Fluid & electrolyte balance and nutrition in OMFS- prashanth panicker.pdf

Fluid & Electrolyte Balance
and Nutrition in OMFS
Dr. Prashanth Panicker
Professor & Consultant,
Kannur Dental & Medical college
Kannur

In OMFS
Dr. PRASANTH PANICKER. BDS,MDS,MBBS,DNB
Professor and Consultant
Dept of Oral and Maxillofacial Surgery
Kannur Medical and Dental College Hospital
Anjarakandy
Kannur

In OMFS

CONTENTS
 INTRODUCTION
 FLUID COMPARTMENTS & COMPOSITION
 EXCHANGE OF FLUIDS ACROSS COMPARTMENTS
 FLUID GAIN V/S FLUID LOSS
 REGULATION OF FLUID &ELECTROLYTE BALANCE
 CAUSE OF FLUID AND ELECTROLYTE IMBALANCE IN SURGICAL PATIENTS
 INTRAVENOUS FLUIDS
 ROUTES OF FLUID AND ELECTROLYTE CORRECTION
 FLUID THERAPY
 ELECTROLYTE IMBALANCE

Introduction
 Fluid & Electrolyte regulation essential for homeostasis
 Perioperative Fluid & Electrolyte disturbance fairly common in surgical
patients
 Understanding the basic evaluation & management of imbalance is
essential for optimum patient care

Fluid Compartments
➢ Intracellular fluid (ICF)
➢ Extracellular fluid (ECF)
 Plasma
 Interstitial fluid (IF)

The ECF and the ICF are two distinct
fluid compartment
• ICF
• The cytosol of cells
• Makes up about two-thirds of the total body water
• ECF
• Major components include the interstitial fluid and plasma
• Minor components include all other extracellular fluids

11
MW (Molecular Weight) = sum of the
weights of atoms in a molecule
mEq (milliequivalents) = MW (in mg)/
valence
mOsm (milliosmoles) = number of
particles in a solution

Composition of body fluid
WATER 25L 12L 3L
CATIONS
Na+ 10 144 140
K+ 150-160 4 4
ANIONS
Cl- 2 114 103
PO4
- 57 1 1
Protein 16 traces 55
Intracellular fluid Interstitial fluid Plasma

Cations and Anions in Body Fluids
Figure 27.2

k+ PO4
---
Protein
Na+
Cl-
Na+
Cl-
Protein
Intracellular
Extracellular
Interstitial Plasma

15
Homeostasis maintained by:
 Ion transport
 Water movement
 Kidney function

Fluid shifts
Intracellular
25 litres
Interstitial
12 litres
IV
3litres
Kidneys Guts Lungs Skin
Extra cellular fluid - 15 litres

17
Movement of body fluids
“ Where sodium goes, water follows.”
Diffusion – movement of particles down a
concentration gradient.
Osmosis – diffusion of water across a
selectively permeable membrane
Active transport – movement of particles
up a concentration gradient ; requires
energy

18
 Fluid compartments are separated by membranes that are
freely permeable to water.
 Movement of fluids due to:
 hydrostatic pressure
 osmotic pressure
 Capillary filtration (hydrostatic) pressure
 Capillary colloid osmotic pressure
 Interstitial hydrostatic pressure
 Tissue colloid osmotic pressure

Osmotic pressure
Na+
Na+
PP
Intracellular Interstitial Intravascular
K+

Hormonal regulation
 ADH
 Atrial Natriuretic peptide
 Renin-Angiotensin-aldosterone system

 Antidiuretic Hormone (ADH)
 Causes body to reabsorb more water
 Released by posterior pituitary
 Works on a negative feedback system
 Aldosterone
 Causes sodium to be reabsorbed, water to be reabsorbed and potassium
to be excreted
 Released by Adrenal glands

Causes of imbalance in
surgical patient
• Patients undergoing surgery do not ingest oral
fluid (in preparation of surgery/ surgery itself)
• External loss of fluid
• Stimulation of stress hormones (ADH,
Aldosterone) in response to surgery
• Fluid loss from surgical drains & fistula

• Patients normal medical treatment (diuretic
& antihypertensive therapy)
• Alteration of osmotic pressure of plasma
due to surgery
• Increased insensible fluid loss
• Sequestration of fluids and electrolytes at
site of surgery(Third space losses).
• The perioperative use of laxatives for bowel
preparation

Most of the fluid imbalance in
surgical patient involve
Extracellular fluid compartment

26
Dysfunction or trauma can cause:
Decreased amount of water in body
Increased amount of Na+ in the body
Increased blood osmolality
Decreased circulating blood volume

Fluid imbalance
Fluid Volume Overload
Fluid Volume Deficit

Fluid Volume Overload
Hypervolemia / Overhydration / Water Toxicity
Causes:
• Excess intake of fluids ( Volume overload)
• Excess intake of sodium
• Compromised regulatory mechanisms
• CHF
• Cirrhosis
• Renal failure
• SIADH
• Normal immediate post-operative response

Mechanism of overhydration
Excessive H2O enters
the ECF
net osmosis into
cells, causing
swelling
ECF is diluted
(hyponatremia)

Pathophysiology of Fluid
Volume Overload
 Normal compensatory mechanisms kick in
 If not treated –
➢ Increased pressure at the arterial end of capillary bed causes movement of
fluid into interstitial spaces
➢ Increased pressure in left ventricle then left atrium
➢ Then back-up into lungs leading to pulmonary edema
➢ Can lead to CHF

Clinical Manifestations
• Weight gain
• Dyspnea
• Cough
• Pulmonary Crackles
• Pleural effusion
• Jugular vein distention
• Edema
• Increased BP
• Loud heart sound

Laboratory evaluation
Blood evaluation
• Decrease Na +
• Decrease BUN,creatinin
• Decrease Haematocrit
• Decrease serum osmolarity
Urine evaluation
• Specific gravity < 1.030 ( normal = 1.010)

Management
• Daily weights
• Strict I&O chart maintenance
• Reduce fluid intake
• Reduce sodium intake
Mild restriction 4-5 gm/day
Moderate restriction 2.0 gm/day
Strict restriction 0.5 gm/day
• Diuretics
• Monitor electrolytes
• Elevate legs, encourage movement

Fluid Volume Deficit
Terminology
Dehydration – extracellular fluid volume
deficit
Hypovolemia –vascular fluid volume deficit
(“isotonic dehydration” - Water and electrolyte losses are equal)
Degree of dehydration Weight loss
Mild 4% of body weight loss
Moderate 6% of body weight loss
Severe > 8% of body weight loss

Excessive loss of H2O from ECF
Cells lose H2O to
ECF by osmosis;
cells shrink
Mechanism of dehydration:

Causes of Fluid Volume
Deficits
Excessive fluid losses
➢ Hemorrhage
➢ Vomiting
➢ Diarrhea
➢ Fever
➢ GI suction
➢ Burns
➢ profuse sweating
➢ diuretic abuse
Water loss exceeds water intake
Lack of intake
➢NPO
➢Tube fed individuals
➢Impaired thirst
mechanism

