fluid and electrolyte balance by dr.naveen

1. FLUID AND ELECTROLYTE
BALANCE
Presenter
Dr Maneesh Kumar Bhardwaj
Dr Naveen Kumar
Moderator: Prof. Mohammad Habib Raza

2. HISTORICAL BACKGROUND
 Earliest authenticated resuscitation in the medical
literature: “miraculous deliverance of Anne Green,”
 By wrenching her teeth apart, poured hot fluid into her
mouth
 Rubbing her fingers, hands, arms, and feet
 Tickling her throat with a feather

3.  Term “shock” first employed in 1743 regarding battlefield
wounds
 In 1830, Herman: first descriptions of intravenous fluid
therapy
 Sydney Ringer: credited for lactated Ringer’s solution
 In 1924, Rudolph Matas: originator of modern fluid
treatment, concept of the continued IV drip

4. INTRODUCTION
WATER CONTENT
Adult males 60-65% of body weight
Adult female 45-50% of body weight
 Water: most abundant constituent in the body
 Obese adult have less TBW per Kg than lean
adult
 Total body water = 0.6 * weight(in kg)

5.  Intravascular (plasma water) : extravascular (interstitial)
spaces - 1:3

6. COMPOSITION OF BODY
FLUIDS

7.  Osmolality: The solute or particle concentration of a
fluid
 Expressed as milliosmoles per kilogram of water
(mosmol/kg)
 Water crosses cell membranes to achieve osmotic
equilibrium (ECF osmolality = ICF osmolality)

8. WATER MOVEMENT ACROSS
THE CAPILLARY WALL
STARLING FORCES :
1.Capillary pressure
2. Plasma colloid osmotic pressure
3. Interstitial fluid pressure
4. Interstitial fluid colloid osmotic pressure

9. WATER BALANCE
• Normal plasma osmolality: 275–290 milliosmol/kg
• In steady state, Water intake = water excretion
• Gastrointestinal excretion: minor component of total
water output, except in patients with vomiting, diarrhea,
or high enterostomy output states
• Evaporative or insensitive water losses: regulation of
core body temperature

10. WATER BALANCE

11. WATER BALANCE
increased

12. WATER BALANCE AND KIDNEY

13.  Primary stimulus for water ingestion: thirst
 Mediated either by an increase in effective osmolality or
a decrease in ECF volume or blood pressure
 Osmoreceptors: stimulated by a rise in tonicity
 Normally, 600 milliosmols must be excreted per day
 Minimum urine output of 500 mL/d required for neutral
solute balance (maximal urine osmolality 1200
milliosmols/kg)

14.  Nonosmotic factors that regulate ADH secretion:
effective circulating (arterial) volume, nausea, pain,
stress, hypoglycemia, pregnancy
 Hemodynamic response: mediated by baroreceptors in
the carotid sinus
 Sensitivity of these receptors is significantly lower than
osmoreceptors

15. FLUID IMBALANCES:
HYPOVOLEMIA
 State of combined salt and water loss exceeding intake,
leading to ECF volume contraction

16. CAUSES OF HYPOVOLEMIA
I. ECF volume contracted
A. Extra renal Na+ loss
1. Gastrointestinal (vomiting, nasogastric suction, fistula, diarrhea)
2. Skin/respiratory (insensible losses, sweat, burns)
3. Hemorrhage
B. Renal Na+ and water loss
1. Diuretics 2. Osmotic diuresis
3. Hypoaldosteronism 4. Salt-wasting nephropathies
C. Renal water loss
1. Diabetes insipidus

17. II. ECF volume normal or expanded
A. Decreased cardiac output
1. Myocardial, valvular, or pericardial disease
B. Redistribution
1. Hypoalbuminemia (hepatic cirrhosis, nephrotic syndrome)
2. Capillary leak (acute pancreatitis, ischemic bowel, rhabdomyolysis)
C. Increased venous capacitance
1. Sepsis

18. CLINICAL FEATURES
 Careful history in determining the etiology of ECF
volume contraction (e.g., vomiting, diarrhea, polyuria)
 Mild: Nonspecific symptoms like fatigue, weakness,
muscle cramps, thirst, and postural dizziness
 Severe: oliguria, cyanosis, abdominal and chest pain,
and confusion or obtundation indicating end-organ
ischemia

