Fluid and electrolyte management is important for perioperative care. Key points include: 1. Body water is divided into intracellular fluid and extracellular fluid. Common IV fluids contain different electrolyte concentrations and osmolarities. 2. Crystalloids expand plasma volume but leave the intravascular space quickly, while colloids remain intravascular longer but do not correct electrolyte deficiencies. 3. Perioperative fluid management aims to replace pre-existing deficits, normal maintenance needs, and abnormal surgical losses like blood loss, third spacing, and insensible losses. Close monitoring of fluid status is important.

1. Fluid And Electrolyte
Management
Presenter
Dr.Mithun.R
Moderator
Dr.Rajeev Sharma

2. Body Water Compartments
• Intracellular water: 2/3 (40%)of TBW
• Extracellular water: 1/3 (20%)of TBW
- Extravascular water[interstitial]: 3/4 (15%)of extracellular
water
- Intravascular water[plasma]: 1/4 (5%)of extracellular
water

3. Electrolyte contents (Commonly used IV fluids)
Solution Electrolyte contents (mEq /l) Osmolarit
* g/L y
(mOsmol.
L-1)
Na+ Cl _ K+ Ca 2+ Glucose* Lactate
Dextrose 5% (D5W) 50 Hypotonic 253
½ NS 77 77 Hypotonic 154
Lactated Ringer 130 109 4 3 28 !! Isotonic 273
N saline 154 154 Isotonic 308
D5 ¼ NS 38.5 38.5 50 !! Isotonic 335
D5 ½ NS 77 77 50 !! Hypertonic 432
3% Saline 513 513 Hypertonic 1026

4. Crystalloids
 Combination of water and electrolytes
Balanced salt solution: electrolyte composition and osmolality similar to
plasma; example: lactated Ringer’s, Plasmlyte, Normosol.
- Hypotonic salt solution: electrolyte composition lower than that of plasma;
example: D5W.
 True solution, No particulate
 Expands IVC adequately (less than colloids), however Small increase in plasma
volume
 Replenishes interstitial compartment
 It leaves IVC faster ( t/2 20-30 minutes)
 Cheap
 Increase GFR
 No risk of allergic reaction

5. Colloids
 Suspension of particle rather than a solution
 High Molecular Weight: Unable to pass through semi permeable membrane
 Remains confined to intra-vascular compartment (at least initially)
 Do not correct water and electrolyte deficiencies
 Examples: hetastarch (Hespan), albumin, dextran

6. Colloids
 Antigenicity & Anaphylactic Reaction
 Blood typing
 Coagulopathy
 Never exceed 1 – 1.5 liter/day (20 ml/kg/day)

7. Colloids
 Most logical choice for intravascular expansion
 Since greater portion remains in IVC & for longer time
( t/2 3-6 hours)
 Less volume is required& initial resuscitation is rapid
 500 ml of colloids expands plasma by 500ml
colloids

8. Colloids (Types)

Blood-derived: Albumin 5%( Heated,
Antigenic)
 Dextran: Dextran 70, Dextran 40

Gelfusine (Anaphylaxis)

Hydroxy ethyl ether
Hetastarch 6%
MW = 450 000
Effective Plasma Expander
Least Antigenicity
&Effect on Coagulation

9. colloid crystalloid
 Advantages : Smaller infused  Advantages : Lower cost. Greater
volume. urinary flow. Replaces interstitial
Prolonged increase in plasma fluid.
volume.
Less cerebral edema.
 Disadvantages :Greater cost
Coagulopathy(dextran>HES).  Disadvantages :Transient
Pulmonary edema hemodynamic improvement.
(capillary leak states). Peripheral edema(protein dilution).
Decreased GFR. Pulmonary edema
Osmotic diuresis (low molecular (protein dilution plus high PAOP)
weight dextran)

10. Practical Fluid Balance
Rule 1
Water without Na expands the TBW (enter both ICF &
ECF in proportion to their initial volume)
H2O H2 O H2 O
ICF ECF

11. Practical Fluid Balance
Rule 2
All infused Na + can not gain access to the ICF Because
of the Sodium Pump
Na +
Na +
Na +
Na +
Na +
Na +
ICF ECF
Isotonic = NO Water Exchange
Isotonic = NO Water Exchange

