Journal of Pediatric Critical Care

P - ISSN : 2349-6592    |    E - ISSN : 2455-7099

Clinical Update
Year : 2019 | Volume : 6 | Issue : 3 | Page : 62 - 69

Practical aspects in Electrolyte Management in PICU

Kundan Mittal1, H K Aggarwal2, Sachin Damke3, Jayant Wagha3

1Senior Professor and in charge PICU and Respiratory Clinic, 2Senior Professor and Nephrologist, PGIMS Rohtak, Haryana, India. 3Professor, Dept. of Pediatrics, Jawaharlal Nehru Medical college, Sawangi, Wardha, Maharashtra, India.

Correspondence Address:

Dr. Kundan Mittal, Senior Professor Pediatrics
Pt B D Sharma, PGIMS, Rohtak, Haryana, India.
Phone : +919416514111, Email :
Received: 14-Apr-19/ Accepted: 14-May-19/Published Online:05-Jun-19

Source of Funding:None Conflict of Interest:None


Fluid and electrolytes management is key to pediatric critical care. These disorders may be primary or secondary to illness, drugs, iatrogenic, or as a result of medical error. The electrolyte disturbances are seen frequently and require aggressive monitoring and management. It is essential to understand normal water and electrolyte physiology and their distribution in human body for the management.

Key words:
Fluid, electrolytes, sodium, potassium

Hyponatremia (serum level <135 mEq/L)
Sodium is primarily present in extravascular compartment and maintains the volume & tonicity of ECF. Sodium is also needed in cell membrane action potential (transmission of nerve conduction and impulses, cellular/enzyme activity, and acid-base balance). Target serum sodium level is 138-142mEq/L (Serum sodium = Total sodium + Total potassium/ TBW). Hyponatremia results due to excessive water intake and impaired and inappropriate urine dilution. Serum sodium value below 120-125 mEq/L is defi ned as severe, 125-130mEq/L moderate and 130-135mEq/L as mild hyponatremia. Also, hyponatremia developing within 48hrs is termed acute and later than 48hrs is termed chronic hyponatremia.True hyponatremia is defi ned as when plasma osmolality is <280mOsm/kg/H2O. Hyponatremia can be further classifi ed as hypertonic ECF (waterloss in excess of sodium), Isotonic ECF (pseudohyponatremia : hyperlipidaemia > 4.6gm/L, hyperproteinaemia >10gm/L, hyperglycaemia >320mg/dL) and hypovolemic ECF (CRSW), euvolemic with no oedema (SIADH, psychotic), hypotonic with oedema(CCF, ARF).
• True hyponatremia (Plasma osmolality <280mOsm/kg H2O): acute (develops <48hrs) or chronic (develops >48hrs)
• Factitious: Hyperlipidaemia, hyperproteinaemia (lipid increase more than 4.6gm/L and protein by 10gm/L will decrease sodium 1mEq/L), hyperglycaemia (trans-locational hyponatremia when osmolality is >320: 100mg/dL increase in plasma glucose will decrease serum sodium 1.6mEq/L and if plasma glucose is >500mg/dL correction factor will be 2.4)
• Dilutional: Serum chloride level will be normal
• Drugs causing hyponatraemia in ICU: Diuretics, sodium valproate, carbamazepine, ACE inhibitors, PPI.

May also be categorized as:
• Hypo-osmolar hypovolemic (urine sodium concentration >20 renal loss in origin and if <20 extra-renal loss in origin). Condition commonly seen in gastrointestinal, kidney and skin disorders.
• Hypo-osmolar euvolemic (urine sodium concentration >20 etiology may be acute or chronic renal failure and if <20 etiology may be nephrotic syndrome, cardiac failure or liver cirrhosis). Classically observed in case of inappropriate kidney water reabsorption (SIADH) or in case of excessive water intake. Absolute criteria for diagnosis includes SIADH is characterised by low plasma osmolality <275mOsm/kg, urine osmolality >100mOsm/kg, urine sodium >30 mmol/L, euvolemia, no recent treatment with diuretics, no adrenal, thyroid and pituitary disorder and relatively plasma urea <3.6mmol/L, uric acid <2.4mmol/L, no response to normal saline infusion, and relative criteria are fractional excretion [(UX/PX) x (Plasma creatinine/Urinary creatinine)] of Na, uric acid, urea less than 0.5%, 12%, 55% respectively).
• Hypo-osmolar Hypervolemic (urine sodium concentration >20). Commonly observed in nephrotic syndrome, liver and heart failure.

