Nutritional support and fluid therapy in surgery

NUTRITION AND FLUID
THERAPY IN SURGERY
CHAIR PERSON : DR. ISHWAR HOSAMANI
PROFESSOR AND UNIT CHIEF
SURGERY B UNIT
KIMS HUBLI
SPEAKER: DR. AJAI SASIDHAR
PG STUDENT
DEPT OF GENERAL SURGERY
KIMS HUBLI

Metabolism in surgical patients
 Metabolic events brought about by :
1. Injury
2. Starvation
 Metabolic response is directed to restore:
1. Homeostasis
2. Repair

Metabolic events following acute stress.
• Ebb Phase
 Occurs the first several hours after injury, typically lasts 2 to 3 days,
and is distinguished by reduced oxygen consumption (VO2), glucose
tolerance, cardiac output, and basal metabolic rate.
• Flow Phase
 Typically starts several days after injury, lasts days to weeks, and
features catabolic breakdown of skeletal muscle, negative nitrogen
balance, hyperglycemia, and increased cardiac output, VO2, and
respiratory rate.

Ebb phase
Phenomenon Effect
 blood glucose
 lactate
free fatty acids
 catecholamine
 glucagon
 cardiac output
Below normal core
temperature
 oxygen consumption
Metabolism in surgical patients

Flow phase
Phenomenon Effect
 catecholamine
 glucagon
 cortisol
 insulin
 cardiac output
 core body
temperature
 aldosterone
 ADH
IL1, IL6, TNF
spillage from
wound
 consumption of
glucose, FFA,
amino acid
 O2
consumption
fluid retention
systemic
inflammatory
response
N or  glucose
N or  FFA
normal lactate
 CO2 production
 heat production
multi-organ failure

Sequence of events
surgical problem
 infection
operation
bleeding
tissue trauma
bacterial
contamination
necrotic debris
local
inflammatory
response
wound
healing
recovery
hypermetabolism
muscle wasting
immunosuppression
mortality
*
*
mortality
food deprivation
wound pain
infection
immobility
Ebb
phas
e
Flow
phas
e
Anabolic
phase
*acute stress

Metabolism of Injured Patient
PHASES:
1. Catabolic phase (Ebb, Adrenergic-Corticoid):
 immediately following surgery or trauma
 characterized w/ hyperglycemia, increase secretion of
urinary nitrogen beyond the level of starvation
 caused by increase glucagon, glucocorticoid,
catecholamines and decrease insulin
 tries to restore circulatory volume and tissue perfusion

PHASES:
2. Early anabolic phase (flow, corticoid-withdrawal):
 tissue perfusion has been restored, may last for days to
months depending on:
a. severity of injury
b. previous health
c. medical intervention
 sharp decline in nitrogen excretion
 nitrogen balance is positive (4g/day) indicating synthesis
of CHON and there is a rapid and progressive gain in weight
and muscular strength

PHASES:
3. Late anabolic phase:
 several months after injury
 occurs once volume deficit have been restored
 slower re-accumulation of CHON
 re-accumulation of body fat

Metabolism in starvation
• Depends on duration of fasting – short term and long term.
• Short term(<5 days)
• Long term

vitamins, minerals, and trace
elements

NUTRITIONAL ASSESSMENT AND
MONITORING

Physical Body Measurements
• Body Weight
• Body weight reflects both fluid balance and nutritional status.
Significant weight loss, particularly if rapid or unplanned, is a
powerful predictor of mortality.

Anthropometric Measurements
• Ideal Body Weight
• Body Mass Index

Ideal Body Weight
• Men: 48 kg for the first 152 cm and 2.7 kg for each inch over 5 ft
• Women:45 kg for the first 152 cm and 2.3 kg for each inch over 5 ft.

Evaluating Caloric Requirements
Harris Benedicts equation

Monitoring Nutritional Status
• Nitrogen balance
• Nitrogen balance can be estimated using equations based on
common measurements, such as urine urea nitrogen (UUN), urine
non urea nitrogen (estimated as 20% of UUN), 24-hour urine output
(UO), and an additional 2 g/day to account for non urinary nitrogen
losses (stool and skin).

• Serial monitoring of total nitrogen balance in patients permits one to
evaluate the response to nutritional support and identify patients at
risk of developing muscle protein loss. Persistent loss of nitrogen and
protein catabolism leads to decreased muscle strength, altered body
composition, increased infectious complications, and subsequent
delayed rehabilitation.

Pediatric Assessment
• Nutritional assessment in children, in addition to clinical history,
physical examination, and biochemical markers, also includes plotting
their growth on percentile charts.

Biochemical Parameters
• serum proteins are commonly used as indicators of nutritional status,
with albumin being the most frequently used.
• Serum proteins with a shorter circulating duration are also used;
these include transferrin (t1/2 = 10 days), prealbumin (t1/2 = 3 days),
and retinol binding protein (t1/2 = 12 to 24 hours), because these are
more sensitive indicators of recent changes.

• Patients with albumin levels below 3 g/dL show an independently
associated increased risk of developing serious complications within
30 days of surgery, including sepsis, acute renal failure, coma, failure
to wean from ventilation, cardiac arrest, pneumonia, and wound
infection.
• But IV administration of albumin is usually ineffective because it
degrades quickly after infusion and does not treat the underlying
cause of malnutrition.

Nutritional Support – When to start ?
• Following surgery, patients who are inadequately fed become
undernourished within 10 days and display a marked increase in
mortality.
• Feeding should therefore be initiated as early as possible.

• If a surgical intervention can be delayed, 10 to 14 days of nutritional
support for patients with severe nutritional risk has been shown to be
beneficial prior to surgery.
• Critical patients and those with a significant loss in body weight or a
premorbid state should receive support almost immediately (<3 days)
after admission.

