This is a lecture note on fluid and electrolytes.

1. Hale Teka, OB-GYN Resident
Fluid and Electorlytes
Hale Teka,
Year-1 Resident,
Mekelle Univeristy,
College of Health Sciences,
Dep't of Obstetrics and Gynecology

2. Hale Teka, OB-GYN Resident
1. To understand the underlying physiology and
pathophysiology of fluid balance for appropriate
fluid therapy
2. To understand properties of IV crystaloids and
colloids
3. Discuss the common electrolyte abnormalities
and their treatments
Objectives

3. Hale Teka, OB-GYN Resident
• Marine life
– Rich in salt and water
• Terrestrial
– Low in salt and water
• Physilogic challenges of evolution in water and
salt maintenance
– External sea
– Internal sea (ECF)
• Constant chemical environment, called the
‘milieu interieur'
Introduction

4. Hale Teka, OB-GYN Resident
• In the Milieu interieur
– Pump sodium and retain potassium
– This is energy consuming process and is
inherent to all cells

5. Hale Teka, OB-GYN Resident
• Fluid balance
– External Balance
• Between external and internal environment
– Internal Balance
• Between various body fluid compartments
of internal environment, examples between
–Intravascular and Interestitial
–ECF and ICF
–ECF and the gut and other internal
spaces

6. Hale Teka, OB-GYN Resident
• Water
– 60% of the body weight of an average adult
• 40% intracellular
– Muscle cells contain 75% water and fat cells have
<5% water
• 20% extracellular
– 5-7% intravascular
» 40-45% intracellular
» 55-60% extracellular
– 14% interestitial
– Lower percentage in obese people and more in
infants
• Adipose tissue contains less water than lean
tissue
Normal Anatomy and Physiology

7. Hale Teka, OB-GYN Resident
• Body Fluid Compartments
Plasma (5
%)
Interstitial
fluid( 15 %)
Intracellular
(40 %)

8. Hale Teka, OB-GYN Resident

9. Hale Teka, OB-GYN Resident
• Functions of body fluid
– Medium for transport
– Cellular metabolism
– Solvent for electrolyte and other constituents
– Helps maintain body temperature
– Helps digestion and elimination
– Acts as lubricant

10. Hale Teka, OB-GYN Resident

11. Hale Teka, OB-GYN Resident
• Cell membrane
– Separates ECF and ICF
– Pumps sodium out ensuring sodium remains
largely in the ECF
• In the ECF: Sodium, Chloride, Bicarbonate
– Draws potassium in to neutralize large
anions such as protein and glycogen, which
cannot escape the cell
• In the ICF: Potassium, protein, glycogen
–Gibbs-Donnan Equilibrium

12. Hale Teka, OB-GYN Resident
• Capillary membrane
– Separates intravascular and extravascular
component
– Has micropores for slow rate scape of
albumin at 5%/hr
• Returned to the circulation via the
lymphatics at the same rate
–Maintained steady state of equilibrium
– Hydrostatic pressure
• Drives fluid out,
– Oncotic pressure
• Draws fluid in
»Starling effect

13. Hale Teka, OB-GYN Resident

14. Hale Teka, OB-GYN Resident
Category of FLuids by Osmolality
• Hypertonic fluids
– Higher concentration of particles
– Have higher osmotic pressure ( ICF TO ECF)
thus cells wil shrink
– Not used for cardiac or renal diseases
– D5% NS,D5%RL

15. Hale Teka, OB-GYN Resident
• Hypotonic Fluids
–Low concentration of fluid
–Have lower osmotic pressure ( ECF TO
ICF) thus cells will swell
–Not used in cases of raised ICP or risks
of raised ICP
–0.33 % NS,0.45 % NS

16. Hale Teka, OB-GYN Resident
• Isotonic Fluid
– Have the same concentration of particles (
280-290 mOsm/Kg)
– Similar osmotic pressure ,cells neither swell
nor shrink
– Expands both intracellular and extracellular
volume
– Commonly used crystalloids
– 0.9 %NS,D5W,RL

17. Hale Teka, OB-GYN Resident
• Other osmotic factors
– Albumin
• Has osmotic properties called colloid pressure
• Draws water from interstitial compartment to
intravascular compartment.
• Helps maintain BP