19.  Diminished skin turgor and dry oral mucous membranes
 Decreased jugular venous pressure, postural
hypotension, and postural tachycardia
 Hypovolemic shock, manifest as hypotension,
tachycardia, cyanosis, cold and clammy extremities,
oliguria, and altered mental status

20. DIAGNOSIS
 Thorough history and physical examination
 Blood urea nitrogen and plasma creatinine
concentrations raised
 BUN:creatinine ratio of 20:1 or higher
 Urine Na+ concentration <20 mmol/L
 Urine osmolality: >450 mosmol/kg
 Specific gravity >1.015

21. CLASSIFICATION OF
HAEMORHAGIC SHOCK

22. TREATMENT
 Therapeutic goal: to restore normovolemia with fluid
similar in composition to that lost and to replace ongoing
losses
 Mild hypovolemia: corrected via the oral route
 Severe hypovolemia: requires intravenous fluid therapy

23.  Normal Needs for 70 kg Man per Day
WATER 2000 ml
URINE 1500 ml
SODIUM 1-1.5 mEq/kg
POTASSIUM 1 mEq/kg

24. FLUID THERAPY
Two components to fluid therapy:
1. Maintenance therapy replaces normal ongoing
losses
2. Replacement therapy corrects any existing water
and electrolyte deficits

25. MAINTENANCE THERAPY
Maintenance IV Fluid Calculation
• 4 mL/kg/hr for first 10 kg
• 2 mL/kg/hr for next 10 kg
• 1 mL/kg/hr for every kg over 20 kg
Eg. Sample Calculation for 45-kg Patient
• 10 kg × 4 mL/kg/hr = 40 mL/hr 10 kg × 2 mL/kg/hr =
20 mL/hr 25 kg × 1 mL/kg/hr = 25 mL/hr Maintenance
rate = 85 mL/hr

26. MAINTENANCE THERAPY

27. REPLACEMENT THERAPY
 Total water loss in the form of vomiting, loose stools,
inadequate intake of fluid, insensible water loss
 Usually given as a bolus of 2 liters
 Free water deficit = (([Na]/140) − 1) × TBW

28. TYPES OF IV FLUID SOLUTIONS
1. Crystalloids: having small “crystalizable” particles like
normal saline, ringer lactate, hypertonic saline
2. Colloids:
• large particles like albumin
• 250ml Albumin = 4L NS
• Adverse effect: anaphylaxis

29. ISOTONIC FLUIDS

30. HYPOTONIC FLUID

31. HYPERTONIC FLUIDS

32. COMPOSITION OF IV FLUIDS

33.  Normal saline (0.9% NaCl): Solution of choice in
normonatremic and most hyponatremic individuals
 Should be administered initially in patients with
hypotension or shock
 Hypernatremia reflects a proportionally greater deficit of
water than Na+
 Require a hypotonic solution such as half-normal saline
or 5% dextrose in water

34. • Patients with significant hemorrhage, anemia, or
intravascular volume depletion: require blood
transfusion or colloid containing solutions (albumin,
dextran)

35. MONITORING FOR PATIENTS IN
SHOCK
 Minimum
● ECG ● Pulse oximetry
● Blood pressure ● Urine output
 Additional modalities
● Central venous pressure
● Invasive blood pressure
● Cardiac output
● Base deficit and serum lactate

36. HYPERVOLEMIA
 ECF Volume excess
 Causes
– Excessive intake of fluids
– Abnormal retention of fluids
• Heart failure
• Renal failure
– Long-term corticosteroid
therapy

37. CLINICAL FEATURES
Cardiovascular
Changes
Respiratory
Changes
Skin
Changes
Neurologic
Changes
GI Changes
o Bounding
pulse
o Distended
neck veins
o ↑ BP
o ↑ respiratory
rate
o Shallow
respirations
o ↑ dyspnea with
exertion or in
the supine
position
o Pulmonary
congestion and
pulmonary
edema
o SOB
o Irritative
cough
o Moist
crackles
o Edematous
may feel cool
o Skin may feel
taut and hard
o Edema-
eyelids,
facial,
dependent
(sacrum),
pitting,
peripheral
extremities
o Altered LOC
o Visual
disturbances
o Skeletal
muscle
weakness
o Cerebral
edema
o Headache
o Confusion
o Lethargy
o Diminished
reflexes
o Seizures,
coma
o Increased
motility
o Enlarged
liver
37

