FLUID, ELECTROLYTES AND ACID BASE BALANCE

Intended Learning Outcome: To

1. Recall the important figures related to major electrolytes and
acid base balance
2. Explain the pathogenesis of each abnormality
3. Describe the manifestations of each abnormality
4. Set a treatment plan for correction of each abnormality or mixed
abnormalities

Definitions:
 Tonicity: is the measure of osmotic pressure between two
solutions, it is influenced only by the solutes that cannot pass
freely through cell membranes, like sodium
 Osmolarity: is the measure of solute concentration per unit
volume, it is influenced by all solutes in a solution
 Osmolality: is the measure of solute concentration per unit mass,
it is more consistent than osmolarity because volume changes
with temperature but not the mass

 Osmolality is the same in both intracellular and extracellular

compartments (ICC & ECC) and is about 190 mOsmol/Kg.
 0.9% Na Cl solution is isoosmolal and isotonic to extra and intra
cellular fluids (ECF & ICF)
 5% Dextrose solution is isoosmolal but hypotonic because it
passes freely and rapidly into the ICC. So it is like infusing plain
water in terms of tonicity. Dextrose and urea are therefore called
the “ineffective osmoles”. Only in severe hyperglycemia, glucose
in the ECF contributes effectively to tonicity.
Water Balance:
• Total body water=60% body wt. (42Lt/70Kg)
• About 2/3 the body water is present intracellular (ICF = 28L) while
the remaining 1/3 is present outside the cells or extra cellular
(ECF= 14 L).
• Output/Input= 2500 mL/day
• Daily water loss includes :
• Urine 30-50 ml/Hr (800 – 1200) ml daily.
• GIT --- 100 - 300 ml in stools.
• Insensible loss 1200 ml where about 800 ml.as invisible
perspiration through the skin by evaporation and 400 ml
through the lungs with the respired air.
• Water moves freely between all compartments; Plasma
osmolality= Body osmolality
• Hyponatremia= relative water excess & hypernatremia = relative
water lack; both occur with pure non-isotonic imbalances

Sodium Balance:
• 1 gm NaCl~ 17 mEq (mmol) Na+ + 17 mEq (mmol) Cl-
• Total body Na= 5000 mEq (about half in bone and half in ECF)
• Pl. [Na+]= 135-145 mEq/Lt, so it is the main ECF cation
• Daily losses: 50-100mEq/day in urine according to intake + 10-80
mEq/d in sweat (average 1 mEq/Kg/d in 5g NaCl)
• Its metabolism and excretion is under the control of
adrenocortical hormones (Aldosterone).
• Sodium is excreted mainly in the urine, but also in sweat in a
concentration about half its concentration in the ECF and in
variable smaller amounts in stools.

Potassium Balance:
• 1gm KCl= 13.5mEq (mmol) K+ + 13.5mEq (mmol)Cl-
• Total body K= 45mEq/Kg (~3,500mEq)
• 2% ECF & 98% Intracellular (150mEq/Lt)
 • About 3/4 of the body potassium is found in the skeletal muscles
and is mobilized with protein catabolism
• Plasma [K+] = 3.5-5 mEq/Lt. ECF K+ is the effective fraction which
affects organ functions especially the myocardium, muscles and
nerves. The ICC is the potassium store.
• Daily losses ~ 60mEq mainly in urine
• Daily needs 0.75mEq/Kg/d= 40-60mEq/d
• Following any trauma including surgical operations there is a
period of increased excretion of potassium the urine .This loss is
greater during the first 24 hours after the insult and will last for
few days in a direct proportion to the severity of the insult.
• Potassium is shifted outside the cells in cases of acidosis, exercise
and cellular break down in cases of trauma or infection.
• At normal pH, each 1mEq plasma[K+] change= 250mEq change in
total body K, so for normal pH, serum [K+] reflects body potassium
• Acidosis causes increased serum [K+]; each 0.06 drop in pH causes
0.6 mEq increase in serum [K+] and vice versa with alkalosis.
• Therefore, acidosis causes transient hyperkalemia and alkalosis
causes transient hypokalemia (uncorrected plasma[K+])