18. Hale Teka, OB-GYN Resident
• Internal Fluid Balance
– Flux of fluid and electrolytes between ECF
and the GIT
– Constant secretion and reabsortion

19. Hale Teka, OB-GYN Resident

20. Hale Teka, OB-GYN Resident
External Fluid Balance

21. Hale Teka, OB-GYN Resident
Intake
• Our intake is governed by
– Insufficient intake
– Increased loss
– High salt intake
• The rule of intake is
– Zero balance in which intake and output are
equal
– Replace insesible and other loses, and meet
the kidney's needs (Volume Obligatoire)
– Physiologic osmolality => 280-290 mOsm/Kg

22. Hale Teka, OB-GYN Resident
• Excessive intake
– Hazardous
– Overwhelm the kidney
– Oedema when the ECF has been expanded
by at least 2-3 litres

23. Hale Teka, OB-GYN Resident
Normal Maintenance Requirements

24. Hale Teka, OB-GYN Resident

25. Hale Teka, OB-GYN Resident
Output
• Insesible loss
– Water loss through the lungs and skin
– 0.5-1 L/day + if hot climate, fever and
exertion 50 mmol/ liter of salt
• GI loss
– Water loss with stool
– Intestines effectively absorb water
– 100-150 mL/day

26. Hale Teka, OB-GYN Resident
• Kidney
– Main organ for regulating fluid and electrolyte
balance as well as excreting the waste
products of metabolism
– controlled by pressure and osmotic sensors
and the resulting changes in the secretion of
hormones

27. Hale Teka, OB-GYN Resident
• Minimal fluctuations in water and salt intake
– small changes in plasma osmolality
• Osmoreceptors triggered
–Changes in thirst and renal excretion of
salt and water
• If blood or ECF volumes are threatened
– Volume receptors are triggered overriding
the osmoreceptors
• In the presence of large volume changes,
therefore, the kidney is less able to adjust
osmolality, which can be important in some
clinical situations

28. Hale Teka, OB-GYN Resident
Electrolyte content of GIT and skin secretions

29. Hale Teka, OB-GYN Resident
• Excessive losses
– Sweating
– Insensible loss in hot climates
– Gastroenteritis

30. Hale Teka, OB-GYN Resident
• Water
– Osmoreceptors are located in the
hypothalamus
• Sense the osmolality of plasma
– Depending on the osmolality hypothalamus
sends signal to the posterior pituitary
• ADH (Vasopressin) stored in the posterior
pituitary
–Osmolality is less => ADH secretion less
–Osmolality is high =>ADH secretion more
– Kidney produces dilute or concentrated urine
accordingly

31. Hale Teka, OB-GYN Resident
• Sodium
– If salt depletion occurs, then the ECF, and
with it the plasma volume, falls
– Pressure sensors in the circulation are
then stimulated and these excite renin
secretion by the kidney
– This, in turn, stimulates aldosterone
secretion by the adrenal gland, which acts
on the renal tubules, causing them to
reabsorb and conserve Na+

32. Hale Teka, OB-GYN Resident
• Potassium
–Normal serum range: 3.5-5.3 mmol/l
–This is achieved by K+/H+ or K+/Na+
exchange in the renal tubules
–In the presence of K+ deficiency, H+ ion
reabsorption is impaired, leading to
hypokalaemic alkalosis
–Risks of not maintaining the normal
range
• Muscular dysfunction
• Potentially fatal cardiac events

33. Hale Teka, OB-GYN Resident
• Response to injury
– Due to neuroendocrine and cytokine changes
– Changes in
• Metabolic
• Water and electrolyte physiology
– Occurs in 3 phases
• Ebb or shock phase
• Flow or catabolic phase
–‘Sodium retention phase’
• Convalescent anabolic phase of
rehabilitation
–‘Sodium diuresis phase’

34. Hale Teka, OB-GYN Resident
“In the presence of the response to
injury, the kidneys are unable to correct
for errors in prescribing!”