38. INVESTIGATION
 Decreased Hematocrit
 Decreased BUN

39. TREATMENT
 Position: Sim-Fowler’s
 Restrict fluid intake
 Diuretics
 Monitor electrolytes, esp. Mg and K
 Vital monitoring
 Input output monitoring

40. ELECTROLYTES
Cations (+)
Sodium
Potassium
Calcium
Magnesium
Anions (-)
Chloride
Bicarbonate
Phosphate
Charged particles in solution:

41. Cations and Anions in Body Fluids
Figure 27–2 (1 of 2)

42. SODIUM
 Major extracellular cation
 Normal range of serum sodium 135 - 145 mEq/L
 Daily sodium requirement: 1-1.5mmol/kg
 Hyponatremia and hypernatremia, controlled by ADH

43. Figure 27–4
SODIUM
REGULATION
So changes in
sodium
concentration are
corrected by ADH

44. HYPONATREMIA
• Serum Na+ level < 135 mEq/L
• Hyponatremia can be
 Mild (130 to 135 mEq/liter)
 Moderate(120 to 130 mEq/liter)
 Severe (<120 mEq/liter)
• Sign & symptoms : <120 mEq/l.(confusion, lethargy,
headache,seizure, coma)

45. Causes :
 Sodium depletion.
 Sodium dilution (Intentional: excessive oral water intake
, Iatrogenic: Intravenous)

46. SODIUM DEPLETION
1.Decrease intake
a) Low Na diet b)Enteral feeds
2. Increase loss
 Gastrointestinal Losses
a) Vomiting b) Prolonged NGT suctioning
c) Diarrhea
 Renal Losses
a) Diuretics b)Primary renal disease
3. Depletional hyponatreamia is often accompanied by
extracellulr volume deficit
.

47. TREATMENT
 Sodium Deficit:
Sodium deficit (mEq) = [Na+] goal − [Na+] plasma x0.6xbodyweight
Ex- 60kg male with s.sodium 125mEq
Sodium deficit (mEq) =(140mEq-125mEq)x.6x60=540mEq
 Infusion of normal saline 0.9%, hypertonic (HTS) may be required.
 HTS is available commercially(in 3%, 5% concentrations)

48. The volume of fluids needed should be taken into
consideration.
Scenario 1:
If patient is hypovolemic :0.9% normal saline is fluid of
choice.
Scenario 2:
If patient is hypervolemic : hypertonic saline (3%HTS,
5%HTS) is fluid of choice

49. • No more than 10 mEq/day of sodium should be corrected
Rapid correction of hyponatremia

Pontine myelinolysis

Seizures, weakness/paresis, akinetic movements,
unresponsiveness

Permanent brain damage

Death

50. HYPERNATREMIA
Sodium concentration > 145 mEq/l
 Moderate hypernatremia (146 to 159 mEq/l)
 Severe hypernatremia (>160 mEq/l)
(confusion, muscle weakness, restlessness, insomnia,
central pontine myelinolysis)

51. • Causes:
 Inadequate water intake
 Decrease ADH synthesis
 Failure of renal tubular cells to respond to ADH
 Increased salt intake or infusion
 Loss of body water.
 Infusion of sodium (like HTS)

52. SIGN AND SYMPTOMS
 Think S-A-L-T
 Skin flushed
 Agitation
 Low grade fever
 Thirst
 Neurological symptoms : due to dehydration of brain
cells (Restlessness, lethargy, ataxia, irritability, tonic
spasms, delirium, seizures, coma)
 Signs of hypovolemia :(Oligouria)

53. TREATMENT
• Correction of hypernatremia depends on volume status.
 Hypovolemic patients: isotonic fluids(D5%)
 Euvolemic : hypotonic fluids(N/2 saline)
 Hypervolemic patients : diuretics.
 Synthetic analogue of ADH: DDAVP(1-desamino-8-D
arginine vasopressin) in diabetic incipidus

54.  Sodium levels should not corrected too rapidly : cause
cerebral edema.
 In acute hypernatremia: 1 to 2 mEq/hr
 In chronic hypernatremia: 0.5 mEq/hr.

