Lec 1 Metabolic response to injury

Metabolic response to injury

DR.Layth Q. Al-Harbawi
M.B.Ch.B;D.S;C.A.B.S.
Arab board of surgery
تسلسل 7
المرحلة الثالثة جراحة نظري
العدد5 19\3\2018

1.homeostasis is the foundation of normal physiology

2. As a result of modern understanding of homestasis minimizing the response by minimal access surgery and stress free perioperative care
3.resuscitation , surgical intervention and critical care can return the severely injured patient to a situation in which homeostasis becomes possible once again.
4. the graded nature of injury response, the more severe the injury the greater response.

Basic concepts inhomeostasis

a. neuroendocrine response to injury or critical illness is biphasic:
*acute phase characterized by actively secreting pituitary and elevate counter regulatory hormones (cortisol,glucagon,adrenaline).
* chronic phase: associated by hypothalamicsuppression and low serum level of the respective target organ hormones.
Changes contribute to chronic wasting.


5. mediators of the metabolic response to injury

*is driven initially by proinflammatory cytokines (e.g.IL1,IL6,and TNFalpha).

*is followed rapidly by increased plasma levels of cytokines antagonists and soluble receptors like IL1 and TNF-SR soluble receptors.
*if prolonged or excessive may evolve into a counter inflammatory syndrome.

B. Systemic inflammatory response syndrom following major injury:

The natural response to injury includes:
1.Immobility/rest
2.Anorexia
3.Catabolism

Physiological response to injury

metabolic response toinjuryin humans divided into:
. ebb phase: begins at the time of injury and
lasts for approximately 24–48 hours.
It may be attenuated by
1proper resuscitation, but not completely abolished. The ebb phase is characterised by hypovolaemia,decreased basal metabolic
rate, reduced cardiac output, hypothermia and lactic acidosis.


are catecholamines, cortisol and aldosterone (following activation
of the renin–angiotensin system)

The main physiological role of the ebb phase is toconserve both circulating volume and energy stores for recovery
and repair..
hormones regulating the ebb phase

Following resuscitation, the ebb phase evolves into a hypermetabolic

flow phase
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
Thisleads to significant weight loss and increased
urinary nitrogen excretion.
,

2. Flow phase

During the metabolic response to injury, the body
reprioritises protein metabolism away from peripheral tissues
and towards key central tissues such as the liver, immune
system and wound. One of the main reasons why the reutilisation
of amino acids derived from muscle proteolysis leads
to net catabolism is that the increased glutamine and alanine
efflux from muscle is derived, in part, from the irreversible
degradation of branched chain amino acids. Ala, alanine;
Gln, glutamine
KEY CATABOLIC ELEMENTS OF THEFLOW PHASE OF THE METABOLICSTRESS RESPONSE


Hypermetabolism
Hypermetabolism following injury:
*Is mainly caused by an acceleration of energy-dependent
metabolic cycles
* Is limited in modern practice on account of elements of
routine critical care

Skeletal muscle wasting

* Provides amino acids for the metabolic support of central organs/tissues
* Is mediated at a molecular level mainly by activation of the
ubiquitin–proteasome pathway
* Can result in immobility and contribute to hypostatic pneumonia and death if prolonged and excessive
Alterations in skeletal muscle protein metabolism

The hepatic acute phase response represents a reprioritisation

of body protein metabolism towards the liver and is characterised
by:
* Positive reactants (e.g. CRP): plasma concentration
*Negative reactants (e.g. albumin): plasma concentration
Alterations in hepatic protein metabolism:the acute phase protein response


Following surgery or trauma, postoperative hyperglycaemia
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.
Insulin resistance

for this phenomenon include the action of proinflammatory

cytokines and the decreased responsiveness of insulin-regulated
glucose transporter proteins. The degree of insulin resistance
is proportional to the magnitude of the injurious process.
Following routine upper abdominal surgery, insulin resistance
may persist for approximately 2 weeks.
Postoperative patients with insulin resistance behave in a
similar manner to individuals with type II diabetes mellitus. The
mainstay of management of insulin resistance is intravenous
insulin infusion.
Suggested mechanisms

*Catabolism leads to a decrease in fat mass and skeletalmuscle mass

* Body weight may paradoxically increase because ofexpansion of extracellular fluid space
CHANGES IN BODY COMPOSITIONFOLLOWING INJURY


• * Continuing haemorrhage
• * Hypothermia
• *Tissue oedema
• *Tissue underperfusion
• *Starvation
• *Immobility
Avoidable factors that compound the responseto injury

*Minimal access techniques

* Blockade of afferent painful stimuli (e.g. epidural analgesia)
* Minimal periods of starvation
* Early mobilisation
A proactive approach to prevent unnecessaryaspects of the surgical stress response