For surgical residents presentation

1. Fluid and Electrolyte
Management in Surgery
Dr. Olofin.K.E

2. OUTLINE
• Introduction
• Distribution of body
water and electrolytes
• Normal fluid and
electrolyte balance
• Disorders in fluid and
electrolyte balance and
causes
– Volume disturbances
• 3rd space fluid loss
– Concentration
disturbances
• Na+ balance
– Composition
disturbances
• K+, Ca2+, Mg2+ and
acid base balance
• Fluid and electrolyte
therapy
• Errors in fluid therapy
• Complications with
intravenous infusion
• Conclusion
• References

3. Introduction
• Fluid and electrolyte management
– Important part of the perioperative management
of the surgical patient
– Critical role in the attenuation of metabolic
response to surgery and trauma in patients

4. • Understanding the daily exchanges of water
and electrolytes is essential in
– maintaining normal concentration of body fluids
and electrolytes
– normal pH
– correct fluid and electrolyte deficits.

5. Distribution of body water and
electrolytes
• Total Body Water (TBW)
• 60% of body weight (adult male)
• 50% of body weight (adult women and older men)
• 45% of body weight (older women)
• In general TBW depends on Age, sex, and
degree of obesity

6. • TBW
• Intracellular –40% (⅔)of TBW = 28L
• Extracellular – 20% (⅓) of TBW = 14L
• Intravascular (plasma) – 4% TBW = 1%
• Extravascular – 16% TBW
• Interstitial – 15% of body weight = 11%
• Transcellular – 1% of body weight = 0.7L
• In Children
• 75 – 80% at birth, decreases steadily to 65% at 1yr
• ECF – 35% at birth, decreases to 20% at 2yrs
• ICF – changes minimally

7. Normal fluid and electrolyte balance
Daily fluid requirements
Water loss Tropics
(ml)
Temperate region
(ml)
Pulmonary and cutaneous 1,700 1,000
Urine 1,500 1,500
Faeces 200 200
Total 3,400 2,700
Water Gains
Endogenous production
from metabolism
200 200
Net requirement 3,200 2,500
Surgical patient- 3,000ml
Pyrexia- 10C→
2.5mL/kg/day to
insensible losses
Tracheostomy on un-
humidified - 1.5L

8. Electrolyte distribution in body fluids
compartments
Ion Intravascular
mmol/L
Interstitial
mmol/L
Intracellular
mmol/L
Na 140 143 8
K 4 4 140
Ca2+ 1.25 0.625 1
Mg 0.7 – 0.9 0.75 15
Cl 95 – 105 115 8
HCO3
- 24 – 27 30 14
PO4
3- 0.8 – 1.4 1.6 25.8
Protein 2 0 9
SO4
2- 1 1 20
Organic acids 3 3 -

9. Electrolyte distribution in body fluids
Sodium Tropics
(mmol)
Temperate
(mmol)
Urine 114 80-110
Sweat 10-16
Faeces 10 10
Total 130-140 90-120
Potassium Tropics
mmol
Temperate
mmol
Urine 50 60
Sweat Negligible Negligible
Faeces 10 10
Total 60 70

10. Disorders in fluid balances
• Classified into:
1. Disturbances of volume – due to loss or addition
of isotonic salt solution
2. Disturbances of concentration – due to addition
or loss of water from the ECF or
depletion/addition of Na+ from the ECF
3. Disturbances of composition:– largely K, Ca, Mg
and Acid – base balance

11. 1. Volume changes
• ECF volume deficit is the most common fluid
disorder in surgical patients.
• Excess or deficit of ECF volume can be diagnosed by
estimating the blood urea nitrogen (BUN)
• BUN rises with sufficient ECF deficit
• The acute loss of an isotonic extracellular fluid like
the intestinal juice results in significant decrease in
the ECF VOLUME and little if any change in the ICF.

12. • The internal fluid shifts are termed Distributional
changes and they create a “Third fluid space”
resulting in the contraction of the Functional
extracellular fluid volume (FECFV)
• Severe volume deficits lead to signs and symptoms
in the CNS & CVS.
• With progressive losses --------> hypovolaemic shock.