Clinical presentation:
Most of clinical symptoms are neurological (brain oedema and alteration in brain excitability) which includes headache, seizure, ataxia, lethargy, depressed refl exes, gait disturbances, osteoporosis, vomiting, muscle cramps, coma, brain herniation, respiratory arrest, and death.

Assessment of a child with hyponatremia:
• Assess volume status: Volume depletion or oedematous (low effective arterial volume) and normal or high effective volume
• Assess serum osmalality
• Pseudo-hyponatremia (Plasma osmolality <275- 290 mOsm/kg H2O)
• Dilutional effect: Effective osmoles (Plasma osmolality >290mOsm/kgH2O)
• Differentiate hyponatremia based on normal, low or high total body sodium [acute hyponatremia (usually symptomatic) occurs within 24hrs and chronic (usually asymptomatic) after 48hrs]
• Measure urinary sodium and osmolality low <100 and high >100)
• Assess fl uid loss, medical conditions and medications. Perform physical examination including vital signs and orthostatic changes
• Perform laboratory tests: serum chemistry, lipid profi le, uric acid, liver, adrenal and thyroid function tests, fractional excretion of sodium, uric acid, phosphate, complete blood count
Point to consider while treating are; severity and duration, neurological features and volume status
Excess sodium defi cit= Sodium concentration desired (135mEq/L) – Sodium concentration present x fD x Weight fD for Na+ = 0.6- 0.7, Cl- = 0.2 – 0.3, HCO3 - = 0.4- 0.5
Give half of defi cit fl uid and 1/3rd of maintenance1st 8hrs and next 16 hrs ½ defi cit + 2/3rd of maintenance. Co rrect hyponatremia slowly, 10-12mEq/L in 24hrs. If child is symptomatic give 1.2ml/kg of 3% saline (0.5mEq/mL) x 120- current sodium over 10 minutes and may be repeated 2-3times (goal is to raise serum sodium 5-6mEq/L in 1-2hrs). (0.1-1mg/kg/day). Never correct 6-8mEq/L in 24hr from baseline. Serum sodium can be measured after 15-20 min of each bolus therapy and 4-6hrly after stopping hypertonic saline therapy. As soon as serum sodium reaches 130mEq/L stop hypertonic saline infusion.In children with acute hyponatremia without moderate to severe symptoms cause-specifi c treatment is advocated and offending factor should be removed. Rarely 3% hypertonic infusion is required. Mo nitor serum sodium 2-4hrly, urine output, volume and acid-base status.Children with SIADH (SIAD) needs fl uid restriction by 50% and occasionally needs sodium supplementation with diuretics. Children with cerebral-renal salt wasting (CSRW) have normal or low volume status, high fractional excretion of uric acid and phosphate, blood urea nitrogen, high urine volume and high Bun/ Creatinine. Treatment include isotonic fl uid (normal saline) and fl udrocortisone (0.1-1mg/kg/day).
When saline is required, the amount of sodium required to achieve the desired level in a patient with both hyponatremia and hypokalaemia should include both sodium and potassium concentrations that should not exceed the total required amount of sodium. In euvolemic chronic hyponatremia loop diuretics [It causes excretion of salt free water with salt concentration approximately half normal saline (75mEq/L of sodium + potassium)] therapy with intravenous normal saline may be useful. Frequently monitor urinary volume, sodium and potassium. Hypovolaemic patient may respond to rapid infusion of normal saline therapy. Symptomatic hypervolemic hyponatraemic patient needs sodium infusion and loop diuretics. Vasopressin antagonist may be tried in some.

