FLUID AND ELECTROLYTES
MANAGEMENT IN SURGERY
DR SALE DANJUMA
DIVISION OF NEUROSURGERY
DEPARTMENT OF SURGERY
BARAU DIKKO TEACHING HOSPITAL
KADUNA STATE UNIVERSITY, KADUNA.
Introduction
Fluid and electrolyte management
• Important part of the perioperative
management of the surgical patient
• Critical factor in some patients as a result of
the response to surgery and trauma
• Understanding of the metabolism of these
fluid and electrolyte is essential to the care of
surgical patients
Distribution of body water
Water ≈ half of adult’s body
TBW – 60% of body weight (young men)
– 50% of body weight (young women
and older men)
– 45% of body weight (older women)
TBW
Intracellular – ⅔ of TBW
Extracellular – ⅓ of TBW
Distribution of body water
Extracellular fluid (ECF)
Intravascular – 4% of body weight (men)
Extravascular
Interstitial – 15% of body weight
Transcellular – 1% of body weight
Transcellular fluid – bone, dense CT, GIT secretions,
CSF, synovial fluid, etc.
Distribution of body water
• TBW is less in obese patients – fat content
• TBW is less in females – relatively smaller
muscle mass and higher fat deposits
In Children
TBW: 75 – 80% at birth, decreases steadily to
65% at 1yr
ECF: 35% at birth, decreases to 20% at 2yrs
ICF – changes minimally
FLUID REQUIREMENT
LOSES TROPICS (ml) TEMPERATE (ml)
Skin and lungs 1,700 1,000
Urine 1,500 1,500
Faeces 200 200
TOTAL 3,400 2,700
GAIN
Endogenous production 200 200
NET REQUIREMENT 3,200 2,500
Electrolyte distribution in body fluids
• Difference in ionic composition of ICF and ECF
due to the cell membrane – semi permeable
• Effective osmotic pressure contributed to by
any substance that does not freely traverse
the cell membrane
Electrolyte distribution in body fluids
Ion Intravascular Interstitial Intracellular
mmol/L mmol/L 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
PO43- 0.8 – 1.4 1.6 25.8
Protein 2 0 9
SO42- 1 1 20
Organic 3 3 -
acids
ELECTROLYTE REQUIREMENTS
LOSES TROPICS (mmol) TEMPERATE (mmol)
SODIUM
Urine 114 80- 110
Sweat 10-16
Faeces 10 10
Total 130 -140 90-120
POTASSIUM
Urine 50 60
Sweat negligible
Faeces 10 10
TOTAL 60 70
Average daily requirements of electrolytes
• Sodium 2-3 mmol/kg body wt
• Potassium 1-2mmol/kg
• Chloride 2-3mmol/kg
• Calcium 0.2-0.3 mEq/kg
• Magnesium 0.25-0.35mEq/kg
• Phosphate 7-9mmol/1000kcal
• *ADJUST IN PRESENCE OF RENAL, HEPATIC OR
CARDIAC FAILURE, AND BY PRE-EXESTING DEFICITS
OR EXCESSES AND ON-GOING LOSSES
ENERGY REQUIREMENT
• Body store of glycogen 400g
• This provides 6694J (1600 kcals)
• Used up in 1st 24hrs of starvation
• After
– 75-90% from fat
– 10 -25% from protein
• With 100 -150g of glucose per day
gluconeogenesis is reduced to the minimum
and acidosis is prevented
COMPOSITION OF COMMON CRYSTALLOIDS
COLLOIDS REPLACEMENT SOLUTIONS
• Hetastarch
• Dextran
• Gelatins
• Red blood cells
• Fresh frozen plasma
• Albumin
Sodium metabolism
Total approx 5000mmol in adults.
20% firmly bound in bone, 80% metabolically available [44%
ECF, 9% ICF, 27% bone (exchangeable)
Predominantly extracellular cation
Total body Na depletion marked by signs of tissue dehydration
Causes – intestinal obstruction with vomiting or aspiration,
high output fistulae, severe diarrhoea [colitis, dysentery,
cholera, SIADH
Na excess caused by excess 0.9% saline in immediate post-op
during phase of Na retention. Marked by pitting oedema, esp
in sacral region, wt increase. However serum Na rarely
elevated since water retention dilutes the blood. Treatment
for Na excess is salt restriction. Occasionally diuretics
especially spironolactone is used.
