Burns ODP3003 PDF

Burns ODP3003  Discuss Discuss types of burns Link to the function of skin in maintaining balance Link (homeostasis) Learning Apply Apply pathophysiology (changes in physiology) during burns Objectives...

Burns ODP3003  Discuss Discuss types of burns Link to the function of skin in maintaining balance Link (homeostasis) Learning Apply Apply pathophysiology (changes in physiology) during burns Objectives Discuss Discuss clinical assessment of burns Discuss clinical management to correct Discuss pathophysiology What is a burn? “A burn is an injury to the skin or other organic tissue primarily caused by heat or due to radiation, radioactivity, electricity, friction or contact with chemicals. Thermal (heat) burns occur when some or all of the cells in the skin or other tissues are destroyed by: hot liquids (scalds) hot solids (contact burns), or flames (flame burns).” (World Health Organization [WHO], 2018:1) The Skin and Homeostasis Largest organ system in the body Epidermis – five layers Dermis – two layers Deepest layers of epidermis regenerate every 2 – 3 weeks Epidermis cannot regenerate without presence (McCann, Watson and Barnes, 2022) of dermal tissue  Layers of skin Depth of burn affected Skin examination Superficial The epidermis is The skin is red and epidermal (for affected, but the painful, but not Classificatio example, sunburn) Superficial dermal dermis is intact. blistered. Capillary refill* blanches then rapidly refills. The epidermis and The skin is red or n of Burns (partial thickness) upper layers of dermis are involved. pale pink and painful with blistering. Capillary refill* blanches but Burns injuries are classified into two regains its colour slowly. groups depending on the amount of Deep dermal The epidermis and The skin appears tissue damage: (partial thickness) the upper and dry, blotchy or Superficial partial-thickness burns deeper layers of the mottled, red, and Full thickness burns dermis are typically painful involved, but not (due to exposed underlying superficial nerves). subcutaneous There may be tissues. blisters. Capillary refill* does not blanch. Full thickness The burn extends The skin is white, through all the brown, or black layers of skin to (charred) in colour, subcutaneous with no blisters. It (National institute for Health and Care Excellence [NICE], tissues. If severe, it may appear dry, 2023) extends into muscle leathery, or waxy Classification of Burns 1st Degree: 2nd Degree 3rd Degree Top layer only Blisters, then top layer Full thickness sensory Red, hot, irritating, starts to slough (Epidermis, Dermis and dry, no blister nerves destroyed) Swelling, Painful, Start to weep fluid Reaches subcutaneous fatty layer Can be deep but not 3rd degree but can lead Black areas, dry areas, to Compartment 2nd degree tissue Syndrome if burn is around edges Pathophysiology: Local Response These three zones of a burn are three dimensional, and loss of tissue in the zone of stasis will lead to the wound deepening as well as widening. Zone of hyperaemia Zone of Stasis (high blood flow (balance) Blood flow increases potentially here due to Zone of Coagulation salvageable tissue. inflammation Central contact point of maximal damage Main aim to increase (Vasodilation & in which cell death, denaturation of proteins in the extracellular matrix, and tissue perfusion here increased circulation damage to the circulation occur Can become from histamine) Irreversible tissue loss irreversible: Will recover, unless it Due to coagulation of protein constituents Infection, becomes systemic hypotension, like sepsis oedema https://www.researchgate.net/publication/363198228/figure/fig1/ AS:11431281129197326@1679491465118/Jacksons-zones-of-injury-with-permission-from- Pathophysiology: Systemic Response The release of cytokines and other inflammatory mediators at the site of injury has a systemic effect once the burn reaches 30% of total body surface area. Cardiovascular changes Capillary permeability: fluid leaks out of vessels leading to loss of intravascular proteins and fluid into the interstitial compartment Peripheral and Splanchnic vasoconstriction: due to the release of catecholamines, vasopressin, and angiotensin-less blood flow to these regions. Reduced cardiac contractility-hence heart rate increases-02 consumption increases ** Together: these changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end organ hypoperfusion. Pathophysiology: Systemic Response Respiratory changes Bronchoconstriction: Inflammatory mediators cause bronchoconstriction (like in anaphylaxis), and in severe burns adult respiratory distress syndrome can occur. Hence, resistance and decreased diffusion of 02 into blood and C02 out. Loss of fluid from vessels: This means less 02 carrying capacity around the system Pathophysiology: Systemic Response Metabolic changes Hypermetabolism: 3-fold increase of metabolic demands, which can lead to muscle, bone, and adipose catabolism (quick breakdown of molecules) (Muscle wastage). Also, due to splanchnic hypoperfusion, early and aggressive enteral feeding is needed to decrease catabolism (quick breakdown of molecules) and maintain gut integrity. Insulin Resistance: Release of adrenaline causes cells inability to bind to insulin (insulin allows glucose to enter cells) Increased glucose production (glycogenolysis): Utilize non-carbohydrate sources (Glycogen) to generate glucose from release of noradrenaline This abnormal production of glucose and the resistance to insulin together lead to a decrease in glucose uptake (process in which glucose is transported into cells) and clearance from the body, resulting in hyperglycaemia. *** Glucose + 02= ATP+C02+H20 Pathophysiology: Systemic Response *** Glucose + 02= ATP+C02+H20 MIXED EVIDENCE ON INSULIN THERAPY “We conclude that in burns there seems to be a signal that insulin administration to a target range of 130 to 150 mg/dl is beneficial in terms of morbidity and mortality without the risk of hypoglycaemia”. (Jeschke, 2013) The standard of care for burned patients experiencing hyperglycaemia associated with the hypermetabolic response is insulin therapy. HOWEVER: Insulin treatment predisposes burn patients to hypoglycaemia, which increases morbidity and mortality. (Hallman et al., 2024) Clinical Assessment – Supporting the Anaesthetist Medics Step by Step guide to provide optimal treatment, including : - Burn Unit Criteria eg. age, 2nd degree >20%, 3rd degree >5%, type (chemical, electrical etc), inhalational injury, circumferential, area (face, hands, feet, genitals, perineum, joints) - A – E survey (airway, breathing, circulation (cannulation & fluid resuscitation), disability(inc. injury), exposure (remove all clothes). Consider HYPOTHERMIA (keep core temp >34°c) - Estimate burned surface area (%TBSA) and degree of burn - Calculate fluid resuscitation eg. Merseyburns app or Parkland Formula (usual practice is to use crystalloid (lactated ringers/ Hartmans or saline / sodium chloride 0.9%) - Routine interventions eg. Monitoring, Arterial line, CVP, ABG(blood gas), NG tube, catheter, microbiology swabs, CBC(complete blood count), U+E etc. Also wash with warm water and re- evaluate TBSA, pain mgmt. - Is surgery needed immediately and secondary survey of cornea etc. - Care plan/ admission/ consent Clinical Management – Airway AIRWAY - Is the patient awake – stridor, hoarseness, wheezing - Do they need intubation (is the ventilator checked, airway equipment to hand, uncut tubes, O2 available, monitor + battery, CO2 line + capnography, difficult airway) - Smaller sized tubes (Swelling- oedema: leaking fluid) - Tracheostomy – consider DAS guidelines Clinical Management – Breathing BREATHING - RESISTANCE? Inflammatory mediators cause bronchoconstriction, hence difficulty breathing and decreased perfusion. Sp02/Capnography/02 via appropriate device until intubation/mechanical ventilation-controlled. - COMPLIANCE?? How much can the lungs stretch? Are the burns 3rd degree and around the chest and back? Short breaths-abnormal posture. - Anaerobic respiration- Less 02 triggers lactic acid release=acidotic PH Surgical Instrumentation ZIMMER DERMATOME WATSON KNIFE Fasciotomy and Escharotomy - FASCIOTOMY - Cut through Fascia (sheet of connective tissue beneath skin that attaches and encloses and separates muscles and organs) (eg.compartment syndrome) - ESCHAROTOMY - Epidermis, dermis and sensory nerves destroyed (full thickness) therefore leathery tissue remains (Eschar) which causes vascular compromise. This is incised until released. Often needed with circumferential burns. Clinical Management – Circulation CIRCULATION - REPLACE LOST FLUID VOLUME: Fluid lost from vascular