12. Practical Fluid
Balance
Rule 3
Change in tonicity of Na solutions (relative to Plasma)
causes water exchange
a. Hypotonic saline (¼ NS)
Hypotonic = Water Exchange
Hypotonic = Water Exchange
H 2O

13. b. Hypertonic solution
Hypertonic = water exchange
Hypertonic = water exchange
H 2O

14. Simple guide line for replacement
 Prolonged vomiting and nasogastric suction : fluid of choice normal
saline. If urine out put is adequate, potassium is added to it after 2 nd day.
Isolyte G can be given in an amount same as upper GI loss, provided
urine output renal status is normal.
 Fluid loss due to small bowel fistulas causing diarrhorea : RL is ideal may
need additional bicarbonate and potassium supplementation to treat
metabolic acidosis and hypokalemia.
 Loss of blood : if volume is less replacement is done with three times
volume of isotonic saline or RL. But if loss is greater , it needs blood or
colloids for replacement.

15. Orthostatic Hypotension
• Systolic blood pressure decrease of greater than 20mmHg from
supine to standing
• Indicates fluid deficit of 6-8% body weight
- Heart rate should increase as a compensatory measure
- If no increase in heart rate, may indicate autonomic dysfunction
or antihypertensive drug therapy

16. Perioperative Fluid Therapy
Pre-existing deficits
Normal maintenance requirements
Abnormal losses

17. Pre-existing losses
 Fasting (maintenance x no. of HR)
 Bowel preparation ---1L fluid loss
 Measurable fluid losses—NG suctioning,vomiting,ostomy output
 Preoperative Bleeding, fistulae
 Diarrhea
 Diuresis – ketosis
 Occult losses

inflammatory traumatic edema

Sequestration in third comp.
 Increased insensible losses (0.5 ml/kg/hr)

Fever (add 12% for 1oC)

Hyperventilation

Sweating

18. Normal Maintenance
requirements
 Hypothetical 2000 ml/ day
 Volume of 30 – 35 ml.kg-1day-1
Weight Rate
 Solutions: D5 or D5 ½ NS
10 kg 4ml/kg/h
10 – 20 kg +2ml/kg/h
> 20kg +1ml/kg/h
 1.5 -2 ml/kg/h

19. Surgical Fluid Losses
 Blood loss
 Obligatory losses of fluids
 Redistribution – third space
 Evaporation

20. Blood Loss
• Replace 3 cc of crystalloid solution per cc of blood loss (crystalloid
solutions leave the intravascular space)
• When using blood products or colloids replace blood loss volume per
volume

21. Third Space Losses
• Isotonic transfer of ECF from functional body fluid compartments to non-
functional compartments.
• Depends on location and duration of surgical procedure, amount of tissue
trauma, ambient temperature, room ventilation.

22. Replacing Third Space Losses
• Superficial surgical trauma: 1-2 ml/kg/hr
• Minimal Surgical Trauma: 3-4 ml/kg/hr
- head and neck, hernia, knee surgery
• Moderate Surgical Trauma: 5-6 ml/kg/hr
- hysterectomy, chest surgery
• Severe surgical trauma: 8-10 ml/kg/hr (or more)
- AAA repair, nehprectomy

23. Monitoring fluid therapy
1.skin and tongue: warm extremities and normal
elasticity of skin. 2.sensorium:improvement of
anxiety and restlessness. 3.urine output: U.O. >30-50ml/hr
in adults or >.5 to 1.0 ml/kg/hr in children in absence of glycosuria or osmotic
diuresis. Increased urine output with decreasing urine specific gravity and
omolality are other dependable parameters
4.pulse rate: correction of tachycardia to pulse rate <110/min. change from
low volume collapsing pulse to bounding pulse
5.blood pressure
6.decreasing hematocrit
7.blood urea and serum creatinine: both will become normal.
8. increase in urinary Na excretion >25 mEq/L

