The surgical inflammatory response can be a type of high-grade acute stress
response associated with an increasingly complex trophic functional system for using
oxygen. This systemic neuro-immune-endocrine response seems to induce the reexpression
of 2 extraembryonic-like functional axes, i.e. coelomic-amniotic and
trophoblastic-yolk-sac-related, within the injured tissues and organs, thus favoring their
re-development. Accordingly, through the up-regulation of two systemic inflammatory
phenotypes, i.e. neurogenic and immune-related, a gestational-like response using
embryonic functions would be induced in the patient's injured tissues and organs, which
would therefore result in their repair. A comparison has been established between the
pahtophysiological mechanisms that are produced during the inflammatory response
and the physiological mechanisms that are expressed during early embryonic
development. Surgical inflammation could be a high-grade stress response whose
pathophysiological mechanisms would be based on the recapitulation of ontogenic and
phylogenetic-related functions. Thus, the ultimate objective of surgical inflammation, as
a gestational process, is creating new tissues/organs for repairing the injured ones. Since
surgical inflammation and early embryonic development share common mechanisms of
production, the factors that hamper the wound healing reaction in surgical patients could
be similar to those that impair the gestational process.
Keywords: Coelomic-amniotic axis, trophoblastic-yolk sac axis, neuro-immuneendocrine
response, gestation, surgical inflammation, poly-traumatized patient,
macrophages, multiple organ dysfunction syndrome, systemic inflammatory
response syndrome, hypercatabolism, ontogeny, phylogenetic evolution.
