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84
Manipal Manual of Surgery
Ventilation: Low PaCO2 suggests respiratory alkalosis.
Acid–base status: The pH shows acidosis. The pH has
decreased, whereas the PaCO
Hence, it is not respiratory acidosis and must be metabolic. The bicarbonate levels are far below normal and
suggests a primary metabolic acidosis. The low PaCO
suggests secondary respiratory alkalosis. The patient has
primary metabolic acidosis with partial compensation.
3. A 65-year-old man with a 40-year history of smoking,
posted for elective herniorrhaphy was sent to the preanaesthetic clinic for evaluation. Since, he gave history
of poor exercise tolerance as evidenced by breathlessness even on mild exertion, and clinical examination
revealed presence of COPD, an arterial blood gas
analysis was done while the patient breathed room
air. The report showed a PaO2 = 55 mmHg, PaCO
= 60 mmHg, pH = 7.34 and [HCO
has also decreased.
2
–
] = 30 mmol/l.
3
1. The normal hydrogen ion concentration of plasma
is ________ nmol/L.
A. 30 B. 40
50 D. 60
C.
2. The most important buffer system in the plasma is:
A. Phosphate buffer system
B.
Ammonia buffer system
C. Proteins
D. Bicarbonate-carbonic acid buffer system
3. pH is the negative logarithm to the base 10 of
hydrogen ion concentration expressed in ________.
A. mol/L B. mmol/L
.
nmol/L D. μmol/L
C
4. The solubility coefficient of carbon dioxide in plasma
________ ml/mmHg/dl.
is
A. 0.3 B. 0.03
.
0.003 D. 3
C
5. The following is true in primary metabolic acidosis
with secondary respiratory alkalosis:
A. pH and PCO
B. pH decreases but PaCO
C. pH and PaCO
D. pH increases but PaCO
are decreased
2
increases
2
are increased
2
decreases
2
Analysis
Oxygenation: The PaO2/FIO2 ratio is 55/0.21 = 262.
Thus, although the PaO2/FIO2 ratio seems adequate,
the actual PaO2 is less than 60 mmHg and suggests
hypoxaemia.
2
2
Ventilation: High PaCO2 suggests respiratory acidosis.
Acid–base status: The pH shows acidosis. The pH has
decreased, whereas the PaCO2 is high. Hence, it is
respiratory acidosis. The bicarbonate levels are high
which suggests metabolic alkalosis. Since, the pH is
acidotic but near normal, the patient must be having
primary respiratory acidosis with compensatory
metabolic alkalosis. He has fully compensated respiratory
acidosis. This picture of chronic hypoxaemia and
hypercarbia is typical of patients suffering from severe
chronic obstructive pulmonary disease.
6. The following is one of the causes of metabolic
acidosis with increased anion gap:
A. Diarrhoea B. Intestinal fistula
.
Pancreatic fistula D. Diabetic ketoacidosis
C
7. The following equation represents the nonlogarithmic
form of acid–base equation:
A. Harrison B. Henderson
C
Hutchinson D. Hanson
.
8. The following may be a cause of respiratory alkalosis:
A. Morphine overdose
B
.
Chronic obstructive pulmonary disease
C. Salicylate poisoning
D. Curare poisoning
9. Following are true for albumin except:
A. First line of treatment in hypovolaemic shock
B. Does not carry risk of transfusion hepatitis
C. Used in nephrotic syndrome
D. It should not be used to treat malnutrition
10. Metabolic acidosis with normal anion gap is also
called:
A. Hyperchloraemic acidosis
B
Hyperkalaemic acidosis
.
C. Hypernatraemic acidosis
D. Hypercalcaemic acidosis
Answers
1. B 2. D 3. A 4. B 5. A 6. D 7. B 8. C 9. A 10. A
Section I • Basic Principles of Surgery
20
Fluids and Electrolytes
Physiology of fluids
Water regulation
Disturbances of volume
Regulation of sodium concentration
SU12.2: Describe and discuss the methods of estimation
and replacement of the fluid and electrolyte requirements
in the surgical patient.
A good understanding of the physiology of fluids and
electrolytes is fundamental to the practice of surgery.
Most surgical conditions are associated with changes
in this balance and it is only appropriate that these are
identified and treated effectively.