Hypernatremia >145mEq/L
Hypernatremia is defi ned as plasma/serum sodium >145mEq/L or serum osmolality>295mosm/kgH2O. Serum sodium is calculated by exchangeable serum sodium + exchangeable serum potassium/Total body water (TBW). Hypernatremia can be associated with normal volume status (diabetes insipidus, low (renal or extra renal fl uid loss) or high-volume status (high salt intake, hypersaline infusion, Cushing syndrome, hypertonic dialysis).

Types of hypernatremia
• Hypovolemic (urine sodium concentration <20mmol/L)
• Euvolemic (urine sodium concentration variable)
• Hypervolemic (urine sodium concentration >20mmol/L)
Clinical manifestations are primarily neurological includes encephalopathy, ataxia, nystagmus, conscious impairment, hypertonia, seizure, coma, intracranial haemorrhage and nausea, vomiting, irritability, weakness.

• Assess volume status, history of volume loss and urine output, medications and medical conditions
• History and clinical examination
• Serum and urine sodium, potassium
• Blood urea, serum creatinine and calcium
• Plasma and urine osmolalities
• Brain imaging as per condition
       Differentiate hypernatremia based on normal, low or high total body sodium
• Total free water defi cit: 10mL/kg/ %- SFD
• Free water defi cit (FWD) = 4 mL x Weight in Kg x (sodium concentration present – sodium concentration desired)
New TBW = Previous TBW x Actual serum sodium/Desired serum sodium New TBW – Previous TBW
• 0.6 x Weight in Kg x 1-(145/serum sodium) x 1000 = mL
• Solute Fluid Defi cit (SFD): Total fl uid defi cit (TFD) – Free water defi cit (FWD)
• Sodium defi cit: SFD in litre x proportion from ECF x serum concentration in ECF
• Check serum sodium 2-4 hourly and fall should be not more than 0.6mEq/L per hour
• If serum sodium is more than 175 mEq/L than resuscitation fl uid should have osmolality approximately 15 mEq/L less
• Use 10ml/kg of normal saline if child is in shock
• Calculate TFW, SFD, and FWD
• First 24hrs give maintenance fl uid + ½ FWD + SFD
• Second 24hrs give ½ FWD + maintenance fl uid
• Always measure serum and urine osmolarity, and urine sodium, chloride
• Correction of underlying etiology
• If child is in shock use normal saline for resuscitation

Potassium is 98% located inside cells (2% extracellular) and essential for generating resting potential in neuronal, cardiac and muscle tissues. It is being regulated tightly in between extracellular and intracellular compartments. Kidneys are primarily responsible for potassium excretion (80%), stool (15%) and skin (5%). Potassium plays crucial role in body cells,nerves, and muscles function. Infants older than 30weeks gestation maintain a positive potassium balance to ensure substrate availability for somatic growth. Hyperosmolality causes rise in potassium level by 0.3-.08mEq/L for rise in effective plasma osmalality by 10mosmol/kg. Also, for every decrease in pH by 0.1 unit increases the serum potassium by 0.6mEq/L.

Hypokalaemia (Serum potassium level <3.5mEq/L)
Mild 3.0-3.5mEq/L, Moderate 2.5-3.0mEq/L, Severe <2.5mEq/L

Clinical Manifestations:
Cardiac arrhythmias and conduction defects, ileus, nephrogenic diabetes insipidus, nocturia,polydipsia, rhabdomyolysis, impaired urine concentration, weakness, paralysis, respiratory muscle failure, ECG changes include prominent U wave, ST segment depression, prolonged QT interval, and T-wave fl attening, decrease insulin release (impaired glucose tolerance and protein synthesis), growth and aldosterone hormone secretion.