55. POTASSIUM
 Major intracellular cation
 Normal K+ levels : 3.5 - 5 mEq/L
 Daily average intake of potassium about 1mmol/kg
 The renin-angiotensin-aldosterone hormone axis is the
key regulator of potassium clearance(causes Na+
reabsorption and K+ excretion)
 Most K+ ingested is excreted by the kidneys

56. HYPOKALEMIA
• Serum K+ < 3.5 mEq /L
Causes:
 Inadequate intake( Dietary, potassium-free intravenous fluids,
potassium-deficient)
 Primary hyperaldosteronism and renin secreting tumors
 Medications : diuretics
 Gastrointestinal losses (diarrhea , vomiting ,high nasogastric
output)
 Renal loss of potassium
 Intracellular-shift (metabolic alkalosis or insulin therapy)

57. SIGN & SYMPTOMS ,ECG
CHANGES
• Hypokalemia is associated with generalized fatigue and
weakness, ileus, acute renal insufficiency.
• K+ <2.5 meq/liter: Rhabdomyolysis
• K+<2 meq/liter: Flaccid paralysis with respiratory
compromise
• ECG will show depressed T waves and U waves.
• CVS: atrial tachycardia, atrioventricular dissociation,
ventricular tachycardia, ventricular fibrillation.

58. TREATMENT
 Increase dietary/oral K+: 40 to 100 mEq/day in two to
four doses
 Change to K+ sparing diuretics
 IV K+ replacement:
 NEVER GIVE IV PUSH POTASSIUM.
 The IV rate is 10 to 20 mEq/hr.
 Concentrations should not exceed 40-60 mEq/L.

59. HYPERKALEMIA
• Serum K+ >5 mEq /L
causes
 Altered kidney function (renal dysfunction or failure)
 Increased intake: Potassium supplementation & Blood
transfusions
 K+ sparing diuretics , beta blockers, cyclosporine, and
tacrolimus.
 Cellular injury (sepsis or ischemia-reperfusion)

60. SIGN, SYMPTOMS AND ECG
CHANGES
• Gastrointestinal: Nausea, vomiting ,colic diarrhea
• Neuromuscular: weakness, paralysis, respiratory failure
• Cardiovascular: Arrhythmia, arrest
• ECG changes:
 Peaked T waves
 Flattened/absent P wave
 Prolonged PR interval
 Widened QRS complex

62. GUIDELINES FOR TREATMENT OF
PATIENTS WITH HYPERKALEMIA

63. From : Sabiston 20th edition

64. CALCIUM
 Divalent cation
 Serum calcium 8.5 to10.5 mg/dL
 About 99% in the bones, 1% circulates in the blood.
 Regulated by:
– Parathyroid hormone
• ↑Blood Ca++ by stimulating osteoclasts
• ↑GI absorption and renal retention
– Calcitonin from the thyroid gland
• Promotes bone formation
• ↑ Renal excretion

65. HYPOCALCEMIA
 Serum calcium < 8.4 mg/dL
Causes:
 Inadequate intake
 Hypoparathyroidism
 Acute pancreatitis(calcium sequestration in the
abdomen)
 Tumor lysis syndrome
 Acute and chronic renal failure

66. • Diagnosis:
 Serum calcium level
 Clinically
– Chvostek’s sign
– Trousseau’s sign

67. TREATMENT
 Orally: Calcium carbonate
 Intravenously :
• Acute symptomatic hypocalcemia (calcium level < 7.0
mg/dL)
• IV calcium gluconate ,The first 100 to 200 mg of
elemental calcium (1 to 2 g calcium gluconate) should be
given during 10 to 20 minutes.
• Followed by a slow calcium infusion at 0.5 to 1.5
mg/kg/hr.

68. HYPERCALCEMIA
• Serum calcium level >10.5 mg/dL
 Mild hypercalcemia : 10.5 to 12 mg/dL
 Moderate hypercalcemia: 12 to 15 mg/dL
 Severe hypercalcemia > 15 mg/dL
 Hypercalcemic crisis > 17 mg/dL(cardiac
tachyarrhythmia, coma,acute renal failure, ileus with
abdominal distention)

69. Causes:
Hyperparathyroidism: parathyroid hyperplasia
 Cancer: Multiple myeloma, lymphoma, and solid tumors
metastatic to bone (particularly breast, lung, and
prostate cancer)
 Milk-alkali syndrome
 Vitamin A and D overdose
 Granulomatous diseases
 Drugs like thiazide diuretics and lithium.

