METABOLIC RESPONSE TO INJURY

MAJ DR BIKASH RAYAMAJHI

METABOLIC RESPONSE TO
TRAUMA (MRT)

MAJ DR BIKASH RAYAMAJHI

INTRODUCTION
Metabolism involves a diverse range of chemical
processes required to sustain life & enable growth,
healing, development, reproduction & homeostasis

Aim to maintain homeostasis

Stress response following injury involves

neuroendocrine, metabolic a% inflammatory
aspects
 More severe injury, greater is the response

Local response is supported by-

generalized neuroendocrine response to conserve

fluid

mobilizeamino acid from protein for

gluconeogenesis & wound repair

mobilize fat for energy production for wound repair

 Early ebb phase

CLASSICALLY DESCRIBED
Begins at the time of injuryBY SIR DAVIS
CUTHBERTSON (1930) INTO:
Last 24-48 hrs

Aim to conserve circulating volume & energy

stores

Reduced oxygen consumption, glucose

tolerance, cardiac output & BMR
 Flow phase
Starts several days after & lasts days to weeks

Concerned with recovery & repair

Catabolic phase -last 3-10 days

Associated with increased level of

catecholamines, cortisol, insulin & glucagon

Protein & fat mobilization, increased urinary

nitrogen excretion, weight loss
 Flow phase

Anabolic phase -may last for weeks

protein & fat are restored & weight regained

INJURY

EBB FLOW RECOVERY

PHASE PHASE

Hours Days Weeks

SHOCK CATABOLIS ANABOLISM

M
 The response of body to injury is considered
under following headings-

Neuroendocrine response

Immunological response

Metabolic response
NEUROENDOCRINE RESPONSE
Earliest pathway to get activated
Injury -> Nociceptive receptors -> Spinal cord ->
Thalamus -> Hypothalamus -> Pituitary

Releaseof CRH -> Triggers release of ACTH

from Ant pituitary -> Secretion of cortisol from
adrenal

Activation of SNS -> release of adrenaline &

glucagon

Increased release of GH & glucagon

 IMMUNE RESPONSE
Immune system of body divided into-
Innate immune system-macrophages

Adaptive immune system- T & B lymphocytes

Medicated by protein signaling compounds called

cytokines

Injury -> Antiinflammatory response -> IL-4, IL-3, IL-9,

IL-13, TGF-B -> CARS

Injury -> proinflammatory response -. IL-1, IL-6, IL-8,

TNF-B -> SIRS
INFLAMMATORY MEDIATORS
Eicosanoids
Serotonin
Histamine
Fatty Acid Metabolites
Kallikrein-Kinin System
Reactive Oxygen Metabolites
Cytokines
Heat Shock Proteins
FACTORS MODIFYING MRT
Severity of injury
Nature of injury
Infection
Complications
Nutritional status
Ambient temperature
Corticosteroids
Age and Sex
Anaesthesia and drugs
CHANGES IN MRT
Pulse & temperature
Pulse rise due to catecholamines
Sympathetic fever for 24 to 48 hours.
Cytokines (IL 1) reset temperature regulating
centers in hypothalamus.
Metabolic rate increase 6-10% per centigrade

Water and salt retention

Oliguria for 48 to 72 hours due to ADH and
aldosterone release.
 Reduction in Neural stimuli Increased
blood volume reaching osmolality
supraoptic stimulate
Stimulation of volume nucleus from osmoreceptors
receptors in atria and injured part in anterior
hypothalamus hypothalamus

ADH production

Reabsorption of water
Reduced inflow pressure Alteration in Na concentration

Reduced Renal Perfusion Macula Densa sensitisation

Increased renin secretion from JGA

Angiotensinogen Angiotensin I

Aldosterone Angiotensin II

Fluid retention Reabsorption of Na and bicarbonate

Increased K and H + excretion

Metabolic Alkalosis
 CARBOHYDRATE METABOLISM
Existing stores for 8 to 12 hours
Period of hyperglycemia following injury

Catecholamines

Increase Suppress Stimulate

Glycogenolysis Insulin Glycogen
release release

Release a.a. Potentiate

from muscles hepatic
gluconeogenesis
Gluconeogenesis
METABOLIC RESPONSE

Carbohydrate Metabolism
Existing stores for 8 to 12 hours

Period of hyperglycemia following injury

Growth Hormones

Inhibit insulin metabolism on glucose

CARBOHYDRATE METABOLISM
Existing stores for 8 to 12 hours
Period of hyperglycemia following injury

Thyroxine

Accelerate gluconeogenesis
PROTEIN METABOLISM
Injury leads to loss of urinary nitrogen in form of urea,
resulting in increased blood urea

Reaches peak in first week, normalizes in 5 to 8 days

If incapable of oral replacement, made worse. So

parenteral feeding indicated
FAT METABOLISM
Principal source of energy following trauma & injury is
adipose tissue

Catecholamines & glucagon activate adenyl cyclase in fat

cells, producing cyclic AMP, leading to breakdown of TG to FA
&Glycerol

FA provides energy for all tissues and hepatic gluconeogenesis

Glycerol provides substrate for gluconeogenesis

Reduced insulin favours lipolysis

CHANGES IN COAGULATION

Following injury, blood becomes hypercoagulable

increasing incidence of DVT & PE

Increased ACTH & cortisol increases number of

platelets adhesiveness

Noradrenaline increases coagulability

REFERENCES
Principles and Practice of surgery. Forrest, Carter and
Macleod.

Clinical Surgery in General. Kirk and Ribbans.

Sabistons Textbook of Surgery.

Metabolic response to injury. T S Walsh.

Thank You