NORMAL PHYSIOLOGY
The human body consists of about 50–70% liquids and
30–50% solids by weight. The liquid portion varies with
age, sex and body habitus. The variation is the result of
individual differences in the fat content of the body
which contains very little water. Hence, thin individuals
have greater total body water (TBW) content as
compared to obese individuals. Similarly, the TBW is
about 50% in women and 60% in men. Neonates have
up to 80% TBW. Of this total body water, intracellular
water constitutes 40% of body weight (2/3rd of TBW)
and the extracellular portion, 20% of body weight
(1/3rd of TBW). The interstitial fluid and plasma
portions of extracellular fluid constitute 15% and 5% of
body weight, respectively (Fig. 20.1).
Composition of Body Fluids
These fluid compartments are separated by semipermeable membranes allowing their fluid composition
to be maintained within distinct limits. Table 20.1 shows
Disturbances in concentration
Disturbance in composition of body fluids
Perioperative fluid therapy
Types of intravenous fluids
Fig. 20.1: Relation of various fluid compartments to body weight.
ICF—intracellular fluid; ISF—interstitial fluid; PV—plasma volume
Table 20.1 Composition of body fluids
Composition Intracellular Extracellular
(mmol/L) (mmol/L)
Cations
Sodium 10 140
Potassium 150 4
Calcium 2 2.5
Magnesium 20 1.5
Anions
Chlorides 10 111
Bicarbonate 10 25
Sulphate 70 1.5
Phosphates 45 1
the composition of the intracellular and extracellular
fluid compartments. The composition of the intra-
85
86
Manipal Manual of Surgery
cellular compartments may vary according to the tissue,
e.g. fat contains very little water.
The tonicity of plasma is determined by the solutes,
sodium and its corresponding anions, chlorides and
bicarbonate, together with substances such as glucose,
urea and proteins. These particles are osmotically active
and hence, tonicity is described in terms of osmolality
(mOsm/kg H
2
O).
Osmolarity is concentration of a solution in terms of
osmoles (or mosmoles) of solute per litre of solution
(solute + water). Osmolality is concentration of a
solution in terms of osmoles (or mosmoles) per
kilogram of solvent. Osmolality is independent of the
temperature of the solution and volume of the solute.
Hence, osmolality is the preferred term in clinical
practice.
Osmolarity: Osmoles per litre
Osmolality: Osmoles per kilogram
Osmolality of a solution can be measured in two
ways:
1. By using the depression of freezing point of the
solution: A solution of 1 Osm/kg freezes at –1.86°C.
Normal plasma freezes at –
Plasma osmolality =
0.54°C.
–0.54
3
10 mOsm/kg
×
–1.86
= 290 mOsm/kg
2. By estimating the solute concentration: Osmolality
can be estimated from the concentration of major
solutes of plasma.
Osmolality = 2 × [Na
+
] mmol/L +
[Glucose (mg%)]
18
[Blood urea (mg%)]
+
6
Example: If a patient’s sodium concentration is
140 mmol/L, blood glucose concentration is 180 mg%
and blood urea is 30 mg%, his plasma osmolality can
be calculated as follows:
Osmolality =
2 ×[140] + +
180 30
18 6
= 280 + 10 + 5 = 295 mOsm/kg
From the equation, it is evident that sodium contributes the most to the osmolality of plasma.
A change in osmolality is usually due to changes
in sodium. The normal range of plasma osmolality is
Section I • Basic Principles of Surgery
285–300 mOsm/kg.
Plasma Colloidal Osmotic Pressure
The plasma proteins normally do not pass out of the
capillaries into the interstitium. These raise the plasma
osmotic pressure above that of the interstitial fluid by
an amount referred to as colloidal osmotic pressure
(plasma oncotic pressure). The normal plasma colloidal
osmotic pressure is 25 mmHg. Albumin is responsible
for 75% of this oncotic pressure.
The body has mechanisms to regulate and maintain
the volume of fluids, their concentration and composition within narrow limits to maintain homeostasis.
Hence, a systematic assessment of fluid status of a
patient involves the assessment of body fluid volume,
its concentration and its composition in that order.
WATER REGULATION (Regulation of Volume)
The primary methods of body water regulation are:
1. Regulating the volume of liquid ingested: When the
extracellular fluid volume reduces, the thirst centre
in the hypothalamus is stimulated which encourages
the person to ingest more water.
2. Regulating the volume of urine excreted: This is
regulated by plasma antidiuretic hormone (ADH). A
reduction in plasma volume releases ADH from the
posterior pituitary which in turn acts on the ADH
receptors in the collecting tubules of the kidney. This
results in increased reabsorption of water and reduced
production of urine. ADH release may also be stimu-
lated by increased plasma osmolality and angiotensin.
