METABOLIC STRESS dr. Sri Mulyati, M.Kes., Sp.GK. CONTENTS METABOLIC STRESS : o DEFINITION o CLINICAL MANIFESTATION o PATHOPHYSIOLOGY o NUTRITION THERAPY
NUTRITION SUPPORT IN SPECIFIC METABOLIC
STRESS CONDITIONS o BURNS o TRAUMA o SPINAL CORD INJURY o PANCREATITIS METABOLIC STRESS METABOLIC STRESS Hypermetabolic, catabolic response to severe injury or disease.
Degree of metabolic stress is correlated to the severity of
the injury.
Energy needs dramatically increase, normal adaptations
do not occur.
The body ≠ utilize nutrients properly & ↑ demand for
calories and protein high nutrition risk PEM. Clinical Manifestation 1) Ebb phase 1st phase of metabolic stress 2-48 h after the injury Characterized by shock hypovolumeia (low blood volume/ECF deficit) & ↓ oxygenation to the tissues. Low blood volume ↓ decrease in cardiac & urinary output. Goals during ebb: 1) Restore blood to the organs 2) Maintain oxygenation of all tissues 3) Stop any hemorrhaging 2) Flow phase 2nd phase of metabolic stress Patient is stabilized hemodynamically. Hypermetabolism, catabolism, and altered immune & hormonal changes occur. Patients can become edematous, so fluid intake should be watched. No set time period for flow phase. 3) Recovery phase End phase of metabolic stress Indicates the resolution of the stress with the return on anabolism and normal metabolic rate. Pathophysiology Metabolic Features of Injury & Infection (Metabolic Stress) HYPERMETABOLISM ↑ metabolic rate ↑ oxygen consumption
PROTEOLYSIS & NITROGEN LOSS
↑ proteolysis & use of amino acids for energy production ↑ ureagenesis & urinary nitrogen excretion ↑ hepatic synthesis of acute phase proteins ↓ hepatic production of albumin & prealbumin
GLUCONEOGENESIS & GLUCOSE UTILIZATION
↑ glycogenolysis ↑ gluconeogenesis ↑ blood glucose levels Nutrition Therapy • Balance between prevention of PEM and complications of nutrition support • Consider status prior to illness, level of injury, current metabolic changes Nutrition Therapy : Assessment Indirect calorimetry most accurate for estimating energy requirements
Energy estimates – equations
Mifflin-St. Jeor or Harris-Benedict Initial caloric goals: 25-35 kcal/kg
Protein : 1.2-1.5 g protein/kg
“Permissive underfeeding” : 14 kcal/kg, 1.2 g protein/kg
Reserved for NPO status, if enteral access not viable or unable to meet needs (volume) Hyperglycemia most critical concern Other concerns: catheter occlusion, infection, hypertriglyceridemia, intestinal atrophy, electrolyte disturbances, refeeding syndrome NUTRITION SUPPORT IN SPECIFIC METABOLIC STRESS CONDITIONS BURNS • Tissue injury caused by exposure to heat, chemicals, radiation, or electricity • Rule of “Nines” used to estimate Body Surface Area (BSA) assessment of extent of injury, basis for fluid and medication recommendations Metabolic stress in burn injury Pathophysiology : • Excessive inflammatory process • Rapid fluid shifts and accumulation • Fluid loss from wound • Hypermetabolism, catabolism, immune, hormonal response • Respiratory complications NUTRITION THERAPY Nutrition Implications : 20% body protein can be lost Fluid imbalance, pain, immobility Wound healing requires optimum nutrition Weight fluctuations (d/t fluid shifts & resuscitation) NUTRITION THERAPY Nutrition Assessment Estimate energy using indirect calorimetry
Energy requirement : 30-35 kcal/kg/d (<40% BSA) & 35-50%
kcal/kg/d (≥40% BSA) Protein 1.2-1.5 g protein/kg (Europe) or more in America Negative nitrogen balance may not be totally prevented Set goal to minimize losses and promote wound healing
Fat <30% Energy requirement
Carbohydrate <5 g/kg/d
Micronutrients : Se, Zn, vitamin B, C, E, β-carotene
NUTRITION THERAPY Nutrition Intervention Nutrition support - enteral • Early feeding associated with prevention of infections and Curling’s ulcer, and reduction in protein catabolism • Focus on higher protein (20-25% of kcal) • Supplemental arginine, glutamine, omega-3 fatty acids PN if enteral cannot meet needs Avoid overfeeding, control hyperglycemia Wean from nutrition support when patients can meet at least 60% of needs orally NEUROLOGIC INJURY Injury to central nervous system, whether from head injury or spinal cord injury, can have a significant impact on a patient’s nutritional status.
Closed head injury often triggers a cascade of systemic &
local metabolic responses that result in a hypermetabolic & hypercatabolic state.
Energy expenditure is dependent on infections, body
temperature, alterations in intracranial pressure (ICP), medications, motor activity, & other injury sustained. Head- injured patients are at particularly high risk for aspiration pneumonia because of gastroparesis & suppressed gag & cough reflexes poor tolerance of gastric enteral feeding postpyloric feeding tubes is recommended Metabolic rate of spinal cord injury patients is dependent on the severity, location & time phase of the injury.
Nutritional consequences of Spinal cord injury :
o ↓ energy expenditure o Negative nitrogen balance o ↓ muscle mass o Hypercalciuria, hypercalcemia, & osteoporosis o Pressure sores & poor wound healing o Neurogenic bladder & bowel resulting in constipation PANCREATITIS Severe pancreatitis causes marked hypermetabolism & hypercatabolism. The goals of nutrition support are to meet the increased metabolic needs as well as limit stimulation of pancreatic secretions Historically, PN & bowel rest have been used to treat severe acute pancreatitis because of concern that EN may stimulate pancreatic secretions. Several studies have shown the jejunal EN was well tolerated & resulted in fewer septic events & overall complications as compared to PN Cephalic & gastric phases of exocrine pancreatic stimulation are avoided by feeding into the jejunum.
No general consensus on type of EN formula to use in
patients with acute pancreatitis.
If PN is necessary, lipid emulsions (along with dextrose &
amino acids) are usually well tolerated. Thank You