35. Hale Teka, OB-GYN Resident
• Transcapillary escape rate of albumin in
response to injury
– Increases from about 5%/h to 13-15%/h
– Albumin leaks out into the interestitial space
• Draws with it sodium and water
– As the return of albumin to the circulation via
the lymphatics is unchanged
– This results in a net contraction of the
intravascular space with intravascular
hypovolaemia and edema in the interestial
space

36. Hale Teka, OB-GYN Resident
Effects of an increase in the transcapillary escape rate of albumin

37. Hale Teka, OB-GYN Resident
• Potassium
– In surgery, sepsis and trauma
• Hypokalemia
–Increased excretion
–During the convalescent period
• Hyperkalemia
–Catabolisim is extreme and renal
function is impaired so potassium level
exceeds the kidney's capacity to excrete

38. Hale Teka, OB-GYN Resident
Assessment, Measurement and Monitoring
• History
– Alerts to likelihood of fluid
• Deficity as in from: Vomiting, diarrhoea,
haemorrhage ...
• Poorly controlled DM
• Burn
• Drugs
• Excess as in from: from intraoperative
fluids
– Autonomic responses
• Sweating

39. Hale Teka, OB-GYN Resident
• Physical Examination
– Autonomic responses
• Pallor and sweating
– Capillary refill
• Slow refill
– Blood pressure
– Skin turgor
– Sunken facies
– Dry mouth
– Edema

40. Hale Teka, OB-GYN Resident
• Urine output
• Weighing
• Fluid balance chart
• Serum biochemistry
• Urine biochemistry

41. Hale Teka, OB-GYN Resident
• Physical Signs of Fluid Deficit
– JVP/CVP
– Pulse Rate
– Blood Pressure followed by pallor and
sweating
– Urine output
– Shock

42. Hale Teka, OB-GYN Resident
• Follow up
– JVP
– Vitals
– Urine output

43. Hale Teka, OB-GYN Resident
• Urine Output
– Prerenal AKI
• Small concentrated urine
• BUN increasing
• Creatinine normal
– Resuscitation
– Intrinsic AKI
• Small concentrated urine
• BUN and Creatining elevated
– Renal replacemnt therapy

44. Hale Teka, OB-GYN Resident
• Fluid balance charts
– Does not consider the insesible losses
• Weight
– Best way of measuring fluid balance
– Does not measure the internal shift
• Invasive monitoring
– Direct fluid therapy in more complex patients
• Laboratory tests
– Hematocrite
– Albumin
– Urea
– Urine to plasma urea concentration
• <15

45. Hale Teka, OB-GYN Resident
– Osmolality
• <350 mOsm/Kg
• >500 mOsm/Kg
– Creatinine
– Creatinine clearance
– Sodium
– Potassium
– Chloride
– Bicarbonate

46. Hale Teka, OB-GYN Resident
• Reference laboratory values for some commonly
measured parameters

47. Hale Teka, OB-GYN Resident

48. Hale Teka, OB-GYN Resident

49. Hale Teka, OB-GYN Resident
Properties of IV Crystalloids and Colloids
• The ability of a solution to expand the plasma
volume is dependent on its
– Volume of distribution and
– Metabolic fate of the solute,
• Colloids
– Intravascular volume expansion
• Crystaloids
– Glucose containing - only as a means to provide free
water

50. Hale Teka, OB-GYN Resident

51. Hale Teka, OB-GYN Resident
• Ideal colloid
– Radily available,
– Have a long shelf life,
– Have no special infusion or storage
requirements and
– Be relatively inexpensive
– Be isooncotic with plasma and
– Be distributed exclusively in the intravascular
compartment

52. Hale Teka, OB-GYN Resident
Volume effects of some colloids

53. Hale Teka, OB-GYN Resident
Advantages and disadvantages of colloids

54. Hale Teka, OB-GYN Resident
Prescription and Administration
• Appropriate fluid and electrolyte
prescriptions may be administered orally,
enterally, subcutaneously, or
intravenously, depending on the clinical
situation

55. Hale Teka, OB-GYN Resident
The relationship between resuscitation,
replacement and maintenance

56. Hale Teka, OB-GYN Resident
• Resuscitation
– Blood loss from injury or surgery, plasma loss
e.g. from burns or acute pancreatitis, or
gastrointestinal or renal losses of salt and
water
– Start with 500 mL balanced crystaloid
– Follow outcome with urine output, JVP, pulse
rate and blood pressure
– If the above parameteres normalize switch to
maintenance

57. Hale Teka, OB-GYN Resident
• In resucitation
– When do we give normal saline?
– When do we avoid Ringer's Lactate?
– When do we give colloids?
– When do we give blood?