Body
weight lost
%
Symptoms
1-2 Thirst, fatigue, weakness, discomfort, loss
of appetite
3-4 Impaired physical performance, dry mouth,
reduction in urine, flushed skin, impatience,
apathy
5-6 Impaired concentration, headache,
irritability, sleepiness, impaired temperature
regulation, increased respiratory rate
7-10 Dizziness, spastic muscles, loss of balance,
delirium, exhaustion, collapse

Laboratory evaluation
Blood evaluation
• Raised Na +
• Raised BUN,creatinin
• Raised Haematocrit
• Raised serum osmolarity
Urine evaluation
• Specific gravity > 1.030 ( normal = 1.010)
• Urine electrolyte concentration indicates conserving values
Tubular activity Sodium
(mEq/L)
Potassium
(mEq/L)
Normal >40 >40
Conserving (early dehydration) 10-30 20-30
Maximal (severe dehydration) <5 15-25

Management of Fluid Volume
Deficit
 Restore Fluids by oral or IV
 Treat underlying cause
 Daily weights
 Accurate I/O chart maintenance
 Monitor closely for overload
 Monitor for worsening condition or hypovolemic shock

Routes of fluid and electrolyte correction
Depends upon:
❑ Pathological state
❑ Symptomatology
❑ Severity of dehydration
Routes:
Oral
In patients who are capable of and can safely drink
Nasogastric tube
In patients who are not able to drink voluntarily
(10-15 ml every 10 min)
Intravenously
In emergency situation & in conditions where meticulous correction
of fluid & electrolyte is necessary

Goals of fluid management
 Attain & maintain normal body fluid composition and
homeostasis
 Correct life threatening imbalances
 Avoid complications of too rapid correction
 Integrate fluid and electrolyte therapy with nutritional
therapy

When choosing and administrating IV fluids it is important to decide
1. From what deficiency the patient suffers
from
2. The compartment that requires
replacement
3. Which fluid is most appropriate
➢ Type of fluid
➢ Rate & Duration of administration
➢ Added electrolytes

IV Fluids
Different solutions with various compositions
are available.
Classification:
Crystalloids
( Fluid containing water and electrolyte(s) &
has LMW)
Colloids
(Fluid containing HMW substances such as
proteins or large glucose polymer)

Crystalloids
 Fluid containing water and electrolytes
 Low molecular weight
 Replace ECF loss
( since most of the fluid loss in
surgical patient is from
extracellular compartment,
crystalloids are most commonly
used replacement fluid)

Classification:
(Based on ionic concentration of the intravenous fluids)
Hypotonic solution (1/2 Normal
saline)
Isotonic solution (NS , RL ,D5W )
Hypertonic solution (3-5 % NaCl)

Isotonic solution
Most of the perioperative loss is isotonic, hence isotonic
soln are most commonly used maintenance fluid
➢ 0.9 % sodium chloride ( Normal saline)
➢ Ringers Lactate Solution (RL)
➢ 5% Dextrose

Normal Saline
Na+ K+ Cl - HCO3
- mOsm
ECF 142 4 103 27 280-310
NS 154 _ 154 _ 308
➢Similar composition as ECF
➢Isotonic to ECF
➢After IV administration NS distributes rapidly into ECF
compartment

ICF interstitial IV
1L of NS administered intravenously
increases :
IV volume by about 220 ml ( 25 %)
Interstitial volume by about 780 ml (75%)
Hence NS expands ECF volume

Ns contains: 154 mmol/L of Na + ( Slightly Higher than ECF)
154 mmol/L of Cl – ( Significantly Higher than ECF)
Administration of large volumes of NS imposes an extra
load of Cl- , leading to mild hyperchloremia
NS is an ideal fluid for correcting Extracellular fluid
deficiency along with :
➢Hyponatremia
➢Hypochloremia
➢Metabolic alkalosis

When NS is used to expand plasma volume :
➢ Plasma volume deficiency = x
➢ Volume of NS to be infused = 3x
( as only 25 % of infused NS reaches plasma)
NOTE: sepsis, burns
increase capillary leakiness
more fluids leak out of IV compartment
volume of NS required for replacement of
plasma volume is more

Ringers lactate (RL)
Named after Sydney Ringer
(Prof. of clinical medicine university college hospital , London)
Na+ K+ Cl- HCO3- mOsm
ECF 142 4 103 27 280-310
RL 130 4 109 28 273
• Similar in composition to ECF .
• RL has minimal effects on normal body composition
and PH even when infused in large quantity.
• Called BALANCED SALT SOLUTION

Buffer : Lactate
Lactate Carbonic acid + CO2
HCO3
- ( BUFFER)
Lactate is used instead of bicarbonate as its more stable in IV fluid
during storage
Indications:
➢ Least effect on ECF composition & most physiologic solution when
large volume necessary
➢ Used in hypovolemic shock while awaiting blood
➢ Suitable for replacing loss due to excessive drainage of intestinal
secretion

ICF interstitial IV
1L of RL administered intravenously increases :
IV volume by about 220 ml ( 25 %)
Interstitial volume by about 780 ml (75%)
Hence RL expands ECF volume

5 % Dextrose (D5W)
 5 Gm / 100 ml of water
 Isotonic to ECF
 Contains dextrose (supplies calories)
 Has no electrolyte
ECF 142 4 103 27 280-310
D5W _ _ _ _ 253

ICF interstitial IV
When administered , dextrose is metabolized
rapidly
Therefore administering D5W is equivalent
to administrating water, which rapidly
distributes evenly throughout the entire body fluid
compartment

Uses :
➢ It is of value for replacing water losses but
has no use as resuscitation fluid to expand
intravascular volume
➢ Used to prevent hypoglycaemia in diabetic
patient who are on insulin
➢ Used to correct hypernatremia
0.45 % NaCl 5% Dextrose
Used in post operative period, to provide
free water for insensible losses & some
sodium for renal adjustment of serum conc.

Hypertonic salt solution
 Less commonly used
 Primarily used for correction of hyponatremia
ECF 142 4 103 27 280-310
3% NaCl 513 - 513 - 1026
(3 – 5 % NaCl)

1L of 3 % NaCl administered intravenously
Decreases:
Intracellular volume by about 1600 ml
Increases :
ECF volume by about 2600 ml
ICF interstitial IV

Hypotonic salt solution
ECF 142 4 103 27 280-310
0.45% NaCl 77 - 77 - 250
Used as a maintenance fluid
Replaced with hypotonic
salt solution
Loss primarily due to water

1L of 0.45 % NaCl administered intravenously
Increases :
ECF volume by about 334 ml
Intracellular volume by about 666 ml

Colloids
 Fluid containing HMW substances such as proteins or
large glucose polymer
 Isotonic solution
 Maintain plasma osmotic pressure and remain
intravascular
 Used to restore Intravascular volume

Classification:
Blood derived colloids
Albumin
Synthetic colloids
➢ Dextrose starch( Dextrans)
➢ Gelatins
• Polygeline ( Haemacele)
• Succinylated Gelatin ( Gelofusine)
➢ Starches
• Hetastarch
• Pentastarch
• Tetrastarch

