Dr. Ahmed Saleem
FICMS
TUCOM / 3rd Year / 2015
THE METABOLIC STRESS RESPONSE
TO SURGERY AND TRAUMA
Homeostasis: the co-ordinated physiological process which maintains most of the steady states of the
organism, through complex homeostatic responses and within this range of responses are the elements of
healing and repair.
The natural physiological response to injury includes the following:
Immobility/rest
Anorexia
Catabolism
These changes are designed to aid survival of moderate injury in the absence of medical intervention.
The ‘Ebb and Flow’ Model
In 1930, Sir David Cuthbertson divided the metabolic response to injury in humans into ‘ebb’ and ‘flow’
phases:
The ebb phase: begins at the time of injury and lasts for approximately 24–48 hours. It may be
attenuated by proper resuscitation, 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 activation of the renin–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.
The flow phase:
Following resuscitation, the ebb phase evolves into a hypermetabolic flow phase, which
corresponds to SIRS. This phase involves the mobilization of body energy stores for recovery
and repair, and the subsequent replacement of lost or damaged tissue.
It is characterized by tissue edema (from vasodilatation and increased capillary leakage),
increased basal metabolic rate (hypermetabolism), increased cardiac output, raised body
temperature, leukocytosis, increased oxygen consumption and increased gluconeogenesis.
The flow phase may be subdivided into an initial catabolic phase, lasting approximately 3–10
days, followed by an anabolic phase, which may last for weeks if extensive recovery and repair
are required following serious injury.
During the catabolic phase, the increased production of counter-regulatory hormones (including
catecholamines, cortisol, insulin and glucagon) and inflammatory cytokines (e.g. IL-1, IL-6 and
TNFα) results in significant fat and protein mobilization, leading to significant weight loss and
increased urinary nitrogen excretion. The increased production of insulin at this time is
associated with significant insulin resistance and, therefore, injured patients often exhibit poor
glycemic control.
The combination of pronounced or prolonged catabolism in association with insulin resistance
places patients within this phase at increased risk of complications, particularly infectious and
cardiovascular. Obviously, the development of complications will further aggravate the
neuroendocrine and inflammatory stress responses, thus creating a vicious catabolic cycle.
Key catabolic elements of the flow phase of the metabolic stress response:
These determine the extent of catabolism and thus govern the metabolic and nutritional care of the surgical
patient and the essence of this coordinated response is to allow the body to reprioritize limited resources
away from peripheral tissues (muscle, adipose tissue, skin) and towards key viscera (liver, immune
system) and the wound:
Hypermetabolism: The majority of trauma patients demonstrate energy expenditures above
predicted healthy resting values. The predominant cause appears to be a complex interaction
between the central control of metabolic rate and peripheral energy utilization.
Alterations in skeletal muscle protein metabolism: During the catabolic phase of the stress
response, muscle wasting occurs as a result of an increase in muscle protein degradation (via
enzymatic pathways), coupled with a decrease in muscle protein synthesis; to provide amino acids
for the metabolic support of central organs/tissues, but can result in immobility and contribute to
hypostatic pneumonia and death if prolonged and excessive.
Alterations in hepatic protein metabolism; the acute phase protein response: The hepatic acute
phase response represents a reprioritization of body protein metabolism towards the liver. In
response to inflammatory conditions, including surgery, trauma, sepsis, cancer or autoimmune
conditions, circulating peripheral blood mononuclear cells secrete a range of proinflammatory
cytokines, including IL-1, IL-6 and TNFα. These cytokines, in particular IL-6, promote the hepatic
synthesis of positive acute phase proteins, e.g. fibrinogen and C-reactive protein (CRP). The acute
phase protein response (APPR) represents a ‘double-edged sword’ for surgical patients as it provides
proteins important for recovery and repair, but only at the expense of valuable lean tissue and
energy reserves. In contrast to the positive acute phase reactants, the plasma concentrations of
other liver export proteins (the negative acute phase reactants) fall acutely following injury, e.g.
albumin.
Insulin resistance: Following surgery or trauma, postoperative hyperglycemia develops as a result of
increased glucose production combined with decreased glucose uptake in peripheral tissues.
Decreased glucose uptake is a result of insulin resistance which is transiently induced within the
stressed patient. Suggested mechanisms for this phenomenon include the action of
proinflammatory cytokines and the decreased responsiveness of insulin-regulated glucose
transporter proteins.
Avoidable factors that compound the response to injury:
Continuing hemorrhage
Hypothermia
Tissue edema
Tissue underperfusion
Starvation
Immobility
Factors to prevent unnecessary aspects of the surgical stress response
Minimal access techniques
Blockade of afferent painful stimuli (e.g. epidural analgesia)
Minimal periods of starvation
Early mobilization