Nutritional

Management
in
Stefania Widya S.
Definition
• Sepsis has historically been defined as an uncontrolled inflammatory
response to infection or trauma.
• It is now understood that sepsis is actually an immunosuppressive
process that prevents an adequate response to infection.
• The Surviving Sepsis Campaign defined severe sepsis as “infection-
induced organ dysfunction or hypoperfusion abnormalities.”
• Septic shock is defined as “severe sepsis with hypotension not
reversed with fluid resuscitation and associated with organ
dysfunction or hypoperfusion abnormalities.”
 Sepsis Etiology
• Infections can lead to sepsis.
• An infection occurs when germs enter a person’s body and multiply,
causing illness, organ and tissue damage, or disease.
• Sepsis is often associated with infections of the lungs (e.g.,
pneumonia), urinary tract (e.g., kidney), skin, and gut. 
• Staphylococcus aureus (staph), Escherichia coli (E. coli), and some
types of Streptococcus (strep) are common germs that can cause
sepsis.
Classifications
 Risk Factors
• Are very young or very old
• Have a compromised immune system
• Are already very sick, often in a hospital's intensive care unit
• Have wounds or injuries, such as burns
• Have invasive devices, such as intravenous catheters or breathing
tubes
 Patophysiology of Sepsis
• sepsis was originally thought to be a result of an overwhelming systemic infection.
• Sepsis is initiated by an originating source of infection and/or trauma.
• When individual cell markers recognize microorganisms, the systemic response causes the
release of inflammatory mediators including TNF, interferon, and interleukins.
• Inflammation results in vascular permeability, which allows the shift of fluid into the lungs and
other third spaces.
• High levels of nitric oxide contribute to this vascular permeability. There is also an imbalance of
coagulation factors that can contribute to production of multiple thrombi.
• As sepsis continues, there is a shift from an inflammatory response to an anti-inflammatory
response with resulting energy (inability to mount an immune response) and organ dysfunction.
• The increased rate of gluconeogenesis results in significant catabolism of skeletal muscle mass.
• These metabolic abnormalities result in hyperglycemia and increased serum lactate
Patofisiologi Sepsis
Kegagalan Organ Pada
Sepsis
Clinical Manifestation
The initial major signs of sepsis include:
• increased white blood cell count (>12,000
mm3),
• increased heart rate (>90 beats per minute)
• respirations (>20 breaths/minute)
• fever (>38 °C) or hypothermia (<36 °C) (8).
• C-reactive protein, fibrinogen, complement
proteins, and other acute-phase proteins
are elevated.
• Other laboratory values may include
increased serum lactate and serum glucose
 Metabolic Stress Conditions
• Sepsis (infection)
• Trauma (including burns)
• Surgery
• Once the systemic response is activated, the physiologic and
metabolic changes that follow are similar and may lead to septic
shock.
 Perubahan
Fisiologis pada
Sepsis
ADH, Antiduretic hormone; NH3, ammonia.
Ebb Phase
• Cuthbertson : two phase theory (Ebb Phase and Flow Phase)
• Ebb phase : 24 - 48 hr since stress
• Increase symphatetic activity and stimulation of hypothalamus
pituary axis Hypometabolism dan penurunan konsumsi oksigen
• Decreased cardiac output
• Lowered body temperature
• Insulin levels drop because glucagon is elevated.
Flow Phase
• Acute atau Flow phase
• Hypermetabolisme, catabolism, increase oxygen consumption
• Catecholamin ↑, Glucocortikoid ↑, Glucagon↑, cytokines ↑, acute phase
protein production
• Follows fluid resuscitation and O2 transport
• Increased cardiac output begins
• Increased body temperature
• Increased energy expenditure
• Total body protein catabolism begins
• Marked increase in glucose production, FFAs, circulating insulin/glucagon/cortisol
 Malnutrition incuded by Sepsis Condition
• Sepsis cause hypermetabolism response in the body
• Pasien dg stress berat berpotensi mengalami malnutrisi, akibat dari :
- Immobility
- Anorexia
- unefficient anabolisme
- increase catabolism
• Hypermetabolic state—stress causes accelerated energy expenditure, glucose
production, glucose cycling in liver and muscle
• Hyperglycemia can occur either from insulin resistance or excess glucose production
via gluconeogenesis and Cori cycle.
• Muscle breakdown accelerated
Perubahan Nutrien di Dalam
Tubuh Pada Kondisi Stres Ber
Starvation Vs Metabolic Stress
Management of Sepsis
Medical and Nutritional Management of Sepsis