Criteria to Initiate Perioperative Nutritional
Support
• Severe nutritional risk expected with at least one of the following:
• Past medical history: Severe undernutrition, chronic disease.
• Involuntary loss >10%-15% of usual body weight within 6 months or
>5% within 1 month.
• Expected blood loss >500 mL during surgery
• Weight of 20% under IB W or BMI <18.5 kg/m2

• Failure to thrive on pediatric growth and development curves (<5th
percentile or a trend line crossing two major percentile lines)
• Serum albumin <3.0 g/dL or transferrin <200 mg/dL in the absence of
an inflammatory state, hepatic dysfunction, or renal dysfunction
• Anticipate that patient will be unable to meet caloric requirements
within 7-10 days perioperatively.
• Catabolic disease (e.g., significant burns or trauma, sepsis, and
pancreatitis)

Principles guiding routes of nutrition
1. Use the oral route if the GI tract is fully functional and there are no
other contraindications to oral feeding.
2. Initiate nutrition via the enteral route if the patient is not expected
to be on a full oral diet within 7 days postsurgery and there are no
GI tract contraindications
3. If the enteral route is contraindicated or not tolerated, use the
parenteral route within 24 to 48 hours in patients who are not
expected to be able to tolerate full enteral nutrition (EN) within 7
days.

4. Administer at least 20% of the caloric and protein requirements
enterally while reaching the required goal with additional PN.
5. Maintain PN until the patient is able to tolerate 75% of calories
through the enteral route and EN until the patient is able to tolerate
75% of calories via the oral route.

Enteral nutrition
• Early (24 to 48 hours) institution of EN following major surgery
minimizes the risk of undernutrition and can reduce the hyper
metabolic response seen after surgery.

Routes of enteral nutrition
• nasogastric (NG),
• nasoduodenal,
• nasojejunal tubes
If requirement is < 4 weeks
• percutaneous gastrostomy
• jejunostomy,
If requirement > 4 weeks

Benefits of enteral feeding
• EN offers the beneficial effects of trophic feedings, which include
structural maintenance and functional support of the intestinal
mucosa, achieved by providing nutrients such as glutamine,
preserving blood supply, and promoting peristalsis.
• Use of EN to protect and maintain the integrity of the intestinal
mucosa may therefore help reduce the risk of sepsis caused by
bacterial translocation.

• In the critically ill patient, EN should be initiated within 48 hours of
injury or admission; average intake delivered within the first week
should be at least 60% to 70% of the total estimated energy
requirements.

Complications of enteral feeding
• Mechanical complication of the tubing.
• Aspiration
• Refeeding Syndrome
• Solute overload

Parenteral Nutrition
• PN is used for patients who meet the criteria for nutritional support
because of temporary or permanent limitation of GI tract function.
• now reserved for patients in whom contraindications to EN are
present.
• To promote gut integrity and motility in patients on PN alone, small
volumes of EN are encouraged, when possible.
• patients should be hemodynamically stable and able to tolerate the
fluid volume and nutrient content of parenteral formulations;

• PN should be used with caution in patients with congestive heart
failure, pulmonary disease, diabetes mellitus, and other metabolic
disorders.

Formulations
• PN includes all IV formulations, emulsions, or admixtures of nutrients
that are administered in an elemental form.
• 2 in 1 solutions contains dextrose and amino acids.
• 3 in 1 solutions contain dextrose amino acids and lipids.

• When calculating TPN requirements, protein requirements are usually
calculated first and subtracted from total calories, with remaining
calorie requirements met with carbohydrate, with or without lipids.
• Protein-fat-glucose caloric ratio has generally approximated 20 : 30 :
50 . Patients with chronic renal failure and hepatic failure have
conventionally been treated with low protein diets.

Complications of parenteral nutrition
• complications arising from line insertion and infection, which include
pneumothorax, hematoma, bacteremia, endocarditis, damage to
vessels and other structures, air embolism, and thrombosis.
• TPN has been associated with increased rates of bacterial
translocation. TPN has also been associated with increased
proinflammatory cytokine levels and increased pulmonary
dysfunction.

• Overfeeding patients can lead to major complications.
• The overfeeding of carbohydrates results in elevated respiratory
quotients, increased fat synthesis, and increased CO2 elimination,
leading to difficulty in weaning from ventilator support.
• Excess carbohydrate or fat can also lead to fat deposition in the liver.
• Excess protein replacement leads to elevations in blood urea nitrogen
levels.

Carbohydrate Content
• Dextrose is D- Glucose.
• Dextrose is the most commonly used carbohydrate substrate and
provides 3.4 kcal/g.
• Concentrated hypertonic dextrose solutions of 20% to 70% are usually
administered via central lines.
• Contraindications to the use of concentrated dextrose solutions
include alcohol withdrawal and delirium tremens in a dehydrated
patient and suspected intracranial or intraspinal haemorrhage.

Lipid content
• IV fat emulsions (IVFEs) provide a dense source of calories and are
particularly useful when carbohydrate administration approaches
maximal limits or blood glucose control is an issue.
• The optimal use of lipid emulsions during parenteral feeding remains
controversial, because of changes in fatty acid metabolism following
severe injuries IVFE may predispose these particular patients to the
adverse effects of lipid infusions.

• Delivery of lipid emulsion has been associated with immune
suppression, modulation of the inflammatory response, and adverse
clinical outcomes.
• In polytrauma patients, infusion of IVFE in the early post-injury period
has been associated with increased length of intensive care unit (ICU)
and hospital stay, prolonged mechanical ventilation, and increased
susceptibility to infection compared with patients not given IVFE until
after 10 days.

• a minimum of 500 mL of lipid emulsion every 2 weeks is
recommended to avoid essential fatty acid deficiency during
parenteral feeding.

Protein Content
• 1.5 to 2.0 g protein/kg IBW/day in fasted surgical patients and up to
3.0 g/kg/day in severely injured patients

Fluid and Electrolytes
• 30 to 40 mL/kg of fluid,
• 1 to 2 mEq/kg of sodium and potassium,
• 10 to 15 mEq of calcium,
• 8 to 20 mEq of magnesium,
• 20 to 40 mmol of phosphate should be administered daily.