Indications of colloids
➢ Severe IV fluid deficits
(eg – Haemorrhagic shock prior to arrival of blood for
transfusion)
➢ Severe hypo-albuminaemia or conditions associated with large
protein losses
( eg – such as burns)
➢ Used in conjunction with crystalloids ( when fluid replacement
exceeds 3-4 L)

ICF interstitial IV
1L of Colloid (Haemaccele) administered
intravenously
Causes volume expansion of 1 L of
Intravascular volume
(The fluid is held intravascularly due to colloidal
particle)

Perioperative fluid therapy:
Guidelines
 Preoperative fluid therapy
 Intraoperative fluid therapy
 Postoperative fluid therapy

Preoperative fluid therapy
 Integral part of surgical care
 Understanding of common fluid disturbances associated with surgical
illness
 Categorized as abnormalities in :
➢ Volume
➢ Concentration
➢ Compositional change

Correction of volume changes
Depletion of extracellular fluid compartment
without change in concentration &
composition is a common problem.
Cause :
External loss of fluid ( eg : Haemorrhage in trauma patient)
Third space loss ( eg : massive infection, severe crush injuries,
Burn )

Quantification of fluid deficits :
➢ Exact quantification impossible & unnecessary
➢ The defect to be estimated clinically
(On the basis of the severity of the clinical sign)
Severity % BW loss Fluid loss Clinical features
Mild 4% 2-3 L Signs/symptoms are
mild/minimal
Moderate 6-8% 4-5 L Tachycardia, Postural
Hypotension, Hypo pyrexia, Dry
tongue, loss of skin turgor
Severe Up to 10% 6-7L Abdominal distension, renal
failure

Management:
Choice of IV fluid replacement depends on concomitant
concentration & compositional abnormality
when pure ECF loss :
Balanced salt solution ( Ringers Lactate)
Continuing therapy
➢ Based on improvement of clinical signs
(Reliance on formula or single clinical sign is perilous)
➢ Stabilization of BP, Pulse ,Urine output ( 30-50
ml/hr)

Correction of concentration changes
(Can present in various combinations along with volume disorder)
➢ Severe hyponatremia with fluid depletion
➢ Moderate hyponatremia with fluid depletion
➢ Hyponatremia with fluid excess
➢ Hypernatremia with fluid depletion

Severe hyponatremia with fluid
depletion
➢ Estimation of Na deficit
Decrease in serum
Na conc. Below
normal
x
Total body water
( In Litres)
➢Immediate correction of Severe Hyponatremia
(3 – 5 % NaCl solution)
➢Half the calculated amount of Na is infused slowly
➢Clinical & chemical evaluation of patient
➢Correction of Fluid deficit ( RL / NS )
➢Small increments of hypertonic salt soln to correct
rest of hyponatremia

Moderate hyponatremia with
fluid depletion
Volume correction started immediately along
with correction of serum Na deficit
(NS is used initially )
The remainder of the volume correction is
done by RL solution

Hyponatremia with fluid
excess
 Restriction of water intake
 Small volume of hypertonic saline infused (Caution : Over infusion will
aggravate volume excess)
Hypernatremia with fluid depletion
• 5 % Dextrose
• Half strength RL
• Half strength NS

Intraoperative fluid
therapy
Causes of fluid loss:
➢ Blood loss during operation
➢ Third space oedema ( Parasitic loss, Sequestration of ECF)
➢ Oedema from excessive dissection

Guidelines for replacement fluid :
➢ Replace ECF loss intraoperatively
➢ Balanced salt soln commonly used ( 0.5 – 1 L/Hr )
➢ Blood to be replaced to maintain acceptable RBC mass irrespective of
any additional fluid & electrolyte therapy

Postoperative fluid therapy
Immediate post operative period ( < 24 hrs)
Involves:
➢ Review of preoperative fluid status
➢ Amount of fluid loss/gain during operation
➢ Clinical examination of patient with assessment of vital signs & urinary
output
Management:
➢ Initial fluid orders to correct any existing deficit
➢ Maintenance fluid to compensate fluid loss postoperatively

Late post operative period
( 24 hrs after surgery)
Accurate measurement & replacement of all
losses
Replacement of measured sensible losses
+
Replacement of insensible losses

Sensible loss
➢ Mainly includes Urinary & GIT Fluid loss
➢ Isotonic (or slightly hypotonic)
Replaced with :
Isotonic Salt solution ( NS or RL Solution)

Insensible loss
Insensible loss = average of 600 ml/day
This may be increased in (maximum of 1500
ml/day)
➢ hypermetabolism
➢ hyperventillation
➢ fever
The insensible loss in mainly pure water
Replaced with 5% Dextrose in water

Rate of fluid administration
Varies depending upon severity & type of
fluid disturbance
In non emergent situation :
administer at steady rate
If given in short period :
Overload
renal excretion of infused salt & water
Fluids of different composition are alternated

Severe deficit
safely replaced with isotonic soln at rate of 2000
ml/ hr
(Constant observation mandatory if rate exceeds 1000 ml/hr)
patient of cardiovascular disorder
➢ Slower, more careful correction
➢ Constant monitoring of cardiopulmonary system

Formula :
For the first 10 kg 4 ml/Kg/hr
For the next 10 kg Add 2 ml/Kg/hr
For each kg above 20 kg Add 1
ml/Kg/hr
For Example: 25 Kg child
First 10 Kg : 4 ml/Kg/hr x 10 Kg = 40 ml/hr
Next 10 Kg : 2 ml/Kg/hr x 10 Kg= 20 ml/hr
Next 5 Kg : 1 ml/Kg/hr x 5 Kg = 5 ml/hr
65 ml/hr

Electrolyte imbalance
Sodium
• Hypernatremia
• Hyponatremia
Potassium
• Hyperkalemia
• Hypokalemia
Magnesium
• Mg excess
• Mg deficiency
Calcium
• Hypocalcaemia
• Hypocalcaemia

Sodium
Serum Na
Normal 135 -150 mEq/L
Hypernatremia >150 mEq/L
Hyponatremia <135 mEq/L
Normal daily intake
100 -150 mg/day( adult)
2.4 mg/Kg/day( infant / child < 20 kg)

Hyponatremia
Clinical features
CNS : lethargy, confusion, seizure
GIT : Nausea, Vomiting , Anorexia
Musculoskeletal : Muscle cramps
Metabolic : Hypothermia
Symptoms rarely develop until serum Na is < 120-125 mEq/ L
Symptoms more severe in acute than chronic hyponatremia

CAUSES OF HYPONATRAEMIA
 LOW EXTRACELLULAR FLUID VOLUME:
1)Volume depletion
2)Salt losing renal diseases
3)Hypoadrenalism
4)Diuretic use
. NORMAL EXTRACELLULAR FLUID VOLUME
1)Hypothyroidism
2)SIADH
.INCREASED EXTRACELLULAR FLUID VOLUME
1)Excessive water administration
2)Cardiac failure
3)Cirrhosis
4)Renal failure

Management
Severe hyponatremia with fluid depletion
➢ Estimation of Na deficit
➢ Immediate correction of Severe
Hyponatremia (3 – 5 % NaCl solution)
➢ Half the calculated amount of Na is infused
slowly
➢ Clinical & chemical evaluation of patient
➢ Correction of Fluid deficit ( RL / NS )
➢ Small increments of hypertonic salt soln to
correct rest of hyponatremia

