The document discusses the metabolic response to injury in the human body. It notes that the severity of injury determines the magnitude of the inflammatory response, with more severe injuries eliciting a stronger response. This response is graded over time, initially mediated by the innate immune system and potentially leading to depressed immunity if prolonged. Key mediators of this response include pro-inflammatory cytokines like IL-1, IL-6, and TNF-α in the initial acute phase response, followed by anti-inflammatory cytokines and receptors if the response is sustained. The metabolic response also occurs in phases, with an initial "ebb" phase of lowered blood pressure, basal metabolic rate and cardiac output followed by a flow phase of response and recovery if resuscitation is

1. METABOLIC
RESPONSE TO INJURY
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2. Homeostasis
 Stress free perioperative
care helps in restoring
homeostasis following
elective Sx.
 Resuscitation, surgical
intervention and critical
care can take back a
severely injured patient to
homeostatic state of the
body.
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3. The graded nature of injury
 The more severe the injury, the greater the
inflammatory response.
 Elective surgery of intermediate severity
slightly raises the To, PR, RR, BMR and WBCc
thus in major Sx, these parameters will be
more accentuated to an extent that SIRS and
MODS may ensue.
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4. The graded nature of injury
 This evolution is as
well graded in terms
of time with the
initial response
being milder and
mediater by the
innate immune
system and later this
may end leading to
depressed immunity.
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5. Mediators of metabolic response to
injury
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SIRS mediated by
IL-1, IL-6 and TNFα
is shortlived.
It is followed by
increased plasma
levels of cytokine
antagonists and
soluble receptors (IL-
1Ra, TNF-sR). If
prolonged, leads to
counter inflammatory
response syndrom.

6. Hormonal mediators of the metabolic
response to injury
 Acute phase:
beneficial
 Chronic
phase:
deleterious
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7. The ebb and flow model: phases of
physiological response to injury
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Ebb phase (from time of
injury to 24-48hrs).
Characterised by ↓BP,
↓BMR, ↓CO, hypovolaemia
and lactic acidosis.
Mediated by
catecholamines, cortisol and
aldosterone. Attenuated with
proper resuscitation.
Follow this link to read and make notes on
metabolic response to injury:
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4379844
/

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