METABOLIC RESPONSE
TO TRAUMA
OUTLINE
Introduction
 Phases of the Metabolic response
 Mechanism/pathway
 Principal Responses
 Determinants of Magnitude of The Responses
 Modification of the metabolic response
 Summary/Conclusion

INTRODUCTION
HOMEOSTASIS- “milieu intérieur”
Body injury / stress of any sort alters body
homeostasis and is usually accompanied by local
and systemic effects aimed to return the body to
status quo.
Cascade of physiological events
brought into play for the “preservation
of self” and homeostasis.
 If uncontrolled may become
detrimental and increase morbidity.
 Seen in trauma, burns, sepsis and
surgery etc.
• Extent of response proportional to
severity of insult

PHASES
The unmodified response divided into two phases the
‘ebb’ & ‘flow’ (Cuthbertson,1930).
Ebb phase = survival phase ( few hours after injury.)
Reversible by early and prompt resuscitation.
Flow phase follows (only attenuated)
2 parts – Catabolic  Metabolic rate
- (negative nitrogen balance and weight loss.
-This phase usually last about a week in mod. trauma
usually longer in severe trauma and if sepsis sets in.
Anabolic phase
- protein and fat stores restoration + weight gain
(positive nitrogen balance).
-The recovery phase usually lasts 2–4 weeks.
PATHWAYS OF METABOLIC RESPONSE
TRIGGER MECHANISM
PRINCIPAL RESPONSES
Hemodynamic response
 Fluid and electrolyte changes
 Altered protein metabolism
 Changes in plasma protein
 Hypermetabolism
 Immunosuppresionn

HEMODYNAMIC RESPONSE
 venous constriction
 increased rate of the sino-atrial node
 More forceful cardiac contraction
 Arteriolar constriction
 MEDIATED BY cathecolamines, ADH,
Aldosterone

FLUID AND ELECTROLYTE CHANGES
 Renals
-↑H₂O & Na⁺ Retention(ECF VOLUME
EXPANSION)
-↑K⁺ Excretion
 Intestine
-↓absorption of H₂O & K⁺
-↑K⁺ Secretion
 Mediated by ADH and aldosteone.
ALTERED PROTEIN METABOLISM & N₂ BALANCE
1.↑pro⁻ turnover: catabolism > anabolism
2.10-15g of N;62.5-96g Pr⁻ ;or 300-450g of mxl tissue loss
Daily, post moderate-severe Ops
3.↑Muscle Proteolysis due to;
-IL-1 (activated macrophages)→ PGE₂ release
- TNF
-Cortisol,Starvation,Fever & immobilization
4. Proteolysis→↑ br Essential AAs; for Gluconeogenesis &
synthesis of Enzymes, Hormones,Plasma pro⁻ ,Acute
phase pro⁻& Collagen for wound healing.
5. Prolonged –ve N₂Bal → Hypoproteinaemia
→Pulm & Cardiovascular failure ,↓ immune fxn
& wound healing
6.Infusion of Pro⁻ , Epidural Anaesthesia, post Op
Analgesia & Laparoscopic surgeries→↓the rate
of post Op Catabolism
CHANGES IN PLASMA PROTEINS
1.↑ in P.P-due to liver stimulation by IL-6,4rm
activated peripheral monocytes
2.Albumin turnover ↑;conc. Falls within 3hrs
due to transcapillary migration,reaches
lowest in 48hrs & rises slowly in 7-14days
3.Transferin;↓by 25-30% in 3-6days
4.Acute phase proteins: ↑ ≥25% following
trauma & sepsis
HYPERMETABOLISM & ENERGY
METABOLISM
1.REE ↑ by 12% for every 1oC rise in temp.
2.Normal REE-6300-7500J/24hrs
3.REE ↑ 10%-major operation,25% -major
#,50-80% in sepsis,40-100% in burns
4.Glycogen reserve provides energy 4 the ist
12-20hrs,hence alternative 4rm fats & protein
5.160g of fats & 70g of protein broken down to
provide dly energy requirement ; may
increase to 250-500g
6.Trigycerides →lipolysis→FFA & glycerol
7.FFA for combustion,glycerol for
gluconeogenesis
8.lipolysis-stimulated by
catecholamines,glucagon,cortisol,GH.inhi
bited by insulin & PG-E
9.Consequences of hypermetabolism-Wt
loss,fatigue
10.Wt loss from lipolysis,protein
catabolism,diminished food intake
↑ SUSCEPTIBILITY TO INFECTIONS
Abnormalities in Macrophages/Monocytes
Function
1.↓ phagocytosis capacity
2.↑ lysosme stability & ↓ oxidative burst
3.Impaired Ag presentation to lymphoctes
4.↓ expression of MHC-II ,MHC-I, HLA-A on
cell surface
5.↓ production of IL-1,IL-6,IL-12,TNF after
initial rise

↑ SUSCEPTIBILITY TO INFECTION
Abnormalities in Lymphocytes Function
1.↓T-lyphocytes prolifferation & reduce T4:T8
ratio.normal-2:1
2.↓NK cell activity & lymphokine activated killer
cell activity
3.Impaired T4,T8 activity
4.Appearance of immature T cells

IMMUNOSUPPRESSION
Causes of Immunosuppression posttrauma
1.Stress Hormones
2.Prostagladin E2
3. Suppressive active glycopeptidesformed in traumatized pxs
4.peri-op blood transfusion
5.Gut integrity breach

OTHER RESPONSES
 Pyrexia
 Insulin resistance
 Changes in iron and zinc metabolism

DETERMINANTS OF MAGNITUDE OF
RESPONSE
 Age
 Sex
 Nutritional state
 Magnitude of trauma
 Concurrent disease
 Environmental Temperature
 Treatment(s)
TREATMENTS / MODIFICATION
Prompt and adequate blood, fluid and elect
replacement
 Spinal anaesthesia and analgesia
 Minimally invasive surgeries
 Antibiotics
 Wound debridement and drainage of septic foci
 Early enteral feeding

CONCLUSION
The profound neuroendocrine and metabolic
responses to injury,though homeostatic in
“intent” can become deleterious if not
controlled
 Understanding the principles & instituting
prompt interventions are important in reducing
associated morbidities.

MERCI BEAUCOUP