Moderate hyponatremia
with fluid depletion
Volume correction started
immediately along with correction
of serum Na deficit
(NS is used initially )
The remainder of the volume
correction is done by RL solution

Hyponatremia with fluid excess
 Restriction of water intake
 Small volume of hypertonic saline infused (Caution : Over
infusion will aggravate volume excess)

Hypernatremia
Clinical features
CNS : restlessness, tremors, weakness,
delirium, maniacal behaviour,
confusion, ataxia, seizure, coma
Renal : oliguria
Tissue: decreased saliva & tears, dry,
sticky & red mucous membrane, Red
swollen tongue, Flushed skin
Metabolic : Hyperthermia

CAUSES FOR HYPERNATRAEMIA
• REDUCED INTAKE
1)Fasting
2)Nausea and vomiting
3)Reduced conscious level
. INCREASED LOSS
1)Sweating
2)Burns
.INAPPROPRIATE URINARY WATER LOSS
1)Diabetes insipidus
2)Diabetes mellitus

Management
(Hypernatremia with fluid depletion)
➢ 5 % Dextrose
➢ Half strength RL
➢ Half strength NS

Potassium
Serum K
Normal 3.5-5.5 mEq/L
Hyperkalemia > 5.5mEq/L
Hypokalemia < 3.5 mEq/L
Normal daily intake
40-60 mEq/L

Hypokalemia
Clinical features :
Cardiac : hypotension, dysrhythmias
Neuromuscular : Weakness, Respiratory
failure
Renal : Polyuria, Metabolic alkalosis

CAUSES OF HYPOKALAEMIA
• Reduced intake
1)Vomiting
2)Gastric aspiration
3)Fistulae
.Urinary losses
1)Metabolic alkalosis
2)Diuretic use

Management
Oral supplementation
➢ Safest method of K replacement
➢ Formulations :
• Potassium chloride ( Metabolic alkalosis)
• Potassium bicarbonate ( Metabolic
acidosis)
Dose varied depending on degree of
hypokalemia

Intravenous supplementation
➢ Used when:
Oral therapy not possible
Rapid replacement is required (serum K+ < 2.5 mEq/L)
➢ Rate of Infusion:
10 mEq/L (In non emergent situation)
20- 40 mEq/L (In emergent situation)

Hyperkalemia
Clinical features :
➢ Cardiac :
bradycardia,
➢ Neuromuscular :
weakness , paresthesis, respiratory failure

CAUSES OF HYPERKALAEMIA
Excessive intravenous/oral intake
Efflux of potassium from cells
1)Haemolysis
2)Massive tissue damage

Treatment :
Acute
➢ 10 % calcium gluconate IV( 10 ml)
➢ 44 mEq (1 amp) Sodium Bicarbonate IV
➢ 40 Mg Frusemide IV
Chronic
➢ Correction of the cause
➢ Reduction of dietary potassium
➢ Loop diuretics

Magnesium
➢ Hyperactive tendon reflex
➢ Muscle tremors
➢ Tetany,
➢ Mental apathy,
➢ Weakness
➢ Lethargy
➢ Weakness
➢ Loss of deep tendon reflex
➢ Severe excess
(Muscular paralysis, respiratory &
cardiac arrest)
Function :
Maintenance of contractility of muscle
Excitability of neural tissue
Clinical Features :
Mg Deficiency Mg Excess

Treatment
Mg Deficiency
➢ Mg
chloride/sulphate
2 mEq / Kg body Wt
(Parentally)
Mg Excess
➢ Stop administration of
Mg
➢ Ca chloride/gluconate
( 5-10 mg IV)
➢ Haemodialysis

Calcium
Hypocalcemia
➢ Numbness & tingling
of circumoral region
tips and toes
➢ Muscle cramp
➢ Tetany
➢ Hyperactive tendon
jerks
Hypercalcemia
➢ Anorexia
➢ Nausea , vomiting
➢ Fatigue, weakness
➢ Headache, back
pain
➢ Polyuria
➢ Polydypsia
Clinical features :

Treatment
Hypocalcemia
➢ IV Calcium gluconate
or calcium chloride
➢ Oral calcium lactate
Hypercalcemia
➢ Organic Phosphate
( Oral / IV )
( Infused slowly over period of
12 hrs once daily for not more
than 2-3 days )

Acid - Base Balance
Normal body PH = 7.36 – 7.44
Buffer system :
Carbonic acid / Bicarbonate system
H2CO3 H+ + HCO3
-

Acid - Base Imbalance
Acidosis
(PH < 7.36)
➢ Metabolic
➢ Respiratory
Alkalosis
(PH > 7.44)
➢ Metabolic
➢ Respiratory

Metabolic Acidosis
Increased plasma H+ conc. (PH < 7.36)
Occur as a result of :
➢ Increased production of lactic acid
 Shock
 Severe hypoxemia
 Severe haemorrhage or anaemia
➢ Accumulation of acid other than lactic acid
 Diabetic ketoacidosis
➢ Increased loss of bicarbonates
 Diarrhoea
 Intestinal fistula

Metabolic Acidosis
Increased plasma H+ conc.
Stimulation of
respiratory centre
➢ Hyperpnoea
➢ Serum PCO2 decreases
Na+ conservation
by kidney
➢ Rise in BP & PR
➢ Concentrated urine

Treatment
Bicarbonate requirement (mmol) :
Body weight (Kg) x Base Deficit (mmol/L) x 0.3
• Infusion of Na Bicarbonate
• Repeated measurements of plasma [HCO3
-] & pH
Bicarbonate solution:
➢Isotonic ( 1.4 % : 163 mmol/L)
➢Hypertonic ( 8.4 % : 1000 mmol/L)

Metabolic Alkalosis
Decreased plasma H+ conc. (PH > 7.44)
Characterised by :
➢Decreased plasma H+ conc.
➢Increased plasma HCO3- conc.
Associated with :
Hypochloremia & Hypokalemia
Common causes in Surgical patients:
➢Vomiting
➢Aspiration of gastric secretion
➢Diuretic administration

Treatment
Chloride responsive alkalosis :
Infusion of 0.9 % saline
In Hypokalemia :
Infusion of KCl
when volume administration contraindicated :
Acetazolamide
Life threatening / emergency :
0.1% HCl in 5% Glucose
(Central vein cannulation ; 0.2 mmol/Kg/h)

Respiratory Acidosis (Hypoventilation)
Interference of gaseous
exchange in lungs
Retention of CO2 Acidosis
Causes:
➢Anesthetized patients
➢Lung disorders (Emphysema, Bropnchopneunonia, Chronic
bronchitis, Pulmonary edema)
➢Depressed respiratory center ( Poisioning : alcohol,
morphine, barbiturates )
➢Airway obstruction

Treatment
 Immediate treatment of pulmonary defect
 Maintain adequate ventilation
 Endotracheal tube & artificial respiration ( Severe Condition)
 Avoid over sedation & over usage of muscle relaxants

Respiratory Alkalosis
Causes :
➢ Excessive manual pulmonary ventilation ( anaesthesia)
➢ Stimulation of respiratory centre
( Pain , CNS injury, Apprehension, High fever)
Treatment :
➢ Treatment of the underlying cause
➢ Frequent blood gas estimation
➢ Appropriate correction of ventilatory pattern
(Hyperventilation)

ENTERAL AND
PARENTERAL
NUTRITION

INTRODUCTION
 Nutritional support is intended to supply all the
essential inorganic and organic nutritional elements
necessary to maintain optimal body composition as
well as positive nitrogen balance.