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Maion F. Winkler and
Ainsley Malone, 2002.
Algoritma Terapi
Gizi Medis Pada
Pasien Kritis
 Timing
• To date, adequately powered studies have not been conducted to
demonstrate a significant difference in mortality when comparing
early versus late EN in critically ill patients
• If the critically ill patient is adequately fluid resuscitated, then EN
should be started within 24 to 48 hours following injury or admission
to the ICU. Early EN is associated with a reduction in infectious
complications and may reduce LOS. The impact of timing of EN on
mortality has not been adequately evaluated.
 Nutrition Delivery Timing

Wrinkle and Malone, 2017. Krause’s Food and Nutrition Therapy

Nutrition
Delivery Route
ASPEN Practice Guidelines for Critical Care
• Patients with critical illnesses are at nutrition risk and should undergo
nutrition screening to identify those who require formal nutrition
assessment with development of a nutrition care plan.
• Specialized nutrition support (SNS) should be initiated when it is
anticipated that critically ill patients will be unable to meet their
nutrient needs orally for a period of 5-10 days.
• EN is the preferred route of feeding in critically ill patients requiring
SNS.
• PN should be reserved for those patients requiring SNS in whom EN is
not possible.
 Nutritional Assessment
• Traditional methods not adequate/reliable
• Urine urea nitrogen (UUN) excretion in
gms per day may be used to evaluate
degree of hypermetabolism:
• 0 –5 = normometabolism
• 5 – 10 = mild hypermetabolism (level 1
stress)
• 10 – 15 = moderate (level 2 stress)
• >15 = severe (level 3 stress)
• Clinical judgment must play a major role
in deciding when to begin/offer nutrition
support
 Energy Need
• Enough but not too much
• Excess calories:
• Hyperglycemia
• Diuresis – complicates fluid/electrolyte balance
• Hepatic steatosis (fatty liver)
• Excess CO2 production
• Exacerbate respiratory insufficiency
• Prolong weaning from mechanical ventilation
• The “gold standard” in estimating energy needs in critical care 
indirect calorimetry
Alternative Methods for Defining Energy Need
ADA Guidelines for Defining Energy Need in
Critically Ill Patients
• If predictive equations are needed in critically ill patients, consider using one
of the following, as they have the best prediction accuracy of equations
studied: Ireton-Jones, 1992, Penn State, 2003a or Swinamer. In some
individuals, errors between predicted and actual energy needs will result in
under- or over-feeding.
• The Harris-Benedict (with or without activity and stress factors), the Ireton-
Jones, 1997, and the Fick equation should not be considered for use in RMR
determination in critically ill patients, as these equations do not have
adequate prediction accuracy. In addition, the Mifflin-St. Jeor equation should
not be considered for use in critically ill patients, as it was developed for
healthy people and has not been well researched in the critically ill
population.
ADA Guidelines for Defining Energy Need in
Critically Ill Patients (Obese)

• If predictive equations are needed for critically ill mechanically

ventilated individuals who are obese, consider using Ireton-Jones,
1992, or Penn State, 1998, as they have the best prediction accuracy
of equations studied. In some individuals, errors between predicted
and actual energy needs will result in under- or over-feeding.