• Factitious
• Redistribution across cells (transcellular)
• Renal Loss (excess mineralocorticoid activity, renal tubular defects, diuretics)
• Endocrinal
• Inadequate dietary intake
• Skin and gastrointestinal loss
• Transcellular distribution

Medications associated with hypokalaemia:
Diuretics, salbutamol, terbutaline, dopamine, insulin, aminoglycosides, amphotericin B, cisplatin, mineralocorticoids

• Clinical details, physical examination including blood pressure
• Rule out spurious cause of hypokalaemia (leukocyte count >100000/cmm). Rise in blood sugar by 100mg/dL will decrease 1.6mEq/L sodium.
• Acid-base analysis, serum sodium, potassium, calcium, magnesium, phosphate, alkaline phosphatase, and uric acid
• Potassium level falls by 0.3mEq/L for every 0.1 rise in pH
• Urinary sodium, potassium, chloride and creatinine level
• Urinary Na+< 100 mEq/24hr and urinary K+<20 mEq/24hr),Cl-<10mEq suspect extrarenal losses
• Urinary Na+ is >100 mEq/24hr and urinary K+>20 mEq/24hr,Cl->10mEq suspect renal loss
• Urine potassium >20mEq/24hr indicates renal etiology of hypokalaemia
• Spot urine potassium/creatinine >200mEq/gm refl ects renal aetiology (since urinary potassium excretion is variable) and <15mEq/gm refl ects extrarenal loss). Normal excretion of potassium and creatinine are 1 and 0.2mEq/kg/day respectively.

1. Identify underlying cause
2. Minimize use of kaliuretic drugs
3. Prefer oral route: 2-4 mEq/kg/day in two to four divided doses. Assess serum K+ after 6hrs of oral dose. Potassium is irritant to gastric mucosa, thus should be given after meal. Do not crush tablets.
4. Initial aim is to raise serum potassium >3mEq/L
5. Intravenous Protocol
    a. Serum Potassium 3.0-3.5 mEq/L give 0.25mEq/kg IV over one hour
    b. Serum Potassium 2.5-3.0 mEq/L give 0.5mEq/kg IV over two hours
    c. Serum Potassium <2.5meq/L mEq/L give 0.75mEq/kg IV over three hours
    d. Infusion in ½ NS under cardiac monitoring and repeat frequent serum potassium level (one to two hourly)
In case of emergency (3- measured K+ x Body weight x 0.04) as bolus in 1-2 minute followed by infusion 0.015mEq/kg/min
    e. Do not raise potassium concentration >60mEq/L infusion through peripheral line and 80mEq/L in central line
    f. Dilute potassium chloride as much as possible
    g. No sodium bicarbonate should be present in infusion
    h. Monitor serum potassium half way of infusion
6. Avoid giving in dextrose containing solutions to minimize insulin release
7. Do not use more than 80 mEq/L of potassium through peripheral line
8. Do not correct metabolic acidosis till serum K+ is >2.8 mEq/L
9. Maximum rise is plasma potassium is seen after completion of infusion, 50% increase is lost after 2-3hours and 1.5-2hours after oral administration.
10. Monitor renal functions
11. Oral and intravenous potassium should not be given simultaneously.

a. Intravenous: 1 ml Potassium chloride contains 2mEq of K+
b. Potassium citrate 1ml = 2mEq
c. Potassium phosphate (94 mg PO 4 and 4.4mmol K + /mL)
d. Potassium gluconate 15mEq/20 ml
e. Potassium citrate 10mEq/5ml
f. Oral: syrup 1 ml contains 2 mEq of K+
g. Food with high potassium content: Orange, banana, baked potato, dates, milk, spinach, tomato, mango.

Hyperkalaemia (serum >5.5mEq/L)
Clinical features:
Weakness, paralysis (cranial nerves and diaphragm are not involved) , depressed refl exes, bundle branch block, decrease heart rate, hypotension, ventricular fi brillation, cardiac dilatation, cardiac arrest, type IV renal tubular acidosis, decrease renal ammoniagenesis, hyperchloremic metabolic acidosis, intermittent intestinal colic, diarrhoea

• Exogenous intake
• Transcellular shift
• Endogenous (release from cells)
• Decreased renal excretion
• Drugs
• Pseudo-hyperkalaemia

