University of Alexandria

High institute of public health

Department of nutrition

Nutrition and Metabolic stress

( sepsis, trauma, burns and surgery )

By Dr: Nahla Mahmoud Elamrawy

Supervisor

Dr: Dalia Tayel

Metabolic Stress:

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.

Metabolic Response to Stress:

Involves most metabolic pathways, accelerated catabolism of lean body

mass, negative nitrogen balance, muscle wasting.

The response to critical illness involves both ebb and flow phases:

Ebb Phase:

Immediate following injury associated with hypovolemia, shock, tissue

hypoxia, decreased cardiac output, decreased oxygen consumption,

Lowered body temperature, Insulin levels drop because glucagon is elevated.

Flow Phase

Follows fluid resuscitation and restoration O2 transport, Increased cardiac

output begins, increased body temperature, increased energy expenditure,

total body protein catabolism begins, marked increase in glucose production,

FFAs release, circulating level of insulin, glucagon and cortisol

Hormonal and Cell-Mediated Response:

There is a marked increase in glucose production and uptake secondary to

gluconeogenesis, and elevated hormonal levels, marked increase in hepatic

amino acid uptake, Protein synthesis, accelerated muscle breakdown.

Hormonal Stress Response:

Aldosterone—corticosteroid that causes renal sodium retention

Antidiuretic hormone )ADH(—stimulates renal tubular water absorption

These conserve water and salt to support circulating blood volume.

ACTH—acts on adrenal cortex to release cortisol (mobilizes amino acids

from skeletal muscles).

Catecholamines—epinephrine and norepinephrine from renal medulla to

stimulate hepatic glycogenolysis, fat mobilization, gluconeogenesis.

Cytokines

Interleukin-1, interleukin-6, and tumor necrosis factor (TNF)

Released by phagocytes in response to tissue damage, infection,

inflammation, and some drugs and chemicals

It stimulate hepatic up take to amino acids, protein synthesis, accelerate ms

breakdown and induce gluconeogenesis.

Skeletal Muscle Proteolysis:

Break down of skeletal muscle protein leads to increases in amino acid

levels, which transaminated with glutamate or pyruvate to form alanine

&glutamine. The muscle preferentially uses branched chain amino acids for

energy through transamination with the formation of branched chain

ketoacids, which can enter the tricyclic acid cycle for energy production.

Metabolic Changes in Starvation:

Starvation vs. Stress

Metabolic response to stress differs from the responses to starvation.

Starvation = decreased energy expenditure, use of alternative fuels,

decreased protein wasting, stored glycogen used in 24 hours

Late starvation = fatty acids, ketones, and glycerol provide energy for

all tissues except brain, nervous system, and RBCs

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 also.

Systemic Inflammatory Response Syndrome:

SIRS describes the inflammatory response that occurs in infection,

pancreatitis, ischemia, burns, multiple trauma, shock, and organ injury.

Patients with SIRS are hypermetabolic.

Multiple Organ Dysfunction Syndrome:

Organ dysfunction that results from direct injury, trauma, or disease or as a

response to inflammation; the response usually is in an organ distant from

the original site of infection or injury.

Diagnosis of Systemic Inflammatory Response Syndrome )SIRS(:

Site of infection established and at least two of the following are present

—Body temperature >38° C or <36° C

—Heart rate >90 beats/minute

—Respiratory rate >20 breaths/min (tachypnea)

—PaCO2 <32 mm Hg (hyperventilation)

—WBC count >12,000/mm3 or <4000/mm3

—Bandemia: presence of >10% bands (immature neutrophils) in the

absence of chemotherapy-induced neutropenia and leukopenia

May be caused by bacterial translocation

Bacterial Translocation:

Changes from acute insult to the gastrointestinal tract that may allow entry

of bacteria from the gut lumen into the body; associated with a systemic

inflammatory response that may contribute to multiple organ dysfunction

syndrome, Well documented in animals, may not occur to the same extent in

humans, early enteral feeding is thought to prevent this.

Causes of hyper metabolic response:

Sepsis, fracture, stress, trauma, burns, major surgery .

Medical management:

Treat cause of hypermetabolism .

Physical therapy and exercise .

Nutritional management:

Meet energy, protein, and micronutrient needs.

Establish and maintain fluid and electrolyte balance.

Plan nutritional therapy (oral, enteral, and/or parental nutrition .

Factors to Consider in Screening an ICU Patient

ICU medical admission

Diagnosis, nutritional status, organ function, pharmacologic agents.

Postoperative ICU admission: Type of Surgery, intraoperative

complications, nutritional status, diagnosis, sepsis.

Burn or trauma admission: Type of trauma, extent of injury, GI function.