permeability-extra uptake on local site (Crystalloid)-calculated - IV Access. - Warmed - Increase stroke volume to maintain BP - Increase 02 carrying capacity Clinical Management – Circulation Thermoregulation - Lost DERMIS? Thermoregulation part. - Less blood volume to peripheries (Peripheral vasoconstriction)= less heat - Fluid leaking out of vessels= not in system - Room temperature above 29 and aiming for patient temperature of 34 min. lethal triad (Hypothermia+ coagulopathy+ metabolic acidosis) Burns= abnormal production of glucose and the resistance to insulin leads to a decrease in glucose uptake and clearance from the body, resulting in hyperglycaemia=metabolic acidosis Clinical Management – Disability Conscious Level - 02 reaching brain decreased-altered consciousness - This coupled with increased demand on body indicates early intubation for controlled ventilation maximizing 02 perfusion. Clinical Management – Exposure Document the full extent of the injuries and there are calculations in departments for burns specifically Skin Grafts ALLOGRAFT - Cadaver or live donor - Enhance granulation - Last between 2 – 4 weeks FULL THICKNESS - Can be Xenograft (different GRAFT species eg Pig) AUTOGRAFT - Split skin graft(meshed – use paraffin oil or saline) - Full thickness graft SPLIT SKIN GRAFT Application to Practice – role of the ODP - Theatre temperature – - Set/instrumentation - Early excision of burns should be above 29°c prep including Watson and immediate grafting - Warm fluids / types of knife / Zimmer improves survival rate fluids Dermatome/ Meshers - Development of grafts (2:1, 4:1, Pie crust) - Airway considerations and how to work with - Dressings/ burn them improves infection - Correct table and swabs / infusions control and therefore attachments for positioning (Jelonet – paraffin survival rates - Consideration of pressure gauze, Kaltostat – area management alginate dressing), - Drugs and infusions staples, local anaesthetic, pressure - Control movement of other dressing, paraffin or staff through theatre to saline for mesher reduce infection risk - Grafts – Allograft or Case Study Critically analyse the clinical management for this patient presenting with burns and apply the anatomy and pathophysiology based on the presenting clinical assessment (30 marks) A 20-year-old female has been admitted to the Emergency Department with 3 rd degree burns to her face, chest and arms following an acid attack whilst on a night out. You have been called as part of the multidisciplinary team to attend. Initial A-E assessment shows: A – cyanosis, swollen lips & tongue B – RR 30, SpO2 poor trace, equal but shallow chest movement, audible wheeze and crackles C – HR – 150, CRT unable to measure centrally due to burns, BP – 103/62, temperature unrecordable due to severity and location of burns D – P on AVPU, no abnormal posturing, glucose 7.5 mmol/l E – full thickness burns to chest and arms. Reference List JESCHKE M. G. 2013. Clinical review: Glucose control in severely burned patients - current best practice. Critical care (London, England), 17(4), 232. https://doi.org/10.1186/cc12678 MCCANN, C., WATSON, A. and BARNES, D., 2022. Major burns: Part 1. Epidemiology, pathophysiology and initial management. BJA Education. 22 (3), pp. 94-103. MCGOVERN, G., PUXTY, K. and PATON, L., 2022. Major burns: part 2. Anaesthesia, intensive care and pain management. BJA Education. 22 (4), pp. 138-145. HALLMAN, T.G., JUQUAN SONG, G.G., PALACKIC, A., WOLF, S.E. & EL AYADI, A. 2024. Metformin is associated with reduced risk of mortality and morbidity in burn patients compared to insulin, Burns. 50 (7), pp.1779-1789. https://doi.org/10.1016/j.burns.2024.05.015. NATIONAL INSTITUTE FOR HEALTH AND CARE EXCELLENCE, 2023. How should I assess a person with a burn? [online]. Available from: https://cks.nice.org.uk/topics/burns-scalds/diagnosis/assessment/#classification-of-burn-depth [Accessed 1 September 2023]. NIELSON, C.B., DUETHMAN, N.C., HOWARD, J.M., MONCURE, M. and WOOD, J.G., 2017. Burns: Pathophysiology of Systemic Complications and Current Management. Journal of Burn Care Research. 38 (1), pp. 496-481. WORLD HEALTH ORGANIZATION, 2018. Burns [online]. Available from: https://www.who.int/news-room/fact-sheets/detail/burns#:~:text=A%20burn%20is%20an%20injury,hot%20liquids%20(scald s) [Accessed 31 August 2023].