METABOLIC RESPONSE TO TRAUMA Flashcards
What is TRAUMA?
Refers to cellular disruption caused by an exchange with environmental energy that is beyond the body’s resilience
What is METABOLIC RESPONSE TO TRAUMA?
Refers to certain physiological responses activated after trauma which serves for “self preservation” and maintenance of homeostasis; but which may become pathological if uncontrolled or prolonged
What is HOMEOSTASIS?
The co-ordinated physiological process which maintains most of the steady states of the organism (Walter Cannon)
AIM OF METABOLIC RESPONSE TO TRAUMA
To maintain homeostasis and aid patient recovery from trauma by:
- Protecting the circulation
- Allowing the body to re-prioritise limited energy resources away from peripheral tissues (muscle, adipose tissue, skin) towards key viscera (immune system, liver and the wound)
- facilitates wound healing
- Restoration of normal function
However, the metabolic response may sometimes be pathological if uncontrolled
What are the PHASES OF METABOLIC RESPONSE? And who classified it?
Classification by Sir David Cuthbertson in 1930
* EBB PHASE
* FLOW PHASE
What is the EBB PHASE?
- Begins immediately after trauma and lasts 24-48hrs
- It conserves both circulating volume and energy stores for recovery and repair
- It can be attenuated by proper pre-operative preparation for elective surgery
- The predominant hormones regulating the ebb phase are catecholamines, cortisol and aldosterone following activation of renin-angiotensin system
What occurs in the EBB phase?
There is decrease in the following:
* Cardiac output
* Oxygen consumption
* Blood pressure
* Tissue perfusion
* Body temperature
Metabolic rate
there is also hypothermia, hypovolaemia and lactic acidosis
What occurs in the FLOW phase?
- Body is hypermetabolic
- cardiac output is increased
- Oxygen consumption is increased
- there is increased glucose production
- Lactic acid may be normal
The flow phase is subdivided into what?
Catabolic phase
Anabolic phase
Discuss the Catabolic phase?
- 3-10 days after injury
- Fat and protein catabolism
- There is weight loss
- Increased urine nitrogen excretion
- Negative nitrogen balance
- Hyperglycaemia from gluconeogenesis and
- increased insulin secretion/resistance
Discuss the Anabolic phase?
- 11- 60days
- Restoration of fat and protein stores
- Weight gain
What causes the activation of metabolic response?
- Pain, anxiety and stress
- Hypovolemia from dehydration and
- hemorrhage
- Hypothermia
- Infection
- Hypoxia
HYPOVOLAEMIA
- These lead to baroreceptor stimulation with sympatho-adrenal response
- it then increased release of catecholamines, aldosterone and ADH:
Sympathetic stimulation: catecholamine causes vasoconstriction - Aldosterone: RAAS: renal artery constriction – reduced renal blood flow – renin activation-angiotensin I –angiotensin II – aldosterone
ADH : Elaborated by the supraoptic and paraventricular nuclei of the hypothalamus and stored in posterior pituitary
-The vasoconstriction from sympathetic stimulation can lead to reduced splanchnic blood flow, with resultant reduced gut perfusion=gut ischaemia=↑ gut bacterial translocation=↑ sepsis
PAIN, FEAR, EMOTION, ANXIETY AND STRESS
- Pain receptor in injured tissue – activation of afferent nerves (C-fibres) & Spinothalamic pathway – impulses are sent to thalamus and Hypothalamus- Sym centre and ant pituitary gland are activated
- There is release of ACTH and GH- Cortisol, Catecholamines, Glucagon release
- Emotion and Fear can also directly stimulate the ant pituitary for ACTH and GH release
METABOLIC RESPONSES
- Fluid and electrolyte response
- Changes in protein metabolism
- Changes in fat metabolism
- Changes in glucose metabolism
- Hypermetabolism
- Endocrine response
- Immunosuppression
- Changes in plasma proteins
- Others
FLUID AND ELECTROLYTE RESPONSE
Sodium and water retention
Potassium loss
Dilutional hyponatraemia
SODIUM AND WATER RETENTION
- Sodium retention is due to influence of aldosterone
- Water retention is due to influence of ADH
- Retention of sodium and water is not an inevitable consequence of operative trauma
- it occurs when the functional extracellular fluid volume (intravascular as well as extravascular) has been compromised either before, during or after operation
- Controlled by aldosterone, ADH and intra-renal hemodynamic mechanism.
