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Medical Management of Trauma and Burns

Nathan Peterson, DVM, DACVECC

VCA West Los Angeles Animal Hospital, Los Angeles, CA, USA

Etiology/Pathophysiology following trauma and contribute to the systemic inflam-
mation and activation of immune cells associated with
The pathophysiology of trauma and burns is complex severe trauma. The culmination of this activation is an
and explains why trauma and burn wounds are capable increased number of circulating polymorphic nucleic
of affecting organs distant from the original insult and cells (PMNs) and additional tissue injury.
why the clinical course of disease can be so variable. Our Concurrent with the systemic inflammatory response
current understanding of the pathophysiology of trauma (SIRS), an anti-inflammatory response called the
is based on the theory that both primary and secondary compensatory anti-inflammatory response syndrome
insults contribute to morbidity and mortality. This is (CARS) is taking place. The purpose of this response is
termed the two‐hit theory. Primary insults (first hits) to minimize the tissue damage induced by the pro-
result in direct tissue injury from the trauma or burn inflammatory response and is achieved through release
(fractures, soft tissue destruction, organ rupture or of anti-inflammatory mediators that reduce the synthe-
vascular disruption). These factors are not under the sis of pro-inflammatory cytokines by their action on
control of the veterinarian. Secondary insults can be transcription factors necessary for their production.
further divided into endogenous or exogenous causes.
Typical endogenous second hits include shock, hypoxia, Coagulation and Inflammation
ischemia/reperfusion injuries, and infection. Exogenous
(interventional) second hits include surgical trauma, Activation of the inflammatory system is closely tied to
anesthetic complications, and transfusion of blood activation of the coagulation and complement cascades.
products. Complement activation occurs through both the con-
tact phase pathway and the classic pathway and results
in recruitment and activation of phagocytic cells, induc-
tion of the hepatic acute phase response, and degranula-
Systemic Inflammatory Response
tion of mast cells. Mast cell degranulation releases
The magnitude of the primary and secondary insults vasoactive mediators including histamine, leading to
determines the systemic inflammatory response of the leukocyte adhesion and increased vascular permeability
host. Immediately following a trauma load, the patient (edema). Activation of the complement system also
begins mounting a systemic response composed of both results in activation of the coagulation cascade although
pro-inflammatory and anti-inflammatory components the most important inciting cause of activation of the
intended to limit entry of microorganisms, on the one coagulation cascade in the context of trauma is through
hand, and limit secondary tissue damage, on the other. the tissue factor pathway. Direct and secondary tissue
The balance, or lack thereof, determines if the patient will injury exposes tissue factor (TF) on the endothelial cell
mount an appropriate response, or whether a pro-inflam- surface which then complexes with factor VII (FVII) and
matory or anti-inflammatory state will predominate. activates the coagulation cascade. In severely trauma-
Plasma levels of primary pro-inflammatory cytokines tized patients, activation of the coagulation cascade can
rise within 1–2 hours following trauma. Secondary result in development of disseminated intravascular
pro-inflammatory cytokines begin to rise several hours coagulation (DIC).

Clinical Small Animal Internal Medicine Volume I, First Edition. Edited by David S. Bruyette.
© 2020 John Wiley & Sons, Inc. Published 2020 by John Wiley & Sons, Inc.
Companion website: www.wiley.com/go/bruyette/clinical