 Severe malnutrition causes widespread organ
dysfunction and increases perioperative morbidity
and mortality rates.
 Nutritional repletion may improve wound healing,
restore immune competence, and reduce morbidity
and mortality rates in critically ill patients.

INDICATIONS FOR
NUTRITIONAL SUPPORT
• Continued recent weight loss of 10% or more in Major
trauma (blunt or penetrating injury, head injury),Burns
(preoperative & continued to postoperative period)
• Severe pancreatitis
• Major elective surgery in severely malnourished
patients
• Hepatic dysfunction
• Renal dysfunction

 Bone marrow transplant recipients undergoing
intensive chemotherapy
 Patients unable to eat or absorb nutrients for an
indefinite period (neurologic impairment,
oropharyngeal dysfunction, short bowel syndrome)
 Well-nourished, minimally stressed patients unable to
eat for 7 to 10 days postoperatively.

Starvation & Trauma
Skeletal muscle
Amino acids
Adipose tissue
Glycerol & FFA
Glycerol
FFA
Glucose
Lactate from tissues
Amino
Acids
Glucose Synthesis
Liver

 Stress starvation in ICU results in accelerated
catabolism – AUTOCANNIBALISM
 Loss of structural proteins leading to death.

Sepsis
Skeletal muscle
Amino acids
Adipose tissue
Protein breakdown
Triglyceride
Glycerol & FFA
Glycerol
FFA
Glucose
Lactate from tissues
Amino
Acids
Glucose Synthesis
Liver
Glycogen
Ketone
Bodies

Body reserves of Nutrients
Aminoacids – a few hours
Carbohydrate – about 12hrs
Fat – 27 -90 days
Thiamine – 30 -60 days
Ascorbic acid – 60 – 120 days
Niacin – 60 – 180 days
Vitamin A – 90 -365 days
Iron – 750 days
Iodine – 1000days
Vit B12 -3yrs

TREATMENT GOALS
 In the early phase – to maintain cellular and tissue
function.
 To minimise the additional catabolic effects of
starvation
 To maintain the patient in a metabolically fed state
 To avoid the toxic effects of nutrient/fluid & electrolyte
excess.

ENTERAL NUTRITION
Enteral refers to feeding via a tube placed into the
gut to deliver liquid formulas containing all essential
nutrients.
➢ It is generally the preferred route because
➢ Natural port of entry for nutrients
➢ sustains the digestive, absorptive, and immunologic
barrier functions of the gastrointestinal tract.

 It is indicated in patients with functioning gut who are
not expected to be on oral diet within 3 days.

Rationale for Enteral nutrition
 Favours intestinal villous
trophy
 Promotes gut motility
 Reduces translocation
of bacteria from gut

 Intestinal structure and enzyme activity is maintained.
 Greater insulin response to enteral than parenteral
nutrition.
 Less tendancy to retain salt and water.

CONTRAINDICATIONS
 Circulatory shock- reduced intestinal perfusion
 Intestinal ischemia/Perforation
 Mechanical bowel obstruction or ileus
 Inability to access the gut eg. severe burns
 Intestinal obstruction

Routes of Access
• For short term use
i. Nasogastric
ii. Nasoduodenal
iii. Nasojejunal
• For long term use (>4wks)
• Gastrostomy/Jejunostomy for endoscopic,
radiologic, or surgical procedures.

 Percutaneous endoscopic gastrostomy is most
commonly performed.
Contraindications:
▪ Gastric cancer
▪ Gastric ulcer
▪ Ascitis
▪ Coagulation disorders

 Percutaneous Endoscopic Jejunostomy
 Indicated if postpyloric feeding is needed
 Allows concomittent jejunal feeding and gastric
decompression

TYPE OF FEEDING TUBE
FEEDING
TUBE SMALL BORE LARGE BORE
(8 to 12 Fr), soft (e.g.,
Silastic)
ADVANTAGES
reduce nasal and
pharyngeal
trauma and
minimize
gastroesophageal
junction
incompetence
ability to quantify residual feedings
and quickly reinitiate nasogastric
suction.
DISADVANTAGES
pulmonary aspiration occasioned
by gastroparesis and incompetence
of the gastroesophageal junction
due to the diameter of the tube.

• Location of Distal end of tube
• Gastroparesis is common in critically ill patients so that
placing the tube distal to the ligament of Treitz (small
intestinal function generally remains intact) prevents
pooling of feeds in the stomach with its risk of
pulmonary aspiration.
• Precaution - Elevate the backrest to a minimum of 300,
and preferably to 450

ADMINISTRATION OF FEEDS
 bolus,
 Intermittent
 continuous

 Bolus feedings are defined as formula
delivered by gravity via a syringe over approximately
15minutes.
 Intermittent feedings are delivered via a feeding
container or bag over 30-45 minutes with or without an
enteral feeding pump.

• Pump-assisted feedings. A pump is generally required
for small-bowel feedings and is preferred for gastric
feedings in critically ill patients.
• Formulas are frequently initiated at full strength at 10-
40mL/h and advanced to the goal rate in increments
of 10-20 mL/h every 8-12 hours as tolerated. This
approach can usually be used with isotonic as well as
high-osmolality or elemental products.

 Children : Bolus feedings may be started with 25% of
the goal volume is divided into the desired number of
daily feedings.
 Formula volume may be increased by 25% per day as
tolerated, divided equally between feedings.

 Pump-assisted feedings. A full-strength, isotonic
formula can be started at 1-2 mL/kg/h and advanced
by 0.5-1 mL/kg every 6-24 hours until the goal volume is
achieved.
 Preterm, critically ill, or malnourished children who
have not been fed enterally for an extended period
may require a lower initial volume of 0.5-1 mL/kg/day
and then

slowly advancing to 20 mL/kg/day.
 Advance nutritive feedings for VLBW and ELBW infants
by a rate of 10-20 mL/kg/day.

 Flushing of feeding tube is important to
prevent clogging.
 Sterile water is recommended for use in adult and
neonatal/pediatric patients before and after
medication administration.