13. Seen in :
• Losses from the GIT due to vomiting, NG suction,
diarrhoea and fistula drainage
• Sequestration of fluid in soft tissue injuries and
infections
• Intra-abdominal and retroperitoneal inflammatory
processes
• Peritonitis
• Intestinal obstruction
• Burns

14. Clinical features
• Dry skin, loss of skin turgor.
• Dry mouth.
• Sunken eyes
• Collapsed peripheral veins.
• Tachycardia.
• Scanty concentrated urine.
• HB & Blood urea are increased

15. Treatment
• Intravenous crystalloids.
• Correct shock- ringer’s lactate, blood
• Choice determined by cause of dehydration.
• Monitoring.
• Urine output – 0.5-1ml/kg/hr (30 – 50ml/hr).,
2mls/kg/hr
• Serum electrolytes and urea.

16. Water intoxication
• Parental administration of hypotonic fluids more
than kidneys can excrete.
• Presence of cardiac, renal, hepatic disease.
Causes
• TURP syndrome.
• Colorectal washouts with water.
• Excessive intravenous fluids e.g. 5% glucose
• SIADH

17. Clinical features
• weight gain
• Added breath sounds
• C.V.P > 15cm of H2O
• CCF when severe

18. Treatment
• Prevention
• Stop IV fluid
• Diuretics
• Mannitol (1gm/kg)

19. 2. Concentration changes
Osmolarity
• Osmolarity – number of osmotically active particles
per litre of solvent
• ECF and ICF contain different types of solute but
concentration of solutes inside and outside the cells
are equal
• Sodium salts, glucose and urea – responsible for
most of the solute particles in the ECF
• Sodium ions account for 90%

20. • Measurement – Osmometer
• Plasma Osmolarity
Posm = 2 X Plasma Na+ + Glucose + BUN
18 2.8
2 – no of anions accompanying Na+
18 and 2.8 – correction factors in converting Glucose and
Urea conc. from mg/dl to mmol/L

21. • Hypo and hypernatraemia can be diagnosed clinically
but the signs and symptoms are not generally
present until derangement is severe.
• With rapid rate of change, the signs and symptoms
tend to occur early and with greater severity

22. Hyponatremia
• Defined as serum [Na+] less than 135 mEq/L
• Water shifts into cells causing cerebral edema
• 125 mEq/L – nausea and malaise
• 120 mEq/L – headache, lethargy, obtundation
• 115 mEq/L – seizure and coma

23. Characterised by :
• CNS signs of increased intracranial pressure and
tissue signs of excessive intracellular water
• Hypertension induced by the rise in ICP
• BP usually returns to normal after correction of Na+
level
• With severe hyponatraemia
– rapid development of oliguric renal failure
– irreversible with delayed therapy.

24. Classifications, aetiology and treatment of Hyponatremia
Hyper-osmotic, Iso-smotic, Hypo-osmotic
Hyperosmotic and Isosmotic Hyponatremia are due
to excessive solutes in plasma.
Hyperosmotic
–Hyperglycemia
• Each 100 mg/dl of glucose reduces [Na+]
by 1.6 mEq/l
–Hypertonic Infusions
• Glycerol
• Mannitol
• Glycine
– Treat underlying cause

25. Iso-osmotic
–Pseudo-hyponatremia necessary
• Hyperlipidemia
• Hyperproteinemia
–Isotonic Infusions containing
• Glycine
• Mannitol
»No treatment

26.  Hypo-osmotic Hyponatremia
Hypovolemic, Euvolemic and Hypervolemic
– Hypovolemic – most common cause
• Excessive renal (diuretic) or GI (emesis, diarrhea) losses
• Asymptomatic – fluid resuscitate with isotonic saline
• Symptomatic or plasma [Na+] less than 110 mEq/L
– Calculate Na+ deficit = 0.6 x wt(kg) x (desired [Na] –
actual [Na]
– Correct at a rate no greater than 0.5 mEq/L/hour or
12 mEq/L/day

27. – Euvolemic – polydipsia, SIADH
• Correct underlying disorder
– Hypervolemic – cirrhosis, heart failure, nephrotic
syndrome
• Correct underlying disorder

28. Hypernatremia
• Defined as serum [Na+] greater than 145 mEq/L
Clinical features:
• Lethargy, weakness, and irritability that progress to
seizure, coma, and death