Calcium Metabolism:
 Calcium is an important cation which is mainly extra cellular. The
plasma level of calcium is about 4.4-5 mEq (2.2 - 2.5 mmol) / Lt.
which is present in three different forms: protein bound, free
ionized and free non ionized. The free ionized component is
necessary for blood coagulation.
 Symptoms of hypocalcaemia may occur in cases of hypo
parathyroid state and in alkalosis.
 Symptoms are due to neuromuscular excitability in the form of
muscle cramps,carpo - pedal spasm and rarely convulsions. ECG
shows prolonged QT interval.
  Treatment is directed to correct the cause: Calcium gluconate
10% slowly IV in acute cases; and vitamin D and calcium
supplement for long term treatment.

Fluid and Electrolyte Abnormalities (Imbalances)

There are four types:
A. Volume abnormalities
B. Concentration abnormalities
C. Mixed volume and concentration abnormalities
D. Composition abnormalities

Volume and concentration abnormalities are due to altered water

content of the body (volume) and altered Na+ concentration in the ECF
(Sodium is the main ECF cation which keeps the ECF osmolality and
tonicity). The normal concentration of Na+ in ECF is the normal tonicity
of the ECP and is equivalent to 0.9% NaCl solution. If the ECF loses or
gains fluid in isotonic concentration (ie. Same concentration of Na + in
ECF), there will be pure volume excess or deficit without change in
tonicity. Concentration abnormalities occur when the ECF tonicity
decreases (due to relative water excess compared to the sodium
content in the ECF) or increases (due to relative water deficiency
compared to the sodium content in the ECF). Since Na concentration in
the interstitial compartment is the same as in the intravascular
compartment, concentration abnormalities are manifest as
hyponatremia or hypernatremia. On the other hand, pure volume
abnormalities show normal plasma sodium levels. Mixed volume and
concentration abnormalities occur when both the volume and the Na +
concentration of the ECF are abnormal. Composition abnormalities are
abnormalities of the body content of any electrolyte other than sodium,
either in excess or in deficiency.The most important is potassium.
A) Volume Abnormalities

1) Non-haemorrhagic Hypovolemia/ Non-haemorrhagic Volume

Depletion/ Isotonic Salt & Water Depletion:

Causes:
• Abnormal losses: Vomiting, GIT obstruction, GIT fistula, ileostomy,
diarrhea, diuresis.
• Third space losses: Paralytic ileus, ascitis, tissue oedema(2ry to
infection/trauma)

Manifestations (according to volume deficit):

 Mild (3-4Lt ECF volume deficit & 450-600mEq Na deficit),
(resembling 15 - 20% blood volume loss):
– Little or no thirst, headache, pylorospasm& vomiting
– Sensation of coldness, pale, cool, clammy skin
– Sunken eyes, drawn in face, furrowed tongue, depressed
fontanells
– Tachycardia, collapsed neck veins, postural hypotension
– Increased haematocrit (in non haemorrhagic) + Normal
serum [Na+]
– Concentrated urine: Urine [Na+]<40mEq/Lt with mild
reduction in volume
 Severe (6-8Lt ECF or more, 900-1200mEq Na, resembling 30-40%
Blood volume): There is Hypoperfusion of vital organs then brain
& heart
– Agitation & confusion then Apathy
– Severe thirst, nausea & vomiting
– Oliguria then anuria
– Severe Pallor, cold & wrinkled skin + slow capillary filling
– Hypotension + Rapid deep breathing (Air hunger)
– Pulse weak & rapid then irregular, later bradycardia &
Cardiac arrest.
 – Marked increase in haematocrit + Some decrease in serum
[Na+]
Treatment:
Substitute by Normal saline or Ringer’s lactate in same amount of
estimated volume deficit
(0.9% Na Cl contains 154 mEq/Lt Na+ + 154 mEq/Lt Cl-)
(Ringer lactate contains 130 mEq/Lt Na+, 4 mEq/Lt K+, 2.7 mEq/Lt Ca2+,
109 mEq/Lt Cl-& 28 mEq/Lt lactate) ‫مهم نييييك‬