• Standard Enteral Formula
• 1. Complete dietary products (+) Suitable for most
patients requiring tube feeding; some can be used orally
• a. Caloric density 1 kcal/mL
• b. Protein 14% cals, caseinates, soy, lactalbumin
• c. CHO 60% cals, hydrolyzed corn starch, maltodextrin,
sucrose
• d. Fat 30% cals, corn, soy, safflower oils
• e. Recommended daily intake of all minerals and vitamins
in >1500 kcal/d
• f. Osmolality (mosmol/kg): 300

• Modified Enteral Formulas
• 1. Caloric density 1.5–2 kcal/mL (+) - Fluid-restricted
patients
• 2. a. High protein 20–25% protein (+) - Critically ill patients
• b. Hydrolyzed protein to small peptides (+) - Impaired
absorption
• c. Arginine, glutamine, nucleotides,
• 3. fat (+++) - Immune-enhancing diets
• d. Branched-chain amino acids, aromatic amino acids
(+++) - Liver failure patients intolerant of 0.8 g/kg protein
• e. Low protein of high biologic value - Renal failure
patient for brief periods if critically ill

• 3 a. Low-fat partial MCT substitution (+) - Fat
malabsorption
• b. Fat >40% cals (++) - Pulmonary failure with CO2
retention on standard formula.
c. Fat from MUFA (++) - Improvement in glycemic
index control in diabetes
• d. Fat from 3 and 6 linoleic acid (+++) - Improved
ventilation in ARDS
• 4. Fiber provided as soy polysaccharide (+) -Improved
laxation

 Enteral feedings should be initiated within 24-48hours.
 A PEG tube is utilized for feedings within several hours
of placement: current literature supports within 2 hours
in adults and 6 hours in infants and children.

• The feedings are initiated with full-strength formula 3-8
times per day, with increase of 60-120 mL every 8-12
hours as tolerated up to the goal volume.
• Diluting formulas increase the risk of intolerance due
to diarrhea secondary to microbial contamination.
• Lower osmolality and higher pH of dilute formulas
support microbial growth better than full-strength
formula.

FORMULATIONS
 Polymeric – high carbohydrate/fat ratio
 Elemental diet – easily absorbable
- Contain oligopeptides, oligosaccharides,
- aminoacids and fat as medium chain triglycerides.
- indicated in patients with short bowel syndrome,bowel
fistula,inflammatory bowel disease & Pancreatic insufficiency.

 Additional water is necessary to meet fluid
requirements.
 it is administered intermittently as flushes throughout
the day.

COMPLICATIONS OF
ENTERAL NUTRITION
• Mechanical
• Tube block (<10%)
• Pulmonary aspiration(<1%)
• Local rhinitis,otitis media
• Leak from ostomy
• Inadvertant intravenous
administration

• Gastrointestinal
• Halitosis – common with elemental diet
• Bloating & vomiting(10-15%)
• Diarrhoea (10 –20%) most common
➢ Over rapid introduction of feeds
➢ Hyperosmolarity
➢ Bacterial contamination

➢ Lactose intolerance
• Metabolic/Electrolytic
• Hyperglycemia(10 -15%)
• Hypernatremia,Hyperkalemia
• Hypercalcemia
• Essential fatty acid deficiency
• Vitamin K deficiency

 Hypophosphatemia
 Cutaneous rashes (fatty acid deficiency)
 Risk of sepsis
 Nonketotic coma (hyperosmolar dehydration from
high glucose load)

PARENTERAL NUTRITION
 Parenteral refers to the infusion of complete nutrient
solutions into the bloodstream via a peripheral vein or,
more commonly, by central venous access to meet
nutritional needs

ABSOLUTE INDICATIONS
 When enteral route is unable to provide or sustain
sufficient caloric intake
 short bowel syndrome
 small bowel obstruction
 active gastrointestinal bleeding
 high-output enteric-cutaneous fistulas

RELATIVE INDICATIONS
 nonhealing moderate-output enteric-cutaneous
fistulas
 the need for bowel “rest” such as during inflammatory
bowel flare-ups and acute radiation enteritis

 marked abdominal distention and ileus due to intra-
abdominal sepsis
 continued distention after relief of intestinal
obstruction
 chylothorax unresponsive to a medium-chain
triglyceride diet

ROUTE OF ADMINISTRATION
 Peripheral Parenteral nutrition
 Total Parenteral nutrition
 Peripheral veins is used mainly for supplementation of short-term
feeding.
 cannot tolerate an osmolarity of more than 750 mOsm/L (the
equivalent of 12.5% dextrose) so that the fluid volume that can be
tolerated limits the caloric intake.

• Central venous catheters are the
main route of TPN administration.
• The preferred entry location is the
subclavian vein
• provides a stable site
• good patient acceptability
• lower infection rates than either the
internal jugular or femoral routes

 To minimize insertion and infectious complications
➢ a skilled individual should insert subclavian catheters
under sterile conditions.
➢ The catheter should be a single-lumen catheter used
only for TPN

FORMULATIONS
 SHORT TERM THERAPY (3 to 5 days in patients without
nutritional deficits)
 after uncomplicated surgical procedures -
hypocaloric, nonnitrogen glucose-electrolyte solutions.
 These solutions provide total fluid and electrolyte
needs and sufficient calories to decrease protein
catabolism and prevent ketosis.

Glucose
(mg/dL)
Sodium
(mEq/L)
Chloride
(mEq/L)
Potassium
(mEq/L)
Magnesium
(mEq/L)
Calcium
(mEq/L)
Lactate
(mEq/L) pH
Osmolarity
(mOsm/L)
5% glucose
in water
5,000 0 0 0 0 0 0 5.0 253
5% glucose
in 0.45%
5,000 77 77 0 0 0 0 4.2 407
5% glucose
in 0.9%
sodium
chloride
0 154 154 0 0 0 0 4.2 561
0.9%
sodium
chloride
0 154 154 0 0 0 0 5.7 308
Lactated
Ringer's
Solution
0 130 109 4 0 3 28 6.7 273
5% glucose
in lactated
Ringer's
Solution
5,000 130 109 4 0 3 28 5.3 527
Normosol-R 0 140 98 5 3 0 * 7.4 295
* Contains 27 mEq/liter of acetate and 23 mEq/liter of gluconate.

 LONG TERM total parenteral nutrition is the technique
of providing total nutrition needs through an infusion of
hypertonic glucose combined with aminoacids
&varying amounts of fat emulsion.

 As per recommendation from the A.S.P.E.N. guidelines
&the American College of Chest Physicians (ACCP),
 total energy requirement of 25 kcal/kg/day.
 Carbohydrate requirement -3.4g/kg/day

Protein requirements
Normal renal function - 1.3 to 2 g/kg/day (moderate to severe
stress)
• In acute renal failure
• 0.8 to 1.2 g/kg/day if patients are not dialyzed.
• 1 to 1.4 g/kg/day in patients receiving dialysis
• 1.5 and 2.5 g/kg/day in patients undergoing continuous renal
replacement therapy (CRRT) .
• chronic kidney disease, the A.S.P.E.N. recommends 0.5 to 0.6 g
of protein/kg/day.

 Cirrhosis
 increased protein/amino acid intakes (1.2-1.5 g/kg/day) to replace
the losses due to ascites formation
 high caloric intake to account for hypermetabolism (25-40 kcal/day
 Hepatic encephalopathy - standard protein intake of 0.8 g/day plus
lactulose & thenbranched-chain amino acid–enriched solutions and
feedings should be considered

 Burn patients are of special concern because of their
very high energy expenditures, transcutaneous losses
of protein, and great fluid requirements.
 If patients are unable to eat, enteral nutrition is the
preferred modality

 Patients with significant burns (>20%) are given early
nutritional support within 16 hours of admission to
reduce the magnitude of stress response.
 To ensure successful administration of many calories of
a high-protein diet, nasoenteric feeding tubes should
be placed into the jejunum.