HISTORY
• The first record available that shows an understanding of the need for fluid in
injured patients was apparently from Ambroise Paré (1510-1590), who urged
the use of clysters (enemas to administer fluid into the rectum) to prevent
“noxious vapors from mounting to the brain.”
• The term shock appears to have been first used in 1743 in a translation of the
French treatise of Henri Francois Le Dran regarding battlefield wounds.
• However, the term can be found in the book Gunshot Wounds of the
Extremities, published in 1815 by Guthrie, who used it to describe the
physiologic instability.

• In 1830, Herman provided one of the first clear descriptions of intravenous (IV)
fluid therapy. In response to a cholera epidemic, he attempted to rehydrate
patients by injecting 6 ounces of water into the vein
• In 1872, Gross defined shock as “a manifestation of the rude unhinging of the
machinery of life.”
• Carl john Wiggers first described the concept of irreversible shock in his 1950
textbook, physiology of shock.
• 0.9% normal saline originated during the cholera pandemic that afflicted Europe
in 1831, but an examination of the composition of the fluids used by physicians
of that era found no resemblance to normal saline. The origin of the concept of
normal saline remains unclear

• Sydney Ringer found three ingredients essential were potassium, calcium, and
bicarbonate. Ringer’s solution soon became ubiquitous in physiologic laboratory
experiments.
• In 1932, attempting to develop an alkalinizing solution to administer to his
acidotic patients, Hartmann modified Ringer’s solution by adding sodium
lactate. The result was lactated Ringer’s (LR), or Hartmann’s solution.
• By world war II, shock was recognized as the single most common cause of
treatable morbidity and mortality. Out of necessity, efforts to make blood
transfusions available heightened and led to the institution of blood banking for
transfusions.

Body fluids
Solid
Component
Intracellular
Fluid
Extracellular
Fluid

• Obesity
• Malnourished
• Newborns/Infants

Body fluid changes
• Diffusion
Form of passive transport that moves solutes from an area of higher concentration to
area of lower concentration
• ACTIVE TRANSPORT
Uses ATP to move solutes from area of low concentrationnto area of high
concentration
• OSMOSIS
Passive movement of fluid across a membrane from area of lower solute
concentration to area of greater solute concentration
• CAPILLARY FILTRATION (kidney)
Movement of fluid through capillary walls through hydrostatic pressure; balanced by
plasma colloid osmotic pressure from albumin that causes reabsorption of fluid and
solutes

MAINTAINING FLUID BALANCE
• KIDNEY
Depending on body requirement of fluid and electrolytes, kidneys reabsorb
more or less than normal, thus maintaining the fluid balance
Kidneys secrete renin, which activates renin-angiotensin-aldosterone system;
aldosterone regulates sodium and water reabsorption by kidneys.
• THIRST
Regulated by hypothalamus; osmotic thirst/ hypovolemic thirst

• HORMONES
 ADH – a.k.a vasopressin, produced by hypothalamus, reduces diuresis if
serum osmolality increases or blood volume decreases.
 RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM – stimulated by increased
blood flow to kidney, causes vasoconstriction and causes sodium and water
reabsorption
 ANP – produced by atria; stops action of renin-angiotensin-aldosterone
system, causes vasodilation and causes excretion of water and sodium

Fluid compartments
PLASMA INTERSTITIAL FLUID INTRACELLULAR FLUID

Electrolytes
OSMOLALITY
The movement of water across a cell membrane depends primarily on
osmosis. This movement is determined by the concentration of the
solutes on each side of the membrane.
Osmolarity is the osmotic activity per volume of solution (solutes plus
water) and is expressed as mOsm/L.
Osmolality is the osmotic activity per volume of water and is expressed
as mOsm/kg H2O.

Osmotic pressure is measured in units of osmoles (osm) or milliosmoles
(mosm) that refer to the actual number of osmotically active particles e.g. 1
mmol of NaCl = 2 mosm.
Calculated serum osmolality = 2 sodium + (glucose/18) + (BUN/2.8)
The osmolality of the intracellular and extracellular fluids is maintained
between 290 and 310 mOsm in each compartment

TONICITY
The relative osmotic activity in the two solutions is called the effective
osmolality, or tonicity.
The solution with the higher osmolality is described as hypertonic, and the
solution with the lower osmolality is described as hypotonic.

Classification of body fluid changes

HYPONATREMIA
Dilutional Depletional

• Hyponatremia also can be seen with an excess of solute relative to
free water, such as with untreated hyperglycemia or mannitol
administration. Glucose exerts an osmotic force in the extracellular
compartment, causing a shift of water from the intracellular to the
extracellular space.
• When hyponatremia in the presence of hyperglycemia is being
evaluated, the corrected sodium concentration should be calculated
as follows:
for every 100-mg/dl increment in plasma glucose above normal, the
plasma sodium should decrease by 1.6 meq/L.

Hyponatremia can be
• mild (130 to 135 mEq/liter)
• moderate(120 to 130 mEq/liter)
• severe (<120 mEq/liter).
Mild hyponatremia and moderate hyponatremia are common but only rarely
symptomatic.
Severe hyponatremia, however, can cause headaches and lethargy; patients can
become comatose or have seizures.

APPROACH
• Hyperosmolar causes, including hyperglycemia or mannitol infusion and
pseudohyponatremia, should be easily excluded.
• Next, depletional versus dilutional causes of hyponatremia are evaluated.
• Depletion is associated with low urine sodium levels (<20 meq/L), whereas
renal sodium wasting shows high urine sodium levels (>20 meq/L).
• Dilutional causes of hyponatremia usually are associated with hypervolemic
circulation. A normal volume status in the setting of hyponatremia should
prompt an evaluation for a SIADH.