24. Post –operative fluid therapy
 Depends upon clinical judgement of the patient’s status
 Goal of fluid therapy: to maintain blood pressure (>100/70 mm of Hg),
pulse rate <120/min and hourly urine flow between 30-50 ml along with
normal temperature, warm skin, normal respiration and sensorium.
 Depends upon type minor, major and nature of surgery
short operative procedure and donot require handling of intestine
or viscera with little morbity will require only maintenance I.V. fluid to
correct for the NPO state. After 4-5 hrs oral fluids is restarted and I.V.
fluid is not needed i.e. hernia, minor orthopedic operations on limbs,
minor plastic surgery
Patients with major surgeries where intestinal viscera need rest
requires postoperative I.V. fluids for a few days. After ensuring normal
movement of intestine, oral fluid intake is restarted.
 Where handling of intestine is not required I.V. fluid is required for 24-48
hrs e.g. cardiac surgery,coronary bypass surgery, total hip replacement

25. Routine postoperative orders of I.V.
fluid for first three days
 First 24 hrs of surgery : 2 liters 5%-dextrose or 1.5 liters 5%-
dextrose +500 ml isotonic saline.
 Second post operative day: 2 liters of 5%-dextrose +1liter
0.9% saline.
 Third post operative day: similar fluid +40-60 mEq potassium
per day.
 Maintenance fluids should be administered at a steady rate
over an 18 to 24 hour period.

26.  Infants respond to dehydration with decreased blood
pressure but without increased heart rate.
 Preoperative fluid deficit replaced with RL or ½ NS

27. Fluid therapy in special
surgical problems
 Turp syndrome: correction of severe and symptomatic
syndrome
hyponatremia should be done with slow administration of 3%
hypertonic saline with I.V. frusemide. Hyper tonic saline must be
given very slowly in divided doses with monitoring of serum
sodium. Rapid administration of saline leads to pulmonary
oedema and central pontine myelinolysis. In general TURP
syndrome can be corrected with 200ml of 3% saline

28. TURP SYNDROME
Defined as serum Na+ <125mEq/L with two or more
clinical symptoms and signs.
Etiology - Intravascular absorption of irrigation fluid
absorption of free water  dilution of serum sodium
Regional anaesthesia preferred over General
anaesthesia.

29. Fluid therapy in neurosurgery
 Isotonic saline, 5% albumin and 6% hestarch are iso to
hyperosmotic,so they have minor effect on the brain’s water
content or ICP. So these lfuids are safe to infuse.
 Osmolality of RL is 274 mOsm/L and 5%-dextrose is 278
mOsmol/L. as both of them are hypotonic, they can increase
ICP and cerebral oedema. So these fluid should be avoided or
should be used judiciously.
 5%- dextrose is hypotonic accelerates ICP and cerebral
oedema.in acute ischemic brain damage produces more
lactic acid free radicals which further damages the brain.

30. Guidelines of fluid management
of increased ICP
 Acute phase: mannitol is main stay of therapy.
Prolonged administration of mannitol should be
avoided.
 Maintenance therapy: fluid restriction and diuretics are
the mainstay of maintenance therapy for ICP. The initial
aim is to produce isovolumic hyperosmolality i.e. elevate
serum osmolality without reducing the intravascular
volume.The best fluid for this purpose is isotonic saline
with added potassium chloride.

31. Fluid therapy in Burns
 Fluid resuscitation in first 24 hours
 Fluid therapy from 24 to 48 hours
 Fluid therapy after first 48 hours
 Indication of I.V. resuscitation are :
1. adults with >15-20% burns
2. child with 10% burns
3. electric burn with haemochromogens in the urine
4. the extremes of age or elderly patients with preexsisting
cardiac or pulmonary disease
 During initial period fluid resusitation sodium rich I.V. fluid
in large quantity is required.

