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Burns (Analgesia (Acute pain can be nocieceptive and/or neuropathic and…
Burns
Analgesia
Acute pain can be nocieceptive and/or neuropathic and may be constant (background), intermittent or procedure related
Although full thickness burns are painless, a mixed picture is common
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With severe pain, achieve analgesia by titration of IV morphine against response (adults 2-5mg 5 mins, kids 50-100mcg/kg 5 mins, IM and SC absorption may be unreliable in the presence of hypovolaemia and vasoconstriction)
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Convert to oral opioids once GI function has returned (feeding, absoption)
Additional non-opioid analgesics (Paracetamol, Pregabalin, Tramadol, Clonidine)
Infection control
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Predisposed to infection (loss of skin protective barrier, immunosuppressive effect from hypermetabolic response)
Reduce risk with: excision of the burn and skin grafting, patient isolation, meticulous attention to infection control procedures
No role for prophylactic Abx (however will require Abx prophylaxis for surgical debridement to cover Staph A, Strep P, Psudomonas and anaerobic Gram -ve bacilli)
Chemical burns
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During the secondary survey, determine the extent of tissue damage by determining:
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Management
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On occasions, administration of a buffer or neutralising agent (where appropriate) to counteract the chemical
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Pathophysiology
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Systemic response
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Cytokines are released from damaged cells, producing a generalised inflammatory response
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Proteinaceous fluid will pass into the interstitial space, which will contribute to tissue oedema and hypoperfusion
CVS: Myocardial depression due to cytokine release, fluid loss also contributes to hypoperfusion
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Metabolic: Hypermetabolism due to catabolic stress hormones (cortisol, adrenaline, glucagon) - results in increased Gluconeogenesis, lipolysis and decreased protein synthesis
Immunological: Downregulated cell-mediated and humoral immunity, leading to increased susceptibility to infection
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