58. Hale Teka, OB-GYN Resident
• Replacement
– Maintenance plus like-for-like water and
electrolyte replacement of any losses

59. Hale Teka, OB-GYN Resident
• Maintenance
– Restore insensible loss
– The average person requires 25-35 ml/kg
water, 1 mmol/kg Na and 1 mmol/kg K+ per
day

60. Hale Teka, OB-GYN Resident
Examples of maintenance fluid regimens
(2-2.5 l/day) suitable for a 70 kg person

61. Hale Teka, OB-GYN Resident

62. Hale Teka, OB-GYN Resident

63. Hale Teka, OB-GYN Resident
Suggested algorithm for resuscitation of
non-haemorrhagic shock

64. Hale Teka, OB-GYN Resident

65. Hale Teka, OB-GYN Resident
Methods of Fluid Administration
• Oral
• Enteral
• Intravenous

66. Hale Teka, OB-GYN Resident
Acid-Base Balance
• Three organs are involved in acid base balance
– Kidney
• Remove acid
• Regenerate bicarbonate
– Lungs
• Remove acid
– Liver
• Removes and recylces lactate

67. Hale Teka, OB-GYN Resident
Normal arterial blood acid-base measurements

68. Hale Teka, OB-GYN Resident
“If the gut works, use
it!”

69. Hale Teka, OB-GYN Resident
• Blood buffering system
– Relative proportions of carbonic acid from carbon
dioxide (CO2) and of bicarbonate (HCO3–)

70. Hale Teka, OB-GYN Resident
– Haemoglobin
– Phosphate (organic and inorganic)
– Bone and its calcium salts

71. Hale Teka, OB-GYN Resident
• The kidney buffering system
– Controls hydrogen (H+) and bicarbonate
(HCO3–) excretion or reabsorption
– Conversion of ammonia (NH3) to ammonium
(NH4+) in the urine

72. Hale Teka, OB-GYN Resident
• The lung buffering system which
controls
– The carbon dioxide (CO2) in the blood,
increasing expired CO2 when more is
produced or to compensate for metabolic
acidosis

73. Hale Teka, OB-GYN Resident
• The liver buffering system
– Removes and recycles the large amounts of
lactate produced by anaerobic respiration (the
Cori cycle)

74. Hale Teka, OB-GYN Resident
• Approaches to acid-base balance
– Schwartz-Bartter approach
– Stewart approach

75. Hale Teka, OB-GYN Resident
• Clinical presentation
– Vomiting/diarrhoea
– Shock
• Cardiogenic
• Septic
• Hypovolaemic
– Acute kidney injury
– Respiratory failure

76. Hale Teka, OB-GYN Resident
– Altered neurological status
• Coma
• Seizures
– Decompensated diabetes
– Hypo- or hyperkalaemia
• Potassium metabolism is intimately linked
with acid-base balance
– Prolonged and excessive infusions of saline

77. Hale Teka, OB-GYN Resident
• If an acid-base disturbance is suspected from
clinical features the following investigations
should be performed initially:
– Urea, creatinine and electrolytes
– Bicarbonate
– Chloride
– Arterial blood gases (including lactate)

78. Hale Teka, OB-GYN Resident
• Step-by-step pathway to identify
underlying cause
– pH to determine whether acidaemia or
alkalaemia
– Change in bicarbonate and base excess =
metabolic proces

79. Hale Teka, OB-GYN Resident
• Change in Pco2 = respiratory process
• Determine whether
– Simple disorder i.e. either metabolic or
respiratory process alone
• Mixed disorder i.e. a combination of a metabolic
and respiratory process occurring together.
There will be evidence of compensatory
changes in either bicarbonate or Pco2
• Calculate the anion gap

80. Hale Teka, OB-GYN Resident
Simple acid-base disorders

81. Hale Teka, OB-GYN Resident
Causes of a metabolic acidosis with a high anion gap

82. Hale Teka, OB-GYN Resident
Causes of metabolic acidosis
(hyperchloraemic) with a normal anion gap

83. Hale Teka, OB-GYN Resident
• Metabolic acidosis with a high anion gap -
– Ketoacidosis,
– Lactic acidosis,
– Poisonings or
– Advanced acute or chronic kidney disease