Sodium retention due to influence of aldosterone
- secreted by zona glomerulosa of adrenal cortex
- Acts on Distal Convoluted Tubules to cause Sodium reabsorption and potassium excretion
STIMULATING/INHIBITING FACTORS
a)Renin angiotensin aldosterone(RAAS) system:
-↓ pressure within renal arterioles →JGA to ↑ renin production
-renin converts angiotensinogen to angiotensin I
-Angiotensin I is converted to angiotensin II by ACE in the lungs
-Angiotensin II causes Aldosterone secretion , ADH release and vasoconstriction
Extracellular Sodium concentration
decrease in extracellular sodium concentration stimulates ↑ aldosterone to conserve sodium
Extracellular Potassium concentration
stimulates release of aldosterone to increase potassium excretion
ACTH
stimulates elaboration of aldosterone
ADH
Causes antidiuresis by increasing permeability of collecting duct
STIMULI
Osmoreceptors
Non-osmotic factors- Arterial receptor system (Baroreceptor stimulation)
Stretch receptors in low pressure vessels
RAAS
Cutaneous and visceral pain, visceral manipulation, stress
Drugs
Intra-renal hemodynamic mechanism
Osmoreceptors
Hyperosmolality (plasma osmolality > 280mOsm/L) , → the osmoreceptors located near the supraoptic and paraventricular nuclei of the hypothalamus to release ADH
Non-osmotic factors- Arterial receptor system (Baroreceptor stimulation)
- Hemorrhage →↓ arterial pressure, → ↓ impulses from the baroreceptors of the carotid sinus and aortic arch to the medulla
- through the reticular formation, the medulla stimulates the hypothalamic nuclei to ↑ADH release
Stretch receptors in low pressure vessels
hypovolemia causes reduced tension in atrial wall, great veins and pulmonary vessels; and these lead to ADH release
RAAS
Angiotensin directly stimulates ADH secretion
Cutaneous and visceral pain, visceral manipulation, stress
directly stimulates ADH secretion
Drugs
Ether, nicotine, morphine and barbiturates also ↑ ADH secretion. (Alcohol inbibits ADH secretion
Intra-renal hemodynamic mechanism
The juxtamedullary nephrons are longer and more efficient in reabsorbing sodium than the cortical nephrons.
Haemorrhage, hypotension and sympathetic stimulation cause redistribution of blood flow from the cortical to the juxtamedullary region, resulting in increased sodium reabsorption.
POTASSIUM LOSS
Aldosterone release: causes sodium reabsorption and potassium loss
However, potassium loss still occurs in absence of sodium retention due to shed blood and breakdown of protein and injured tissues
During the anabolic phase, when protein is replenished, potassium is required and renal excretion is diminished
CHANGES IN PROTEIN METABOLISM
Protein catabolism and anabolism are increased, but catabolism is greater than anabolism leading to negative nitrogen balance
Proteolysis is aided by
Hormones: Cortisol, Glucagon, Adrenaline (GH causes proteogenesis, not proteolysis)
Fever: there is a linear relationship btw ↑temp. & proteolysis
Exercise: i-NOS →↑NO and hydroxyl radicals =↑ proteolysis after exercise
Starvation and immobilization of illness
CHANGES IN PLASMA PROTEIN: Albumin
-turnover increases, its plasma concentration decreases to 25-30% due transcapillary escape
-Lowest level is reached in 48hrs,then rises and return to normal in 7-14days
CHANGES IN PLASMA PROTEIN: ACUTE PHASE PROTEIN
These are plasma proteins whose levels rise by at least 25% following trauma or during sepsis
2 types –positive and negative acute phase proteins
Positive acute-phase proteins (after injury)
● C-reactive protein
● Haptoglobins
● Ferritin
● Fibrinogen
● a1-Antitrypsin
● a2-Macroglobulin
● Plasminogen
Negative acute-phase proteins (after injury)
● Albumin
● Transferrin
CHANGES IN LIPID METABOLISM
Lipids are non-protein, non-CHO fuel sources
Lipolysis minimizes protein catabolism in the injured patient.