• Urgent ECG: Narrow based, peaked, tented symmetrical T-wave with shortened QT interval, broad fl at P wave, prolonged PR interval, widened QRS complex, sine wave pattern. These ECG changes may be modifi ed by serum calcium, sodium level, ECF, rate of rise in potassium, and pH.
• Clinical details including drug intake, review risk factors and diseases responsible for hyperkalaemia
• ABG and serum electrolytes including chloride, magnesium and calcium level
• Measure Urine pH, potassium/Urine creatinine ratio, chloride
• Calculate GFR
• Plasma aldosterone, renin and cortisol level

Goals of management
• Membrane stabilization
• Cell uptake
• Removal of potassium from body

Goals of management
• Antagonising the effect of hyperkalaemia
• Redistribution of ECF potassium in cells
• Elimination of potassium from body Various methods are;
• Stop all exogenous potassium and offending agents.
• If no heart or heart rate <60/min start cardiopulmonary resuscitation.
• Continue cardiac monitoring using multiparamonitor.
• Give intravenous calcium gluconate 10% (50- 100mg/kg or 0.6mL/kg) or calcium chloride (10- 25mg/kg or 0.2mL/kg) intravenously over 2-3 minutes and faster if life threatening arrhythmias are present or severe hyperkalaemia with ECG changes. Calcium gluconate is preferred over calcium chloride due to risk of tissue necrosis. Onset of effect in 3-5 minutes and last for 60minutes. Repeat dose of calcium may be given if there is no change in ECG within 5min.
• Hypertonic saline 3% may be given intravenous, onset of action is immediate and duration is unknown.
• Insulin+ glucose infusion: Give regular insulin 0.1U/kg + 25% glucose, 0.5 g/kg (2 mL/kg of 25%) over 30 minutes. Intravenous glucose is not indicated when plasma glucose level is > 250mg/ dL. Shift in potassium begins in 15min and peak at 60minutes. Effect lasts for 1-3hours. Expected fall in serum potassium is 0.5-1.5mEq/L. Follow glucose monitoring hourly.
• Increase intracellular pH by increasing minute ventilation (in ventilated children) or give sodium bicarbonate 1-2mmol/kg intravenously over 10min (if pH < 7.2 and renal functions are good). Sodium bicarbonate may not be effective in patient not having metabolic acidosis.
• Nebulised salbutamol in the dose of 2.5 mg for children <25 kg and 5.0 mg for children > 50kg is also given in non-life-threatening situations or IV salbutamol 4-5μg/kg.Peak effects seen within 30 minutes after IV infusion and at 90 minutes of nebulization Expected fall in serum potassium is 0.5-1.5mEq/L by 30-60min and effect lasts for 2hours.
• Furosemide, loop diuretics 1-2 mg/kg and mannitol 0.5g/kg in children with intact renal functions.
• Normal saline 10mL/kg may be given as bolus.
• Fludrocortisone in case of mineralocorticoid defi ciency or resistance.
• Kayexalate is given 1g/kg orally or as retention enema dissolved in 70% sorbitol. Onset of action starts within 1-2hr and effect lasts for 4-6 hrs. Use cautiously in patient with GI problems. Two new potassium binding agents patiromer and sodium zirconium cyclosilicate have been introduced and are under FDA review.
• Dialysis is [haemodialysis is more effective (removes potassium 25-30mEq/hr compared to peritoneal dialysis which removes 10-15mEq/ hr) than peritoneal dialysis]recommended in refractory cases and the effect is immediate and last for 2-8hrs.
• Drugs causing hyperkalaemia: Potassium sparing diuretics, ACE inhibitors, Beta blockers, trimethoprim/ sulfamethoxazole, heparin, NSAIDs.

Phosphate constitute approximately 1% of total body weight (85% in bones and teeth, 14% in soft tissues, and 1% in ECF). The concentration of intracellular phosphate is higher than plasma concentration. 70% of phosphate is in organic form and 30% in physiologically active inorganic form of which 10% is bound to albumin.

It is defi ned as serum phosphate level <2.5mg/dL (mild 2.0-2.5mg/dL, moderate 1.0-1.9mg/dL and severe <1.0mg/dL).