2) Hypervolemia/ Volume Overload/ Isotonic Salt & Water

Excess:
Causes:
• Over infusion of saline esp. in early post-operative period
• Acute renal failure
Manifestations:
<3Lt ECF excess (450mEq Na+ excess):
– Slight puffiness of face
> 3Lt ECF slow development:
– Minimal dependant pitting oedema (pretibial or presacral)
– Weight gain, increased tension of fontanells
– Increased urine output
– Normal haematocrit and serum [Na+]
> 3Lt. ECF due to rapid infusion:
– Congestive heart failure:
• Pleural effusion and dyspnoea
• Engorged neck veins
– Pulmonary oedema:
• Dyspnoea and orthopnoea
• Pulmonary crepitations
– Increased CVP
– Decreased haematocrit but normal serum [Na+]
Treatment:
Sodium restriction plus diuretics
B) Concentration Abnormalities

1) Hyponatremia: due to relative water excess

Causes:
Occurs when ECF losses (eg. GIT losses) are compensated for by
drinking water or by IV 5% dextrose or hypotonic saline (eg.
Compensating by 5% dextrose with intestinal obstruction)
Manifestation:
– (CNS irritation) Nausea, vomiting, confusion, convulsions &
coma
Treatment:
• Water restriction & Normal saline 1½ volume of maintenance
needs
• Osmotic diuresis or dialysis if patient isanuric
• 200 mL of hypertonic saline very slow infusion for convulsions

2) Hypernatremia: due to relative water deficiency

Causes:
Compensation for low salt water losses (like excessive sweating,
tracheostomy, fever, severe diarrhea, severe diuresis) by isotonic or
hypertonic saline solutions.
Manifestations:
– Thirst & Dry mouth
– Increased urine sp. Gravity
– (CNS depression) Apathy, stupor & coma
– Hypernatremia ( every 3 mEq/Lt increase in serum [Na+]= 1Lt
relative pure water deficiency)
Treatment:
Oral water or IV 5% dextrose solution
C) Mixed Volume and Concentration Abnormalities

The manifestations are an algebraic summation of the previously

mentioned two abnormalities and the treatment is a combination of
both.

1) Hypovolemia with Hyponatremia:

Occurs when GIT losses are partially compensated for by hypotonic
solutions like drinking water or infusing dextrose or hypotonic saline.

2) Hypervolemia with Hyponatremia (Water intoxication)

Causes
• Increased IV hypotonic solutions
• Enemas with plain water esp. children
• Bladder irrigation with hypotonic soln.
• Increased water by NGT in comatosed
• ADH sedreatingtumours
• Head trauma (increased ADH production)
• Severe Hyperglycemia (increased ECF osmotic pressure)

3) Hypovolemia with Hypernatremia (rare):

Causes:
Lack of water intake
– Comatosed
– Esophageal obstruction
Increased output with inadequate water replacement (eg. Excessive
sweating, tracheostomy, severe diuresis, fever, severe diarrhea)
 4) Hypervolemia with Hypernatremia:
Causes:
Compensation for low salt water losses (like excessive sweating,
tracheostomy, fever) by excessive large volumes of isotonic or
hypertonic saline solutions.

D) Composition Abnormalities

1) Potassium Depletion (Hypokalemia):

Unlike sodium, decreased plasma concentration of K+ reflects its body
content. Therefore, hypokalemia is a manifestation of K+ depletion.
Manifestations:
A. Excessive losses (Potassium depletion)
– Intestinal Losses: obstruction, fistulae, diarrhoea, villous
adenomas –mucus secreating
– K losing diuretics
– Hperaldosteronism
B. Intracellular shift
– Alkalosis
Manifestations:
• Slurred speech and confusion
• Malaise, drowsiness, lost reflexes
• Atonia (Neuromuscular depression) including respiratory muscles
causing poor ventilation and chest infection.
• Intestinal atony (ileus) & abdominal distension
• Pseudodiabetic glycosuria (due to inability to transfer glucose
intracellularly)
• Low bl. Pressure, widened QRS complex & depressed ST segment
• Hypokalemia
 Treatment: (hypokalemia ↓)
• Establish urine output
• Oral potassium if possible
• IV K given on 5% dextrose, concentration not more than 60mEq/Lt
and rate by infusion pump not exceeding 40mEq/hr under ECG
monitoring in ICU
• IV slow K replacement (half deficit, after pH correction + expected
losses + daily need) over the first 24 hours then reassessment
• Correction of acid base imbalance simultaneously

