Burns - Building SCHEMATA with Burns Slides PDF

Building SCHEMATA with Burns Slides BURNS: 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. (remember 6 things) First, we need to understand layers of skin and how they work (for ho...

Building SCHEMATA with Burns Slides BURNS: 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. (remember 6 things) First, we need to understand layers of skin and how they work (for homeostasis-to keep us in balance) Key aspects to take from this:  EPIDERMIS: - 5 layers -deeper layers continuously divide and migrate to the top layer and we shed away.  DERMIS: Mainly involved in thermoregulation: Think about it: We sweat to release heat (sweat=plasma in blood)/Piloerection to raise hair (goose pumps) to preserve heat (we get goose pumps and hair erects on our arms (or face if you’re hairy) to trap air cos air is a super insulator of heat. - Dermis also has nerves; blood vessels and glands so are in charge of regenerating epidermis cells. (So it is important in the regeneration of the outer layer of skin when burns are superficial) Building SCHEMATA with Burns Slides Classifications of Burns: 1st Degree: Superficial epidermal (rash, sunburn etc)-no damage to dermis. 2nd Degree: 1. Superficial dermal (Blisters, red, peeling): Blanches (when you press skin and it goes white first) and has capillary refill. Weep fluid-swelling-painful 2. deep dermal (dry, mottled, red-may be blisters too): No blanch at capillary refill-no damage to underlying tissue 3rd degree: FULL THICKNESS (Epidermis & dermis: nerves destroyed-so painless)- black leathery waxy looking. Reaches subcutaneous tissue or even bone and muscle. LOCAL Response (What happens at the site of the burns/s?) (Pathophysiology) Zone of coagulation (clot)—This occurs at the point of maximum damage. Tissue is damaged at the point of injury due to coagulation (clotting) of the constituent proteins. Zone of stasis (balance)—The surrounding zone of stasis is characterised by decreased tissue perfusion. The tissue in this zone is potentially salvageable. The main aim of burns resuscitation is to increase tissue perfusion here and prevent any damage becoming irreversible. Additional insults—such as prolonged hypotension, infection, or oedema—can convert this zone into an area of complete tissue loss. Zone of hyperaemia (High blood flow)—In this outermost zone tissue perfusion is increased. Natural response to inflammation-blood flows quickly to the local site. The tissue here will invariably recover unless there is severe sepsis or prolonged hypoperfusion. 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. Building SCHEMATA with Burns Slides Systemic Response (Pathophysiology) 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 is increased (leaking fluid out of vessels), so proteins and fluid is outside the vessels instead of inside to run round full system. Peripheral (Outer parts) and splanchnic (supplies blood to digestive system) vasoconstriction occurs (So blood gets pulled from peripheries and splanchnic to supply main organs). Myocardial contractility is decreased, possibly due to release of tumour necrosis factor α. These changes, coupled with fluid loss from the burn wound, result in systemic hypotension and end organ hypoperfusion. In other words: Circulation problem is from fluid loss to the local site (hyperaemia) & vascular permeability. But the local site demands more fluid to keep the dermis/epidermis alive (recreation)-so more fluid demand causes less for organs (Hypoperfusion of organs) and less in the system (Systemic hypotension)- So reduced stroke volume & contractility (Will probably raise HR for homeostasis of cardiac output-BP)-First 24-72 hours Respiratory changes—Inflammatory mediators cause bronchoconstriction (similar to in anaphylaxis), and in severe burns adult respiratory distress syndrome can occur. Think about RESISTANCE (in breathing like asthma)-struggle to breath and diffuse gases. Plus less 02 carrying capacity will deplete 02. Metabolic changes—The basal metabolic rate increases up to three times its original rate. So everything is being metabolised too quickly but because there is less blood flow to splanchnic (Supply to digestive system), early and more feeding is required to decrease catabolism (quick breakdown of molecules) and maintain gut integrity. In other words, your demand for 02, ATP for energy, fluid etc will increase by 3-fold! At the same time: thinking of 02+glucose=ATP+C02 Burn patients