- Similar responses seen to trauma, burns, sepsis and surgery
- Involves both local and systemic reactions
- Extent of response proportional to severity of insult
- An appropriate response maintains homeostasis and allows wound healing
- An excessive response can produce a systemic response
- This can cause the systemic inflammatory response syndrome (SIRS)
- Multiple organs dysfunction syndrome (MODS) can result from SIRS
Initiation of response
- Several factors can initiate the physiological response to trauma
- Multiple simultaneous factors can have a synergistic effect/li>
- Important factors are:
- Tissue injury
- Infection
- Hypovolaemia
- Hypoxia or hypercarbia
Control of response
- Four systems control the response to trauma
- Sympathetic nervous system
- Acute phase response
- Endocrine response
- Vascular endothelium
Sympathetic nervous system
- Has direct actions via the release of noradrenaline from sympathetic nerves
- Has indirect action via the release of adrenaline from the adrenal medulla
- Produces cardiovascular, visceral and metabolic actions
- Blood diverted from skin and visceral organs
- Heart rate and myocardial contractility are increased
- Bronchodilation occurs and gastrointestinal motility is reduced
- Insulin production is reduced and glucagons production increased
- Increased glycogenolysis increases blood sugar levels
Acute phase response
- Tissue injury results in cytokine release
- Important cytokines include TNF-alpha, IL-1, IL-2, IL-6, interferon and prostaglandins
- Cytokines have mainly paracrine actions
- Important in regulating the inflammatory response
- Overflow of cytokines into systemic circulation is important factor in SIRS
- Cytokines stimulate the production of acute phase proteins such as:
- C-reactive protein
- Fibrinogen
- Complement C3
- Haptoglobin
Endocrine response
- The hypothalamus, pituitary, adrenal axis is important
- Trauma increases ACTH and cortisol production
- Steroids have a permissive action in many metabolic responses
- Catabolic action increases protein breakdown
- Insulin antagonism increases blood sugar levels
- Anti-inflammatory actions reduce vascular permeability
- Aldosterone increases sodium reabsorption
- Vasopressin increases water reabsorption and produces vasoconstriction
- Histamine increases vascular permeability
- Total T4, total and free T3 levels are reduced
Vascular endothelium
- Nitric oxide produces vasodilatation
- Platelet activating factor augments the cytokine response
- Prostaglandins produce vasodilatation and induce platelet aggregation
Outcome or response
- Inflammatory response produces clinically apparent local and systemic effects
- The local response is usually the cardinal signs of inflammation
- The systemic response includes:
- Increased ECF volume and hypovolaemia
- Increased vascular permeability and oedema
- Early reduced urine output and increased urine osmolality
- Reduced ‘free’ water clearance
- Late diuresis and increased sodium loss
- Pyrexia in the absence of infection
- Early reduction in metabolic rate
- Late increased metabolism, negative nitrogen balance and weight loss
- Lipolysis and ketosis
- Gluconeogenesis via amino acid breakdown
- Reduced serum albumin
- Hyponatraemia due to impaired sodium pump action
- Acid-base disturbance – usually a metabolic alkalosis or acidosis
- Immunosuppression
- Hypoxia and coagulopathy
Limitation of response
- Inflammatory response can be limited by
- Reducing degree of trauma with appropriate and careful surgery
- Reducing infection with wound care and antibiotics
- Maintaining enteral nutrition
- Controlling pain
- Correcting hypovolaemia
- Correcting acid-base disturbance
- Correcting hypoxia
Bibliography
Foex B A. Systemic
response to trauma. Br Med Bull 1999;
76: 352-354
Street S J, Plank L D,
Hill G L. Overview of modern management of patients
with critical injury or severe sepsis. World J Surg 2000;
24: 673-680.
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