• Shift from extracellular to intracellular compartment
• Decreased intestinal absorption
• Increased renal loss
• Drugs
• Miscellaneous

Clinical manifestations are;
• Neurological: Confusion, irritability, seizure, ataxia
• Cardiac: Cardiomyopathy and decreased cardiac output
• Respiratory: Muscle weakness, respiratory failure, hypoxia
• Bone and skeletal muscle: Pain, rickets, osteomalacia, osteopenia, muscle weakness, rhabdomyolysis.
• Hematologic: Decreased RBC life span, haemolysis, increased oxygen affi nity, thrombocytopenia
• Biochemical: Decreased glucose metabolism, hypomagnesemia, decreased GFR, hypercalciuria, hypophosphaturia

Diagnostic workup
• Serum phosphate, magnesium, calcium, alkaline phosphatase, PTH, and vitamin D3
• Urine phosphate, urinary fraction excretion of phosphate FEPO4 (<5 non-renal, >5 renal etiology), and creatinine
• Imaging studies

Intravenous phosphate 0.16-0.32mmol/kg over 4-6hr (sodium phosphate and potassium phosphate contain 3mmol/mL phosphate and 1mmol contains 3.1mg/dL phosphate) is recommended in symptomatic patients.

It is defi ned as serum level >4.5mg/dL. Causes of true hyperphosphatemia include addition of phosphate from ICF to ECF, decrease renal excretion and drugs effects. Treatment modalities include dietary restriction, use of phosphate binders, rehydration, and rarely haemodialysis. Hypocalcaemia should be managed aggressively.

Magnesium is second most common cation next to potassium in intracellular compartment. 67% magnesium is present in bone, 20% in muscles, 12% other tissues, and 1% in extracellular fl uid. Normal magnesium level is 1.7-2.7mg/dL (1.4-2.3mEq/L) and hypomagnesaemia is defi ned as serum magnesium <1.7mg/dL.

Etiology of hypomagnesaemia
• Decreased intake
• Reduced intestinal absorption
• Increased urinary loss
• Drugs
• Miscellaneous
Clinical manifestation includes nausea, vomiting, muscle weakness, seizures, tremors, cardiac arrhythmias, hyperrefl exia, muscle fasciculations, prolonged QT interval, hypertension, positive Chvostek sign, and death.
• History and physical examination
• Laboratory estimation magnesium, calcium, phosphate, albumin, urinary magnesium and creatinine
• Fractional excretion of magnesium (<5 consider GI loss or cellular uptake and >5 renal loss)
    o Serum magnesium may be normal despite defi cit. In such cases, magnesium loading test (2.4 mg/kg of elemental magnesium in D5W to be infused over a 4 h period, and <70% urinary excretion indicates magnesium defi ciency).

a. Intravenous: magnesium sulphate 50% (500 mg/ mL) and magnesium sulphate 12.5% (120 mg/ mL)
b. Oral: magnesium chloride (64 mg), magnesium oxide-400 (241 mg), magnesium gluconate (27 mg), magnesium carbonate, citrate and lactate.
• Severe symptomatic (<1.0mg/dL): Intravenous 25-50 mg/kg/dose diluted in isotonic saline to10% (osmolality 4000 mOsm/L) over 15-30 minutes (monitor for hypotension, dysrhythmia, skeletal muscle weakness and respiratory depression). Potassium and calcium defi ciency may coexist and it is advisable in severe case fi rst treat symptomatic severe hypomagnesemia. Dose of magnesium is reduced (50%) in renal impairment patients.
• In life threatening situations like torsede pointes and arrhythmia after giving intravenous dose over 2-5 minutes start infusion over next 6 hrs.
• Extreme precaution while using in patients with renal insuffi ciency. Dose may be reduced to half in renal diseases.
• Serial monitoring of serum magnesium.
• Calcium should be available as antidote.
• Correct hypokalaemia and hypocalcaemia.
• In less emergent situations magnesium (>1.0mg/ dL) hemodynamically stable patients dose can be given 0ver 12-24hr.
• Mild asymptomatic patients can be treated with oral medications at a dose of 20-40 mg/kg of elemental magnesium.