• Because overfeeding is more problematic than underfeeding, could

possibly use adjusted weight or 20-21 kcal/kg actual BW in obese pts
 Carbohydrates
• Should provide 60 – 70% calories
• Maximum rate of glucose
oxidation = ~5 – 7 mg/kg/min or
7 g/kg/day*
• Blood glucose levels should be
monitored and nutrition regimen
and insulin adjusted to maintain
glucose below 150 mg/dl
Fats
• Can be used to provide needed
energy and essential fatty acids
• Should provide 15 – 40% of calories
• Limit to 2.5g/kg/day or possibly 1
g/kg/day IV*
• Caution with use of fats in stressed
& trauma pts
• There is evidence that high fat
feedings (especially LCT) cause
immunosuppression
• New formulas focus on omega-3s
 Protein
• 1.5 – 2.0 g/kg/day to start; monitor response
• A recent systematic review of protein requirements in critical illness concluded that protein
delivery of 2.0 to 2.5 g/kg/day is safe and may be optimal for most critically ill patients except
for those withrefractory hypotension, overwhelming sepsis, or severe liver disease (Hoffer
and Bistrian, 2012).
• Administration of excessive amounts of protein does not decrease the characteristic net
negative nitrogen balance seen among hypermetabolic patients.
• Giving exogenous aa’s decreases negative N balance by supplying liver aa’s for protein
synthesis
• Alterations in glutamine metabolism can occur in critical care, possibly affecting gut function
• PN solutions traditionally have not contained glutamine because of instability in solution
• Animal and human studies suggest that supplemental GLN in PN may have beneficial effects
• Those benefits have not been demonstrated in EN
 Fluids and
Vitamin and Fiber
Electrolytes
Fluid • Micronutrient needs are elevated
during acute illness because of
• 30-40 mL/kg or increased urinary and cutaneous losses
• 1 to 1.5mL/kcal expended and diminished GI absorption, altered
distribution, and altered serum carrier
protein concentrations.
Electrolytes/Vitamins/Trace • With increased caloric intake there may
Elements be an increased need for B vitamins,
particularly thiamin and niacin.
• Enteral feedings: begin with
• Catabolism and loss of lean body tissue
RDA/AI values increase the loss of potassium,
• PN: use PN dosing guidelines magnesium, phosphorus, and zinc.
 Cautious Re/Early Feeding in Sepsis
• EN is the preferred route of feeding for the critically ill patient who cannot eat
food and yet has good intestinal function.
• During sepsis, the GI tract and liver are susceptible to ischemia due to increased
oxygen consumption and decreased blood flow
• Enteral nutrition delivered to septic patients given vasoactive drugs may
exacerbate this
• EN should be initiated cautiously after hemodynamic stability is established
• Intake of 50% to 65% of goal calories during the first week of hospitalization is
thought to be sufficient to achieve the clinical benefit of EN
• Immune modulating enteral formulations that contain arginine, glutamine,
nucleic acids, antioxidants, and omega-3 fatty acids should not be used routinely
for ICU patients with sepsis because they may worsen the inflammatory response
(SCCM and A.S.P.E.N., 2009).
Major Burns
Overview
• Burn injury causes a persistent and prolonged hypermetabolic state
and increased metabolism that results in increased muscle wasting
and cachexia.
• Metabolic rates of burn patients can surpass twice normal, and failure
to fulfill these energy requirements causes impaired wound healing,
organ dysfunction, and susceptibility to infection
Clinical Consideration in Major Burns
• Cutaneous exudative losses of fluids containing large quantities of
protein, minerals and micronutrients, which cause acute deficiency
syndromes.
• Venous access is more difficult due to the destruction of the skin at
the puncture sites (higher risk of catheter related infection).
• The surface to repair is extensive and explains the requirement for
prolonged nutritional support, which is rare in other trauma.
• Burn patients stay for much longer periods in intensive care units
(ICU) compared with other trauma, and require more prolonged
nutritional support.
Metabolic Implication of Burns
Classification of burn
How to Calculate Total Body
Surface Area (TBSA)
Lund and Browder Chart

The Lund and Browder chart is more accurate, and can be used in children as it takes into account the person's
age, and the different proportions of the head and legs in growing children.
Palmar Method
• For small or scattered burns, or for
assessing the amount of unburnt
skin in very extensive burns, the
person's palmar surface (including
fingers) can be used as a guide.
• It is equivalent to around 0.8% of the
person's total body surface area.
Nutritional Assessment in Burn Patients
• Weight may fluctuate considerably due to fluid shifts and
resuscitation.
• High protein losses from wounds and the overall acute inflammatory
response can affect accurate interpretation of the protein markers
albumin, prealbumin, or C-reactive protein in relationship to
nutritional status.
• the goal should be to minimize losses and promote wound healing.
Assessment Indicator Checklist
• Height and pre-burn weight. Fluid resuscitation can cause significant
oedema and make assessing pre-burn weight difficult.
• Details of previous nutritional status
• %TBSA of burn and site of injury
• Gastrointestinal function
• Pain control
• Pre-existing medical conditions
• Usual diet and any specific dietary needs
Nutrition Diagnosis
Common nutrition diagnoses that occur for the burn patientn include:
• increased energy expenditure;
• increased nutrient needs;
• impaired nutrient utilization;
• altered GI function;
• Involuntary weight loss;
• and altered nutrition-related laboratory values.
Nutritional Intervention
• Many burn patients will be able to eat food
• Nutrition counseling should focus on selection of high protein and calorically
dense food and fluids.
• Enteral nutrition should be considered for those patients who are unable to
eat or cannot achieve adequate intake by food alone.
• Weight maintenance should be the goal for overweight patients until the
healing process is complete.
• Obese individuals may be at higher risk of wound infection and graft
disruption.
• The energy requirement for the obese burned person is probably more than
that calculated when ideal body weight is used but less than that calculated
when actual body weight is used.
Energy Requirement