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 = normal metabolism

5 – 10 = mild hypermetabolism (level 1 stress)

10 – 15 = moderate (level 2 stress)

>15 = severe (level 3 stress).

Energy:

Enough but not too much for nonobese:25-30 kcal/kg/day

& obese:18-20 kcal/kg/day.

Excess calories:

Hyperglycemia, Diuresis : complicates fluid/electrolyte balance

Hepatic steatosis (fatty liver), excess CO2 production,

Exacerbate respiratory insufficiency, Prolong weaning from mechanical

ventilation.

It prefer to use Penn state equation, Swinamer equation rather than the static

variables of weight and height to measure energy needs.

Objectives:

First, fluid resuscitation and treatment of cause of hypermetabolism

When hemodynamically stable, begin nutrition support

Nutrition support may not result in positive nitrogen balance may slow loss

of protein, Undernutrition can lead to decrease in protein synthesis,

weakness, Multiple organ dysfunction syndrome, death.

Carbohydrate:

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.

Fat:

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 patients:

There is evidence that high fat feedings (especially LCT) cause

immunosuppression .

New formulas focus on omega-3s

Protein:

Amino acids are supplied to critically ill patient to support the synthesis of

the protein required for defense and recovery, to spare lean body mass, and

to reduce the amount of endogenous protein catabolism.

They need about1.5 – 2.0 g/kg/day .

Giving exogenous amino acids decreases negative N balance by supplying

liver with substrates for protein synthesis.

Vitamins, Minerals, and Trace Elements:

No specific guidelines exist for the provision of them in metabolically

stressed individuals, but with increased caloric intake there may be an

increased need for B vitamins, particularly thiamin and niacin.

Specialized Nutrients in Critical Care:

Include supplemental branched chain amino acids, glutamine,

arginine, omega-3 fatty acids, RNA, others

Most studies used more than one nutrient, making assessment of

efficacy of specific supplements impossible

Immune-enhancing formulas may reduce infectious complications in

critically ill pts but not alter mortality

Mortality may actually be increased in some subgroups (septic

patients)

Supplemental Glutamine )GLN( in Critical Care:

Alterations in glutamine metabolism can occur in critical care,

possibly affecting gut function

Parenteral nutrition solutions traditionally have not contained

glutamine because of instability in solution

Animal and human studies suggest that supplemental GLN in

Parenteral nutrition may have beneficial effects.

Those benefits have not been demonstrated in enteral nutrition.

Enteral nutrition)EN( versus Parenteral nutrition)PN( in Critical Care:

Adequately powered trials have not been found to enable evaluation

of the impact of EN versus PN on mortality in critically ill patients

Enteral nutrition is associated with reductions in infectious

complications in critically ill patients, when compared to PN

Enteral nutrition is associated with reduced cost of medical care in

critically ill patients, when compared to PN

If the critically ill ICU patient is hemodynamically stable with a

functional GI tract, then EN is recommended over PN. Patients who received

EN experienced less septic morbidity and fewer infectious complications

than patients who received PN. In the critically ill patient, EN is associated

with significant cost savings when compared to PN.

Burn:

[Potential] Beneficial Effects of Postburn Early Enteral Nutrition:

Nutrient needs satisfied

Improved tube feeding tolerance

Decreased incidence of bacterial translocation

Decreased number of infectious episodes

Decreased antibiotic therapy

Improved nitrogen balance

Reduced urinary catecholamines

Diminished serum glucagon

Suppressed hypermetabolic response

Enhanced visceral protein status

Medical nutritional therapy:

In fluid-resuscitated, critically ill patients, EN started within 24-48 hours

following injury or admission to the ICU reduces the incidence of infectious

complications.

Energy requirements:

The increased energy needs of the burned patient vary according to the size

of the burn, it measured by curreri formula:

Energy=24kcal x usual body wt (kg) + 40kcal x %TBSA burned.

Energy sources:

Carbohydrate: Hyperglycemia (up to 200-220 mg/dl) in critically ill

patients was once considered acceptable ,

New goal is to keep BG as close to normal as possible. Target: <150

mg/dl, we Can use intermediate insulin morning and evening once

feedings are tolerated and stable.

Survival is decreased in critically ill patients with hyperglycemia

Controlling BG is associated with fewer infectious complications in

critically ill patients There is fair evidence that controlling BG values in

critically ill patients leads to a decrease in ICU duration, reduced number

of days on mechanical ventilation, and cost of medical care.

Fats: omega-3 improve immune response and tube feeding tolerance but

it not added during the early stages because of their antiinflammatory

effect.

The administration both enterally & parenterally, of low fat formula

results in less pneumonia, improved respiratory function, faster recovery

of nutrition status and a shorter length of care.