DISTURBANCES OF VOLUME
A decrease in the circulating volume is called hypovolaemia and an increase, hypervolaemia.
HYPOVOLAEMIA
This is common in surgical patients. The assessment of
acute loss of blood volume is detailed in Chapter 12.
The reduction in blood volume due to loss of water can
be in the following ways:
. Gut—vomiting, diarrhoea, fistulae
a
b. Skin and lungs—0.5 ml/kg/h normally, increases by
12% for every 1°C rise in body temperature.
c. Sequestration of fluid in third space refers to non-
contributory fluid space that is unavailable to the
circulatory system.
Assessment of Dehydration
This is a clinical assessment based upon:
1. History: Severity and duration of loss of fluid.
Fluids and Electrolytes
87
Table 20.2 Assessment of dehydration
Degree of Loss of body Clinical features
dehydration weight (%)
Mild 5 Reduced skin turgor, sunken
eyes, dry mucous membranes
Moderate 10 Oliguria, hypotension and
tachycardia in addition to the
above
Severe 15 Profound oliguria and com-
promised cardiovascular
function
2. Examination: Thirst, dryness of mucosa, loss of skin
turgor, orthostatic hypotension, tachycardia, reduced
jugular venous pressures and decreased urine output
in the presence of normal renal function. Dehydration
can be classified as given in Table 20.2.
Laboratory Assessment
Haemoconcentration leads to falsely elevated haemoglobin, packed cell volume estimations and increased
blood urea concentration. The kidneys reabsorb more
water than usual leading to increased urine osmolality
(>650 mOsm/kg).
REGULATION OF SODIUM CONCENTRATION
Water constitutes the major component of all body fluids
but the composition varies with the fluid compartment.
The most abundant cation of extracellular fluid is
sodium and is the prime determinant of ECF volume.
Ninety per cent of the ECF osmolality is due to sodium.
The human body has no known mechanism to
regulate sodium intake. The body regulates sodium
output by:
• Regulating glomerular filtration rate
• Regulating plasma aldosterone levels
Addition or loss of water produces a change in the
concentration of the solute. The quantity of solute
relative to the volume of water is thereby increased (ECF
is concentrated) or decreased (ECF is diluted) with loss
or addition of water, respectively. Changes in concentration are generally changes in water balance rather than
changes in sodium regulation. Since the changes in
volume and concentration are interdependent and the
changes in water content are not easily measured, an
estimate of the fluid volume and concentration is usually
made by using the measured sodium levels and serum
osmolality.
HYPERVOLAEMIA
Causes
1. Excessive infusion of intravenous fluids.
. Retention of water in abnormal conditions, such as
2
cardiac, renal and hepatic failure.
3. Absorption of irrigation fluid as during transurethral
resection of prostate using distilled water.
Diagnosis
• History and physical examination can lead to the
cause.
• Physical examination: Distended neck veins, pedal
oedema, body weight gain.
• Circulatory overload:
Hypertension, tachycardia, pulmonary oedema
–
– Confusion, restlessness, convulsions and coma.
The development of these signs depends on the rate
and volume of fluid overload, renal function and
cardiovascular reserve.
Management
1. Treat the cause
2. Restriction of water and salt
3. Diuretics (or dialysis, if necessary) to remove excess
water.
DISTURBANCES IN CONCENTRATION
HYPONATRAEMIA
Hyponatraemia is defined as a sodium level less than
135
mmol/L. It may occur as a result of water retention,
sodium loss, or both. True hyponatraemia is always
associated with low plasma osmolality. It may be
associated with expanded, contracted or a normal
extracellular volume.
Causes
Assessment of hyponatraemia should begin with an
estimation of the extracellular fluid volume (clinically
and if necessary, using central venous catheters). Thus,
true hyponatraemia can be of three types: Hypervolaemic hyponatraemia, hypovolaemic hyponatraemia
and normovolaemic hyponatraemia (Fig. 20.2).
I. Hypervolaemic Hyponatraemia
Hypervolaemic hyponatraemia may be associated with
clinical features of hypervolaemia, such as oedema.