70. • Signs and symptoms of hypercalcemia:
 Nonspecific: nausea, vomiting, altered mental status,
constipation, depression, lethargy
 Myalgias, arthralgias
 Polyuria, headache
 Abdominal and flank pain (renal stones)
 Coma.
• Abdominal groans, psychic moans, and renal stones.

71. TREATMENT
 Drink plenty of fluids
 IV NS 200-300ml/hr ,maintain urine output 100-150 ml/hr
 loop diuretics: furosemide
 Exogenous Calcitonin
 Excision of parathyroid glands
 Malignant neoplasm : surgical excision, radiation therapy,
or chemotherapy.
 Bisphosphonates : reduce osteoclast-mediated release of
calcium from bone
 Chelating agents (EDTA or phosphate salts)

72. MAGNESIUM
• Divalent cation
• Serum magnesium 1.5 and 2.0 mEq/liter.
 Helps produce ATP
 Role in protein synthesis & carbohydrate metabolism
 Regulates muscle contractions

73. HYPOMAGNESEMIA
 Serum Mg2+ level<1.5mEq/L
 Symptomatic<1.2 mEq/L
Causes
 Poor dietary intake
 Poor GI absorption
 Excessive GI/urinary losses(diuretics)

74. TREATMENT
1. For asymptomatic and mild hypomagnesemia
administer oral mg.
2. For severe deficit (<1meq/L) or symptomatic patient:
 8 to 12 g of magnesium sulfate in the first 24 hours
followed by 4 to 6 g/day for 3 or 4 days to replete body
stores.
Monitor by
 Deep tendon reflexes
 Urine output
 Serum Magnesium levels

75. HYPERMAGNESEMIA
 Serum Mg2+ level > 2 mEq/L
 Not common
 Renal dysfunction/failure is most common cause
 IV magnesium overdose
 Chronic oral ingestion of magnesium

76. SIGN, SYMPTOMS AND ECG
CHANGES
 Decreased neuromuscular activity
 Loss of deep tendon reflexes
 Occasionally nausea/vomiting ,ileus ,urinary retention
 Bradycardia , complete heart block and cardiac arrest
 ECG: prolonged PR interval, increased QRS duration,
and prolonged QT interval

77. ECG CHANGES

78. TREATMENT
 Stop all infusion of magnesium
 Increased fluids if renal function normal
 Loop diuretic if no response to fluids
 IV Calcium gluconate for toxicity 10% (10 to 20 ml
during 10 mint.)
 Hemodialysis in patients with renal insufficiency

80. • Case Scenario : in a 60kg man with intestinal obstruction
 NG Aspirate- 2 L
 Urine output- 1.2 L
 Electrolyte: Na and K with in normal limits
 Insensible fluid loss-800ml
 Total volume required- 2L+1.2L+0.8L=4.0L

81. Total volume required=4L
Electrolyte requirement: loss by NG aspirate
Na+=120meq/l and k+=10meq/l
2L NG loss Na+=240meq
K+=20meq
Daily requirement: Na+ 1-1.5meq/kg=60-90meq
k +1meq/kg= 60meq
Total Na+ =240+60=300meq
k+ =20+60=80meq
500ml of 0.9%saline has 77meq Na+(154meq/L)

82. • Hence to give 300meq of Na+ 2L(77x4=308) of 0.9% saline
required
• Therefore remaining 2L is 5% dextrose additional 4 amp of K+
(20x4=80meq) have to be added in 4 unit of 5% dextrose
• So 4 unit saline and 4 unit 5% dextrose required with 1 amp of
kcl in each dextrose unit

83. TAKE HOME MESSAGE
• Fluid therapy has to be carefully adjusted to body weight,
losses and electrolyte levels
• Hypervolemia can be because of decreased body fluids
and sodium loss
• Categorize the hemorrhagic shock and treat accordingly
• NEVER GIVE IV PUSH POTASSIUM
• Never overtreat electrolyte imbalances as may lead to
sudden death

84. REFRENCES
 The biological basis of modern surgical practice ,
sabiston textbook of surgery
 Bailey & love’s short practice of surgery
 Harrison’s Principles of internal medicine
 Internet