption)
– Can also be given as retention enema consisting 50gm resin and
50 ml of 70% sorbitol mixed in 150ml water every 4-6 hourly.
– Each enema generally lowers levels by 0.5-1 mEq/L within 1-2
hrs and effect lasts for 4-6 hours.
– Adverse effects – anorexia, nausea, vomiting and constipation.
– Should be cautiously used in CHF patients.

70. TREATMENT OF HYPERKALEMIA
• DIALYSIS: -
– Most rapid and effective way of lowering potassium
levels.
– Should be reserved for patients with renal failure and
those with severe life threatening hyperkalemia
unresponsive to conservative measures.
– Peritoneal dialysis also remove potassium but is only
15-20 % as effective as hemodialysis.

71. CALCIUM
• Essential for bone formation and neuromuscular
function.
• Parathyroid hormone (PTH) and Vitamin D (1,25(OH)2
D-3) are main factors that maintain normal serum ionized
Calcium.
• Normal adult human body contains ~ 1.2 – 1.4 Kg Ca
• So it is most abundant cation in body.
• 99% present in bone.
• Normal range = 9.5-10.5 mg/dl
• 40% is bound to albumin and 50-55% in ionized form

72. CALCIUM

73. CALCIUM
• Ionized free form is the physiologically active form (4.8
mg/dl)
• Total serum calcium does not always reflect ionized Ca
level.
• Hypoproteinemia leads to reduced protein bound and
total serum calcium but the ionized Ca remains
unchanged.
• Correction for total serum Ca level in Hypoalbuminemia :
add 1mg/dl to serum Ca level for each 1gm/dl reduction
in serum albumin level below 4 gm/dl.

74. CAUSES OF HYPERCALCEMIA
• Increased bone turnover :
– Primary and secondary hyperparathyroidism
– Malignancy (lung,breast, kidney, multiple myeloma)
– Thyrotoxicosis
– Lithium therapy
• Increased intestinal absorption
– Vitamin D intoxication
– Milk alkali syndrome
– Granulomatous disease ( i.e. Sarcoidosis)
• Decreased renal excretion
– Familial hypocalciuric hypercalcemia
– Thiazide diuretics
– Acute adrenal insufficiency

75. CLINICAL FEATURES OF HYPERCALCEMIA
• Secondary to underlying disorders.
• Secondary to Hypercalcemia :
– Mild hypercalcemia is asymptomatic.
– Severe Hypercalcemia may manifest as :
• CNS symptoms : weakness, fatigue, depression,
confusion, stupor or coma.
• GI symptoms : constipation, anorexia, nausea
and vomiting, abdominal pain
• Renal symtoms : polyria, nocturia and calculi
formation.
• Cardiac : more prone to digitalis toxicity

76. DIAGNOSIS OF HYPERCALCEMIA
• Primary hyperparathyroidism and malignancy account
for 90% of cases.
• History
• Physical examination
• Imaging (eg.Cxray)

77. TREATMENT OF HYPERCALCEMIA
A. Measures to increase urinary excretion :
– Volume restoration, expansion and saline diuresis
are most useful and effective measures to correct
hypercalcemia.
– 0.9% NaCl corrects dehydration, expands volume
and causes natriuresis and Ca secretion in urine.(4-6
L/day)
– Forced diuresis with Frusemide (20-160 mg IV 8
houly after volume expansion)
– Haemodialysis

78. TREATMENT OF HYPERCALCEMIA
B. Measures to inhibit bone resorption :
– Bisphosphonates :Pamidronate is most potent and
widely used in hypercalcemia due to bone
resorption. Dose – 90mg IV over 4 hours, maximal
effect in 2-3 days and effect lasts for few weeks .
– Plicamycin – highly toxic
– Calcitonin – inhibits bone resorption and increases
urinary clcium excretion. Rapid onset of action. So
useful in acute conditions only. Dose 4 IU/kg s/c 12
hourly

79. TREATMENT OF HYPERCALCEMIA
C. Measures to decrease intestinal absorption :
– Glucocrticoids : decreases intestinal absorption
and increases urinary excretion. Effective in
hypercalcemia due to vitamin intoxication,
sarcoidosis, and malignancies but donot alter
calcium levels in primary hyperthyroidism or in
normal person.
Dose – 200-300 mg Hydrocortisone IV 6 hrly for 3-5 days
– Oral phosphate : inhibits calcium absorption and
promotes calcium deposition in bone and soft
tissues. Should be used only when serum
phosphorus < 3 mg/dl and normal renal function.