Rousseau, Anne-Françoise., Losser, Marie-Reine., Ichai, Carole., Berger, Mette M. ESPEN endorsed recommendations:
Nutritional therapy in major burns . Clinical Nutrition 32 (2013) 497-502
 Energy Requirement Calculation Checklist
When calculating requirements, it is important that the following points
are considered:
• Use of ideal / usual body weight (except with use of Ireton-Jones
equation for spontaneously breathing patients)
• Reassessing as wounds are closed and healed
• Ensuring at least twice weekly re-evaluation
• Consider graft mesh size
• Consider the impact and continuum of physiotherapy
andoccupational therapy using the activity factors
Toronto
Formula
Modified
Schofield
Equation
Ireton-Jones
Equation
Curreri Formula

• Note: The Curreri Formula is well known to overestimate requirements. This may be due to
advances in the medical management of burns which have reduced the hypermetabolism
associated with a burn injury, e.g. early excision and grafting, wound dressings and environmental
temperature control
Fluid Requirement
• The volume of fluid needed is based on the age and weight of the patient
and the extent of the injury designated by percentage of total body
surface area (TBSA) burned.

• Once resuscitation is complete, ample fluids must be given to cover

maintenance requirements and evaporative losses that continue through
open wounds.
• Evaporative water loss can be estimated at 2 to 3.1 mL/kg
 Protein
• High protein delivery of 1.5-3.0 g/kg ideal body weight/day or 20-25%
of total energy is required for burn patients.
• Non-protein calorie to nitrogen ratio should be maintained between
150:1 and 100:1 whilst in the Burn Unit, according to the percentage
TBSA and each stage of injury, as follows:

Deitch EA. Nutritional support of the burn patient. Critical Care Clinics 1995; 11: 735-750
Carbs and Fats
• Carbohydrate
Glucose infusion or delivery should be no more than 5-7 mg/kg/min
(about 50% CHO as energy).

• Fat:
Fat should constitute no more than 25-30% as energy, but in fact 15-
20% of non-protein energy as fat is optimal.
 Micronutrient
Regarding vitamin requirements, the clinical studies have mainly
investigated vitamin B, C, and E.
• Additional thiamin intake normalizes lactate and pyruvate
metabolism.
• Clinical benefits have been shown with reduction of oxidative stress,
and improved wound healing using doses of vitamin C and E 1.5
times higher than recommended daily intakes in children and adults.

Rousseau, Anne-Françoise., Losser, Marie-Reine., Ichai, Carole., Berger, Mette M. ESPEN endorsed recommendations:
Nutritional therapy in major burns . Clinical Nutrition 32 (2013) 497-502
 Micronutrient
• Copper, selenium and zinc are lost in large amounts through
cutaneous exudates: depletion of body stores must be anticipated by
early substitution in patients with major burns.
• Copper is of special importance in burns as collagen is dependent on
it for maturation.
• Selenium is essential for glutathione peroxidase activity
• zinc for immunity and cell replications.
• Magnesium and phosphorus losses through exudates are extensive
and explain, to a large extent, the increased requirements in burns
Berger, Meete. Basics in clinical nutrition: Nutritional support in burn patients. the European e-Journal of Clinical
Nutrition and Metabolism 4 (2009) e308–e312
Nutraceutical
 Glutamine and Arginine
• Both amino acids are conditionally essential after injury.
• They improve the function of the gut mucosa as well as immune
function which may help to reduce septic complications in burned
patients.
• Up to 30 g day1 of glutamine and of arginine have been
recommended
 Omega 3
• These fatty acids are potential immunomodulatory and
antiinflammatory agents in a dose of up to 3–5 g day
Monitoring and Evaluation
• In adults, re-calculation of nutritional requirements using an equation
should occur on a routine basis as wound size, and thus metabolism
changes with skin grafting, reepitheliazation and graft loss.
• Weekly serum transferrin and prealbumin should be tested, as they
are indicators of visceral protein status. Both serum transferrin and
prealbumin are negative acute phase reactants and thus decline
markedly in the acute post burn phase
Any Questions?