32.  RL is the most preferred fluid for initial fluid resuscitation
 Volume required=4×%BSA×body weight 24 hrs period from
the time of burn accident
 Out of total fluid requirement for 24hours half is given first 8
hrs post burns and remaining half is given over the next 16
hrs
 Electrolyte-free fluid i.e 5%-dextrose are avoided for initial
fluid resuscitation
 Colloid infusion is either ineffective or destructive in early
period
 BT is usually avoided initially

33.  During the second post burns day the volume of fluid infused
per hour should be roughly reduced by 25-50%
 Fluid infused – 5% dextrose but if sodium supplementation is
needed RL or .45% saline can be added
 The amount colloid infused after 24 hrs depends on degree of
burns volume roughly 0.3-0.5 ml/kg/% of burns. Among
colloids infusion albumin is often preferred

34. Fluid therapy after 48 hrs
 Is the sum of normal maintenance requirements plus
replacements of abnormal losses
 Maintenance requirement contains water, sodium 3mEq/kg
and potassium 2mEq/kg
 5% dextrose volume required is 1ml/kg/% burns. Albumin
with aim to maintain serum albumin >2.5gm/dl.

35. Summary
• Fluid therapy is critically important during the perioperative
period.
• The most important goal is to maintain hemodynamic
stability and protect vital organs from hypoperfusion (heart,
liver, brain, kidneys).
• All sources of fluid losses must be accounted for.

37. SODIUM (Na + )
 Major cation of ECF ; Normal – 135-145mEq/L
 Determines ECF & ICF Osmolality
Serum osmolality = 2x Na + + glucose/18 +
urea/2.8
Normal – 275-290mOsm/kg
 Maintain ECF volume and thus Blood pressure

38. HYPONATREMIA (Na+< 135mEq/L+)
Hypervolemic Euvolemic
Hypovolemic
•CHF
Extra renal loss
•SIADH
Renal loss
•Hypothyroidism
(urine Na+
•Nephrotic syndrome (urine Na+ >15mEq/L)
<15mEq/L ) •Glucocorticoid
•Excessive diuretics
•Cirrhosis
deficiency
•Salt losing
TURP syndrome
Vomiting
• •Psychogenic polydypsia
Diarrhoea
•
Renal Failure
• nephropathy
•Pseudohyponatremi
( urine Na+ >20mEq/L) •Diabetic ketoacidosis
•Peritonitis a
•Cerebral salt wasting
Normal osmolality
•Tube drainage
Fistula
• syndromehyperlipidemia
obstruction
• hyperproteinaemia
Burn wound
•  High osmolality

39. CLINICAL FEATURES
Mild Moderate Severe
135-130 130-125 <125mEq/L
mEq/L mEq/L
Anorexia Personality Drowsiness
Changes
Headache Muscle Cramp Diminished
reflexes
Nausea Muscular Convulsions
weakness
Vomiting Confusion Coma
lethargy Ataxia Death

40. TREATMENT
HYPONATREMIA (correct underlying
etiology)
HYPOVOLEMIA OEDEMATOUS
EUVOLEMIA
Salt and water No salt Water restriction
supplementation Water restriction
Loop diuretics

41. TREATMENT
 Chronic asymptomatic hyponatremia (>48hrs):
 Rate of correction - 0.5 to 1.0
mEq/L/hour.
 MAX 8mEq/L per day.
 Rapid correction  Central pontine
demyelination
Dysarthria, dysphagia, flaccid paralysis or coma

42. TREATMENT
 ACUTE hyponatremia with severe neurological
symptoms
 Rapid correction with hypertonic saline
 1.5 – 2mEq/L /hr for first 3-4 hours
 Other supportive therapy for neurological symptoms
 Correct until

Symptoms subside

Safe plasma Na+ concentration : 120-125mEq/L
 Na+ Requirement = (140- Na+ )x Body weight x 0.6

43. HYPERNATREMIA
(Na + >145mEq/L)
 Etiology – Usually : water deficit
 Excess water loss

Insensible loss
 Dermal -: heat exposure, severe burns
 Respiratory -: patients on mechanical
ventilators.