80. TREATMENT OF HYPERCALCEMIA
D. Specific treatment :
– Discontinue drug responsible.
– Surgical treatment of hyperparathyroidism
– Specific treatment for malignancy

81. HYPOCALCEMIA

82. CAUSES OF HYPOCALCEMIA
• Hypoalbuminemia
• Hypoparathyroidism
– Post surgical
– Hypomagnesemia
– Idiopathic
• Defect in Vitamin D metabolism
– Nutritional, lack of sunlight exposure
– Malabsorption
– Liver disorders, renal failure
– Vitamin D depenedent rickets
• Miscellaneous
– Metabolic or respiratory alkalosis
– Sepsis, toxic shock syndrome, burns, acute pancreatitis,
massive transfusion of citrated blood

83. CLINICAL FEATURES OF HYPOCALCEMIA
• Vary with degree and rate of onset.
• Due to increased neuromuscular excitability.
• Weakness, circumoral and distal extremity parasthesias,
muscle spasms, carpopedal spasm, tetany and mental
changes such as irritability, depression and psychosis.
• On physical examination, patient may have increased
DTR’s or signs of latent tetany (Chevostek sign,
Trousseau sign)
• ECG – prolonged QT interval.
• Severe hypocalcemia may cause lethargy, confusion,
laryngeal spasm, seizure or reversible heart failure.
• Chronic state due to hypoparathyroidism may cause
catarcts and basal ganglia calcification.

84. DIAGNOSIS OF HYPOCALCEMIA
• Detailed History
• Physical examination
• Serum albumin
• Serum HCO3.
• Serum Magnesium
• Serum PTH

85. TREATMENT OF HYPOCALCEMIA
A. Acute management :
• Symptomatic hypocalcemia should be treated as an
emergency with 10% calcium gluconate (90 mg
elemental calcium/10ml) 10-20 ml IV, slowly over 10
mins.
• May also require infusion of 60 ml of calcium
gluconate in 500 ml 5% dextrose (Ca concentration
1mg/ml at rate 0.5-2 mg/kg/hour)
• If IV calcium doesnot relieve tetany, then rule out
(and correct) hypomagnesemia.
• When citrated blood is transfused rapidly,
hypocalcemia can occur. So for every 4 units of
blood, give 10ml of 10% calcium gluconate.

86. TREATMENT OF HYPOCALCEMIA
A. Long term management :
• Treatment of underlying etiology.
• Calcium supplementation : oral elemental calcium
1 to 3 gm per day. Calcium is best absorbed when
taken between meals.
• Vitamin D supplementation :
• Calcitriol [1,25(OH)2 D3] is the most potent of
vitamin D preparations.

87. MAGNESIUM

88. MAGNESIUM
• 4th most common cation of body (after Na, K, and Ca)
• 2nd most common intracellular cation (after K)
• Commonest intracellular divalent cation.
• 60 % of body Mg is in bones
• Normal serum Mg level = 1.4-2.2 mEq/L (1.8-3.0 mg/dl)
• Since clinical effects of Magnesium disorders are
determined primarily by tissue magnesium content,
serum Mg levels have limited diagnostic value.
• Mg plays an important role in neuromuscular function
and maintenance of cardiovascular tone.

89. CAUSES OF HYPERMAGNESEMIA
• Serum Mg levels > 3 mg/dl.
• Rarely seen in clinical practice if renal function is normal
• Seen in : -
• Renal failure patients, receiving Mg containing antacids,
laxative or IV fluids is the most common cause.
• Treatment of pre-eclampsia with IV Mg sulphate.
• ARF with acute rhabdomyolysis.
• DKA without treatment.

