Bailey and Love Explained| Chapter 46: Burns| Explained with Podcasts

0:00 Okay, let's unpack this. We are tackling a u a really complex and profoundly urgent area of medicine today. >> Yeah. >> Burn injuries, >> right? >> And a major burn. It's so much more than just a skin problem. It's an immediate life-threatening multi-system trauma. >> It really is. >> So, our mission for this deep dive is to take chapter 46 from the sources, the definitive surgical guide, and really distill the absolute critical structure you need. We're aiming for a thorough understanding of the pathophysiology, the acute assessment, and all the intricate multidisciplinary treatment that's required right through to reconstruction. >> And we want you to be able to instantly access this to recall it for revision, but also for clinical application. >> Exactly. >> And the reason this knowledge is so vital is, you know, the sheer scale of

0:46 the clinical problem. While advancements over the last 50 years have um radically reduced mortality, the incidence is still staggering. >> Give us the numbers. In a country like the UK, we're talking about approximately 175,000 people visiting A&E departments every year with burns. That translates to about 13,000 admissions. And here's the really crucial vulnerability marker. Half of those admissions are victims under the age of 16. >> Half >> half. That volume coupled with the immediate life threat means that structured immediate care is the absolute standard. >> Absolutely. So the clinical context is our starting point specifically looking at how the mechanism of injury shifts so dramatically based on the patient's age.

1:32 It tells us a lot, doesn't it? >> It does. It tells you the story. When we look at children, the overwhelming majority of burns, well over half, are scolds. >> So hot drinks, bath water. >> Exactly. Think hot drinks spilled from kettles, bath water that's too hot, or steam. It's typically a domestic accident profile where you get this immediate fast energy transfer causing a superficial or deep partial thickness injury. >> And as they get older, >> as we move into adolescence, the mechanism begins to involve well higher energy injuries, often due to risk-taking or experimentation with flammable liquids or matches. For the large adult population and particularly the elderly, we see flame burns becoming more frequent. But we also see these critical contact burns, >> but falling against a radiator. >> Precisely. patients falling against a hot radiator or heater and being unable to extract themselves. And this is often

2:19 a flash point for recognizing an underlying frailty or an inability to self-care that needs immediate social services intervention. >> That focus on vulnerable groups, the very young and the very old brings up a really serious ethical and legal duty for every clinician. Screening for non-acal injury or NAI. >> 100%. >> What are the signs? which should immediately put the team on high alert and trigger a senior staff consultation. >> This is a non-negotiable step in the assessment. The source lists four primary warning signs and any one of them must raise concern. First, a delay in presentation. >> They didn't bring the child in right away. >> Exactly. Or a perceived lack of appropriate concern from the caregiver, you know, relative to the severity of the injury. Second, and this is probably

3:05 the most common red flag, is an inconsistency between the history provided and the actual burn pattern or depth. >> The story just doesn't fit the injury. >> It just doesn't add up. Third, the presence of other unexplained injuries, maybe bruises in various stages of healing or you notice previous fractures in the notes. And fourth, a pattern of frequent hospital attendances. Recognizing these patterns is absolutely paramount. >> It's our duty of safeguarding. >> It is. Now, stepping away from the immediate safeguarding issues, the sources note that in the general adult population, burns often reveal significant underlying co-orbidities. >> They really do. I mean, studies show that in some trauma populations, underlying factors like severe mental disease, including attempted suicide, or assault, epilepsy, or chronic alcohol or

3:52 drug abuse, are associated with as many as 80% of burn patients admitted to the hospital. >> 80%. That's huge. >> It's a massive number. These conditions inherently increase the risk because they impair judgment, reaction time or the ability to escape a hazardous environment. And you have to manage these underlying issues alongside the acute injury >> and occupational injuries. >> Yes, the majority of those. So, electrical and chemical burns tend to occur in working age adults. >> It's a huge public health issue. It requires that multiddisciplinary input from day one. But on a positive note, our sources do highlight some major public health successes in prevention. What specific measures have actually worked? >> Well, prevention is always the gold standard, right? These injuries are so devastating. Summary box 46.2

4:39 reviews the success of legislation. Things like mandating flame retardant clothes and furniture and uh product design changes >> like cordless kettles. >> Exactly. Cordless kettles have made a huge difference in reducing scalds and public education has been hugely effective. specifically campaigns that emphasize setting water thermostats to no more than 60° C. >> And those simple slogans, >> those slogans stick. Hot water burns like fire. That simple step drastically reduces the time needed for hot water to cause a full thickness injury, especially in a child's delicate skin. >> That's a great synthesis of the context. >> Yeah. >> So, let's move immediately into the core science. >> Yeah. >> The pathophysiology. As we established, this is a multi-system injury driven by this massive overdrive switch, the