TREATMENT
• Free water restriction
Na requirement = (desired Na – actual Na) X TBW
• If neurologic symptoms are present, 3% normal saline should be used to
increase the sodium by no more than 1 meq/L per hour until the serum sodium
level reaches 130 meq/L or neurologic symptoms are improved.
• Correction of asymptomatic hyponatremia should increase the sodium level by
no more than 0.5 meq/L per hour to a maximum increase of 12 meq/L per day

• The rapid correction of hyponatremia can lead to pontine myelinolysis,
with seizures, weakness, paresis, akinetic movements, and
unresponsiveness, and may result in permanent brain damage and
death. Serial magnetic resonance imaging may be necessary to confirm
the diagnosis.
• Tolvaptan (oral) - vasopressin antagonist, causing increased water loss;
15mg OD

HYPERNATREMIA
Hypervolemic Hypovolemic

TREATMENT
• Hypernatremia is less common than hyponatremia, but has a worse prognosis,
and is an independent predictor of mortality in critical illness.
• In hypovolemic patients, volume should be restored with normal saline before
the concentration abnormality is addressed.
• The water deficit is replaced using a hypotonic fluid such as 5% dextrose, 5%
dextrose in ¼ normal saline, or enterally administered water.
• The formula used to estimate the amount of water required to correct
hypernatremia is as follows:
Water deficit (L) = (serum sodium -140)/ 140 × TBW
Estimate TBW as 50% of lean body mass in men and 40% in women

• The rate of fluid administration should be titrated to achieve a decrease
in serum sodium concentration of no more than 1 mEq/h and 12 mEq/d
for the treatment of acute symptomatic hypernatremia.
• 0.7 mEq/h correction should be undertaken for chronic hypernatremia ,
because overly rapid correction can lead to cerebral edema and
herniation.

hypovolemia
RENAL Causes
• Osmotic diuresis (DM)
• Drugs (e.g. diuretics)
EXTRARENAL Causes
• GI Losses
• Haemorrhage
• Third-space fluid shifts
• Fistulas

True volume depletion, or hypovolemia, refers to a state of combined salt and
water loss that leads to contraction of the ECFV.
Once a volume deficit is diagnosed, prompt fluid replacement should be
instituted, usually with an isotonic crystalloid, depending on the measured serum
electrolyte values.
Patients with cardiovascular signs of volume deficit should receive a bolus of 1 to
2L (30 ml/kg bolus) of isotonic fluid followed by a continuous infusion.
Resuscitation should be guided by the reversal of the signs of volume deficit –
• vital signs
• maintenance of adequate urine output (½–1 mL/kg per hour in an adult,

• In the case of arterial hemorrhage, ‘Relative bradycardia’ is defined as a heart
rate lower than 100 beats/min when the systolic BP is less than 90 mm Hg.
When bleeding patients have relative bradycardia, their mortality rate is lower.
Interestingly, up to 44% of hypotensive patients have relative bradycardia.
However, patients with a heart rate lower than 60 beats/min are usually
moribund.
• Arterial bleeding often stops temporarily on its own; the transected artery will
spasm and thrombose. Arterial bleeding, if constant, results in rapid
hypotension
• Venous bleeding, however, is slower; the human body compensates, and
sometimes large volumes of blood are lost before hypotension ensues.
• Hypotension has been traditionally set, arbitrarily, at 90 mm Hg and below.

• Capillary Haemorrhage is bright red ooze. If continuing for many hours can be
serious, as in hemophilia
• Primary Haemorrhage – occurs at time of injury or operation
• Reactionary Haemorrhage – may follow primary haemorrhage within 24 hours
(usually 4-6 hours) mainly due to slipping of ligature, dislodgement of clot, or
cessation of reflex vasospasm.
• Rise of BP on recovery from shock
• Restlessness, coughing, vomiting

• Secondary Haemorrhage – 7-14 days after, due to infection and sloughing of
part of wall of artery
• Pressure of a drainage tube, fragment of bone,
• ligature in infected area
• Cancer
• It is heralded by ‘warning’ haemorrhages, which are bright red stains on the
dressing, followed by sudden severe haemorrhage

Massive blood loss
• Loss of entire blood volume within 24 hours
• Loss of 50% of blood volume within 3 hours
• Ongoing blood loss of 150 ml/min
• Rapid blood loss leading of circulatory failure

Lethal triad
ACIDOSIS
HYPOTHERMIA COAGULOPATHY

• Common in resuscitated patients who are bleeding or in shock from various
factors.
• Inadequate tissue perfusion results in acidosis caused by lactate production.
• In the shock state, the delivery of nutrients to the cells is thought to be
inadequate, so adenosine triphosphate (ATP) production decreases. The human
body relies on ATP production to maintain homeostatic temperatures.
• The resulting hypothermia then affects the efficiency of enzymes, which work
best at 37° C. Coagulation cascade depends on enzymes affected by
hypothermia; can contribute to uncontrolled bleeding from injuries or the
surgery itself.

CRYSTALLOIDS
• Normal Saline used most commonly
• Ringer’s lactate – useful in massive transfusions, because of its ability to buffer
metabolic acidosis. There is a theoretical risk of hyperkalemia, in cases of AKI
COLLOIDS
• Synthetic colloids like Hestarch, hextend can be used, however may be
associated with coagulopathy and increased risk of acute kidney injury.
HYPERTONIC SALINE
• Additional benefit of acting as an osmotic agent to decrease cerebral edema,
decreased incidence of ARDS
BLOOD PRODUCTS
• PRBCs are only indicated if patients fail to respond to crystalloid bolus.