90. CLINICAL FEATURES OF HYPERMAGNESEMIA
• Neuromuscular manifestations : muscular weakness,
lethargy, loss of DTRs, respiratory depression and
respiratory failure.
• Cardiac manifestations : hypotension due to peripheral
vasodilatation, bradyarrhythmia, and in severe cases
cardiac asystole.
• ECG changes : prolonged PR interval, increased QRS
duration and QT interval, complete heart block
• Hypocalcemia may occur due to hypermagnesemia
induced decreased secretion of PTH and end organ
resistance of PTH.

91. TREATMENT OF HYPERMAGNESEMIA
1. Eliminate source : stop Mg containing antacids,
laxatives etc
2. 10 % Ca Gluconate, 10-20 ml IV slowly over 10 mins
will effectively correct hypotensionby lowering Mg
levels.
3. If renal function is normal, IV Furosemide after
rehydration with Normal Saline will enhance renal
excretion.
4. Hemodialysis is the treatment of choice in renal failure
patients.
5. Supportive treatment like Artificial respiration in case of
respiratory failure.

92. HYPOMAGNESEMIA

93. CAUSES OF HYPOMAGNESEMIA
• Serum Mg levels < 1.5 mEq/L (1.8 mg/dl).
• Symptomatic hypomagnesemia = Mg < 1 mEq/L
• Common causes are :
1. Increased renal excretion : loop diuretics, osmotic
diuretics, hypercalcemia, acute pancreatitis
2. Increased GI losses : malabsorption syndrome,
vomiting or nasogastric aspiration
3. Poor intake : prolonged malnutrition
4. Chronic alcoholism
5. Others : primary aldosteronism, hypoparathyroidism,
drugs like Aminoglycosides, Cisplatin, Amphotericin B
etc.

94. CLINICAL FEATURES OF HYPOMAGNESEMIA
• Rarely occurs as a single entity. It often causes
hypocalcemia and hypokalemia which contribute the
clinical picture.
• Neuromuscular manifestations : lethargy, confusion,
tremor, fasciculations,ataxia, tetany and seizures.
• Cardiac manifestations : ECG changes : prolonged PR
interval and QT interval.
• Metabolic abnormalities : hypocalcemia, hypokalemia,

95. TREATMENT OF HYPOMAGNESEMIA
1. Correct underlying etiology and coexisting
hypocalcemia and hypokalemia.
2. Magnesium Sulphate : available as powder as well as
10% or 50% solution.
– 5 ml of 10% or 1 ml of 50% contains 4 mEq magnesium.
– 1 gram MgSO4 = 8.1 mEq of magnesium
3. Mild deficiency (Mg ~ 1.8 mg/dl) needs oral
supplementation of 2gms three times a day without
producing diarrhoea. Mg rich diet include green
vegetables, nuts and legumes, chocolate and fruits
such as banana, grapes and oranges

96. TREATMENT OF HYPOMAGNESEMIA
4. Severe Mg deficiency (Mg level < 1.2 mg/dl) needs
parenteral Mg supplementation.
– 2 gram MgSO4 (4 ml of 50%, 16 mEq) is given
slowly over 10 minutes. Followed by 1 mEq/kg/24 hrs
as slow continuous infusion or IM injection.
– For IV infusion, 10 ml of 50% MgSO4 is added to
500 ml NS which will contain 40 mEq Magnesium.
– Alternatively, 2 gm MgSO4 is given every 6 to 8 hrs
as im injections.

97. TREATMENT OF HYPOMAGNESEMIA
• Caution and monitoring of MgSO4 therapy :
 Check DTR every 15 mins. Disappearance of
Patellar reflex is a useful clinical sign to detect onset
of Mg intoxication. If Knee jerk on examination prior
to a repeat dose is absent, no additional Mg should
be given until they return.
 Periodic monitoring of Mg levels is essential.
 Mg therapy is contraindicated in heart block or in
patients with extreme myocaridal damage.
Maintain urine output at minimum rate of 100 ml
every 4 hours.

98. THANK YOU

99. REFERENCES
• Practical guidelines on Fluid therapy 2nd edition
• Clinical practice guideline on diagnosis and treatment of
hyponatraemia - Eur J Endocrinol March 1, 2014 170G1-
G47
• New European guidelines management of Hyponatremia
2014
• Neurology Clinics – neurology and systemic disease Feb
2010 .vol28
• Harrison’s principles of internal medicine 18 th edition