Acute hypervolaemia (e.g. TURP syndrome—acute
absorption of hypotonic fluids into the intravascular
compartment) may result in cerebral oedema and
pulmonary oedema. As plasma osmolality decreases,
water moves from the extracellular space into the cells
Section I • Basic Principles of Surgery
88
Manipal Manual of Surgery
Fig. 20.2: Evaluation of hyponatraemia
leading to oedema. The expansion of brain cells is
responsible for the symptomatology of water
intoxication: Nausea, vomiting, lethargy, confusion,
+
restlessness, etc. If severe ([Na
] <100 mmol/L), it can
result in seizures and coma. Chronic hypervolaemia as
in congestive cardiac failure, cirrhosis and nephrotic
syndrome may manifest with pedal oedema and
elevated jugular venous pressures until decompensation
occurs. The urinary sodium concentration is less than
15 mmol/L.
Treatment
Acute hyponatraemia (duration <72 h) can be safely
corrected more quickly than chronic hyponatraemia.
The following factors must be evaluated: Patient’s
volume status, duration and magnitude of the hyponatraemia and the degree and severity of clinical symptoms.
Fluid restriction, diuretics and correction of the
Section I • Basic Principles of Surgery
underlying condition may be adequate in most cases.
A combination of intravenous normal saline and diuresis
with a loop diuretic (e.g. frusemide) also elevates serum
sodium concentration.
Acute symptomatic hyponatraemia is a medical
emergency. It should be treated with hypertonic saline
(1.6% or 3%). Concomitant use of loop diuretics
increases free water excretion and also decreases the
risks of fluid overload.
The sodium concentration must be corrected to relieve
symptoms and to a concentration of 125 mmol/L.
Patients who are acutely symptomatic, the treatment
goal is to increase the serum sodium by approximately
1–2 mEq/L/h until the neurologic symptoms subside.
The correction should be slow and over a period of
12–24 hours with frequent checks of sodium concentration (every 2–4 h) to avoid overcorrection.
Avoid an absolute increase in serum sodium of more
than 15–20 mEq/L in a 24-hour period. If sodium
correction is undertaken too rapidly, the resulting
Fluids and Electrolytes
89
osmolality changes in the extracellular fluid can cause
central pontine myelinolysis. This condition is serious
and can be irreversible.
The following equation can aid in the estimation of a
sodium deficit to help determine the rate of saline infusion:
Calculated sodium deficit = (140 – current serum Na
+
× (body weight in kg) × 0.6
A litre of normal saline (0.9%) contains 154 mEq
sodium chloride (NaCl) and 3% saline 500 mEq NaCl.
In chronic severe hyponatraemia (i.e. serum sodium
<115 mEq/L), the rate of correction should be slow and
should not exceed 0.5–1.0 mEq/L/h, with a total
increase not to exceed 10 mEq/L/day.
II. Hypovolaemic Hyponatraemia
Hypovolaemia corrected inappropriately with
hypotonic fluids such as 5% dextrose may result in
hyponatraemia. The hypovolaemia may be due to renal
causes such as diuresis or a salt-losing kidney. The
urinary concentration of sodium is more than 20 mmol/L
in these patients. Extrarenal loss of volume as in
diarrhoea, vomiting or 3rd space loss may result in
urinary concentration less than 20 mmol/L. All these
are termed depletional syndromes and require saline
infusion.
Treatment
Based upon the volume status, administer isotonic saline
to patients with hypotonic hyponatremia who are
hypovolaemic to re-expand the contracted intravascular
volume.
III. Normovolaemic Hyponatraemia
Occasionally, hyponatraemia may exist with normovolaemia. In such situations,
the plasma osmolality must
be estimated. If it is low, renal failure or the syndrome
of inappropriate ADH secretion (SIADH) may be
considered.
Treatment
For patients who have hypotonic hyponatraemia and
normovolaemic (euvolaemic), asymptomatic, and
are
mildly hyponatraemic, water restriction (1 L/day) is
generally the treatment of choice. For instance, a fluid
restriction to 1 L/day is enough to raise the serum sodium
in most patients. This approach is recommended for
patients with asymptomatic SIADH. Pharmacological
agents can be used in some cases of more refractory
SIADH, allowing more liberal fluid intake. Demeclocycline is the drug of choice to increase the diluting
capacity of the kidneys by achieving vasopressin
antagonism and a functional diabetes insipidus.
Pseudohyponatraemia
Occasionally, the hyponatraemia is only an apparent
one due to the accumulation of
other solutes such as
glucose, urea, plasma proteins or lipids. The plasma
osmolality is either high or normal in these patients.
