Metabolic and Physiological

changes in trauma
• Response is changing with time gradually
• Severe injury = more response
• CVS, inflammatory, metabolic
Phases of response
• Curthberson, 1942
HYPERMETABOLISM
Cardiovascular responses
Mediators of metabolic responses
• Neuroendocrine
• Upregulation symphtoadrenal axis
• Stimulate hypothalamic-pituitary axis
• Cytokines
Metabolism post trauma
• To mobilize stored energy for hemostasis and healing
• Lipid
• Lipolysis
• Protein
• Proteolysis
• Carbohydrate
• Glycogenolysis
• Insulin resistance
• Gluconeogenesis
Lipid
• Primary energy source, 50 – 80% from TG,
greater energy yield
• Accelerated in the early period ↑ ACTH,
cortisol, catecholamine, glucagon, growth
hormone, and insulin levels
• Energy for gluconeogenesis in liver from fat
oxidation
• Ketogenesis reduced in major trauma, shock
and sepsis d/t increased use of free fatty acids
Protein
• Proteolysis by glucocorticoid action
• Trauma with no oral nutrition = lose 15% of his
body mass in 10 days.
• not long-term fuel reserves, excess protein losses are
incompatible with life
• Amino a.  acute phase proteins, albumin,
fibrinogen, glycoproteins, complement factors.
• Absorption (intestine) & release (skeletal muscle)
glutamine and alanine increased
Carbohydrate
• First metabolic change = gluconeogenesis, driven by
stress hormones and cytokines
• Glucose can be used in hypoxic tissue and
inflammatory cells
• Fat cannot reach because capillaries not yet developed /
damaged
• In certain period of glycolysis oxygen is not required
• Glycogenolysis in liver  glucose
• In skeletal muscle for the local muscle only
• Insulin resistance
• IL1 and TNF suppress insulin secretion.
• ↑counter-regulatory hormones result in stress
hyperglycemia
Strategy to reduce response