NUTRITION AND FLUID THERAPY IN SURGERY

CHAIR PERSON : DR. ISHWAR HOSAMANIPROFESSOR AND UNIT CHIEF

SURGERY B UNITKIMS HUBLI

SPEAKER: DR. AJAI SASIDHARPG STUDENT

DEPT OF GENERAL SURGERYKIMS HUBLI

Metabolism in surgical patients Metabolic events brought about by :

1. Injury2. Starvation

Metabolic response is directed to restore:1. Homeostasis2. 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 phasePhenomenon 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 glucoseN or FFAnormal lactate

CO2 production

heat production

multi-organ failure

Sequence of events

surgical problem infection

operation

bleeding tissue trauma

bacterial contaminationnecrotic debris

local inflammatory

response

wound healing

recovery

hypermetabolism

muscle wastingimmunosuppression

mortality

*

*mortality

food deprivation

wound pain

infection

immobility

Ebb phas

e

Flow phas

e

Anabolic phase

*acute stress

Metabolism of Injured PatientPHASES: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

Metabolism of Injured PatientPHASES:2. Early anabolic phase (flow, corticoid-withdrawal):

tissue perfusion has been restored, may last for days to months depending on:

a. severity of injuryb. previous healthc. 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

Metabolism of Injured PatientPHASES: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 traceelements

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.

Body Mass Index

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 NutritionalSupport• 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 nutrition1. 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.

For a 70 kg man,

For 2 in 1 solutions

For 3 in 1 solutions

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.

Metabolic complications of PN

Metabolic complications of PN

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.

Fluid therapy In Surgery

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 Com-ponent

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 TRANSPORTUses ATP to move solutes from area of low concentrationnto area of high concentration

• OSMOSISPassive 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

• KIDNEYDepending on body requirement of fluid and electrolytes, kidneys reabsorb more or less than normal, thus maintaining the fluid balanceKidneys secrete renin, which activates renin-angiotensin-aldosterone system; aldosterone regulates sodium and water reabsorption by kidneys.

• THIRSTRegulated 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

ElectrolytesOSMOLALITYThe 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

TONICITYThe 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.

Disturbances in VOLUME

Disturbances in CONCENTRATION

Disturbances in COMPOSITION

Classification of body fluid changes

Disturbances in concentration

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.

Disturbances in VOLUME

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,

SHOCK

• 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 triadACIDOSIS

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 AKICOLLOIDS• 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 ARDSBLOOD PRODUCTS• PRBCs are only indicated if patients fail to respond to crystalloid bolus.

• AcidosisThe 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)

• Hypothermia

• 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 days5. Unexplained metabolic acidosis: A pH ≤7.30 or a base deficit ≥5.0 mEq/L6. 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 SHOCKFluid 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

HYPERKALEMIA

HYPOKALEMIA

• 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 doseso 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 coagulationDaily 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.

Most cases of hyperphosphatemia are asymptomatic, but significant prolonged hyperphosphatemia can lead to metastatic deposition of soft tissue calcium-phosphorus complexes.

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 excretiono alcohol abuse, o diuretic use, o administration of amphotericin Bo 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

Fluid and electrolyte therapy

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 starchesGelatinsDextranAlbumin.

• 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

HYPOTONIC0.45% NaCl

2.5% Dextrose

HYPERTONIC

5% Dextrose in Half Normal Saline

5% Dextrose in Normal Saline

10% Dextrose

CRYSTALLOIDS

PlasmaAlbuminDextranHestarchHextend

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

Intravascular Fluid

5% Dextrose 666 249 83

Crystalloid 0 750 250

ColloidImmediate 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, ARDSHowever 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 absent3. There is no renal

impairment, 4. minimal interaction

with coagulation 5. no tissue accumulation, 6. and no allergic reactions

• Colloids are1. 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 therapyIV 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 = 25mLMaintenance 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