• Acidosis
The best fundamental approach to metabolic acidosis from shock is to treat the
underlying cause of shock. Treating acidosis with sodium bicarbonate may have a
benefit in an unintended and unrecognized way.
1. Sodium bicarbonate
2. THAM (tromethamine; tris[hydroxymethyl]aminomethane) buffers CO2 and
acids.
The initial loading dose of THAM acetate (0.3 M) for the treatment of acidemia
may be estimated as follows:
THAM (in mL of 0.3M solution) = lean body weight in kg X base deficit (in mmol /
liter)

• COAGULOPATHY
• The use of rFVIIa may be particularly useful for patients with traumatic
brain injuries (TBIs).
• Factor IX, or prothrombin complex concentrate (PCC), has become popular
for the treatment of surgical coagulopathy.
• FFP
• Tranexamic Acid – inhibits plasminogen activation and plasmin activity, thus
prevents fibrinolysis rather than promoting coagulation. CRASH-2 trial
found benefit of tranexamic acid in trauma patients, only if given within 3
hours of injury.

OXYGEN DELIVERY OPTIMIZATION (SUPERNORMALISATION)
• The optimization process involves administering a rapid bolus of fluid so that it
raises wedge pressure.
• Also rapid bolus of fluid increases cardiac output, thereby increasing effective
delivery of oxygen
• Add hemoglobin . If the hemoglobin level increased from 8.0 to 10 dL/liter, by
transfusing 2 units of blood, oxygen delivery would increase by 25%.

SEPTIC SHOCK
• Bacteremia - Presence of bacteria in blood, as evidenced by positive blood
cultures
• Septicemia - Presence of microbes or their toxins in blood
• Systemic inflammatory response syndrome (SIRS) - Two or more of the following
conditions:
1. Fever (oral temperature >38°C) or hypothermia (<36°C)
2. Tachypnea (>24 breaths/min)
3. Tachycardia (heart rate >90 beats/min)
4. Leukocytosis (>12,000/μL), leukopenia (<4,000/μL), or >10% bands
• Sepsis - SIRS that has a proven or suspected microbial etiology

• Severe sepsis - Sepsis with one or more signs of organ dysfunction:
1. Cardiovascular: Arterial systolic blood pressure ≤90 mmHg or mean arterial
pressure ≤70 mmHg that responds to administration of intravenous fluid
2. Renal: Urine output <0.5 mL/kg per hour for 1 h despite adequate fluid
resuscitation
3. Respiratory: PaO2/FIO2 ≤250
4. Hematologic: Platelet count <80,000/μL or 50% decrease in platelet count
from highest value recorded over previous 3 days
5. Unexplained metabolic acidosis: A pH ≤7.30 or a base deficit ≥5.0 mEq/L
6. Adequate fluid resuscitation: Central venous pressure ≥8 mmHg

• Septic shock - Sepsis with hypotension (arterial blood pressure <90 mmHg
systolic, or 40 mmHg less than patient’s normal blood pressure)
for at least 1 h despite adequate fluid resuscitation;
or Need for vasopressors to maintain systolic blood pressure
≥90 mmHg or mean arterial pressure ≥70 mmHg

INTERNATIONAL GUIDELINES FOR MANAGEMENT OF
SEVERE SEPSIS AND SEPTIC SHOCK
Fluid Therapy
• ✓ Fluid-resuscitate using crystalloids or colloids (1B).
• ✓ Target a CVP of ≥8 cm H2O (≥12 cm H2O if mechanically
ventilated) (1C).
• ✓ Use of fluid challenge technique while associated with a
hemodynamic improvement (1D).
• ✓ Give fluid challenges of 1000 mL of crystalloids or 300- 500 mL
or colloids over 30 min. More rapid and larger volumes may be
required in sepsis-induced tissue hypoperfusion (1D).
• ✓ Rate of fluid administration should be reduced if cardiac filling
pressures increase without concurrent hemodynamic
improvement (1D).

 Vasopressors
✓Maintain MAP ≥ 65 mm H g (1C).
✓Norepinephrine and dopamine centrally administered are the initial
vasopressors of choice (1c).
• Epinephrine, phenylephrine, or vasopressin should not be administered as
the initial vasopressor in septic shock (2c).
• Vasopressin, 0.03 units/min, may be subsequently added to norepinephrine
with anticipation of an effect equivalent to norepinephrine alone.
• Use epinephrine as the first alternative agent in septic shock when blood
pressure is poorly responsive to norepinephrine or dopamine. (2b).
✓Do not use low-dose dopamine for renal protection (1a).
✓In patients requiring vasopressors, insert an arterial catheter as soon as practical
(1d)

 Inotropic therapy
• ✓Use dobutamine in patients with myocardial dysfunction as
supported by elevated cardiac filling pressures and low cardiac
outputs (1C).

 Steroids
• Consider IV hydrocortisone for adult septic shock when hypotension
responds poorly to adequate fluid resuscitation and vasopressors (1C).
• Hydrocortisone is preferred to dexamethasone (2b).
• Steroid therapy may be weaned once vasopressors are no longer
required (2d).
• ✓Hydrocortisone does should be ≤300mg/day (1a).
• ✓Do not use corticosteroids to treat sepsis in the absence of shock.

 Recombinant human activated protein C
• Consider RHAPC in adult patients with sepsis-induced organ dysfunction with
clinical assessment of high risk of death (multiorgan failure) if there are no
contraindications (2B, 2C postoperative patients).
• ✓Adult patients with severe sepsis and low risk of death (one organ failure)
should not receive RHAPC (1a).