84. Hale Teka, OB-GYN Resident
Causes of metabolic alkalosis

85. Hale Teka, OB-GYN Resident
Oliguria

86. Hale Teka, OB-GYN Resident

87. Hale Teka, OB-GYN Resident

88. Hale Teka, OB-GYN Resident

89. Hale Teka, OB-GYN Resident
Disorers of Serum Electrolytes
• Sodium (Na+)
– Total body sodium is 3000-4000 mmol,
– of which only 60% is exchangeable, the
remainder being locked mainly in bone
– Salt balance is about maintenance of volume,
whereas water balance is more concerned
with osmolality

90. Hale Teka, OB-GYN Resident
• The serum Na concentration on its own ,
cannot be used to diagnose the state of
Na balance

91. Hale Teka, OB-GYN Resident
• Hyponatraemia
–Severe Hyponatraemia (serum Na+
<120 mmol/l)
• Cerebral oedema and brain damage
• Too rapid correction of severe
hyponatraemia
– Neurological damage (osmotic demyelination)
–It is advised that hyponatraemia be
corrected at a rate not exceeding 10
mmol/l/day.

92. Hale Teka, OB-GYN Resident
• Clinical Feature
– Mild and Gradual
• Asymptomatic
– Moderate
• Headache,
• Confusion
– Severe and rapid
• Seizure
• Coma
– Emergency Rx
• Hypertonic Saline

93. Hale Teka, OB-GYN Resident
• False hyponatremia
– Severe hyperlipidaemia
– Hyperglycaemia
– Hyperproteinemia

94. Hale Teka, OB-GYN Resident
Approach to Hyponatremia
Serum
Osmolality
High
Sr Glucose
Increased
Low
ECF
Volume
High
Edematous
States
Low
Urine Na
< 10
Skin/ GI Loss
>20
Renal Loss
Norma
l
SIADH/, Drugs,
Thyroid
Norma
l
Sr Lipids
Sr Proteins

95. Hale Teka, OB-GYN Resident
• Determine serum Osmolality
– High and Normal osmolality are “artifacts” of
increase Glucose, Lipids, Proteins.
• With Low Osmolality, determine if ECF status is
high, low or normal
– High
• Edematous states
– Low
• Renal or Extra-Renal Na loss
– Normal
• SIADH, Drugs, Thyroid, Water Intoxication

96. Hale Teka, OB-GYN Resident
• Treatment :
– True volume depletion
• Administer saline
• 1 L ~ 1 meq
• Suppression of ADH secretion
– Edematous patients
• Free water restriction to below the daily UOP
• Generally < 800 ml/d
– Treat with 3% normal saline if:
• Serum sodium < 120 mEq/L or
• With neurologic symptoms

97. Hale Teka, OB-GYN Resident
• Mild
– > 130 meq/l
– Water restriction
– Oral salt tablets
• Moderate
– 120 – 130 meq/l
– Water restriction
– Hypertonic saline if symptomatic
• Severe
– < 120 meq/l
– Hypertonic saline

98. Hale Teka, OB-GYN Resident
• Hyponatremia with positive water and
sodium balance
– Infusions of hypotonic fluids post-operatively

99. Hale Teka, OB-GYN Resident
• With positive water and normal or slightly
negative salt balance
– inappropriate ADH secretion, classically
associated with oat cell carcinoma of the lung

100. Hale Teka, OB-GYN Resident
• With normal water balance and negative
salt balance
– This classically occurs in Addison’s disease

101. Hale Teka, OB-GYN Resident
• With water excess and negative sodium
balance
– This occurs when excess salt losses from the
GI tract or the kidneys (diuretics or tubular
disease) are combined with excess water or
hypotonic fluid intake by mouth or other
routes

102. Hale Teka, OB-GYN Resident
• In critical illness
– In critical illness ‘sick cell syndrome’.

103. Hale Teka, OB-GYN Resident
• Hypernatraemia
– Most common cause is net loss of hypotonic
fluid from the GI tract e.g. vomiting and
diarrhoea
– Due to the osmotic diuresis associated with
uncontrolled diabetes
– Large fluid losses from sweat
– Primary hyperaldosteronism
– Treatment is with hypotonic fluids orally,
enterally or intravenously

104. Hale Teka, OB-GYN Resident
Treatment
• Step 1:
– Focus on the treatment of water deficit.
– Estimate the TBW as 50 % of lean body
mass in men and as 40% in women
• Alternative formula:
– 3 ml/kg of electrolyte free fluid decreases
the serum sodium by 1 meq/L
• Plus insensible loss: 30 t0 40 ml/hr