5:26 inflammatory cascade, >> right? >> Let's begin at the site of injury, >> the skin. What vital functions are immediately lost when the skin is destroyed by heat? >> Well, the skin is the body's primary control center and barrier. When it's burned, you instantly lose that waterproofing layer, which compromises the patients fluid status. You lose UV protection, immune response mechanisms resident in the skin and the critical ability to thermmorreulate, >> which is a major factor driving hypothermia, >> a huge factor. You also lose vitamin D production, but crucially for the long term, you lose the skin's elastic role in facilitating movement, sensation, and you know, acceptable cosmetics. Losing that protective barrier sets the stage for every single complication that follows, especially infection and massive fluid loss. >> And here's where it gets truly life-threatening. inhalation injury.

6:14 This is the critical factor that dictates immediate airway management. The sources describe this as a triple threat. >> The triple threat is a perfect way to describe it. It's a combination of three distinct injury types that happen when a patient is trapped in an enclosed space with fire. First, upper airway injury from hot gases. >> Okay. >> Second, lower airway injury from smoke particles and steam. And third, metabolic poisoning from gases like carbon monoxide and cyanide. And the key history point there is trapped in an enclosed space. >> Absolutely. The significance of a patient being trapped even for a few minutes cannot be overstated. It just drastically increases the risk of all three. >> So let's focus on the first two. How do we differentiate the upper from the lower injury. >> The upper airway injury is usually

6:59 purely thermal. It's caused by inhaling superheated air or steam. This heat targets the superglottic region so above the vocal cords leading rapidly to superglotic airway burns and massive leneal edema. >> Swelling that can just completely block off the airway. >> Exactly. The lower airway injury however is predominantly chemical. It involves inhaling toxic steam and smoke particles deep into the lungs. This causes subglottic burns, sloughing and loss of the respiratory epithelium, chemical pneuminitis, and ultimately acute respiratory failure. >> And then there's the immediate non-therrmal killer, metabolic poisoning. We're talking about gases released during combustion. >> Precisely. And carbon monoxide, CO, is the most common cause of immediate death

7:45 in house fires. It's odorless, colorless, and incredibly lethal >> because it binds to hemoglobin so much more readily than oxygen. >> So much more. It has an affinity for ariththraite hemoglobin that is approximately 250 times greater than oxygen. It essentially hijacks the red blood cells forming caroxy hemoglobin which cannot transport oxygen. >> So the delivery truck is still running but it's carrying the wrong payload. >> Exactly. And it's even worse than that. CO doesn't just block oxygen transport. It actively inhibits the binding of oxygen to cytochrome oxidase in the mitochondria. >> So it's double hit. >> It's a double hit. It directly impairs cellular respiration. So even the limited oxygen that does get delivered can't be used efficiently by the cells. The immediate treatment is just high flow high concentration oxygen to

8:32 rapidly displace it. >> And the second major poison we have to anticipate >> hydrogen cyanide or HCN. This is released from burning nitrogen containing polymers. So things like plastics and synthetic fabrics which are common in modern homes. >> Right? >> The HCN poisoning mechanism is similar to CO at the cellular level. It combines with the iron in the mitochondrial cytochrome A3 complex inhibiting the electron transport chain. So if CO stops the delivery, HCN shuts down the internal factory production line entirely. >> And they both present with that profound metabolic acidosis. >> They do. Recognizing both is vital. >> So we have chemical toxicity and swelling. But there's also a purely mechanical threat related to the full thickness burn itself. >> The mechanical block. Yes, this is a physical phenomena. When full thickness

9:17 skin is burned, the underlying collagen fibers coagulate. The resulting tissue, the cher is rigid, stiff, and leathery. It loses all elasticity. >> And if that's circumferential, >> if that cher extends completely around the chest wall, combined with the massive subcutaneous edema that follows, it can physically prevent the ribs from expanding fully during inspiration. This rapidly compromises ventilation and respiration and demands immediate surgical intervention. That sets us up for the massive systemic response, the shock and inflammation phase. Why does a localized burn lead to such catastrophic fluid shifts across the whole body? >> The systemic response is dictated by an immediate and massive inflammatory cascade. Heat injury and altered