2) Hyperkalemia:
Causes:
A. Body Potassium Excess
– Iatrogenic: excessive IV/oral K therapy
– Renal failure (oliguria & anuria)
– Hypoaldosteronism
B. Extracellular shift
– Acidosis
– Intravascular haemolysis
– Crush injuries
Manifestations:
• Dysrythmias, peaking of T wave, cardiac standstill
• Nausea, vomiting, colics&diarrhoea
• Sudden flacid paralysis from legs to trunk to arms
• Respiratory paralysis
• Hyperkalemia
Treatment:
• 100mL 50% Dextrose + 20% regular insulin IV infusion over 30 min
to shift K+ into the cells.
• Correct associated acidosis by slow NaHCO3 IV infusion
• Calcium gluconate slow IV infusion to antagonize the effect on cell
membranes
• Try to establish good urine output, if not then dialysis
 • Other measures but slow:
• Ion exchange resins as sodium polystyrene
• Sulphonate 50 gm. Enema.

Acid Base Balance & Disturbances (Imbalances)

General:
• Normal Arterial pH= 7.36-7.44 (7.4+0.04)
• Normal arterial HCO3- : 22-25 mEq/Lt
• Normal arterial PCO2 : 31-42 mmHg
• Normal arterial PO2 : 80-110 mmHg
• In metabolic acidosis, HCO3- deceases & in metabolic alkalosis
HCO3- increases
• In respiratory acidosis PCO2increases & in respiratory alkalosis
PCO2 decreases

The Regulatory Mechanisms are

A-Buffer system
B-Respiratory mechanism through CO2 washout.
C-Renal mechanism which excretes acids and conserve fixed
bases.

The Buffer system:

The buffer system includes 4 types:-
1- Carbonic acid and bicarbonates in a ratio of 20:1 under
normal conditions at pH within the normal range.
• It acts mainly in the extra cellular compartment.
• Any strong acid formed in the body is replaced by the weak
carbonic acid which is easily changed to water and C02 which
is easily excreted through the lungs with expiration.
2-Phosphate buffer which acts mainly inside the cells.
3-Proteins which act as a buffer through the amphoteric nature
of amino acids that can react with both acids and bases.
 4-Haemoglobindue to its high binding capacity for hydrogen ions
and transporting power for carbon-dioxide.

Acid Base Imbalances:

Are one or combination of two of four types:
• Respiratory acidosis occurs due to CO2 retention in hypoventilation
(Inadequate alveolar ventilation) as in:
o Airway obstruction
o Painful deep breathing
o Obstructive pulmonary disease
o Respiratory muscle paralysis
o Ineffective breathing (Flail chest)
• Metabolic acidosis due to increased fixed acids are in the body as in
o Renal: acute & chronic failure, renal tubular acidosis
o Non-gastric GIT losses: fistulae, diarrhoea
o Acid generation: tissue hypoxia (shock & sepsis), diab.
Ketoacidosis, Parentralhyperalimentation (acidic amino acids)
• Respiratory alkalosis occurs as a result of excess loss of carbon
dioxide due to hyperventilation as in:
o Sepsis & hyperpyrexia
o Hypoxia due to shock
o Pulmonary embolism
o Hyperventilation during artificial breathing
• Metabolic alkalosiswhich is due to excessive gain of fixed base as
sodium bicarbonate or loss of fixed acid as in losing HCl in vomiting
leading to hypochloremic acidosis as in:
o Gastric losses: Pyloric obstruction, NGT aspiration
o Diuretic induced hypokalemia: K+ shifts extracellular and H+
intracellular (intracellular acidosis)
Blood arterial samples in different imbalances:
Imbalance Diagnostic Finding If partially
Compensated