44. 
Renal loss
 Diabetes insipidus
 central (ADH deficiency): pituitary surgery, basal skull
fracture and severe head injury
 Nephrogenic – drugs (lithium, demeclocycline,
amphoteracin B,) hypokalemia, hypercalcemia etc
 Excessive diuretics
 Uncontrolled diabetes mellitus

Gastrointestinal loss : osmotic diarrhoea

45.  Water deficit due to impaired thirst
 Primary hypodypsia, confused or
comatous condition
 Sodium Retention
 Excessive I.V. Hypertonic NaCl or NaHCO3

46. CLINICAL FEATURES
 Polyuria and thirst
 Neurological symptoms: altered mental
status, weakness, neuromuscular irritability,
focal neurological deficit, seizures & coma

Hypertonicity  contracts ICF volume  brain cell
volume  subarachnoid or intra-cerebral hemorrhage

47. TREATMENT
 Restoration of ECF volume:
 Water deficit :
Plasma Na+ concentration – 140 X total body
water
140
 Rate of correction : 0.5mEq/L/hr and not more than 12 mEq/l
over 24 hours

48. ANAESTHETIC
IMPLICATION
 Increases the MAC of inhaled anaesthetic
agents:
 Enhanced sodium conductance during
depolarisation of excitatory membranes.

49. POTASSIUM
 Determines excitability of nerves and muscle cells
including the myocardium.
 Most abundant intracellular cation: 98% intracellular.

50. Hypokalemia (K+ < 3.5mEq/L)
Etiology
Poor Non renal Renal loss Redistribution
intake loss
•Anorexia •Vomiting Diuretics
• Metabolic
nervosa • diarrhoea osmotic diuresis
• alkalosis, insulin,
Starvation
• excessive
• • salt wasting nephropathy β2 agonist,
alcoholism
• sweating, • Mineralocorticoid excess Hypokalemic
large
• (primary or secondary), periodic
nasogastric Cushing’s syndrome, paralysis,
aspiration • Steroid therapy Vitamin B12
** Surgical stress reduces
Magnesium deficiency
•
therapy,
serum K by 0.5 mEq/L
+
Amphoteracin B
•
Li overdose

51. Clinical Features
 Commonly : Fatigue, myalgia and muscular weakness of lower
extremity
 Smooth Muscle : Constipation, ileus or urinary retention
 Progressive weakness, hyporeflexia, hypoventilation( due to
respiratory muscle involvement)
 Polyuria due to nephrogenic diabetes insipidus
 Increased ammoniagenesis : precipitates hepatic
encephalopathy in patients with hepatic failure

52.  Arrythmia
 Early changes

Flattening or inversion of T waves

Prominent U waves

ST segment depression

Prolonged QT interval
Flattening of T waves

53. Flat T waves
U waves

54.  SEVERE HYPOKALEMIA
 Prolonged PR interval
 Decreased voltage
 Widening of QRS
 Ventricular arrythmia :VPC, ventricular
tachycardia

55. TREATMENT
 Prevention of K+ Depletion
 Patients receiving Digitalis, long term diuretics or
large dose steroids
 Beware in special conditions like
 hepatic failure, previous myocardial infarction or IHD,
Diabetes Mellitus
 Post operative patients should receive 40 -50

56. TREATMENT
 When to Treat
 3.5 to 4 mEq/L :

No potassium supplementation

Add potassium sparing diuretics or decrease
dose of diuretics
 3 to 3.5 mEq/L :

Treat in high risk groups
 <3 mEq/L :

Needs definitive treatment

57. IV KCl Therapy
 Reserved for symptomatic and severe cases
 Common Guidelines
 Continuous ECG monitoring
 Avoid till urine output is established
 Don’t give > 10- 20 mEq/L/ hour (typically 0.5mEq/kg/hr)
( 10ml of 15% KCL – 20 mEq/L)
 Don’t give > 40 mEq/L
 Don’t give more than 240mEq/ day

58. TREATMENT
 Treatment of acidosis with NaHCO3 may
aggravate or precipitate hypokalemia.
 KCL infusion : In NaCl not in 5% Dextrose
D5  insulin release  K+ shift ICS 
aggravates hypokalemia(0.2-1.4mEq/L)
 20mEq/hr of K Cl raises K+ by 0.25mEq/L
80% of this enters cells.