29. Classifications, aetiology and treatment of
Hypernatremia
• Hypovolemic – loss of hypotonic fluids
– Diuresis, vomiting, diarrhea
– Replace the free water deficit
– 0.6 x weight (kg) x ([Na+]/140 -1)
• Hypervolemic – gain of hypertonic fluids
– Hypertonic saline administration
– Diuretics (lasix) to excrete sodium in urine
combined with hypotonic saline for partial volume
replacement

30. • Isovolemic
– Diabetes Insipidus
– Loss of hypotonic urine secondary to lack of ADH
production (central) or lack of response to ADH by
kidney (nephrogenic)
– Hallmark is hypotonic urine (200-500 mOsm/L)
with hypertonic plasma
– Treat by correcting free water deficit
– In central DI must also administer 5 – 10 units of
DDAVP Q6H to prevent ongoing free water loss

31. 3. Composition changes
• Abnormalities of composition of major importance
are changes of
– potassium
– calcium
– magnesium
– changes in Acid-base balance.

32. Potassium
• Major cation of intracellular water – 98% at
concentration of 150mEq/L
• Normal dietary intake – 50-100mEq/day
• Severe injury, surgical stress, acidosis and catabolic
state can result in the release of significant amount
from the intracellular space into the extracellular
space

33. Hyperkalaemia (>5.5mmol/l)
• Signs limited to the CVS and GIT
• GIT symptoms – nausea, vomiting, intermittent
intestinal colic and diarrhoea
• CVS signs apparent on ECG –
– Tall peaked T waves
– Widened QRS complex
– Depressed ST segments

36. Hypokalaemia (<3.5mmol/l)
• Due to excessive renal excretion of K+
• Prolonged administration of K+ free parenteral fluids
with continued obligatory renal loss of K+
(>20mEq/day)
• Parenteral nutrition with inadequate K+ replacement
• Loss of GIT secretions
• Hyperthroidism, B-adrenergics, insulin,alkalosis

37. Hypokalaemia
Signs
• Failure of normal contractility of skeletal, smooth
and cardiac muscles i.e. weakness leading to flaccid
paralysis, diminished/absent tendon reflexes and
paralytic ileus
• ECG signs – arrhythmias, low voltage ECG, flat T
waves and depressed ST segments

38. Treatment
• Prevention i.e. replace GIT fluid loss volume for
volume
• K deficit(mmol) = (desired – actual)x 0.3 x wt(kg)
• Give K+ not more than 40mEq/L of fluid
• Rate not exceeding 20mEq/hour
• Don’t give oliguric patients and post op patient
within 24hrs post surgery

39. Calcium
• Majority of Calcium in the body is in the form of
PO4
3- and CO3
2-
• Normal daily intake : 1 – 3g/day
• ≥ 200mg excreted in the urine daily, the rest is lost in
the GIT
• Half of the serum calcium exists in unionised form
bound to plasma proteins
• 45% exists in ionised form and is responsible for
neuromuscular stability

40. • Acidosis increases the ionised fraction while alkalosis
decreases it
• Disturbances of calcium metabolism are generally
not problematic in the postoperative patient
• Therefore, routine administration of Ca2+ to the
surgical patient is not needed in the absence of
specific indications

41. Hypocalcaemia
• Serum levels < 8mg/100ml
• Features –
– Circumoral numbness
– Numbness of fingers and toes
– Hyperactive tendon reflexes
– +ve Chvostek’s sign
– Tetany, carpopedal spasms
– Convulsions (with severe deficits)
– Prolonged Q-T interval on the ECG

42. Hypocalcaemia
Causes
• Acute pancreatitis
• Massive soft tissue infections – necrotising fascitis
• ARF and CRF
• Pancreatic and small bowel fistulas
• Hypoparathyroidism
• Severe depletion of magnesium
Give Calcium salts – gluconate and chloride – IV ,
- lactate – orally
Correct underlying cause and the deficit

43. Hypercalcaemia
• Symptoms
– Easy fatigability
– Lassitude
– Weakness
– Anorexia, nausea and vomiting
– Weight loss
In severe cases
- lassitude, somnambulism, stupor, coma
- Headaches, skeletal pains, thirst, polydipsia,
polyuria