Met. Acidosis pH - PCO2

HCO3
Met. Alkalosis pH - PCO2
HCO3
Resp. Acidosis pH PCO2 -
HCO3
Resp. Alkalosis pH PCO2 -
HCO3

Mixed Acidosis pH -
HCO3
PCO2
Mixed Alkalosis pH -
HCO3
PCO2
Principles of Infusion Therapy

Indications:
Infusion therapy should be used if the oral route cannot be used or
it cannot cope with the normal body requirement either:
 To correct preexisting deficits.
 To give the normal daily requirement.
 To replace losses.

Precautions during IV fluid therapy:

 Clinical observation and assessment.
 Accurate clear fluid chart for the intake and output daily.
 Body weight changes.
 Check blood chemistry for plasma level of :-
o Sodium 135-145 m mol/L
 o Potassium 3.5 – 5 m mol/L
o Chloride 95 – 105 m mol/L
o Urea 1-7 m mol /L.

Plan of fluid therapy:

• Volume abnormality with concentration abnormality are
corrected first with synchronous correction of acid base
imbalances
• Then composition abnormalities are corrected next

Complications of infusion therapy:

 Circulatory over load: The use of C.V.P line should prevent this
hazard.
 Electrolyte and acid base imbalances: Repeated arterial samples
for electrolytes and blood gases with ECG monitoring should
prevent this hazard.
 Pyrogenic reaction
 Biochemical disturbances.
 Hypoproteinaemia
 From the cannula as :
o Thrombophlebitis.
o Sepsis.
o Air embolism.

Solutions for I.V. Therapy:

A- Crystalloid: diffuse rapidly from the circulation.
 Normal Saline contains 0.9% sodium chloride i.e. 153
mmol sodium per liter. – It is isotonic.
 Dextrose 5% contains 200 calories per liter.
 Dextrose-Saline contains 4.3 dextrose with 0.18%
sodium chloride i.e. one fifth of the amount of
sodium in normal saline.
  Ringers lactate contains :
Sodium --- 130 m mol/L
Potassium --- 4 m mol /L
Chloride --- 110 m mol/L
Lactates --- 28 m mol/L
B- Colloids: Due to large molecular weight is retained in the
circulation.
 Plasma
 Dextran: A polysaccharide with two different
molecular weights; high (70000) and low (40000).
 It reduces the blood viscosity and improves the
microcirculation.
 It interferes with coagulation and blood typing so take
blood sample for grouping before starting the infusion.
 Ask yourself always :
o How much fluid is needed?
o Which solution should be used?
o What are the possible complications?
Surgical Nutrition
Intended Learning Outcome: To
1. Set a list of the common indications and contraindications of
surgical nutrition
2. Recall the possible complications
3. Enumerate the routes of administration
4. Explain how to assess and monitor the nutritional status
5. Decide for which type of surgical nutrition in a particular
situation and justify your decision
6. Calculate the nutritional needs for a given patient
Definition:
Surgical nutrition is any additional nutritional support to the surgical
patient due to inadequate normal oral intake.

General Conditions Suggesting Initiation of Nutritional Support:

Poor nutritional status (oral intake <50% of energy needs)
• Catabolic disease (burn, sepsis, pancreatitis)
• Significant weight loss (>10%)
• Anticipated duration of starvation longer than 5-7 days
• More than 5-7 days starvation
• Nonfunctioning gastrointestinal tract
• Serum albumin <3 g/dL in the absence of an inflammatory state

Specific Conditions Suggesting Initiation of Nutrition Support:

• Proximal intestinal fistula
• Inflammatory bowel disease
• Massive intestinal resection(<100 cm small bowel remains)
• Paralytic ileus/obstruction
• Severe pancreatitis

Contra-indications to Parenteral Nutrition (PN):