59. HYPERKALEMIA (K+ >
5.5mEq/L)
 Etiology
•Increased intake
I.V fluids containing potassium
I.V.fluid Isolyte- Isolyte Isolyte- Isolyte- Ringer’
s M -P G E s
lactate
Potassiu
m 35.0 20.0 17.0 10.0 4.0
(mEq/L)
High potassium containing foods
Potassium containing Drugs

60. HYPERKALEMIA
• Tissue breakdown
 Bleeding into soft tissue, G.I.tract or body cavities
 Hemolysis, Rhabdomyolysis
 Catabolic State
• Shift of potassium

Tissue damage

Metabolic acidosis

Uncontrolled Diabetes due to insulin deficiency

Aldosterone Deficiency

Hyperkalemic periodic paralysis, Succinylcholine

61. HYPERKALEMIA
• Impaired Excretion
 Acute renal failure or chronic renal failure
 Drugs : Potassium sparing diuretic, ACE inhibitors, AT-
II inhibitors, NSAIDS, heparin, cyclosporine
 Reduced tubular excretion : Addison’s disease,
hyporeninemic hypoaldosteronism and amyloidosis
 Effective circulatory volume depletion
• Pseuhohyperkalemia
 Traumatic haemolysis during blood drawing
 Thrombocytosis, marked leucocytosis

62. CLINICAL FEATURES
 Muscle weakness  hyporeflexia  paralysis affecting legs, trunk
and arms (in that order) and at last respiratory muscles.
 Muscles supplied by cranial nerves are spared
 Cardiac Arrythmia
 6-7 mEq/L : Tall peaked T waves
7-8 mEq/L : loss of P waves, widening of QRS complex
8-10 mEq/L : QRS merges with T waves forming sine waves
>9mEq/L : AV dissociation, Ventricular tachycardia or
fibrillation , Diastolic arrest.

64. CLINICAL FEATURES
 Lethal hyperkalemia during anaesthesia:
Reperfusion of a large vascular bed after a
period of ischemia. ( usually 4 hrs)
 Ischemia  acidosis  shift of K+ from ICF to
ECF

65. TREATMENT
 Stop exogenous sources : K+ containing IV fluids, drugs etc.
 For mild elevation (5 to 6 mEq/L), remove potassium from the body with
 Diuretics : 40-80mg I.V
 Cation exchange Resins:
 Sodium polystyrene sulphonate (Kayexalate ) 15 to 30 g in 50 to 100 mL
of 20% sorbitol either orally or by retention enema.

Exchange sodium for potassium in G.I.tract
 Each gram binds 1mEq of K+ and releases 2-3mEq of sodium.
 Caution : CHF and volume overload patients

66. …TREATMENT
 For moderate elevation (6 to 7 mEq/L) , shift potassium
intracellularly with
 Glucose plus insulin:
 mix 25 g (50 mL of D50) glucose and 10-20 U regular
insulin and give IV over 15 to 30 minutes
 Initial bolus followed by continuous infusion with 5%
dextrose @ 100ml/hr to avoid late hypoglycemia.
 K+ falls by 0.5-1.5mEq/L. effect begins in 15 mins and
peaks at 60 mins. Lasts for 4-6 hours.

67. …TREATMENT
 Sodium bicarbonate: 50 mEq IV over 5-10
minutes
 less effective for treatment of patients with renal
failure : do not tolerate the sodium load and
resultant volume expansion
 Nebulized albuterol: 10 to 20 mg nebulized over
15 minutes or inj Salbutamol 0.5mg by I.V.infusion

Preferred in ESRD for rapid lowering

Tachycardia : I.V therapy > nebulization.

68. …TREATMENT
 Severe elevation (7 mEq/L with toxic ECG
changes)
 Calcium chloride (10%) 500 to 1000 mg (5 to 10 mL) IV
over 2 to 5 minutes or Calcium Gluconate 10% 10-20ml
over 5-10mins
 to reduce the effects of potassium at the myocardial cell
membrane (lowers risk of ventricular fibrillation [VF])
 Avoid if patient is on digitalis.

69. TREATMENT
 Dialysis
 Hemodialysis: removal rate – 35mEq/hr
 Peritoneal dialysis : 15 -20% as effective
as hemodialysis.

70. CALCIUM 10+/-0.5 mg/dl
 Mediates :
 Muscle contraction
 Exocrine, endocrine and neurocrine secretions
 Cell growth
 Transport and secretion of fluid and electrolytes.
 99% present in bones, 1% in cells and 0.15% in ECF.