105. Hale Teka, OB-GYN Resident
• Step 2: The rate of correction:
– Acute hypernatremia
• Not more than 1 mEq/h and 12 mEq/d.
– Chronic hypernatremia
• 0.7 mEq/L/h
– Overly rapid correction can lead to cerebral
edema and herniation
– In hypovolemic patients, volume should be
restored with normal saline
– Then change to hypotonic fluids such as 5%
dextrose, or enteral water

106. Hale Teka, OB-GYN Resident
• Chloride (Cl–)
– The main anion of the ECF at a concentration
of 95-105 mmol/l
– It is important to remember that while the
concentration of Na+ in 0.9% saline is 10%
higher than that in plasma, the concentration
of Cl– is 50% higher
– pH of NaCl is 5.5

107. Hale Teka, OB-GYN Resident
• Potassium (K+)
– The total body K+
• 3000 and 3500 mmol
• ICF: 120 -145 mmol/l, where it is the chief
cation
• ECF, 3.5-5.2 mmol/l

108. Hale Teka, OB-GYN Resident
• Hyperkalaemia
– Serum K+ rises with renal failure and
catabolic states
– Clinical Features
• Nausea/vomiting, colic, diarrhea
• Weakness, paralysis, respiratory failure
• Arrhythmia, arrest

109. Hale Teka, OB-GYN Resident
• Treatment
– Fluids
– Glucose
– Insulin
– Bicarbonate
– Calcium gluconate
– Renal replacement

110. Hale Teka, OB-GYN Resident
• ECG changes associated with hyperkalemia
– Peaked T waves (early change)
– Flattened P wave
– Prolonged PR interval (first-degree block)
– Widened QRS complex
– Sine wave formation
– Ventricular fibrillation

111. Hale Teka, OB-GYN Resident
• The goal of therapy :
– Reduce the total body potassium
– Shift potassium from extracellular to intracellular
– Protect the cells from the effects of increased
potassium
– All exogenous sources of potassium be discontinued

112. Hale Teka, OB-GYN Resident
Treatment of hyperkalemia
Potassium removal
Kayexalate
Oral administration is 15–30 g in 50–100 mL of 20% sorbitol
Rectal administration is 50 g in 200 mL 20% sorbitol
Dialysis
Shift potassium
• 10 units of regular insulin in 500 mL of 10 percent dextrose, given over 60
minutes
Bicarbonate 1 ampule intravenous
Counteract cardiac effects
• Calcium gluconate 1000 mg (10 mL of a 10 percent solution) infused over two
to three minutes

113. Hale Teka, OB-GYN Resident
Hypokalemia
Causes of Hypokalemia
Inadequate intake
Dietary, potassium-free intravenous fluids, potassium-
deficient total parenteral
nutrition
Excessive potassium excretion
Hyperaldosteronism
Medications
Gastrointestinal losses
Direct loss of potassium from gastrointestinal fluid (diarrhea)
Gastric fluid, either as vomiting or high nasogastric
output
Renal loss of potassium

114. Hale Teka, OB-GYN Resident
• ECG changes suggestive of
hypokalemia:
– U waves
– T-wave flattening
– ST-segment changes

115. Hale Teka, OB-GYN Resident
• Treatment:
– Oral repletion is adequate for mild and asymptomatic
hypokalemia.
– If intravenous repletion is required, usually no more
than 10 to 20 mEq/h is advisable in an unmonitored
setting.
– This amount can be increased to 40 mEq/h when
accompanied by ECG monitoring.
– Caution should be exercised when oliguria or
impaired renal function is coexistent

116. Hale Teka, OB-GYN Resident
Treatment of hypokalemia
Serum potassium level <3.5 mEq/L:
Asymptomatic, tolerating enteral nutrition:
KC1 40 mEq per enteral access x 1 dose
Asymptomatic, not tolerating enteral nutrition:
==> KCl 20 mEq IV q2h x 2 doses
 Symptomatic:
==> KCl 20 mEq IV q1h x 4 doses
Recheck potassium level 2 hours after end of infusion; if <3.5
mEq/L and asymptomatic, replace as per above protocol

117. Hale Teka, OB-GYN Resident
• Mild (3.0 to 3.4 meq/L.):
– Potassium chloride PO – 20 to 80 meq/day in divided
doses
– 1 to 1.5 meq/L increase- after an oral dose of 40 to 60
meq
• Moderate ( 2.5 to 3.0) & Severe ( < 2.5 meq/L):
– Potassium chloride IV- 20 meq/L Q two to three hours
– Measure the serum k+ level Q two to three hours.