Other causes of hyponatremia
Pseudohyponatremia (normal plasma osmolarity)
Hyperlipidemia, hyperproteinemia
Dilutional hyponatremia (increased plasma osmolarity)
Hyperglycemia, mannitol
True hyponatremia (reduced plasma osmolarity)
Reduction in ECF volume
Plasma, GI, skin, or renal losses (diuretics)
Expanded ECF volume
Congestive heart failure
Hypoproteinemic states (cirrhosis, nephrotic syndrome, malnutrition)
Normal ECF volume
SIADH
Pulmonary or CNS lesions
Endocrine disorders (hypothyroidism, hypoadrenalism)
Drugs (e.g., morphine, tricyclic antidepressants, clofibrate,
antineoplastic agents, chlorpropamide, aminophylline, indomethacin)
Miscellaneous (pain, nausea)
Potassium metabolism
35-45 mmol/kg in body
75% within muscle mass
50-60mmol present in extracellular fluid where it useful in glucose uptake
and glycogen synthesis
Intracellular K : N ratio of 3.5:1 essential for optimal protein synthesis
K depletion caused by diabetic coma treated by saline infusion [acute];
diuretics, diarrhoea of villous adenomas and ulcerative colitis, Cronkhite-
Canada syndrome, prologed naso-gastric aspiration and high intestinal
fistulae [chronic]. It is associated with malaise, weakness, ileus, paradoxic
aciduria with metabolic acidosis, pseudodiabetic glycosuria, urinary K
<40mmol/L
K excess marked by weakness, areflexia, paraesthesias and respiratory
paralysis
K deficit treated by infusion of K chloride or acetate over the day , or oral
as KCl, milk, fruit juices, honey and meat extracts
K excess treated with ion exchange resins [low, chronic] or dialysis
In emergencies [arrhythmia] intravenous calcium gluconate, Na
bicarbonate, 50% dextrose with insulin provide temporary relief
For patients on parenteral nutrition add 30-50 mmol/day to cover for
anabolic needs
Calcium metabolism
Total body store – 1000 – 1500g
Plasma – 2.2 – 2.5 mmol/L
3 forms – bound, free non-ionized and free ionized
[active component, falls with alkalinity]
Controlled by PTH, Vitamin D, calcitonin, bone
metabolism, massive (ACD) blood transfusion renal
function, immobilization
Tetany, nephrolithiasis, psychiatric, bone pains
Magnesium metabolism
• 1000 mmol total. 60% firmly bound to bone.
• 0.7 -0.9 mmol/L in plasma
• Def. – prolonged loss of secretions [fistulae,
ulcerative colitis, prolonged Mg-free fluid admin.,
massive small gut resection, cirrhosis and parathyroid
disease
• CNS irritability, lowered blood pressure, cardiac
arrhythmias
• Treatment – add 20 mmol Mg sulfate to dextrose
over 24hrs.
• Essential in hyperalimentation
Osmolality
• ECF and ICF contain different types of solute
but conc. of solutes inside and outside the
cells are equal
• Concentration difference exists only
transiently because they create an extremely
strong force for water movement across cell
membranes
• Osmolality – no of milliosmoles of solute
particles per litre of solution
Osmolality
• Sodium salts, glucose and urea – responsible for most
of the solute particles in the ECF
• Measurement – osmometer
• Plasma osmolality
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
Body fluid changes
Classified into three groups
Disturbances of volume – due to loss or addition
of isotonic salt solution
Disturbances of concentration – due to addition
or loss of water from the ECF or depletion of
Na+ from the ECF
Disturbances of composition:– Acid – base
balance
Volume changes
- Excess or deficit of ECF volume can be
diagnosed by estimating the blood urea
nitrogen (BUN)
- BUN rises with sufficient ECF deficit
- Concentration of blood cells and plasma
proteins increases with ECF deficit and
decreases with ECF excess
- Concentration of Na+ is not related to the
volume status of the ECF
Volume changes
ECF volume deficit is the most common fluid
disorder in surgical patients.
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
Volume changes
• Severe volume depletion depresses all body
systems and interferes with the clinical
evaluation of a patient.
Concentration changes
• Serum Na+ level is used to estimate total body
fluid osmolality
• 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
Hyponatraemia
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.
Potassium
• Major cation of intracellular water – 98% at
concentration of 150mEq/L
• Normal dietary intake – 50-100mEq/day
• Intracellular and extracellular distribution
influenced by many factors :
Release of significant amount from
intracellular space into the extracellular space
in response to severe injury, surgical stress,
acidosis and catabolic state.