 Antibiotic
Sepsis without a clear Focus
(1) piperacillin-tazobactam (3.375 g q4–6h); or
(2) imipenem-cilastatin (0.5 g q6h) or meropenem (1 g q8h); or
(3) cefepime (2 g q12h).
If the patient is allergic to β-lactam agents, use ciprofloxacin (400 mg q12h) or
levofloxacin (500–750 mg q12h) plus clindamycin (600 mg q8h).
Vancomycin (15 mg/kg q12h) should be added to each of the above regimens.

hypervolemia
• Excess isotonic fluid in extracellular space
• Can lead to cardiac failure, pulmonary edema
• Severe hypervolemia when there is more than 10% weight
gain

Water intoxication
• When excess fluid moves from extracellular space to the intracellular space due
to low osmolality of extracellular fluid.
• SIADH
• Rapid infusion of hypotonic solutions
• TURP
• Increases ICP leading to seizures, coma
• S. Na < 125 mEq/L
• S. osmolality <280 mOsm/kg

Changes in composition of body fluids
• Main intracellular cation
• Regulates cell excitability
• Extracellular potassium (2% of total potassium) is maintained by
renal excretion of potassium, normal range 3.5 – 5 mEq/L.
POTASSIUM

• Hypokalemia can occur due to intracellular shifts from metabolic
alkalosis or insulin therapy.
• The change in potassium associated with alkalosis can be calculated
by the following formula:
Potassium decreases by 0.3 meq/L for every 0.1 increase in ph above
normal.
• Drugs that induce magnesium depletion (amphotericin,
aminoglycosides, cisplatin, and ifosfamide) cause renal potassium
wastage. In such cases potassium repletion is difficult unless
hypomagnesemia is first corrected.

• Serum potassium level <4.0 meq/L:
o Asymptomatic, tolerating enteral nutrition: Oral 40 to 100 mEq/day, in two to
four doses.
o Asymptomatic, not tolerating enteral nutrition: KCl 20 meq IV q2h X 2 doses
o Symptomatic: KCl 20 meq IV q1h X 4 doses
• Recheck potassium level 2h after end of infusion; if K <3.5 mEq/L and
asymptomatic, replace as per above protocol.

CALCIUM
• Major cation in teeth and bones
• Acts as enzyme activator within cells
• Required for muscle contractility
• Aids in coagulation
Daily calcium intake is 1 to 3 g/d.
Most of this is excreted via the bowel, with urinary excretion relatively low.
Disturbances in metabolism are relatively long term and less important in the
acute surgical setting. However, attention to the critical role of ionized calcium in
neuromuscular function often is required.

• Serum calcium (<1% of body’s calcium) is distributed among three forms:
• protein found (40%)
• complexed to phosphate and other anions (10%)
• ionized (50%)
• It is the ionized fraction that is responsible for neuromuscular stability and can
be measured directly.
• Normal range of total serum Calcium 8.9 – 10.1 mg/dl
• Normal range of ionized calcium is 4.4 – 5.3 mg/dl

• When total serum calcium levels are measured:
Corrected iCa 2+ = total [Ca]+(0.8×[4.5 − albumin level])
• Changes in ph will affect the ionized calcium concentration. Acidosis decreases
protein binding, thereby increasing the ionized fraction of calcium.

HYPERCALCEMIA
• Hypercalcemia is defined as a serum calcium level above the normal range of
8.5 to 10.5 meq/L or an increase in the ionized calcium level above 4.2 to 4.8
mg/dl.
• Primary hyperparathyroidism in the outpatient setting and malignancy in
hospitalized patients, from either bony metastasis or secretion of parathyroid
hormone–related protein, account for most cases of symptomatic
hypercalcemia.

• Treatment is required when hypercalcemia is symptomatic, which usually occurs
when the serum level exceeds 12 mg/dl.
• The critical level for serum calcium is 15 mg/dl, when symptoms noted earlier
may rapidly progress to death.
• The initial treatment is aimed at repleting the associated volume deficit and
then inducing a brisk diuresis with normal saline.

Etiology:
• Pancreatitis
• massive soft tissue infections
such as necrotizing fasciitis,
• renal failure,
• pancreatic and small bowel
fistulas,
• hypoparathyroidism,
Hypocalcemia rarely results solely
from decreased intake, because
bone reabsorption can maintain
normal levels for prolonged
periods
• abnormalities in magnesium levels
• tumor lysis syndrome.
• transient hypocalcemia commonly
occurs after removal of a
parathyroid adenoma due to
atrophy of the remaining glands and
avid bone remineralization, and
sometimes requires high-dose
calcium supplementation
• malignancies associated with
increased osteoblastic activity, such
as breast and prostate cancer, can
lead to hypocalcemia from
increased bone formation.
• Massive blood transfusion with
citrate binding is another
mechanism.
HYPOCALCEMIA

• Hypocalcemia is defined as a serum calcium level below 8.5 meq/L or a
decrease in the ionized calcium level below 4.2 mg/dl
• Asymptomatic hypocalcemia may occur when hypoproteinemia results in
a normal ionized calcium level. Conversely, Symptoms can develop with a
normal serum calcium level during alkalosis, which decreases ionized
calcium.
• Neuromuscular and cardiac symptoms do not occur until the ionized
Fraction falls below 2.5 mg/dl.

• Clinical Findings may include
• paresthesias of the face and
extremities,
• Muscle cramps, carpopedal spasm,
• stridor,
• seizures.
• hyperreflexia
• hyperreflexia
• Chvostek’s sign (spasm resulting
from tapping over the facial Nerve)
and
• trousseau’s sign (spasm resulting
from pressure applied to the
nerves and vessels of the upper
extremity with A blood pressure
cuff
• decreased Cardiac contractility and
heart failure.

Ionised calcium level <4.0 mg/dl
• Tolerating enteral nutrition: Calcium carbonate suspension 1250
mg/5ml q6h per oral; recheck ionized calcium level in 3 days
• Not tolerating enteral nutrition: Calcium gluconate 2 g IV over 1 h X 1
dose; recheck ionized calcium level in 3 days
• Associated deficits in magnesium, potassium, and pH must also be
corrected.

phosphorus
• Phosphorus is the primary intracellular divalent anion and is abundant in
metabolically active cells.
• Phosphorus is involved in energy production during glycolysis and is found in
high-energy phosphate products such as adenosine triphosphate.
• Acts as a hydrogen buffer
• Serum phosphate levels are tightly controlled by renal excretion.
• Normal range of serum Phosphorus is 2.5 – 4.5 mg/dl or 1.8 – 2.6 mEq/L

Hyperphosphatemia can be due to decreased urinary excretion,
increased intake, or endogenous mobilization of phosphorus.
• impaired renal function.
• Hypoparathyroidism or hyperthyroidism
• cell destruction
• rhabdomyolysis, tumor lysis syndrome, hemolysis,
• sepsis, severe
• hypothermia, and malignant hyperthermia.
• Excessive phosphate administration from IV hyperalimentation
solutions or phosphorus containing laxatives may also lead to
elevated phosphate levels.
HYPERPHOSPHATAEMIA

• Phosphate binders such as sucralfate or aluminum-containing
antacids can be used to lower serum phosphorus levels.
• Calcium acetate tablets also are useful when hypocalcemia is
simultaneously present.
• Sevalemer – phosphate binder, given orally
• Dialysis usually is reserved for patients with renal failure.