10:02 proteins activate numerous pathways including neuropeptides, compliment activation, and most importantly, the activation of the Hegman factor. >> And the Hegman factor is the real initiator here. It's the initiator of so many proteins driven cascades involving thrombin and calocrine pathways which just quickly leads to a state of profound physiological chaos >> and the crucial clinical endpoint of all this system activation. >> Vastly increased vascular permeability. The endothelial cells of the capillaries effectively open up. Water salutes and high molecular weight proteins move rapidly out of the intravascular space and into the interstitial or extravascular space. >> The infamous fluid shift. >> That's it. This results in the massive generalized edema we see in severe burn patients. The volume of fluid lost is

10:48 directly proportional to the area of the burn leading to hypoalymic or burn shock. >> And that fluid loss is why we have that 15% TBSA threshold. Right. >> Precisely. We know that fluid loss sufficient to con burn shock requiring immediate intravenous resuscitation occurs when the burn exceeds 15% of the total body surface area in adults or 10% TBSA in the elderly and children. Below those levels, oral fluids are usually okay >> as long as they have salt. >> As long as they have adequate salt. Yes. >> Let's talk about the hidden dangers, the impacts on the GI tract and the immune system, which aren't always obvious in that first acute hour. >> The immune system takes a massive immediate hit. Large burns cause a profound reduction in cell mediated immunity. The patient is effectively immunompromised and therefore highly

11:34 susceptible to bacterial and fungal infections. >> Coming from where? often from the wound itself, the lungs, especially post inhalation injury or from invasive monitoring lines and catheterss. >> And the gut, which can often seem stable at first, can become a real source of trouble. >> It absolutely can. The systemic inflammatory response and shock lead to microvascular damage and eskeeia in the gut mucosa. This reduces gut motility leading to gastric stasis and impairs nutrient absorption. But critically that damaged mucosal barrier increases the transllocation of commensal gut bacteria into the systemic circulation >> providing a persistent and dangerous source of sepsis. >> Exactly. >> And that swelling in the gut can even compromise breathing compounding the primary respiratory problems. >> Yes. Through the development of

12:20 abdominal compartment syndrome. Gut mucosal swelling plus peritineal edema from the fluid shift increases intraabdominal pressure. This pressure pushes up on the diaphragm, physically splining it, >> making it harder for the ventilator to work. >> Much harder. You need much higher inspiratory pressures to achieve adequate ventilation, further stressing the lungs. >> Finally, let's revisit that peripheral circulation issue. The limbthreatening tourniquet effect caused by circumferential burns. >> This is a true surgical emergency. The rigid non-elastic full thickness cher on a limb physically restricts the underlying tissues. As the massive fluid shift and edema progress, the pressure beneath that fixed usher just increases relentlessly >> and it cuts off the blood supply. >> It compromises arterial and venus flow

13:07 causing limbthreatening eskeeia unless that cher is immediately relieved. >> That sets the stage perfectly for the acute management structure. So we're moving to section three, immediate care. If I'm the first responder or the receiving physician in the ED, what's the one thing that gets missed most often in that initial chaotic hour that can really change the patients long-term outcome? >> The thing most frequently done incorrectly or missed entirely is the effective immediate cooling of the burn coupled with the prevention of hypothermia. >> People forget about the hypothermia risk. >> They do. They focus too much on the fire and not enough on the physiology. The sequence of care must be deliberate. >> Okay, lay out that sequence for us. The key principles of that critical first hour. >> First, rescuer safety. Essential for electrical, chemical, or ongoing

13:53 hazards. Second, stop the burning process. Remove the patient from the source. Stop, drop, and roll for flame. >> Simple but vital. >> Third, perform a rapid primary survey, your ABCs, and look for other injuries. We can't miss coexisting trauma like fractures or blast injuries. Fourth, cool the burn. This is so critical. It provides powerful analesia and significantly slows the delayed microvascular damage potentially salvaging viable tissue. >> And how long and what temperature for cooling? >> Cooling should be for a minimum of 20 minutes and it's effective up to about an hour post injury. The water must be tepid around 15° C. And here is the crucial caveat. We must avoid hypothermia especially in kids and the elderly. That significantly compounds the systemic injury.