Such hyponatraemia is called pseudohyponatraemia.
)
Serum osmolality is governed by contributions from
all molecules in the body that cannot easily move
between the intracellular and extracellular spaces.
Sodium is the most abundant electrolyte but glucose,
urea, plasma proteins and lipids are also important.
Normally, their concentrations are small and contribute
to the plasma osmolality only to a small extent.
However, when the concentrations of these molecules
increase to very high levels, the relative concentration
of sodium in unit volume of serum may reduce. The
actual amount of sodium is normal in these patients and
hence the term pseudohyponatraemia. High blood
sugar level or uraemia leads to higher plasma osmolality
but high plasma protein or lipid levels is associated with
normal plasma osmolality.
Treatment
The treatment of pseudohyponatraemia mainly involves
treatment of the cause and supportive therapy.
HYPERNATRAEMIA
Hypernatraemia is defined as a plasma sodium concentration
of more than 150 mmol/L and may result from
pure water loss, hypotonic fluid loss or salt gain.
Causes of Hyper
natraemia
I. Pure water depletion
. Extrarenal loss Failure of water intake (coma,
1
elderly, postoperative patients)
Mucocutaneous loss—fever
2. Renal loss Diabetes insipidus, chronic renal
failure
II. Hypotonic fluid loss
1. Extrarenal loss Gastrointestinal (vomiting,
diarrhoea)
Excessive sweating
2. Renal loss Osmotic diuresis (glucose, urea,
mannitol)
3. Salt gain Iatrogenic (sodium bicarbonate,
hypertonic saline), salt ingestion
steroid excess
The hypertonicity of plasma leads to cellular dehydration. Clinical evidence of dehydration may not be
apparent until 10–15% of body weight has been lost.
Rehydration should be slow to prevent cerebral oedema.
Section I • Basic Principles of Surgery
90
Manipal Manual of Surgery
The diagnosis can be established by measuring
plasma and urine osmolalities and urine output.
• Uosm > Posm and ↓ urine output → Extrarenal
causes (e.g. diarrhoea, fistulae)
• Uosm > Posm and ↑ urine output → Osmotic
diuresis
• Uosm < Posm and ↑ urine output →↑ ADH or
renal response to ADH.
Treatment
1. Administration of water orally/nasogastric tube
. Administration of IV fluid—5% dextrose or 0.45%
2
saline
3. Change in serum sodium should not be more than
1–2 mmol/L/h. Rapid rehydration can cause cerebral
oedema.
DISTURBANCES IN COMPOSITION OF BODY FLUIDS
POTASSIUM BALANCE
The normal potassium level is 3.5–5.5 mmol/L.
Hypokalaemia and hyperkalaemia are two clinically
important disturbances.
Hypokalaemia (Key Box 20.1)
This is defined as a plasma concentration of potassium
less than 3.5 mmol/L.
Symptoms
• Anorexia, nausea
• Muscle weakness, paralytic ileus
• Altered cardiac conduction: Delayed repolarisation,
reduced height of ‘T’ wave, presence of ‘U’ wave,
wide QRS complexes and arrhythmias.
Management
• Diagnosis and treatment of the cause
• Repletion of body stores
• Potassium supplements, in the form of milk, fruit
juice, tender coconut water.
Key Box 20.1
Causes of Hypokalaemia
Reduced intake
Tissue redistribution: Insulin therapy, alkalaemia, β
adrenergic agonists, familial periodic paralysis
Increased loss: Gastrointestinal losses—diarrhoea,
vomiting, fistulae
Renal causes: Diuretics, renal artery stenosis, diuretic
Section I • Basic Principles of Surgery
phase of renal failure
• Syrup potassium chloride orally—15 ml contains
20 mmol of potassium.
• If the patient cannot take orally or the hypokalaemia
is severe, intravenous potassium chloride is usually
given at a rate of 0.2 mmol/kg/h. If there are lifethreatening arrhythmias, it may be given at a rate
not exceeding 0.5 mmol/kg/h under electrocardiographic monitoring and serial measurements.
Hyperkalaemia
This is defined as a plasma concentration of potassium
more than 5.5 mmol/l.