Chronic hypophosphatemia
• Decreased GI uptake due to
malabsorption
• administration of phosphate
binders
• malnutrition
Acute hypophosphatemia
• Intracellular shift of phosphorus
• respiratory alkalosis,
• insulin therapy,
• refeeding syndrome,
• hungry bone syndrome.
HYPOPHOSPHATAEMIA

• Clinical manifestations of hypophosphatemia usually are absent
until levels fall significantly.
• Symptoms are related to adverse effects on the oxygen availability
of tissue and to a decrease in high-energy phosphates.
• Cardiac dysfunction
• Muscle weakness.

Phosphate level 1.0 – 2.5 mg/dl:
• Tolerating enteral nutrition: Neutra-Phos 2 packets q6h per oral
• Not tolerating enteral nutrition: KPHO4 or NaPO4 0.15 mmol/kg IV
over 6 h X 1dose
• Recheck potassium level in 3 days

Phosphate level < 1.0 mg/dl:
• Tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg over 6 h X 1 dose
• Recheck phosphate level 4h after end of infusion; if <2.5 mg/dl, begin
Neutra-Phos 2 packets q6h
• Not tolerating enteral nutrition: KPHO4 or NaPO4 0.25 mmol/kg (LBW) over 6h X
1 dose; recheck phosphate level 4 h after end of infusion
• If <2.5 mg/dl, then KPHO4 or NaPO4 0.15 mmol/kg (LBW) IV over 6 h X 1
dose

magnesium
• Approximately one half of the total body content is incorporated in bone and is
slowly exchangeable.
• Normal range of serum Mg 1.5 – 2.5 mEq/l
• Of the fraction found in the extracellular space, one third is bound to serum
albumin.
• The magnesium ion is essential for proper function of many enzyme systems
particularly protein synthesis
• Modifies nerve impulse transmission and skeletal muscle response

• Severe renal insufficiency
• Magnesium-containing antacids and laxatives can produce toxic levels in
patients with renal failure.
HYPERMAGNESEMIA

• Treatment for hypermagnesemia consists of measures to eliminate
exogenous sources of magnesium, correct concurrent volume deficits,
and correct acidosis if present.
• To manage acute symptoms, calcium chloride (5 to 10 ml) should be
administered to immediately antagonize the cardiovascular effects.
• If elevated levels or symptoms persist, hemodialysis may be necessary

• Poor intake
o starvation,
o alcoholism,
o Prolonged IV fluid therapy,
o TPN with inadequate
supplementation of magnesium.
• GI losses
• acute pancreatitis.
• Increased renal excretion
o alcohol abuse,
o diuretic use,
o administration of amphotericin B
o primary aldosteronism,
HYPOMAGNESEMIA

• positive chvostek’s and trousseau’s signs
• Delirium and seizures.
it can produce hypocalcemia and lead to persistent hypokalemia. When
hypokalemia or hypocalcemia coexists with hypomagnesemia, magnesium should
be aggressively replaced to assist in restoring potassium or calcium homeostasis.

• Magnesium level 1.0 – 1.8 mEq/L:
• Magnesium sulphate 0.5 mEq/kg in NS 250 ml infused IV over 24 h X 3 d
• Recheck Mg Level in 3 d
• Magnesium level , 1.0 mEq/L:
• Magnesium sulphate 1 mEq/kg in NS 250 ml infused IV over 24 h X 1 d, then
0.5 mEq/kg in NS 250 ml infused IV over 24 h X 2 d
• Recheck Mg level in 3 d
• If patient is tolerating orally: milk of magnesia 15 ml (approx. 49mEq Mg) q24h;
hold for diarrhoea

Classification of IV Fluids
• Crystalloids:
Hypotonic- 2.5% dextrose ,1/2 NS
Isotonic- 0.9%Nacl, ringer lactate, ringer acetate
Hypertonic- 3%,5%, 7.5% Nacl. D5 1/2 NS OR 1/4NS
• Colloids:
Hydroxyethyl starches
Gelatins
Dextran
Albumin.

• Crystalloids are aqueous solutions of inorganic and small organic
molecules, the main solute being either normal saline or glucose.
Depending on the concentration of the solute, crystalloid
solutions are isotonic, hypotonic, and hypertonic.
• Colloids, in contrast, are homogeneous noncrystalline substances
containing large molecules.