71. HYPOCALCEMIA
 Weakness
 Circumoral and distal paraesthesia
 Muscle spasm : carpopedal spasm, tetany.
 Mental changes: irritability, depression and
psychosis.

72. CHOVSTEK’S SIGN

73. TROUSSEAU’S SIGN

74. ECG CHANGES

75. …. CLINICAL FEATURES
 Severe hypocalcemia : lethargy, confusion ,
laryngospasm, seizures or irreversible heart
failure.
 Cataract and calcification of basal ganglia.

76. TREATMENT
 Acute Management
 10% calcium gluconate, : 10ml – 93mg of elemental calcium
 10% calcium chloride: 10ml - 273mg of elemental calcium
 10% calcium gluconate 10-20 ml IV over 10 minutes.
+ IV infusion of 540 to 720 mg of elemental calcium (58
to 77 mL of 10% calcium gluconate) in 500 to 1000 mL D5W @
0.5 to 2 mg/kg/ hour (10 to 15 mg/kg). OR
 10% calcium chloride 5 mL () over 10 minutes, followed by
36.6 mL (1 g) over the next 6 to 12 hours IV.

77. TREATMENT
 Measure serum calcium every 4 to 6hours.
 Aim to maintain the total serum calcium concentration at 7
to 9 mg/dL.
 Correct abnormalities in magnesium, potassium, and pH
simultaneously.
 Massive transfusion : for every 4 units of blood or rate>
1.5ml/kg/min – 10ml of 10% calcium gluconate.
 Extravasated calcium chloride – severe tissue
destruction : Calcium gluconate preferred for peripheral
venous administration.

78. HYPERCALCEMIA
 Serum calcium - 12 to 15 mg/dL.
 Neurologic symptoms :
 Depression, weakness, fatigue, and confusion at lower
levels.
 At higher levels : Hallucinations, disorientation,
hypotonicity, seizures, and coma.
 Renal
 Polyuria , nocturia, stone formation

79. CLINICAL FEATURES
 Cardiovascular symptoms:
 Upto 15mg/dl myocardial contractility increases
 The QT interval typically shortens when the serum calcium
is> 13mg/dL.
 PR and QRS intervals are prolonged.
 Atrioventricularblock may develop and progress to
complete heartblock and even cardiac arrest when the total
serum calcium is > 15 to 20 mg/dL.
 Hypercalcemia can worsen digitalis toxicity and may cause
hypertension.

80. CLINICAL FEATURES
 Gastrointestinal symptoms:
 Dysphagia
 Constipation
 peptic ulcers, and
 pancreatitis
 Muscle weakness due to hypercalcemia:
 decrease doses of non depolarising muscle relaxant.

81. TREATMENT
 Treat if
 Symptomatic and > 12mg/dl
 >15mg/dl
 Immediate therapy
 Restore intravascular volume & promote excretion

infusion of 0.9% saline at 300 to 500mL/h (saline diuresis)
until any fluid deficit is replaced and diuresis occurs (urine
output 200 to 300 mL/h).

After adequate rehydration rate to 100 to 200 mL/h.

82. TREATMENT
 Hemodialysis is the treatment of choice to rapidly
decrease serum calcium in patients with heart failure or
renal insufficiency.
 Chelating agents (eg, 50 mmol PO4 over 8 to 12hours or
EDTA 10 to 50 mg/kg over 4 hours) may be used for
extreme conditions.
 Furosemide (1 mg/kg IV) but avoid thiazide diuretics.

83. MAGNESIUM
 Magnesium is the fourth most common mineral and the
second most abundant intracellular cation (after potassium) in
the human body.
 Normal serum Mg2+ 1.8 – 3mg/dl
 Magnesium is necessary for the
 movement of sodium, potassium, and calcium into and out of
cells
 magnesium plays an important role in stabilizing excitable
membranes.