14:39 >> What follows cooling? >> Fifth, give oxygen. Anyone trapped in an enclosed space or presenting with altered consciousness must be placed on high flow oxygen immediately. Sixth, elevate. >> Life saving for an airway. >> Life-saving for a potentially burned airway if you sit the patient up and it greatly reduces swelling and discomfort in burned limbs. And seventh, analesia via opiates are preferred for larger burns. Avoid IM injections because of poor absorption and shock. >> Okay, so the patient arrives in hospital. The management immediately shifts into that standard advanced trauma life support structure, the ATLS approach. >> That structure is completely non-negotiable for any major trauma patient. A for airway, B for breathing, C for circulation, D for disability, E for exposure and environmental control

15:26 fighting that hypothermia and F for the formal calculation and initiation of fluid resuscitation. >> And the secondary survey has to continue. >> Absolutely. Ensuring all secondary injuries are identified. Before we dive into the specifics of A, B, and C, let's quickly remind the listener of the four major determinants of the outcome which guide the severity assessment. >> The severity is really dictated by the interaction of these four factors. The percentage of total body surface area or TBSA involved, the actual depth of the burns, >> superficial versus full thickness. >> Exactly. The presence of any inhalational injury, and finally, the patient's age and any pre-existing coorbidities. These factors determine whether we manage the patient locally or transfer them to a specialist unit. >> Which brings us to that crucial referral decision. Which patients must be

16:11 admitted to a specialist burns unit? >> The criteria are very clearly defined. This includes any suspected airway or inhalational injury, any burn that meets the threshold for fluid resuscitation. So that 15% in adults, 10% in a child, >> any patient likely to require surgery or burns to critical cosmetic and functional areas. So the face, hands, feet or perennium. Additionally, suspicion of NI patients at the extremes of age, high tension electrical burns or specific chemical burns like concentrated hydrofuloric acid all need immediate transfer. >> Let's focus on the airway. You emphasize that the swelling is a race against time with occlusion happening typically between 4 and 24 hours. What are the key indicators that we cannot wait for? >> We have to be proactive not reactive.

16:58 The classic symptoms, horarsseness, a change in voice, stridor and profound anxiety. These are very late signs of leneal edema. >> If you hear stridor, you're already behind. >> You're way behind. Intubation may already be impossible due to the severe swelling. >> So the strategy is early elective intubation ET. >> Exactly. ET is the treatment of choice for any suspected airway burn, especially if the patient has deep facial burns or a history of being trapped. This allows a calm planned intubation by an experienced anesthetist. The tube is usually kept in place for about 48 hours until the swelling starts to go down >> in the backup plan. >> If for any reason intubation is delayed or complicated, that equipment for an emergency criccoathyroidtomy must be at the bedside and ready for immediate use. No exceptions. >> Okay, moving to breathing. Once the

17:45 airway is secure, how do we manage the true lower airway inhalational injury? Initial suspicion is based on the history trapped in fire for more than a couple of minutes and physical signs like soot in the nose or oraferings. Symptoms of chemical pneumminitis like patchy consolidation on a chest x-ray can be delayed by 24 hours up to 5 days. >> And the management is primarily supportive. What does supportive entail here? >> It means maintaining a secure airway, rigorous chest physiootherapy and administering nebulizers with warm humidified oxygen. We monitor them clinically and with frequent blood gas measurements. For severe injuries that need ICU, we employ more advanced therapeutic strategies. >> Tell me more about that advanced strategy. It sounds like we are fighting two different battles simultaneously in

18:31 the lower lung. >> We are. We're fighting blockages and inflammation. The chemical injury causes the sliffing epithelium to mix with proteinatious exidate forming these thick obstructive fibbrin casts deep in the small airways. >> So you have to break those up. >> You do. Our strategy uses nebulized heperin to prevent the formation of those fibbrin casts. We enhance its effect by simultaneously giving the mucalytic agent an acetylcysteine which helps break up and clear the thickened mucus and debris. Bronco dilators like albuterol are also helpful. >> Let's shift back to the poisons CO and HCN. How do we confirm and treat them once a patient is in the hospital? >> For carbon monoxide, diagnosis is confirmed by measuring caroxymoglobin levels. If the level is above 10%

19:16 treatment is high inspired oxygen. We continue this for 24 hours to aggressively speed up the displacement of CCSC from hemoglobin. >> And for cyanide >> for hydrogen cyanide poisoning which you should suspect if there is severe metabolic acidosis without an obvious cause. The modern treatment involves a administration of hydroxycobalamin. It's essentially a form of vitamin B12. >> And how does that work? >> It binds directly with cyanide to form cyanocobalamin. This is a water- soluble non-toxic complex that is then safely excreted in the urine. It's a very rapid and effective detoxification pathway. >> Finally, addressing that mechanical block from the usher that compromises breathing. >> Right. If the full thickness burn is circumferential across the chest wall, it acts like a corset physically restricting lung movement. This shows up