Protein:

Adequate of protein and energy intake is best evaluated by monitoring

wound healing, graft and basic nutrition assessment parameters. Wound

healing or graft may be delayed if weight loss exceeds 10% of usual wt.

Nitrogen balance often is used to evaluate the efficacy of nutritional

regimen, but it cannot be considered accurate without accounting for

wound losses. This formulas are used to estimate wound nitrogen losses:

<10% open wound=0.02 g nitrogen/kg/day.

11% to 30% open wound=0.05 g nitrogen/kg/day.

>30% open wound=0.12 g nitrogen/kg/day.

Nitrogen excretion should be decreased as the wounds heals or are

grafted.

Vitamin and minerals:

vitamin C is important in collagen synthesis and immune function and

required in increased amount of wound healing, its usual doses 500 mg

twice daily .

Vitamin A also important for immune function and epithelialization,

provision of 5000 units of vitamin A per 1000 calories of enteral nutrition

Administration of calcium to treat hypocalcemia, and supplemental

magnesium & phosphorus are given to prevent gastrointestinal irritation.

Traumatic Brain Injury )TBI(:Severely hyper metabolic and catabolic

The more severe the head injury, the greater the release of catecholamines

(norepinephrine and epinephrine) and cortisol and the greater the hyper

metabolic response.

Patients with neurologic impairment are at nutrition risk and should undergo

nutrition screening to identify those who require formal nutrition assessment

with development of a nutrition care plan. NS should be initiated early in

patients with moderate or severe TBI.

PN should be administered to patients with TBI if NS is indicated and EN

does not meet the nutritional requirements. Indirect calorimetry should be

utilized, if available, to accurately determine nutrition requirements in

patients with TBI.

Swallowing function should be evaluated to determine the safety of oral

feedings and risk of aspiration before the initiation of an oral diet.

Perioperative Nutrition Suppor:t

Preoperative nutritional support should be administered to moderately-

severely malnourished pts undergoing major gastrointestinal surgery for 7 to

14 days if the operation can be safely postponed.

PN should not be routinely given in the immediate postoperative period to

patients undergoing major gastrointestinal procedures.

Postoperative nutritional support should be administered to patients who will

be unable to meet their nutrient needs orally for a period of 7 to 10 days.

Postoperative Nutrition Support:

Introduction of solid foods depends on condition of gastrointestinal tract

Oral feeding may be delayed for first 24 – 48 hours post surgery until return

of bowel sounds, passage of flatus or soft abdomen.

Traditional practice has been to progress from clear liquids, to full liquids, to

solid foods, However, there is no physiological reason not to initiate solid

foods once small amounts of liquids are tolerated.

Energy Requirements in Surgery: Can use estimate of 25-30 kcal/kg to

begin and monitor response to therapy.

Hypocaloric Feedings Have Been Recommended in:

Class III obesity (BMI>40

Refeeding syndrome

Severe malnutrition

Trauma patients following shock resuscitation

Hemodynamic instability

Acute respiratory distress syndrome or COPD

MODS, SIRS or sepsis

Monitoring Response to MNT in Critical Care:

Evaluating patient position should be part of an EN monitoring plan. To

decrease the incidence of aspiration pneumonia and reflux of gastric

contents into the esophagus and pharnyx, critically ill patients should be

placed in a 45-degree head of bed elevation, if not contraindicated.

Intake and output: stooling, fluid balance

Tolerance of feeding regimen (abdominal exam, gastric residuals)

Amount of nutrition prescription delivered; support is often interrupted due

to surgeries, dressing changes, intolerance, and therapy.

References

1- Journals. Cambridge.org/production/action/cjogetfultext.

2- www.Medunc.edu/nutrition/stress-handout .

3- www.guideline.gov/summary/summary.aspxess .

4- Alexander JW: nutritional pharmacology in surgical patient,Amjf surg

183:349,2002.

5- American Dietetic Association: Evidence analysis library,

www.eatright.org,accessed December 1,2006.

6- ASPEN Board of Directors: Guidelines for the use of parenteral and

enteral nutrition in adult and pediatric patient FPENF parenter Enteral

nutr 26:1s.

7- Cunningham j et al : caloric and protein provision for recovery from

sever burn in infants and young children,Amf Clin Nutr 51:553,1990.

8- Finny sj et al: Glucose control and mortality in critically ill patient ,

fAMA 290:2041,2003.

9- Ireton jones C, JD: improved equations for predicting energy

expenditure in patient : Nutr Clin Pract 17:29,2002.

10- Twyman D: Nutritional management of critically ill neurologic

patient, Crit Care Clin 13:39,1997.