INITIATING PARENTERAL
NUTRITION
 As per ASPEN guidelines,no more than 150 to 200 g/day of glucose
initially to ensure tolerance of PN.
 to infuse only 1 L of the TPN on the first day (i.e., 42 mL/hour) and
reaching goal rate on day 2 or 3, depending on the patient's
tolerance of volume and macronutrients.
Central line placement should be verified by radiography before
initiating TPN.

A 1.2-micron filter is used to reduce the chance for infusing
particulates, microorganisms, and pyrogens.
(smaller than 1.2 micron may filter out the fat emulsions in a three-in-
one formula).
A 0.22-micron filter may be used alternately for a two-in-one formula.

 PPN formula is not as calorie dense and contains less
protein & so can be initiated at goal rate (assuming
the patient is able to tolerate the fluid load).
 The PN administration set must be changed every 24
hours using aseptic techniques and universal
precautions

 if the PN does not contain fat emulsions (i.e., the two-
in-one formulation); then the administration set should
be changed every 72 hours.
 the administration set used in infusing the IVFE
separately must be discarded after use or at least
every 12 hours.

Electrolytes/additive Suggested amounts
Sodium 1–2 mEq/kg/d
Potassium 1–2 mEq/kg/d
Chloride Default salt
Acetate (Ac) Add if patient has metabolic acidosis

Calcium gluconate 10–15 mEq/d Use ionized calcium as a guide
rather than total calcium.
Magnesium sulfate 8–20 mEq/d Intracellular cation. It can accumulate
in renal failure; 1 g = 8 mEq.
Phosphorus 20–40 mmol/d Major intracellular anion. May be
given as KPO4 (4.4 mEq K+/3 mmol
PO4
–) or NaPO4 (4 mEq Na+/3 mmol
PO4
–) depending on cation deficiency.
Amount of calcium or phosphorus in
total PN is limited by the calcium-
phosphate solubility curve.
Insulin Add 50%–70% of insulin sliding scale
needs
Use amounts of insulin used by the
sliding scale used in the last 24 h to
guide how much to add to the PN bag.
Start conservatively with 50%–70%
of total insulin used during last 24 h.
H2 blocker Add total daily dose Continuous infusion of H2 blocker is
superior in keeping pH elevated
compared to intermittent dosing.a
Protein pump inhibitors are not
compatible in total PN.

Trace Mineral Intake
Zinc 2.5–4 mg/d, an additional 10–15 mg/d per L of stool or ileostomy
output
Copper 0.5–1.5 mg/d, possibility of retention in biliary tract obstruction
Manganese 0.1–0.3 mg/d, possibility of retention in biliary tract obstruction
Chromium 10–15 g/d
Selenium 20–100 g/d, necessary for long-term PN, optional for short-term
TPN
Molybdenum 20–120 g/d, necessary for long-term PN, optional for short-term PN
Iodine 75–150 g/d, necessary for long-term PN, optional for short-term PN

• Intralipid
• a fat emulsion that is used to prevent or correct
essential fatty acid deficiency.
• to provide calories during prolonged total parenteral
nutrition.
• As intralipid is isotonic with plasma, it is suitable for
peripheral infusion.
• If sufficient calories can be provided by this method,
the use of hypertonic glucose (>10%) by way of a
central vein catheter can be avoided.

• The transitional period is the time during which enteral
feeding is started and PN is discontinued.
• Patients who are young, have no history of
malignancy, and were well nourished before PN was
started can have their PN discontinued as soon as
they are able to tolerate solid food.
• PN can be discontinued once 60% of energy needs is
met enterally.

 In older debilitated patients who have a history of
malnutrition and malignancy, transitioning to enteral
feeds may be more challenging.
 Factors such as aspiration risk, appetite, strength, and
ileus play a role in whether patients can be
successfully transitioned to enteral feeds

• Rebound hypoglycemia - from rapid cessation of PN.
• So the TPN should be decreased by half for 1 to 2 hours
before discontinuation if the current infusion rate is >42
mL/hour.
• This will allow time for the body to adjust its insulin secretion
to decreasing amounts of circulating dextrose and avoid
hypoglycemia.

 10% Dextrose (D10W) or 10% dextrose with 0.9% sodium
chloride (D10NS) should be infused at the same rate
as the TPN to avoid rebound hypoglycemia.
 5% Dextrose can be substituted in place of PPN, not
for rebound hypoglycemia, but more for maintaining
caloric intake.

Cyclic Parenteral Nutrition
Totalvolume is infused over a shorter period (12 or 14
hours), starting in the evening and finishing in the
morning.
• Cyclic PN allows patients to be more mobile during
the day, as well as have more of an appetite.
• Other benefits include less deterioration of liver
function.

 Full support means that the total amount of protein and calories will
be provided.
 In this case, it is important to make sure that the TPN is already
concentrated, since the patient will be receiving the same volume
that was previously given over 24 hours over a shorter period of
time.
 If the goal is to have the patient eat more but not get behind in
nutrition, then one can provide 50% of assessed needs as cyclic PN
while the patient is fed orally or enterally.

 For example :
 Amino acids base solution: Travasol 10% Dextrose base solution 70%
 Intralipid base solution 20%
 Assessed caloric needs: 2,000 kcal/day
 Assessed protein needs: 130 g/day

• STEP 1: Assess calories and volume provided by protein
(4 kcal/g).
• 4 kcal/1 g = x/130 g (see Table 65.2)
• x = 520 kcal (from protein)
• Travasol 10% = 10 g/100 mL = 130 g/xx
• xx = 1300 mL(volume of 130 g protein

 STEP 2: Assess amount of nonprotein calories required.
 Nonprotein calories should be 15% to 30% fat based.
 the remaining (70%–85% of nonprotein calories) should
be dextrose based.

 2,000 kcal (total caloric needs) - 520 kcal (calories
from proteins) = y
 y = 1,480 kcal (nonprotein calories needed)
 1,480 kcal × 0.2 (i.e., 20% calories from fat) ~ 300 kcal
(fat calories)
 1,480 kcal - 300 kcal = 1,180 kcal (dextrose calories

• STEP 3: Assess volume contributed by dextrose (3.4 kcal/g) and fat
calories
• Fat calories = 300 kcal
• Intralipid = 20% or 2 kcal/mL
• 300 kcal = 150 mL fat volume
• Since 20% is 20 g/100 mL, 150 mL = 30 g fat
• Dextrose calories = 1,180 kcal ÷ 3.4 kcal/g = 347 g
• Dextrose 70% = 70 g/100 mL = 347 g/z
• z = 495.7 or ~ 496 mL (volume from dextrose)

• STEP 4: Add up the protein, fat, and dextrose volume
to calculate minimum amount of fluid needed to
make the TPN formula.
• 1,300 mL (from AA) + 150 mL (from fat) + 496 mL (from
dextrose) = 1,946 mL
• 1,946 mL/day ÷ 24 hour/day = ~81 mL/hour.
• The 1,946-mL volume represents the minimum amount
of volume needed to make the TPN (i.e., the TPN is
“concentrated”).

