The metabolic stress response to surgery and trauma

The metabolic stress response to surgery and trauma

Neuroendocrine response to injury / critical illness is biphasic :
-acute phase. Characterized by actively secreting pituit and elevated counter –regulatory hormones( cortisol, glucagon, adrenaline). Changes are thought to be beneficial for short term survival.
- chronic phase. Associated with hypothalamic suppression and low serum levels of the respective target organ hormones.changes contribute to chronic wasting.
The innate immune system (principally macrophages ) interacts in a complex manner with the adaptive immune system (T cells,B cells in co generating the metabolic response to injury.
The metabolic stress response to surgery and trauma: the Ebb AND flow ‘ Model
; these changes are designed to aid survival of moderate injury in the absence of medical intervention.
The innate immune system (principally macrophages) interacts in a complex manner with the adaptive immune system (T cells, B cells) in co-generating the metabolic response to injury). Pro-inflammatory cytokines including interleukin-1 (IL-1), tumour necrosis factor alpha (TNF?), IL-6 and IL-8 are produced within the first 24 hours and act directly on the hypothalamus to cause pyrexia. Such cytokines also augment the hypothalamic stress response and act directly on skeletal muscle to induce proteolysis while inducing acute phase protein production in the liver. Within hours of the upregulation of pro-inflammatory cytokines, endogenous cytokine antagonists enter the circulation [e.g. interleukin-1 receptor antagonist (IL-1Ra) and TNFsoluble receptors (TNF-sR-55 and 75)] and act to control the pro-inflammatory response

The ebb phase begins at the time of injury and last 24-48 hrs it may be attenuated by resuscit .but not completely abolished.
The Ebb phase is characterized by hypovolemia, decreased basal metabolic rate, reduced cardiac output,hypothermia and lactic acidosis.The predominant hormones regulating the Ebb phase are catecholamines,cortisol and aldosterone(following the activation of the rennin- angiotensin system). The magnitude of this neuroendocrine response depends on the degree of blood loss and the stimulation of somatic afferent nerves at the site of injury. The main physiological role of the ebb phase is to conserve both circulating volume and energy stores for recovery and repair.
Following resusc. ,the ebb p. evolves into a hypermetabolic flow phase.This phase involves the mobilization of body energy for srecovery and repair and the subsequent replacement of lost or damaged tissue.It is subdivided into a- initial catabolic phase ,lasting 3- 10 days , followed by anabolic phase which may last for weeks if excessive recovery and repair are required following serious injury.