Hyperkalaemia
• 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
Hyperkalaemia
Treatment
- Withhold exogenously administered K+
- Correct the underlying cause
- Iron exchange resins
- Dialysis when indicated
- Give HCO3- , glucose and insulin
-Give 1g of 10% calcium gluconate under ECG
monitoring to suppress the myocardial effects of K+
temporarily
Hypokalaemia
• Due to excessive renal excretion of K+
• Movement of K+ into the cells
• 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
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
Hypokalaemia
Treatment
• Prevention i.e. replace GIT fluid loss volume
for volume
• Give K+ not more than 40mEq/L of fluid
• Rate not exceeding 20mEq/hour
• Don’t give oliguric patients and within 24hrs
post operatively
Calcium
• Majority of Calcium in the body is in the form
of PO43- and CO32-
• 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
Calcium
• 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
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
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
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
Hypercalcaemia
Causes
• Hyperparathyroidism
• Cancer with bony metastasis e.g. Breast Ca
Treatment
• Inorganic PO43- 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+
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
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
Magnesium
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+
Acid – Base Balance
Intracellular Buffers:– Proteins
Extracellular Buffers:– Bicarbonate –
Carbonic acid system
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
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
Respiratory Acidosis
Management
• Take measures to ensure adequate ventilation
• Prompt correction of the pulmonary defect
when feasible
– Head injury may worsen hypoxic brain damage
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
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
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
Metabolic Acidosis
• Most common cause of severe metabolic
acidosis in surgical patients is acute circulatory
failure with accumulation of lactic acid
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.
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.
Metabolic Alkalosis
• Caused by persistent vomiting as seen in
gastric outlet obstruction and intestinal
obstruction as well as in prolonged nasogastric
drainage
Fluid Consumption/Production
Production
• Average – 2,000 – 2,500mls/day
• Orally – 1,500mls
– The rest from food
Daily fluid losses
– Stool – 250mls
– Urine – 800 – 1,500mls
– Insensible losses (skin, lungs): 600 – 900mls
• Increases with increased environmental temperature –
250mls/°C rise/day
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.
Fluid and Electrolyte Therapy
• Ringers lactate - an ideal isotonic
solution/physiological fluid that is close to the
plasma compared to isotonic NaCl whose Cl- conc. is
154mEq/L and is higher than the conc. in blood
imposing an appreciable load on the kidneys of
excess Cl- that can’t be excreted rapidly leading to a
dilutional acidosis.
• Normal saline is however good for the correction of
an ECF volume deficit in the presence of
hyponatraemia, hypochloraemia and metabolic
alkalosis.
Preoperative fluid therapy
• Preoperative and fluid correction – an integral
part of surgical care
• Safe approach – proper understanding of fluid
disturbances associated with surgical illness
and adherence to guidelines
Preoperative fluid therapy
• Fluid replacement depends on existence of
concomitant concentration and compositional
abnormalities
e.g Hypernatr. + Vol. deficit –dextrose
Hypernatr. + Vol. excess–restrict water
Intraoperative fluid therapy
• Inadequate preoperative ECF Volume
replacement can cause hypotension under
anaesthesia
• Intraoperative correction of vol. deficit with a
balanced salt solution will remove post
operative salt intolerance
Intraoperative fluid therapy
• Routes of intraoperative fluid losses
- Blood loss
- Oedema from extensive dissection
- Fluid collection within the lumen and wall
of small bowel
- Accumulation of fluid in the peritoneal
cavity
- Fluid loss from the wound – very small
Intraoperative fluid therapy
• The use of albumin solutions with balanced
salt solutions to replace ECF deficits during
surgery is not necessary and is potentially
harmful
Intraoperative fluid therapy
• Guidelines
- Blood should be replaced as lost
- Fluid replacement should begin during
the operative procedure
Postoperative therapy
• Immediate postoperative period
-Give fluid only after proper evaluation
-Correct existing deficit in addition to
maintenance as proper replacement
during this period will facilitate subsequent
fluid management
*Do not give potassium within the first 24hrs
after surgery unless there is a deficit
Postoperative fluid therapy
• Late postoperative period
- There is a problem of accurate
measurement and replacement of all
losses during this postoperative
convalescent phase
- Measure and replace sensible losses
(from GIT)
- Estimate and replace insensible losses
- Identify and correct any electrolyte deficit and
give maintenance
Fluid and Electrolyte Management in
Surgery
• Fluid and Electrolytes in the Paediatric and
Elderly patients need to be administered with
caution
• Essential to the successful management of
fluid and electrolyte abnormalities in them is
adequate monitoring of their
cardiopulmonary status especially the
neonates
•
MANAGEMENT
History
duration of illness
duration and approximate amount of loss
• Clinical observation
general condition
mental state
skin
Tongue
subcutaneous veins
eyes
PR, BP
• Investigation
serum electrolyte and blood urea
PCV, Hb
arterial blood gases
• Treatment
replace what is lost
monitor- input/output
CVP 10-15cm H2O
Urine output 0.5 -1mls/Kg/hr in adults
1-2mls/Kg/hr in children
2-4mls/kg/hr in newborn
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