• STEP 5: Put it all together:
• Amino acids = 130 g
• Dextrose = 347 g
• Fat emulsion = 30 g
• Rate = 81 mL/hour (i.e., 1,946 mL over 24 hours)
• This formula will provide 1,997 kcal + 130 g protein over
24 hours

• If100 mL/hour of fluid is required (i.e., 2,400 mL over 24
hours, sterile water is added to make up the balance)
without affecting the amount of calories and proteins
given to the patient.
• Since 81 mL/hour (1,946 mL) represents the minimum
volume needed to make the above TPN, it is not
possible to go below 81 mL/hour without decreasing
the calories and proteins given to the patient

• Travamulsion is an intravenous fat emulsion that is 56%
linoleic acid.
• Adverse effects
• ↑ plasma triglycerides
• Hepatomegaly
• altered liver function tests
• decreased pulmonary diffusing capacity,
• thrombocytopenia, and anemia may occasionally
occur

 Hence periodic liver function tests and platelet counts
should be performed during long-term total parenteral
nutrition.

GLUTAMINE
added to both enteral and parenteral nutrition which
helps to maintain gut integrity .
 Glutamine is the most abundant free amino acid in the
blood and skeletal muscle.
 a primary fuel for rapidly dividing cells such as
enterocytes and immunocytes & a precursor of
purines, pyrimidines, and nucleotides.

 It is synthesized primarily in skeletal muscle & is
involved in the interorgan transport of nitrogen.
During severe stress decreased glutamine synthesis
occurs.

 Glutamine is rather insoluble, so it is difficult to
administer.
 TPN solutions enriched with glutamate, arginine, and
aspartate increases glutamine concentrations.
 In critically ill patients, about 30 g/day or 0.5
g/kg/day of glutamine is needed to meet both basal
and increased enterocyte requirements

ARGININE
 essential amino acid.
 About 5% to 6% of arginine comes from intake of
proteins, and the rest is synthesized by the body via
the urea cycle.
 Arginine is important in ammonia detoxification, as
well as producing nitric oxide.
 mediates vasodilatory effects of endotoxin

Nucleotides
• Nucleotides are structural units for nucleic acids and various
enzymes involved in energy transfer.
• are essential for the formation of new cells (e.g., intestinal
epithelium).
• in the synthesis of protein, lipids, and carbohydrates
• Nucleotides are of interest because supplementation of infant
formulas with nucleotides enhances bifidobacteria growth in the
gastrointestinal tract.
• Bifidobacteria decrease the colonic lumen pH and inhibit growth
of enteric bacteria .

Refeeding syndrome
 Imbalance of electrolytes as well as vitamins, micronutrients, and
fluids that occurs within the first few days of refeeding malnourished
patients.
 nutrients replete the intracellular space .
 The main biochemical findings include
 hypophosphatemia (intracellular shift plus depletion of phosphorus
substrate to synthesize adenosine triphosphate [ATP]).

 Hypomagnesemia (intracellular shift plus magnesium is
a cofactor in many enzymatic functions).
 Hypokalemia (intracellular shift of potassium with
insulin secretion as a response to dextrose infusion).
 Patients may exhibit respiratory distress, cardiac
arrhythmias, congestive heart failure, hemolytic
anemia, or paresthesias, or they may die.

• The three most important steps in preventing refeeding
are
• (a) high-risk patients (chronic alcoholism, kwashiorkor,
marasmus, rapid refeeding) and those receiving high
TPN rates must be identified
• (b) baseline electrolytes must be checked before the
initiation of PN and low magnesium, phosphorus, or
potassium levels must be corrected immediately.
• (c) the TPN rate should be advanced slowly (<150
g/day of carbohydrates) as tolerated over several
days before going to the goal rate

 Twice weekly
➢ Hb,Full blood count
➢ Liver function tests
➢ Prothrombin time
➢ Calcium,Phosphate

• Weekly
➢ Zinc,magnesium
As indicated
➢ Blood culture
➢ Arterial blood acid base analysis
➢ Iron & iron binding capacity
➢ Folate,VitB12

 Abrupt withdrawal of TPN can precipitate
hypoglycemia due to high circulating insulin levels.
 10% glucose can be temporarily substituted for the
TPN and gradually decreased.
 Serum glucose measurements should generally be
measured every 4 h until they stabilize.

ANAESTHETIC MANAGEMENT
 Patients who are receiving TPN often require surgical
procedures.
 Careful preoperative evaluation is necessary because
of potentially serious complications that can be
associated with TPN.

• Metabolic abnormalities,if any should be corrected
preoperatively.
• Hypophosphatemia is a serious and often
unrecognized complication that can contribute to
postoperative muscle weakness and respiratory
failure.

• When TPN infusions are suddenly stopped or
decreased perioperatively, hypoglycemia may
develop.
▪ If the TPN solution is continued unchanged,
excessive hyperglycemia resulting in
hyperosmolar nonketotic coma or ketoacidosis
(in diabetics) is also possible.
▪ It is safe to discontinue TPN completely before
surgery.
• Blood Glucose should be maintained between
100 – 150 mg/dl

 Separate infusions should be used for injection of
anesthetic agents and administration of other
perioperative fluids and blood to decrease the
likelihood of catheter sepsis

COMPLICATIONS OF
PARENTERAL NUTRITION

 Catheter-related
 Pneumothorax
 Hemothorax
 Chylothorax
 Hydrothorax
 Air embolism

 Cardiac tamponade
 Thrombosis
 Subclavian vein
 Vena cava
 Pulmonary thromboembolism
 Catheter sepsis

• Metabolic
• Azotemia
• Hepatic dysfunction
• Cholestasis
• Hyperglycemia
• Hyperosmolar coma
• Diabetic ketoacidosis
• Excessive CO2 production due to metabolism of large
quantities of glucose may result in need to initiate
mechanical ventilation or failure to wean from
mechanical support)

• Hypoglycemia
• Metabolic acidosis or alkalosis
• Hypernatremia
• Hyperkalemia
• Hypokalemia
• Hypocalcemia
• Hypophosphatemia

• Hyperlipidemia
• Pancreatitis
• Fat embolism syndrome
• Anemia
• Iron
• Folate
• B12

 Vitamin D deficiency
 Vitamin K deficiency
 Essential fatty acid deficiency
 Hypervitaminosis A
 Hypervitaminosis D

BURNS
 Burn patients are of special concern because of their
very high energy expenditures, transcutaneous losses
of protein, and great fluid requirements.
 If patients are unable to eat, enteral nutrition is the
preferred modality

References
• Principles and practice of surgery :O James
Garden ;4th edition
• Text book of medicine :K V Krishna Das ;Vol 1 ,
4th edition
• Anaesthesia: Ronald D Miller ; 5th edition , Vol 1
• Text book of anaesthesia :Alan R Aitkenhead,
David J R , Fraham Smith ;4th edition
• Clinician’s manual of OMFS: Paul H Kwon,
Laskin
• Principles and practice of medicine : Davidson

Text book of surgery :Sabiston
Text book of surgery : Das
Medicine : Kumar & Clark

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