ISOTONIC
5%Dextrose
0.9% NaCl
Ringer’s Lactate
HYPOTONIC
0.45% NaCl
2.5% Dextrose
HYPERTONIC
5% Dextrose in Half Normal Saline
5% Dextrose in Normal Saline
10% Dextrose
CRYSTALLOIDS

Plasma
Albumin
Dextran
Hestarch
Hextend
Colloids are used as volume expanders. Due to their molecular weight, they are
confined to the intravascular space, and their infusion results in more efficient
transient plasma volume expansion.
COLLOIDS

Distribution of IV Fluids in Body Compartments
Distribution of 1,000 mL of
fluid given IV
Intracellular
Fluid
Interstitial
Fluid
Intravascula
r Fluid
5% Dextrose 666 249 83
Crystalloid 0 750 250
Colloid
Immediate 0 0 1,000
After 4
hours
0 750 250
Blood 0 0 1,000

Advantages of Colloids
• Intravascular volume can be expanded more rapidly.
• Smaller total volume of fluid required to chieve adequate perfusion
• Less third-spacing, low incidence of complications like bowel edema, abdominal
compartment syndrome, ARDS
However numerous studies examining use of colloids in resuscitation of critically
ill and injured have failed to demonstrate statistically significant benefit

CRYSTALLOIDS V/S COLLOIDS
• Crystalloids are
1. inexpensive
2. adverse effects are rare
or absent
3. There is no renal
impairment,
4. minimal interaction
with coagulation
5. no tissue accumulation,
6. and no allergic reactions
• Colloids are
1. better volume-
expanding
properties,
2. minor edema
formation
3. improved
microcirculation.
4. Improve tissue
oxygenation.
5. expensive

• 5% Dextrose: Solution is isotonic initially, becomes hypotonic when dextrose
is metabolized; not used for resuscitation, can cause hyperglycemia.
• Normal Saline: The high chloride concentration imposes a significant chloride
load on the kidneys and may lead to a hyperchloremic metabolic acidosis.
Sodium chloride is an ideal solution, however, for correcting volume deficits
associated with hyponatremia, hypochloremia, and metabolic alkalosis.
• Ringer’s Lactate: useful in replacing GI losses and correcting extracellular
volume deficits
• renal failure
• liver failure
• Alkalosis
• Using lactated ringer’s may be deleterious in hypovolemic shock because
it activates the inflammatory response and induces apoptosis.

• Half Normal Saline: Useful for replacement of ongoing GI losses as well as for
maintenance fluid therapy in the postoperative period; used in hypertonic
dehydration
• 5% D in Normal Saline:
• Used in hypotonic Dehydration
• SIADH
• Should not be used in patients with cardiac or renal disease

• Hypertonic saline solutions (3.5% and 5%)
• severe sodium deficit
• closed head injuries
• Albumin: 5% solution (osmolality of 300 mOsm/L) or 25% solution
(osmolality of 1500 mOsm/L
• allergic reactions.
• renal failure and impair pulmonary function when used for
resuscitation in hemorrhagic shock
• Hypoproteinemia

• Dextrans: They lead to initial volume expansion due to their osmotic effect
but are associated with alterations in blood viscosity. Thus dextrans are used
primarily to lower blood viscosity rather than as volume expanders. Dextrans
have been used, in association with hypertonic saline, to help maintain
intravascular volume.
• Hydroxyethyl starch solutions or Hetastarches:
• Hemostatic derangements related to decreases in von Willebrand’s
factor and factor VIII, and its use has been associated with
postoperative bleeding in cardiac and neurosurgery patients.
• Hetastarch also can induce renal dysfunction.
• Hyperchloremic acidosis (due to its high chloride content).

• Hextend: No adverse effects on coagulation with hextend other
than the known effects of hemodilution
• Gelatins: Gelofusine has been used abroad with mixed, it has been
shown to impair whole blood coagulation time in human
volunteers.

Pre-operative fluid therapy
IV Fluid Calculation
• 4 mL/kg for first 10 kg
• 2 mL/kg for next 10 kg
• 1 mL/kg for every kg over 20 kg
E.g. for 45-kg patient:
• 10 kg × 4 mL / kg = 40 mL
• 10 kg × 2mL / kg = 20 mL
• 25 kg ×1mL / kg = 25mL
Maintenance rate = 85mL/hr, 2000 ml/day

• Alternative approach is to replace the calculated daily water losses in urine,
stool, and insensible loss with a hypotonic saline solution.
• An appropriate choice of 5% dextrose in 0.45% sodium chloride at 100 ml/h
as initial therapy, with potassium added for patients with normal renal
function.
• Volume deficits should be considered in patients who have obvious GI
losses, such as through emesis or diarrhea, as well as in patients with poor
oral intake secondary to their disease.

Intra-operative fluid therapy
• With the induction of anesthesia, compensatory mechanisms are lost, and
hypotension will develop if volume deficits are not appropriately
corrected.
• In addition to measured blood loss, major open abdominal surgeries are
associated with continued extracellular losses in the form of bowel wall
edema, peritoneal fluid, and the wound edema during surgery.

• Large soft tissue wounds, complex fractures with associated soft tissue
injury, and burns are all associated with additional third-space losses that
must be considered in the operating room. These functional losses have
been referred to as parasitic losses, sequestration, or third-space edema,
because the lost volume no longer participates in the normal functions of
the ECF.
• Replacement of ECF during surgery often requires 500 to 1000 ml/h of a
balanced salt solution to support homeostasis.

Post-operative fluid therapy
• Postoperative fluid therapy should be based on the patient’s current
estimated volume status and projected ongoing fluid losses.
• Any deficits from either preoperative or intraoperative losses, third-
space losses should be included in fluid replacement strategies.
• The adequacy of resuscitation should be guided by the restoration of
acceptable values for vital signs and urine output.
• If uncertainty exists, particularly in patients with renal or cardiac
dysfunction, a central venous catheter may be inserted to help guide
fluid therapy.

• In the initial postoperative period, an isotonic solution should be
administered.
• After the initial 24 to 48 hours, fluids can be changed to 5% dextrose in 0.45%
saline in patients unable to tolerate enteral nutrition.
• If normal renal function and adequate urine output are present, potassium
may be added to the IV fluids.
• Daily fluid orders should begin with assessment of the patient’s volume
status and assessment of electrolyte abnormalities. All measured losses,
including losses through vomiting, nasogastric suctioning, drains, and urine
output, as well as insensible losses, are replaced with the appropriate
parenteral solutions.

Complications of i.v. therapy
• Infiltration
• Extravasation
• Infection
• Thrombophlebitis
• Severed catheter
• Fluid overload
• Air embolism

Nutritional support and fluid therapy in surgery

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