44. Hypercalcaemia
Causes
• Hyperparathyroidism
• Cancer with bony metastasis e.g. Breast Ca
Treatment
• Inorganic PO4
3- given IV/orally lowers Ca2+ levels
• Large doses of furosemide
• Prevention is the main treatment of hypercalcaemia
due to metastatic cancer
– Low calcium diet, adequate hydration to promote
urinary excretion of Ca2+

45. Magnesium
• Total body content – 2000mEq
• Half of this is in bone
• Distribution similar to potassium – mostly
intracellular
• Serum concentration between 1.5 –2.5mEq/L
• Normal dietary intake – 20mEq/day
• Largely excreted in the faeces

46. Magnesium
Deficiency
• Seen in starvation, malabsorption syndromes, GIT
losses, parenteral nutrition, acute pancreatitis, DKA
during treatment , primary aldosteronism and
chronic alcoholism
Symptoms and signs similar to hypocalcaemia

47. Treatment
• Parenteral MgSO4 or MgCl2 solution
• Monitor HR, BP, respiratory rate and ECG with large
doses
• Never to be given in the phase of oliguria or severe
volume deficit to avoid toxicity
Excess – rare but seen in renal insufficiency
- Correct acidosis
- Correct pre existing ECF volume deficit
-Withhold exogenous Mg2+

48. Acid – Base Balance
Intracellular Buffers:– Proteins +PO4
Extracellular Buffers:– Bicarbonate –
Carbonic acid system

49. Respiratory Acidosis
• Caused by retention of CO2 secondary to decreased
alveolar ventilation
• Pco2 is elevated and plasma HCO3
- conc. is normal
• Chronic respiratory acidosis - Pco2 ↑, HCO3
- ↑ with
renal compensation

50. Respiratory acidosis
Causes
• Conditions causing inadequate ventilation
– Airway obstruction
– Pneumonia
– Atelectasis
– Pleural effusion
– Hypoventilation due to pain of abdominal incisions
or abdominal distension limiting diaphragmatic
excursions

51. Respiratory Acidosis
Management
• Take measures to ensure adequate ventilation
• Prompt correction of the pulmonary defect when
feasible
– Head injury may worsen hypoxic brain damage

52. Respiratory Alkalosis
Causes – hyperventilation due to
– Apprehension
– Pains
– Hypoxia
– CNS injury
– Assisted ventilation
They all cause rapid depression of the arterial Pco2
and elevation of pH.
Acute phase – normal HCO3
- conc.
Later – HCO3
- falls with renal compensation

53. Respiratory Alkalosis
Management
• Measurement/monitoring of blood gases
• Appropriate corrections of ventilatory pattern when
indicated
• Severe and persistent respiratory alkalosis – difficult
to correct and has poor prognosis because of the
underlying cause – hyperventilation from intracranial
injury
•Treatment – directed towards the underlying
cause

54. Metabolic Acidosis
• Due to retention or production of acids or loss of
HCO3
-
• Causes – any condition causing elevated anion gap
– Shock or inadequate tissue perfusion
– Starvation
– Alcohol intoxication
– Renal failure
– Uraemia
– Aspirin poisoning

55. Metabolic Acidosis
• Most common cause of severe metabolic acidosis in
surgical patients is acute circulatory failure with
accumulation of lactic acid

56. Metabolic Acidosis
Treatment
• Directed towards correcting the underlying cause
• Reserve HCO3
- therapy for severe metabolic acidosis
• Discourage routine use of NaHCO3 during
resuscitation of patients in hypovolaemic shock
particularly after cardiac arrest
• Frequent measurements of HCO3
- and blood pH are
the best guides of therapy.

57. Metabolic Alkalosis
• Results from the loss of fixed acids or gain of HCO3
-
and is aggravated by any existing K+ deficit.
• Respiratory compensation is small but compensation
is generally through the renal mechanisms.
• Caused by persistent vomiting as seen in gastric
outlet obstruction and intestinal obstruction as well
as in prolonged nasogastric drainage

58. Fluid and Electrolyte Therapy
Parenteral solutions –
• Vary in composition to satisfy various fluid
requirements in the surgical patient.
• Given a situation, a typical fluid will correct the
abnormalities with minimal demands on the kidneys.
• The choice of a particular fluid depends on the
volume status of the patient and the type of
concentration or compositional abnormality present.