Symptomatic hypermagnesemia occurs once levels are >5mg/dL and otherwise >2.7mg/dL is labelled as hypermagnesemia. Signs and symptoms are nausea, vomiting, decreased tendon refl exes, neuromuscular block, bradycardia, myocardial depression, and prolonged QT interval. In asymptomatic patients remove the cause and may need volume expansion and loop diuretics therapy. In symptomatic patients give intravenous calcium gluconate (50-100mg/kg over 4hr) to antagonize cardiac and neuromuscular effects. Haemodialysis is advised in children with renal insuffi ciency.

99% of body calcium is present in bone, 1% teeth, soft tissue and plasma. Calcium in plasma is present in three forms [50%in ionized form and is physiologically active, 40% bound to protein (mainly albumin) and 10% bound to anions (phosphate, bicarbonate, lactate and citrate)]. Every 1gm decrease in albumin, calcium decreases by 0.8mg/dL. Normal calcium level is 8.8- 9.4mg/dL and the ionized calcium value is 1.22mM in children below 6 years and 1.15mM later.

Hypocalcaemia (<8.5mg/dL)
Hypocalcaemia is important complication in severe critical illness including septic shock and calcium homeostasis is maintained by interrelationship among intestinal absorption, bone turn over and renal excretion.

Clinical manifestations:
• Nervous system: Irritability, tonic-clonic seizure, pseudo-tumour cerebri, altered mental status
• Cardiovascular: Arrhythmias, hypotension, prolonged QT interval, cardiomyopathy
• Neuromuscular: Muscle weakness, positive Chvostek sign

• Pseudo-hypocalcaemia
• Low or normal PTH level
• High PTH level
• Drugs
• Miscellaneous

Obtain clinical details including physical examination and vitals
Rule out pseudo-hypocalcaemia
Determine serum total, ionized calcium, albumin, magnesium, phosphate, vitamin D3, PTH level and liver function tests

Formulation of calcium
1. Intravenous
a. Calcium chloride (10%) contains 100 mg/mL of calcium salt or 27.2 mg/mL or elemental calcium.
b. Calcium gluconate (10%) contains 100 mg/mL calcium salt or 9 g/mL of elemental calcium.

2. Oral:
Calcium glubionate (64 mg/g), calcium gluconate (94 mg/g), calcium lactate (130 mg/g), calcium citrate (211 mg/g), calcium acetate (253 mg/g), and calcium carbonate (400 mg/g).
• For symptomatic patients use intravenous calcium gluconate 50-200 mg/kg or 9-18 mg/ kg of elemental calcium diluted in 5% dextrose intravenously slowly over 5-10 minutes under ECG monitoring (look for bradycardia and ventricular irritability) since both solutions have high osmolality (calcium chloride 2000 mOsmol/L and calcium gluconate 680 mOsmol/L). Calcium level starts falling after 30 minutes or calcium chloride 10-20mg/kg/IV over 5-10min through central line.
• Treatment is guide by ionized calcium level.
• If hypocalcaemia persists start infusion 0.3 - 2 mg/kg/hr and monitor plasma calcium 4hrly.
• Remove offending agent or drug.
• Treat hypomagnesaemia if present
• Give calcitriol 0.01 – 0.05 μg/kg/BID till calcium normalizes
• Later start oral calcium 45 – 65 mg/kg/d elemental calcium

Hypercalcaemia is defi ned as serum calcium >10.2mg/ dL with normal albumin level [mild (10.3-11.9mg/ dL), moderate (12.0-13.9), and severe(>14mg/dL)] and affects kidney, brain, peripheral nerves, and gut. Diagnostic workup clinical details, physical examination, estimation of electrolytes, phosphate, alkaline phosphatase, PTH, vitamin D3, 24hr urinary calcium and fractional excretion calcium, complete blood count, ECG, chest x-ray. Treatment includes hydration with normal saline (200-250mL/kg/day) with furosemide induced diuretics (1-2mg/kg/IV every 6hrly), haemodialysis, decrease intestinal absorption (hydrocortisone 1mg/kg/6hrly) and decrease bone reabsorption (calcitonin 10U/kg/IV, zoledronate, gallium citrate).

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