NUTRITON AND METABOLIC STRESS

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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.

Immediate Physiologic and Metabolic Changes after Injury or Burn

ADH, Antiduretic hormone; NH3, ammonia.

Metabolic Response to StressMetabolic Response to Stress

Involves most metabolic pathways Accelerated metabolism of LBM Negative nitrogen balance Muscle wasting

Ebb PhaseEbb Phase

Immediate—hypovolemia, shock, tissue hypoxia

Decreased cardiac output Decreased oxygen consumption Lowered body temperature Insulin levels drop because glucagon is

elevated.

Immediate—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 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

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

Skeletal Muscle Proteolysis

From Simmons RL, Steed DL: Basic science review for surgeons, Philadelphia, 1992, WB Saunders.

Metabolic Changes in StarvationMetabolic Changes in Starvation

Hormonal Stress ResponseHormonal 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

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

Hormonal Stress Response—cont’dHormonal Stress Response—cont’d 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

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

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

Bacterial Translocation across Microvilli and How It Spreads into the Bloodstream

Hypermetabolic Response to Stress—CauseHypermetabolic Response to Stress—Cause

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.

Hypermetabolic Response to Stress—PathophysiologyHypermetabolic Response to Stress—Pathophysiology

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000.

Hypermetabolic Response to Stress—Medical and Nutritional Management

Algorithm content developed by John Anderson, PhD, and Sanford C. Garner, PhD, 2000. Updated by Maion F. Winkler and Ainsley Malone, 2002.

NUTRITIONAL ASSESSMENT

Clinical judgment must play a major role in deciding when to begin/offer nutrition support

Determination of Nutrient Requirements Energy Protein Vitamins, Minerals, Trace Elements Nonprotein Substrate

– Carbohydrate– Fat

Energy

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

Indirect Calorimetry

Better estimate in critically ill hypermetabolic patient

The “gold standard” in estimating energy needs in critical care

Can be used in both mechanically ventilated and spontaneously breathing patients (ventilated patients most accurate)

Equipment is expensive and not readily available in many facilities

Indirect Calorimetry

Requires appropriate calibration of equipment, attainment of a steady state for measurement, and appropriate timing of measurement

Requires interpretation by trained clinician Inaccurate in patients requiring inspired

oxygen (FiO2>60%), and with air leaks via the entrotracheal tube cuff, chest tubes or bronchopleural fistula

Indications for Indirect Calorimetry

Patients with altered body composition (underweight, obese, limb amputation, peripheral edema, ascites)

Difficulty weaning from mechanical ventilation Patients s/p organ transplant Patients with sepsis or hypercatabolic states

(pancreatitis, trauma, burns, ARDS) Failure to respond to standard nutrition support

Malone AM. Methods of assessing energy expenditure in the intensive care unit. Nutr Clin Pract 17:21-28, 2002.

Nutrient Guidelines: 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

*ASPEN BOD. JPEN 26;22SA, 1992

Nutrient Guidelines: 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 pts – There is evidence that high fat feedings

(especially LCT) cause immunosuppression – New formulas focus on omega-3s

*ASPEN BOD. JPEN 26;22SA, 1992

Nutrient Guidelines: Protein

1.5 – 2.0 g/kg/day to start; monitor response Nonprotein calorie/gram of nitrogen ratio

for critically ill = 100:1 Giving exogenous aa’s decreases negative

N balance by supplying liver aa’s for protein synthesis

ASPEN BOD. JPEN 26;22SA, 1992

Fluid and Electrolytes

Fluid 30-40 mL/kg or 1 to 1.5mL/kcal expended

Electrolytes/Vitamins/Trace Elements Enteral feedings: begin with RDA/AI

values PN: use PN dosing guidelines

ASPEN BOD. JPEN 26;23SA, 1992

Supplemental Glutamine (GLN) in Critical Care 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

Glutamine Metabolism

NH2, Amine; NH3, ammonia.

MNT in Selected Populations in Critical Care

Acute Spinal Cord Injury

Source: www.spinal-cord-injury-resources.com/ spinal-i...

Acute Spinal Cord Injury (SCI)

Energy requirement for SCI = H/B x 1.1 x 1.2 (Barco et al, NCP 17;309-313, 2002)

Pt with multi-traumas in addition to SCI may have higher needs

Protein needs: 2 g/kg (Rodriguez DJ et al, JPEN 15:319-322, 1991

Nutrition Support in Surgery/Trauma

Graphic source www.nlm.nih.gov/.../ gallery/image/surgery.gif

Postoperative Nutrition Support Introduction of solid foods depends on condition

of GI 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 or Trauma Will vary with type of surgery, degree of trauma Use Ireton-Jones 1992 or Penn State if data is

available* Can use estimate of 25-30 kcals/kg to begin and

monitor response to therapy** Indirect calorimetry yields most accurate

estimates, particularly in pts difficult to assess

*ADA Evidence Analysis Library, accessed 10-06**ASPEN Nutrition Support Practice Manual, 2nd Edition, p. 278

Hypocaloric Feedings

Hypocaloric feedings have been recommended in specific patient populations

Aggressive protein provision (1.5-2.0 gm/kg/day

ASPEN Nutrition Support Practice Manual, 2nd Edition, p. 279

Zaloga GD. Permissive underfeeding. New Horizons 1994

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

Protein or Nitrogen Requirements in SurgeryProtein or Nitrogen Requirements in Surgery 1.2 to 1.5 g protein/kg BW

for anabolism mild or moderate stress Nitrogen requirement estimated from

energy requirements

1.2 to 1.5 g protein/kg BW

for anabolism mild or moderate stress Nitrogen requirement estimated from

energy requirements

NUTRITON AND METABOLIC STRESS

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