59. Maintenance of balance by
1.Normal daily requirement
2.Replacement of loss (due to disease or surgery or
both)
•Normal fluid requirement:
In the tropics: 3 litres/24 hrs:
(1 L N/S + 2 L of 5% D/w)
In temperate regions: 2.5 L/24 hrs (0.5 L N/S + 2 L 5%
D/w

60. • Electrolytes: daily requirements
• 1.5 – 2.3 grams of sodium/day/adult (2.3 grams
equivalent to one teaspoonful of salt
• This is equiv to 1.5 mmol–2.3 mmol
• N/saline = 154 mmol/litre !

61. • Using body weight - 100ml/kg for 1st 10 kg.
+ 50ml/kg for 2nd 10 kg.
+ 25ml/kg for each subsequent kg. > 20
•Determinations using body wt over-estimate
needs in obese pts and under-estimate in thin
pts
•Also by fluid shifts that accompany onset of
anabolism
– For adults [rough estimate]
•30-35ml/kg/day

62. • Using body surface area:--1500ml/surface area in m2
– Both formulae assume 1200-1500ml/day of urine,
500-1000ml/day of insensible loss and addition of
350-500ml/day from catabolic oxidation of body
fat
– Converting from parenteral nutrition to anabolic
status, add 500-800ml to accommodate loss from
catabolic oxidation and extra for new body cell
mass anabolism

63. For maintenance, give:
 4.3% dex-in-0.18 saline
 Osmolality = 300
 For both children and adults

64. Fluid & electrolyte therapy for different surgical
conditions:
1.Dehydration (vomiting, diarrhoea, faecal fistula):
• N/s only until urine output normal
• Then, maintenance fluid
2.Shock: same as above
3. Gastric outlet obstruction:
• Fluid of choice in goo is N/saline, not ringer’s
lactate (b/cos in goo, there is alkalosis. Ringer’s
lactate will worsen it)

65. • In resuscitation
• Use ringer’s lactate or N/s
• Ringer’s lactate is better than N/s
• NORMAL URINE OUTPUT = 30-50ml/hr (0.5 ml–1
ml/kg/hr) = NORMAL TISSUE PERFUSION=ADEQUATE
RESUSCITATION

66. • 5%, 10%, 50% dextrose; darrows:
• 5% dex post-op = protein-sparing
• 10% dex = augment liver storage
• 50% dextrose = hypoglycamia
• Darrows = augment potassium

67. Composition of Parenteral Fluids (mEq/L)
Fluid Na+ K+ Ca2+ Cl- HCO3- CHO pH
ECF 142 4 5 103 27 7.4
LR 130 4 2.7 109 28 6.5
0.9%(0.45) NaCl 154(77) 154(77) 4.5
4.3% D/S
.2% NaCl 30 30 4.5
3%(5) NaCl 513(855) 513(855) 4.5
5% Albumin 145 7.4
Badoe’s 43.3 16 1.3 51.7 9

68. Errors in fluid therapy
 5% Dex in N/s is hypertonic. It has a diuretic effect
 5% Dex in water is hypotonic. In large volumes, will
cause cerebral oedema and hyponatraemia.
Treatment: diuretics, then N/saline
 Darrow's before adequate urine output – very
serious error!
 Ringer’s lactate in alkalosis
 Starting fluid before blood is taken for blood
chemistry

69. Complications of intravenous fluid
therapy
• Thrombophlebitis
• Local sepsis
• Septicaemia
• Overloading
• Air embolism

70. Conclusion
• Versatility in fluid management is a
prerequisite for successful management of
patients

71. References
• Baja’s principles and practice of surgery E. A.Badoe
.Et al 5th edition.
• Fluids and electrolyte metabolism Dr.O. A. Atoyebi,
(FMCS) Professor of surgery College registrar 2009
• Principles of fluid and electrolyte management in
surgery Prof G. U. Chianakwana FWACS, FRCS
(IRELAND) WASC update course 2019
• Bailey & love's short practice of surgery, 27th edition
edited by norman S. Williams, P. Ronan
o'connell, andrew mccaskie

72. THANK YOU