The Surgical Stress Response
Last updated 5th Feb 2018 - Tom Heaton
Surgery leads to a complex number of physiological responses which can have adaptive and maladaptive effects.
These include a number of neurological, hormonal, metabolic and immunological changes to the trauma of surgery.
Similar changes are found in response to other ‘insults’ such as severe trauma, infection and extreme exercise..
In many cases these responses can cause problems, and an understanding of them and how to approach them is essential for anaesthesia.
An increased focus on this is a key part of the enhanced recovery after surgery (ERAS) approach.
These include a number of neurological, hormonal, metabolic and immunological changes to the trauma of surgery.
Similar changes are found in response to other ‘insults’ such as severe trauma, infection and extreme exercise..
In many cases these responses can cause problems, and an understanding of them and how to approach them is essential for anaesthesia.
An increased focus on this is a key part of the enhanced recovery after surgery (ERAS) approach.
Trigger
The trigger is primarily from the insult itself.
Nociceptive stimuli from the site of injury will be transmitted via the somatic and autonomic nervous system, to higher brain centres.
Local changes, such as cytokine production may also play a role in the trigger of the stress response, with IL1 and IL6 being recognised. .
Much of the stress response is orchestrated by the hypothalamus, which leads a number of the hormonal changes through the hypothalamic-pituitary-organ axis.
The sympathetic nervous system is also activated in this way.
Nociceptive stimuli from the site of injury will be transmitted via the somatic and autonomic nervous system, to higher brain centres.
Local changes, such as cytokine production may also play a role in the trigger of the stress response, with IL1 and IL6 being recognised. .
Much of the stress response is orchestrated by the hypothalamus, which leads a number of the hormonal changes through the hypothalamic-pituitary-organ axis.
The sympathetic nervous system is also activated in this way.
Sympathetic Nervous System
The sympathetic arm of the autonomic nervous system has a significant role in the stress response.
Many of these effects can be seen as initially adaptive to deal with the consequences of trauma.
It is stimulated by:
The response includes:
Many of these effects can be seen as initially adaptive to deal with the consequences of trauma.
It is stimulated by:
- Hypotension - mediated by baroreceptors
- Hypoxia
- Acidaemia
- Pain
- Anxiety
- Hypothalamus directly
The response includes:
- Alpha 1 adrenoceptor effects
- Vasoconstriction (peripheral and splanchnic)
- GI smooth muscle relaxation
- Glycogenolysis
- Vasoconstriction (peripheral and splanchnic)
- Beta adrenoceptor effects
- Tachycardia
- Increased inotropy
- Metabolic effects
- Tachycardia
- Increased cardiac output
- Hypertension
- Tachycardia
- Renin-angiotensin system activation
- Salt/water retention
- Elevated glucose, lactate and fatty acid levels
- Increased glucagon release
Metabolic/Hormonal
The overall metabolic picture is one of substrate mobilisation to provide the body’s tissues with ample resources to deal with the trauma.
Some of the changes include:
There are several drivers of these changes:
Some of the changes include:
- Protein catabolism
- Fat catabolism
- Increased gluconeogenesis
- Increased ketone production from fatty acid mobilisation
There are several drivers of these changes:
- ACTH production increases
- Increased levels of ACTH very rapidly after trauma
- Stimulates increased production of cortisol from the adrenal cortex
- Cortisol drives number of changes
- Anti-inflammatory/immunomodulatory - negative feedback effect
- Insulin resistance
- Salt/water retention
- Anti-inflammatory/immunomodulatory - negative feedback effect
- Increased levels of ACTH very rapidly after trauma
- Antidiuretic hormone (ADH)
- Salt/water retention
- Salt/water retention
- Growth hormone (GH)
- Rise in proportion to the degree of tissue damage
- Effects via insulin-like growth factors (particularly IGF-1)
- More protective effect on protein catabolism
- Anti-insulin effect, promote glucose as a substrate
- Glycogenolysis
- Rise in proportion to the degree of tissue damage
- Insulin
- Demonstrates an inappropriate response to hyperglycemia
- Peripheral resistance and inhibition of release from other stress response arms e.g. SNS
- Demonstrates an inappropriate response to hyperglycemia
- Acute phase proteins e.g. CRP, fibrinogen
- Increased production by the liver
- Role is to optimise haemostasis, promote healing and reduce tissue damage
- Increased production by the liver
Haematological/Immunological
These changes include:
- Leukocytosis - granulocyte and lymphocyte proliferation
- Hypercoagulability and fibrinolysis - effects of the acute phase proteins
- Immunosuppression - from cortisol
Adverse Effects
Whilst some of the effects can be seen to be adaptive from an evolutionary perspective, in modern healthcare, some of the maladaptive aspects are very relevant.
These include:
These include:
- Increased oxygen demand
- Hypoxaemia
- Myocardial ischaemia
- Hypoxaemia
- Reduced gut blood flow
- Impaired perfusion of anastomosis
- Impaired perfusion of anastomosis
- Excess utilisation of substrates
- Loss of lean muscle mass
- General/respiratory weakness
- Loss of lean muscle mass
- Hypercoagulability
- Increased risk of thromboembolic disease
- Increased risk of thromboembolic disease
- Sodium/water retention
- Increased tissue oedema
- Organ dysfunction
- Anastomotic risk
- Increased tissue oedema
Links & References
- Matthews, C. Enhanced recovery after surgery (ERAS). Anaesthesia tutorial of the week. 2010. http://www.frca.co.uk/Documents/204%20Enhanced%20recovery%20after%20surgery%20(ERAS).pdf
- Nicholson, G. Hormonal, metabolic & inflammatory response to surgery. e-LFH. 2012.