• Functioning gastrointestinal tract
• Treatment anticipated for <5 days in patients without severe
malnutrition
• Inability to obtain venous access
• Poor prognosis that does not warrant aggressive nutrition support
• When the risks of PN are judged to exceed the potential benefits

Methods of Nutritional Assessment:

• Clinical history
• Indirect calorimetry: Oxygen consumption, determination of
respiratory quotient
• Anthropomorphic measurements: Ideal body weight, skinfold
thickness
• Biochemical measurements: Albumin, transferrin, prealbumin
• Measurement of nitrogen balance
• Measurements of immunologic function

Routes of Feeding:
• Enteral vs Parenteral
• If you can use the gut, use it
• Enteral is much more cost effective with fewer complications than
parenteral—it is also thought to preserve gut barrier function

Enteral Feeding:
Nasogastric
• Short term, requires fully functional GI tract, can be inserted orally
• Insertion method: blindly at bedside; by radiology or endoscopically
• Benefits: easily inserted and replaced; can use bolus feeds
• Complications: sinusitis, aspiration, airway obstruction (postcricoid
ulceration), nasal neucrosis, pneumothorax, displacement, occlusion

Nasoenteric
• Short term; used in patients with aspiration risk or poor gastric
emptying; requires continuous infusion
• Insertion methods: blindly at bedside, in OR, endoscopically,
radiologically
• Benefits: reduces aspiration risk; some tubes allow suction of
stomach while simultaneously feeding small bowel
• Complications: sinusitis, aspiration, airway obstruction (postcricoid
ulceration), nasal neucrosis, pneumothorax, displacement (esp into
stomach), occlusion, pneumotosis, intestinal ischemia/infarction,
blockage, unable to check residuals
Gastrostomy
• Long term tube; requires well emptying stomach; not a good choice
for patients with significant reflux and aspiration
• Insertion methods: surgically, endoscopically, radiologically
• Benefits: allows bolus feeding, can be placed at bedside, low profile
tubes may decrease dislodgement
• Complications: bleeding, retching, abdominal wall infection,
perforation of other abdominal organs, migration of parts of the
tube, aspiration, dislodgement, occlusion, bowel obstruction,
pneoumoperitoneum, dislodgment/malposition
Transgastricjejunostomy
• Long term; requires continuous infusion; use in patients with
aspiration risk or poor gastric emptying
• Insertion: surgically, radiologically, endoscopically
• Benefits: reduces aspiration risk, allows suction of stomach while
feeding small bowel; may be used immediately after placement; may
be converted to g-tube
• Complications: same as gastrostomy
Jejunostomy
• Short or long term; requires continuous infusion;use in patients with
aspiration risk or poor gastric emptying; difficult to replace
• Insertion: surgically, endoscopically, radiologically
• Benefits: reduces aspiration risk, may be used immediately after
insertion
• Complications: same as g-tube but also higher obstruction risk

Types of Parenteral Nutrition (PN):

Delivery of nutrients intravenously, e.g. via the bloodstream.
– Central Parenteral Nutrition: often called Total Parenteral
Nutrition (TPN); delivered into a central vein
– Peripheral Parenteral Nutrition (PPN): delivered into a
smaller or peripheral vein
Venous Sites for Access to the Superior Vena Cava

PN through Central Catheter:

• May be delivered in the hospital setting via internal jugular or
subclavian vein catheters and rarely femoral lines
• Peripherally inserted central catheters (PICC) are inserted via the
cephalic and basilic veins

PICC Lines (peripherally inserted central catheter):

• PICC lines may be used in ambulatory settings or for long term
therapy
• Used for delivery of medication as well as PN
• Inserted in the cephalic, basilic, median basilic, or median cephalic
veins and threaded into the superior vena cava
• Can remain in place for up to 1 year with proper maintenance and
without complications
Centrally Inserted Central Catheter:
• Internal Jugular (most common)
• Subclavian vein
– Must be placed in sterile environment
– Generally, placed radiologically
– Confirm placement with chest x-ray
– Can change over a wire to replace