84. Mg 2+ in ANAESTHESIA
 PNS –
 interferes with release of neurotransmitters at all synaptic juctions
 Potentiates action of local anaesthetics.
 Neuromuscular Junction
 Significant presynaptic neuromuscular blockade
 Enhance action of nondepolarizing muscle relaxant
 Precipitate weakness in patients with myasthenia gravis and
Eaton-Lambert syndrome
 Prolongs action of depolarizing neuromuscular blockers.
 Prevents K+ release by succinylcholine

85. Mg 2+ in ANAESTHESIA
 Severe acute asthma – effective
bronchodilator
 Obstetric practice
 Powerful tocolytic – Manage premature
labour.
 Prophylaxis and treatment of eclampsia.

86. HYPOMAGNESEMIA
<1.8mg/dl
 Muscular tremors and fasciculations
 Ocular nystagmus
 Tetany
 Altered mental state
 Cardiac arrhythmias such as torsades de pointes
(multifocal ventricular tachycardia)
 Ataxia, vertigo, seizures, and dysphagia.

87. TREATMENT
 For severe or symptomatic hypomagnesemia: 1 to
2 g of IV MgSO4 over 5 to 60 minutes.
 Followed by continuous infusion of 1mEq/kg/24hours.
 For torsades de pointes with cardiac arrest : 1 to 2
g of MgSO4 IV push over 5 to 20 minutes.
 For seizures - give 2 g IV MgSO4 over 10 min.
 Administration of calcium is usually appropriate
because most patients with hypomagnesemia are
also hypocalcemic.

88. TREATMENT
 Caution and monitoring MgSO4 therapy
 Check deep tendon reflex every 15mins (knee
jerk)
 Periodic monitoring of serum Mg concentration.
 Reduce dose in renal failure.
 Contraindicated in heart block or extreme
myocardial damage
 Maintain urine output – 100ml/4hours
 Overtreatment  10% calcium gluconate 10-20ml
followed by fluid loading and diuretics.

89. HYPERMAGNESEMIA
(>3mg/dl)
 Etiology
 Renal failure patients : most common cause
 Treatment of pre-eclampsia with I.V MgSO4.
 ARF with acute rhabdomyolysis
 Diabetic ketoacidosis without treatment.

90. CLINICAL FEATURES
 Neuromuscular Manifestations
 Muscular weakness muscular paresis leading to
respiratory depression and respiratory failure.
No effect on central respiratory drive.
 Cardiac manifestation
 Hypotension: peripheral vasodilatation
 Bradyarrhythmia
 Cardiac asystole

91.  ECG changes
 Prolonged PR interval,
 QRS duration and QT interval
 Complete heart block

92. TREATMENT
 Eliminate source
 10% calcium chloride (5 to 10 mL [500 to 1000 mg] IV) or 10%
calcium gluconate will often correct lethal arrhythmias.
 IV saline diuresis (administration of IV normal saline and furosemide
[1 mg/kg]) can be used to increase renal excretion of magnesium
until dialysis can be performed.
 Dialysis is the treatment of choice for severe hypermagnesemia.
 Artificial respiration

93. PHOSPHORUS
 Major Buffer anion for ICF & ECF
 Rapid shifting can occur
 Functions
 Muscle, red blood cells & nervous system
 Maintains acid-base balance
 Adequate renal function necessary to maintain
normal balance
 90% excreted by kidneys

94.  PTH regulates levels
 Increases resorption from bone
 Inhibits reabsorption in renal tubules
 Increases absorption from GI tract
 Calcium and phosphate or inversely proportional
 PTH = PO4³¯& Ca+
 Normal: 2.8 - 4.5 mg /dl

95. HYPOPHOSPHATEMIA < 2.8mg/d
l
 Paresthesia
 Muscle pain/weakness
 Acute respiratory failure
 Confusion/coma
 Cardiac: arrhythmias, decreased SV

96. TREATMENT
 Diet/supplements (mild)
 IV replacement (severe)
 Major nursing role is teaching diet
 Monitor for diarrhea if on supplements


97. HYPERPHOSPHATEMIA
(> 4.5mg/dl)
 Tachycardia
 Restlessness
 Anorexia, Nausea and vomiting
 Tetany
 Tingling & numbness of fingers/lips
 Muscle spasms

98. TREATMENT
 Diet restrictions
 Milk, meat,fish
 Administer phosphate binding products
 Calcium acetate and calcium carbonate or
aluminum hydroxide
 Dialysis in severe renal failure.