Lipolysis of triglyceride stored in adipose tissue takes place to yield fatty acid and glycerol
Lipolysis isstimulated by the Sym nervous system & Hormones (catecholamines, glucagon, cortisol and growth hormone)
Lipolysis is inhibited by Insulin and PGE2
CHANGES IN GLUCOSE METABOLISM
Glycogenolysis -Glycogenolysis is aided by epinephrine and glucagon
Gluconeogenesis-derived from lipolysis of TG in adipose tissue, amino acids derived from proteolysis and lactate/pyruvate derived from glucose metabolism in TCA cycle
Facilitated
by adrenaline, Glucagon, GH & Cortisol
The glucose derived is utilized mainly by obligatory glucose-dependent cells
The heart, skeletal muscle, liver and other tissues utilize mainly fatty acids from triglycerides and ketone bodies
CYTOKINES
They are short-acting, soluble, low molecular weight polypeptides
They regulate the intensity and duration of the immune response and also mediate cell-cell communication
Cytokines have autocrine, paracrine, and endocrine effects
Autocrine: refers to self-stimulating effect through cellular production of a factor acting on a receptor specific for it
Paracrine: relates to an hormone-like function in which the effects are restricted to the local environment
Endocrine: secreted into the systemic circulation for its action at a distant site
Pro-inflammatory cytokines include
TNF-alpha, IL-1, IL-2, IL-6, IL-12
Anti-inflammatory cytokines include
IL-4 and IL-10
What can cause pyrexia after injury?
Stimulation of the pre-optic area of the hypothalamus by IL-1 and TNF causes pyrexia after injury
FACTORS INFLUENCING MAGNITUDE OF RESPONSE: Patient related
- Genetic predisposition: how an individual responds to injury and infection is related to gene subtypes
- Coexisting disease: such as cancer and chronic inflammatory disease
- Drug treatments: Pre-existing anti-inflammatory or immunosuppressive therapy, such as steroids.
- Nutritional status: Malnourished patients have decreased immune function and deficiency in important substrates. Poor response & poor outcome
Discuss TRUAMA/SURGERY RELATED injuries
- Severity of injury: Greater tissue damage associated with a greater response
- Nature of injury: Some types of tissue injury cause a proportionate metabolic response. E.g. major burn injury is associated with a major response
- Ischaemia–reperfusion injury: If resuscitation is not quick &/or effective, reperfusion of previously ischaemic tissues can set off a cascade of inflammation that further injures organs.
- Temperature: Extreme hypothermia and hyperthermia are both detrimental
- Infection: The occurrence of infection is often associated with an exaggerated response to injury b/c of massive inflammatory response
- Anaesthetic techniques: drugs, such as opioids, can reduce the release of stress hormones.
- Regional anaesthetic techniques for major surgery reduces the release of cortisol, adrenaline (epinephrine) and other hormones, but has little effect on cytokine responses.
What are Pre-op METHODS OF ALLEVIATING THE METABOLIC RESPONSE?
- Patient education and counseling - Reducing anxiety = ↓ cathecolamines, cortisol and GH secretion levels
- Prompt and adequate fluid and electrolyte resuscitation -This minimizes responses such as salt and water retention
- Adequate analgesia: to control pain
- Correct hypoxia
- Commence appropriate antibiotics as indicated
- Nutritional control
What are Intra-op METHODS OF ALLEVIATING THE METABOLIC RESPONSE?
- Anaesthesia with reduced stimulation of the sympathetic system is preferred
- Regional anaesthesia is preferred: reduces morbidity by 30%. Eg LA, Subarachnoid block, Epidural block
- Hypotensive anaesthesia: to minimize blood loss
- Appropriate prophylactic antibiotic therapy at induction of anaesthesia
- Secure hemostasis, ensure bloodless tissue planes
- Minimal tissue disruption: minimally invasive surgery
- Fluid mgt, Autologous blood transfusion if transfusion indicated
What are Post-op METHODS OF ALLEVIATING THE METABOLIC RESPONSE?
- Ensure fluid and electrolyte balance
- Adequate analgesia
- Nutritional supplementation : Early enteral feeding