Clinical Features
• Vague muscle weakness, flaccid paralysis
Electrocardiographic Changes
• Tall, peaked ‘T’ waves with shortened QT interval
(6–7 mmol/l)
• Wide QRS complex, widening and then loss of ‘P’
wave (8–10 mmol/l)
• Wide QRS complex, merge into ‘T’ waves (sine wave
pattern)
+
• Ventricular fibrillation (K
>10 mmol/l)
Treatment of Hyperkalaemia
1. Calcium gluconate (10%): 10–30 ml.
2
. Sodium bicarbonate: 1–2 mmol/kg over 10–15 minutes.
3. 100 ml of 50% dextrose with 10–12 units of insulin
over 15–20 minutes.
4. Hyperventilation
5. Salbutamol nebulisation
6. Calcium exchange resins
7. Peritoneal or haemodialysis
A 21-year-old lady was found to be collapsed as she was
feeding her 15-day-old baby in the nephrology ward. On
arrival, the cardiac arrest response team found her to
have ventricular tachycardia without pulse. Cardiopulmonary resuscitation was given and she was shifted to
the intensive care unit after return of spontaneous
circulation. Investigations showed that her potassium
level was 1.6 mmol/L. She had been admitted to the
nephrology unit for postpartum acute renal failure. She
2
had been dialysed three times following which she had
gone into the diuretic phase of recovery from acute renal
failure. She was putting out about 5 litres of urine per day
in the last two days. Her hypokalaemia was corrected
over 2–3 days. She recovered completely and could be
discharged from the ward in 5 days time.
Fluids and Electrolytes
91
MAGNESIUM
It is the second most abundant intracellular cation. The
normal serum magnesium concentration is 0.7–1 mmol/L.
Most of it is present in the muscle and bone. Only about
1% is intravascular. Consequently, the serum concentration does not reflect body stores.
Role of magnesium in the body: Magnesium is
required for the functioning of most enzyme systems
including Na, K-ATPase, for synthesis of proteins, DNA,
RNA, and parathormone. It also prevents influx of
calcium into the cell.
Magnesium is a muscle relaxant and produces vasodilatation, cardiac depression, bronchodilatation and
tocolysis.
Hypomagnesaemia
Serum concentration <0.7 mmol/L.
Causes
• Inadequate intake as in prolonged starvation or
malabsorption, inappropriate fluid therapy.
• Excessive losses through nasogastric drainage,
diarrhoea or diuresis.
• Redistribution as with insulin infusion or massive
transfusion.
Clinical Features
• Predominantly neurological or neuromuscular
abnormalities—muscular weakness, cramps
• Anorexia, lethargy and weight loss
• Hyperirritability, hyperexcitability, muscle spasms,
stridor, tetany and convulsions
• Hypertension, pulmonary oedema
• Prolonged PR and QT intervals, ST depression and
flattening of T waves
• Supraventricular and ventricular tachyarrhythmias
• Features of hypokalaemia and hypocalcaemia can
also be seen.
Treatment
Magnesium sulphate is available as 50% (500 mg/ml)
solution. Each ml contains 2 mmol of magnesium. In hypomagnaesemia, 8 mmol can be diluted in 50 ml of 5%
dextrose or 0.9% saline and given over 30 minutes. If the
patient has life-threatening arrhythmias, such as pulseless ventricular tachycardia due to hypomagnesaemia
(torsade de pointes),
and is unresponsive to defibrillation
and epinephrine, it can be given as a bolus of 2 g.
Hypermagnesaemia
Most common cause: Iatrogenic.
Clinical Uses of Magnesium
• Antiarrhythmic agent for ventricular arrhythmias
(torsade de pointes)
• As an antihypertensive, particularly for pre-
eclampsia and eclampsia
• As an anticonvulsant
• As a bronchodilator
Clinical features of hypermagnesaemia depend on
plasma concentration
• 4–5 mmol/L—muscle weakness and loss of tendon
reflexes
• 6–7.5 mmol/L—respiratory arrest
• 10 mmol/L—cardiac arrest.
Hence, when patients are administered magnesium
in large doses or as prolonged infusions, their ankle jerks
must be monitored. If found sluggish, further doses or
the infusion must be stopped.
CALCIUM
• Calcium is the most abundant mineral in the body.
Ninety-nine per cent is deposited in the skeleton. In
addition, calcium ions are important for the control
of muscular and neural activities, in blood clotting,
as cofactors for enzymatic reactions and as second
messengers.
• Calcium homeostasis reflects a balance between
reserves in the bone, rate of absorption across the
digestive tract, and rate of loss from the kidneys.
• The hormones parathyroid hormone (PTH), vitamin
D and calcitonin maintain calcium homeostasis in the
ECF. Parathyroid hormone and vitamin D raise Ca
2+
concentrations and calcitonin lowers it.