Implanted Central Venous Catheters (e.g. Hickman, Groshong, Port-A-

Cath):
• For prolonged TPN:
– Also for fluids, chemotherapy, blood draws
• Catheter inserted ‘operatively’
• Placed with fluoroscopic guidance
• Implanted into a subcutaneous tunnel

Parenteral Base Solutions:

• Carbohydrate
o Available in concentrations from 5% to 70%
o D30, D50 and D70 used for manual mixing
• Amino acids
o Available in 3, 3.5, 5, 7, 8.5, 10, 15, 20% solutions
o 8.5% and 10% generally used for manual mixing
• Fat
o 10% emulsions = 1.1 kcal/ml
o 20% emulsions = 2 kcal/ml
o 30% emulsions = 3 kcal/ml (used only in mixing TNA, not for
direct venous delivery)
PN solutions are hypertonic

Other Requirements:
• Fluid
– 30 to 50 ml/kg/d (2 to 3 L/day)
– 5% D is added to PN admixture to meet fluid requirements
• Electrolytes
– Use acetate or chloride forms to manage metabolic acidosis or
alkalosis(in patients with normal electrolytes
– acetate : chloride 1:2)
• Vitamins: multivitamin formulations
• Trace elements

Stress Factors Used in Calculation of Total Energy Expenditure:

Clinical condition Stress factor
• Starvation 0.8–1.0
• Elective operation 1.0–1.1
• Peritonitis or other infections 1.1–1.3
• Sepsis 1.3–1.4
• Pancreatitis 1.3–1.8

Estimated Protein Requirements in Various Disease States:

Clinical condition Protein requirements
(g/kg ideal body weight/day)
Healthy, nonstressed 0.8
Mild metabolic stress 1.0 – 1.1
(elective hospitalization
Moderate metabolic stress 1.2 – 1.4
(complicated postoperative care,
infection)
Severe metabolic stress 1.5 – 2.5
(major trauma, pancreatitis,
sepsis)

Suggested Sequence for the Initiation of Parenteral Nutrition Therapy:

PARAMETER DAY 1 DAY 2 DAY 3
Volume (mL/24 hr) 1000 1000-1500 1500-2000

Calories (% of goal) 50% 75% 100%

Dextrose (g/24 hr) 100 - 150 150 - 200 200 - 350
Amino acids 50%-100% 100% 100%
Fat No Perhaps Often

Infusion Schedules:
– Continuous PN
Non-interrupted infusion of a PN solution over 24 hours via a central
or peripheral venous access
– Cyclic PN
The intermittent administration of PN via a central or peripheral
venous access, usually over a period of 12 – 18 hours

Routine Physiologic and Laboratory Monitoring:

– Clinical:
Daily fluid balance, body weight, evidence of infection
– Laboratory:
Baseline: Electrolytes, BUN, creatinine, glucose, calcium, magnesium,
inorganic phosphate, liver function (bilirubin, alanine transaminase,
aspartate transaminase, alkaline phosphatase), triglyceride, albumin,
prothrombin time
 Every 6 to 12 hours: Glucose, usually for the initial 3 to 5 days or until
stable
Daily until stable: Electrolytes, BUN, creatinine, glucose, calcium,
magnesium, PO4
Weekly: Liver function, triglyceride, albumin, prothrombin time

Complications of PN:
• Infectious
• Catheter and systemic infections
• Mechanical
• Catheter obstruction
• Catheter migration
• Pneumothorax
• Haemothorax
• Hydrothorax: solution (TPN)
• Intravascular misplacement: often IJ
• Catheter embolism: sheared tip
• Air embolism
• Venous thrombosis
• Metabolic
• Bone disease
• Hepatobiliary disease
• Renal disease
• Fluid overload
• Dehydration
• Electrolyte imbalance
Na, K, Mg, PO4, Ca
• Metabolic acidosis
• Hyperglycemia / hypoglycemia
• Hyperlipidemia
• Hypercapnea
• Vitamin/trace element deficiencies
• Essential fatty acid deficiency