are utilizing non-carbohydrate sources to generate glucose (gluconeogenesis) resulting in an increase in glucose production (glycogenolysis). These patients also have high insulin resistance, resulting in a poor response to insulin. This abnormal production of glucose and the resistance to insulin leads to a decrease in glucose uptake (absorption into Building SCHEMATA with Burns Slides cells) and clearance from the body, resulting in hyperglycemia. Due to the extreme damage caused by burn trauma, patients can remain in a hypermetabolic and catabolic state long after the wounds have healed. **All this happens from release of hormones, such as adrenaline, noradrenaline, cortisol, glycogen Treatment: Step-by-step 1. Look at where the burns are and how much of the body’s surface area is covered with the burns. 2. Establish the degree of damage from burns: Is it superficial (epidermis); 2 nd degree (dermis as well-does it blanch while doing a CRT? This will allow you to detect if the impact is of deep dermis (no blanch) or superficial dermis). 3. If airway (face, neck, chest), then you need to consider AIRWAY management (apply pulse oximeter; Look, feel, listen). If stridor, wheeze, audible sounds plus low sats-Consider RSI with ET tube-Follow DAS guidelines and get Difficult intubation trolley-as this will be a difficult airway- You may need fibre-optic scope-smaller ET tubes-tracheostomy.  REMEMBER: A true RSI includes rapid acting drugs as well since the patient may not be fasted being an emergency. 4. BREATHING: Especially during 3rd degree burns (but also with severe 2nd degree) black, tight, leathery black scab looking layer may be present. Now this is hard and not elasticated like our skin. If that is around your chest-how will you expand your chest to inhale air (we increase our surface area to lower air pressure inside our chest so the outside air-which is now greater- can flow in-see Boyles law in BREATHING slides). If there is trouble like this the patient may present with dyspnoea (short fast breathes) to expel the load of C02 build-up (which is what triggers us to breath remember). At the same time, it will impair gaseous exchange because the breath is not deep enough- so then we now get respiratory acidosis-I guess (from anaerobic respiration)- without enough 02 in blood. 5. CIRCULATION: Because of the cytokines and inflammatory mediators- vascular permeability happens-leading to fluid maldistribution and oedema. Also the uptake and demand for fluid to the burns site increases-though cleverly, or systemic response triggers peripheral vasoconstriction to conserve fluid for the main organs-so in all we need to replace volume because as we know loss of STROKE VOLUME-will increase HR to maintain cardiac output-so the BP remains stable. We need IV access to infuse fluid (this has to be calculated though). Building SCHEMATA with Burns Slides  Don’t forget Temperature: The patient will get hypothermic, especially if they have lost the DERMIS as this has key homeostatic parts for thermoregulation which are now destroyed-Even though peripheral vasoconstriction will prevent excessive heat loss-they still have less volume (volume=heat). In a 3 rd degree burn-layers of epidermis and dermis are lost-the patient will get very cold very quickly. Keep the room temperature above 29 and aim for a temperature over 34 for this patient. Also: remember the lethal triad (Hypothermia+ coagulation+ metabolic acidosis) IS BAD! Leads to death! I know you might be thinking that well-they don’t have metabolic acidosis, but actually, during burns, an abnormal production of glucose and the resistance to insulin leads to a decrease in glucose uptake and clearance from the body, resulting in hyperglycaemia.  You will need to take bloods-consider arterial lines-CVP lines-gases. 6. DISABILITY: Mainly conscious level- if your patient is not getting enough 02, then how are they going to keep consciousness???? The brain needs 20% of our overall 02. So just bear this in mind. 7. EXPOSURE: This is when you may be documenting the full extent of the injuries and there are calculations in departments for burns specifically. Extra reading: https://www.bmj.com/content/328/7453/1427?hwshib2=authn %3A1708470189%3A20240219%253A41a152d1-997d-477f-a679-f68afa76abfd %3A0%3A0%3A0%3A4cn7vVbDA3yGKJ5uMcvItA%3D%3D Burn Evaluation and Management - StatPearls - NCBI Bookshelf (nih.gov) The Impact of Hyperglycemia in Burn Trauma - Monarch Medical Technologies (monarchmedtech.com)