• Calcium absorption from the digestive tract and
reabsorption along the distal convoluted tubule are
stimulated by PTH from the parathyroid glands and
calcitriol from the kidneys. The average daily requirement of calcium in an adult is 0.8–1.2 g/day.
• Half the serum calcium is bound to albumin and as
albumin levels become low, this bound fraction is
lower leading to a low total serum calcium concentration.
• Hence, the serum calcium level should be related to
the albumin levels and corrected as follows:
• Corrected calcium (mg/dl) = measured total Ca (mg/
dl) + 0.8 (4.0 – serum albumin [g/dl])
• Free ionic calcium is important for the electrical
activity of the nerves and m
uscles and is more reliable
(Normal: 1.0–1.4 mmol/L).
Section I • Basic Principles of Surgery
92
Manipal Manual of Surgery
Hypercalcaemia (Key Box 20.2)
2+
Hypercalcaemia exists when the Ca
concentration of
the ECF is above 11 mg%.
Key Box 20.2
Causes of Hypercalcaemia
Hyperparathyroidism
Malignant cancers of the breast, lung, kidney or bone
marrow
Features
Severe hypercalcaemia (12–13 mg%) causes symptoms,
such as fatigue, confusion, cardiac arrhythmias, and
calcification of the kidneys and soft tissues throughout
the body (moans, stones and groans).
Hypocalcaemia (Key Box 20.3)
Hypocalcaemia exists when calcium level is <9 mg%.
mmol/L).
Key Box 20.3
Causes of Hypocalcaemia
Hypoparathyroidism
Vitamin D deficiency
Chronic renal failure
Features
Muscle spasms, stridor, generalised convulsions,
myocardial depression, cardiac arrhythmia and
osteoporosis.
SU1.3: Describe basic concepts of perioperative care.
PERIOPERATIVE FLUID THERAPY
A patient undergoing surgery needs intravenous fluids
to replace volume deficit acquired during starvation,
normal maintenance for the duration of surgery and
volume lost during surgery. Depending on the extent
of dissection, fluid accumulates in these tissues in the
form of oedema (third space losses). In addition, blood
loss also needs to be replaced.
Perioperative fluid therapy in a patient whose body
homeostasis is normal.
The replacement is as follows:
1. Fluid requirement during starvation:
• Patients awaiting anaesthesia and surgery are kept
fasting for at least two hours for clear fluids. This
Section I • Basic Principles of Surgery
could be longer in patients requiring bowel surgeries.
• People need fluids to cover insensible losses
(through skin and respiratory tract) and urine
output. This is 1–1.5 ml/kg/h.
• The volume deficit that occurs due to fasting before
surgery is replaced. The current fasting guidelines
allow patients to drink clear fluids up to 2 hours
prior to surgery. Hence, the patients should not be
dehydrated.
• If there are any signs of hypovolaemia due to
vomiting, diarrhea, bowel preparation or any other
cause, the patient may need to be administered
additional fluids.
2. Maintenance requirement: The average daily require-
of water for an average-sized adult is 2000 ml.
ment
In general, a volume of 25–30 ml/kg/day meets
the daily maintenance needs. This is calculated as
1–1.5 ml/kg/h. The maintenance fluids are given to
cover insensible losses and urine output as mentioned
before.
3. Third space losses:
• The third space refers to accumulation of fluid in
spaces that are not in continuity with plasma.
• During surgery, there could be loss of fluid into
interstitial space leading to oedema. It is difficult
to quantify how much fluid seeps into the third
space during surgery but it is proportional to the
extent of dissection during surgery. It was believed
that the third space losses could be as much as
4, 6, or 8 ml/kg/h for surgeries with minimal,
moderate or large amount of dissection.
• This is currently considered as an overestimation.
Excessive fluid administration can lead to loss
of endothelial glycocalyx and oedema. Inadequate
fluid therapy can give rise to hypoperfusion, renal
failure and organ dysfunction.
• The current opinion is that maintenance fluids
should be given as described earlier and fluids
boluses of 250 ml must be given as required by
monitoring the haemodynamic effects.
• When in doubt, passive leg raising can increase
venous return and help in decision-making.
• Usually, urine output is measured during major
surgery and an output of 0.5–1 ml/kg/h is desired.
However, intraoperative urine output has no
correlation to the incidence of postoperative renal
failure and hence should not be used as a guide to
intraoperative fluid therapy.