118. Hale Teka, OB-GYN Resident
• Calcium:
– Mainly stored within the bone matrix.
– Only less than 1% found in the extracellular
fluid.
– Serum calcium is distributed among three
forms:
• Protein-bound (40%)
• Complexed to phosphate and other anions
(10%)
• Ionized (50%).

119. Hale Teka, OB-GYN Resident
–It is the ionized fraction that is
responsible for neuromuscular stability
and can be measured directly.
–Total : 2.2 – 2.9 mmol/L ( 8.5 – 10.5
mg/dl )
–Ionized : 1.1 – 1.4 mmol/L ( 4.2 – 4.8
mg/dl )

120. Hale Teka, OB-GYN Resident
• Hypercalcemia :
– Serum calcium T > 2.9 or i >1.4 mmol/L
– Mild: < 3.0 mmol/L
– Moderate: 3.0 – 3.5 mmol/L
– Severe: > 3.5 mmol/L
 Causes:
– Primary hyperparathyroidism
– Malignancy

121. Hale Teka, OB-GYN Resident
– ECG Changes
• Shortened QT interval
• Prolonged PR and QRS
intervals
• Increased QRS voltage
• T-wave flattening and
widening
• AV block

122. Hale Teka, OB-GYN Resident
• Treatment :
– required when hypercalcemia is symptomatic,
which usually occurs when the serum level
exceeds 3 mmol/L.
– Treat volume deficit:
• Isotonic saline at an initial rate of 200 to
300 mL/hour
• Then adjusted to maintain the UOP at 100
to 150 mL/hour.
– Calcitonin:
• Increase renal calcium excretion
• Decrease bone resorption
– Bisphosphonates : Decrease bone resorption

123. Hale Teka, OB-GYN Resident
• Hypocalcemia:
– Serum calcium level below- 2.2 mmol/L
– or ionized calcium level below- 1.1 mmol/L
• Causes:
– Hypoparathyroidism
– Pancreatitis
– Massive soft tissue infections such as necrotizing
fasciitis
– Renal failure
– Pancreatic and small bowel fistulas
– Toxic shock syndrome

124. Hale Teka, OB-GYN Resident
Hypocalcemia
Symptoms do not occur until the ionized fraction falls below o.8
mmol/L.
Neuromuscular:
• paresthesias of the face and extremities
• muscle cramps
• carpopedal spasm
• Stridor
• Tetany
• seizures
• hyperreflexia
Cardiac
• Decreased contractility
• heart failure
124

125. Hale Teka, OB-GYN Resident
Hypocalcemia
Chvostek's
sign :
• Spasm resulting from tapping over the
facial nerve.
Trousseau's
sign :
• Spasm resulting from pressure applied to
the nerves and vessels of the upper
extremity, as when obtaining a blood
pressure.
125

126. Hale Teka, OB-GYN Resident
• Treatment:
– Oral calcium:
• Asymptomatic hypocalcemia
– IV- calcium :
• Acute symptomatic hypocalcemia
• Not tolerating oral calcium
• Serum ca++ < 1.9 mmol/L
– 10 ml of 10 % calcium gluconate, in 50 mL of
5 % DW infused over 10 to 20 minutes.

127. Hale Teka, OB-GYN Resident
• Magnesium (Mg2+)
– 0.7-1.2 mmol/l
– 0.4 mmol/l

128. Hale Teka, OB-GYN Resident
• Phosphate (PO42–)
– 0.89 -1.44 mmol/l
– 0.32 mmol/l

129. Hale Teka, OB-GYN Resident
References
1. Basic Concepts of Fluid and Electrolyte Theray,
2. UpToDate 21.2
3. Schwartz's Text of Surgery 8th Edition
4. Harrison Textbook of Internal Medicine, 18th
Edition
5. Guyton Textbook of Medical Physiology, 11th
Edition
6. Seminars

130. Hale Teka, OB-GYN Resident
Thank you very much!