• In complicated and extensive surgeries or in
patients with compromised cardiac status or renal
failure, more sophisticated monitoring techniques
such as central venous pressure, stroke volume
variation or inferior vena caval diameter measurements may be required.
Fluids and Electrolytes
93
4. Blood loss is replaced by compatible blood transfusion
(homologous or autologous), if the haematocrit falls
below 25%. Blood loss is replaced with an equal amount
of colloids or 2–3 times the volume with crystalloids, if
the haematocrit is >25% in an otherwise healthy
individual. Crystalloids are electrolyte solutions that
distribute themselves throughout the body water and
hence, a larger volume needs to be given.
Perioperative Fluid Therapy in Patients with
Disturbed
Fluid Balance
Derangements of fluid therapy can be classified as:
. Disturbances of volume
a
b. Disturbances of concentration
c. Disturbances of composition.
In the evaluation of a patient with a suspected
problem in fluid and electrolyte or acid–base balance,
careful sequential analysis of the volume, concentration
and composition must be done in that order. This must
be followed by appropriate therapy (as described earlier
in this chapter). Also refer to Chapter 17 for management
of shock.
TYPES OF INTRAVENOUS FLUIDS (Table 20.3)
These can
be broadly divided into three groups:
Crystalloids, colloids and special purpose solutions.
Crystalloids
These are essentially solutions of
electrolytes in water,
e.g. Ringer lactate. Some also contain dextrose, e.g.
dextrose saline, 5% dextrose and paediatric maintenance
solutions. They vary in the content of different electrolytes.
Ringer lactate:
• This is also called a balanced salt solution as this is a
solution
of electrolytes in water, with a composition
very similar to extracellular fluid.
Table 20.3 Intravenous fluids
Solution pH Osmol- [Na+][K+] [Ca++] [Cl ] Other
arity compo(mOs- nents
m/l)
Plasma 7.4 291 140 4 2.5 103 Many
Ringer 6.75 273 130 4 2.7 109 Lactate as
lactate bicarbo-
Isotonic 5.5 308 154 – – 154 –
saline
Plasmalyte 7.4 295 140 5 0 98 [Mg
5% 4.5 253 – – – – Dextrose
dextrose 5 g/L
others
nate
++
] 2
• This is the solution of choice to replace third space
losses.
• It has a pH of 6.5. It contains Na
Ringer lactate does not provide any calories.
+
131 mmol/L, K
5 mmol/L, Ca++ 2 mmol/L, chloride 111 mmol/L and
lactate 29 mmol/L (lactate gets converted to
bicarbonate in the body).
• It has an osmolarity of around 270–278 mOsm/L and
hence is
marginally hypo-osmolar.
Normal saline:
• Normal saline is a misnomer; it is ideally called
isotonic
saline or 0.9% saline.
• It contains 154 mmol each of sodium and chloride
per litre of
solution. It has a pH of 5.
• Its osmolarity is 308 mOsm/L. This does not provide
any
energy.
• Isotonic saline may be used as replacement solution.
However, large amounts of isotonic saline infusion
can cause hyperchloraemic metabolic acidosis.
5% dextrose:
• Each 100 ml contains 5 g of dextrose. It has a pH of 4.
One litre of 5% dextrose will provide 200 kcal of
energy.
• It may be used to replace insensible free water loss.
Once the dextrose is metabolised, only water remains.
Hence, it is called a hypotonic solution.
• It may be used to dilute inotropes, vasopressors, ino-
dilators, sodium nitroprusside, aminophylline, etc.
• It may be used as part of glucose-insulin-potassium
solution.
Newer solutions:
• Ringer’s acetate is similar to Ringer lactate but the
has been replaced by acetate. The lactate in
lactate
Ringer lactate can cause confusion during serum
lactate measurements in sepsis. This is avoided by
using acetate.
• Plasmalyte is a crystalloid where the amount of
chloride has
been further reduced and calcium has
been replaced with magnesium. It also has gluconate
and acetate instead of lactate.
• The newer solutions are increasingly being used
especially
in critically ill patients and when large
amounts need to be given.
Colloids
• Colloids are suspensions of large molecules in
solution,
usually in saline.
• Unlike the ions in crystalloids, such as saline or Ringer
lactate, these
molecules cannot cross the cell mem-
brane. They remain in the intravascular compartment
+
Section I • Basic Principles of Surgery