20:02 clinically as rising CO2 levels and if they're ventilated, extremely high peak inspiratory pressures. >> And the fix is immediate. Immediate eststerotomy scoring cuts made through the full thickness of the burn skin down to the subcutaneous fat to allow the chest wall to spring open. This should immediately drop airway pressures and improve respiration. So now we have the patient breathing and stable. The next fundamental pillar is the assessment of burn size and depth because this dictates our entire fluid plan and surgical strategy. Why is burn size estimation the first question in a referral? It's the driving variable for resuscitation and transfer planning. It's measured as the percentage of total body surface area or TBSA. If you get this number wrong, you get the fluid rate wrong and that mistake can be

20:48 lethal. >> What are the quick estimate tools available to clinicians in the field? >> For smaller scattered burns, say up to about 10% TBSA. The quickest estimate is the patient's hand. The area from the distal wrist crease to the fingertips of the patient is approximately 1% TBSA. And then the classic, the Wallace rule of nines. >> The rule of nines is an excellent, quick, and reliable approximation for adults. It divides the body into sections representing 9% or multiples thereof. Nine for the head, nine for each arm, 18 for the front of the torso, 18 for the back, 18 for each leg, >> but it has some notorious limitations. >> It does. It tends to slightly overestimate the burn size, which can lead to over resuscitation. Crucially, it's inaccurate in obese patients

21:34 because the proportions change and it is completely unsuitable for children under 10. >> Which brings us to the gold standard, the London Browder chart. >> This chart developed in the 1940s remains the definitive assessment tool in specialist units. It's a detailed schematic that subdivides the body into much smaller units, allowing for incredibly precise percentage calculation, and its greatest utility is in pediatrics. >> Why is it so necessary for children? because the proportions change yearly. For an infant at birth, the head represents a massive 18% TBSA, twice that of an adult. The London Brower chart accounts for this growth. For every year of age, 1% is subtracted from the head and half a percent is added to each lower limb until about age 10. This accuracy is absolutely essential.

22:20 >> Once we have the size, the next crucial element is depth. What's the fundamental principle that determines how deep the injury goes? It is entirely a time temperature relationship. The two variables determine the severity. For example, skin kept at 44° C will suffer irreversible changes after about 6 hours. But if you increase that to 70°, it takes just 1 second. >> Give us a specific example that brings home the urgency of getting patients out of hot water quickly. >> Okay. Consider water at 65° C, which is common if a thermostat is set too high. 7 seconds of exposure causes a superficial partial thickness burn. Increase that exposure time to 45 seconds and you have a full thickness injury. That difference is huge. >> We need to be able to clinically differentiate these three key depths in

23:06 real time. Let's start with the least severe superficial partial thickness burns. >> This is the group A burn. Damage only extends into the papillary dermis. Clinically, you see a pink, moist, highly painful wound, often with blistering. Crucially, the capillary refill is clearly visible. The burn blanches with pressure. >> It goes white when you press it. >> Exactly. Sensation is normal. These are burns that heal spontaneously, usually within two weeks, with minimal to no scarring. >> Next, the deep partial thickness burn. >> This is group B territory. Damage extends deeper into the reticular dermis. The exposed dermis is less moist, often modeled white or red. And the key clinical sign is the capillary staining. It is fixed and does not blanch easily with pressure.

23:52 >> So, it stays red. It stays red. Sensation is reduced. The patient often can't distinguish sharp from blunt touch. These burns take three weeks or more to heal and almost always result in hypertrophic scarring if not treated surgically. >> And the most severe, the full thickness burn. >> Again, group B, the entire dermis is destroyed down to the fat or fascia. Clinically, the tissue is hard, rigid, leathery, thatcher we talked about. The appearance can be waxy white, mahogany brown, or charred black. There's absolutely no capillary return and you might see thrombos vessels >> and no sensation >> completely anesthetic because all the nerve endings are destroyed. You can stick a needle deep into it without pain or bleeding. >> So that distinction between group A and group B is the whole ball game for treatment planning. The quick takeaway

24:38 is if it blanches, we support it. If it doesn't blanch or it's white, hard, and numb, we are likely scheduling surgery. >> That is the core clinical decision. Group A heals spontaneously and needs local support. Group B, if left alone, underos months of degradation and poor secondary healing. Our goal is to surgically abort that toxic process and replace the burn tissue as quickly as possible. >> Now we move to section six, fluid resuscitation. Once we have that TBSA calculation, we have the fluid rate. What are the key thresholds? >> IV fluids are required for any adult with burns greater than 15% TBSA and any child with burns greater than 10%. If you are attempting oral resuscitation below those thresholds, you have to add salt solutions like dioralite because drinking plain water can lead to fatal

25:24 hyperetriia. >> And we must always remember that the fluid calculation starts from the time of the burn, not the time of arrival. >> That's right. Any delay in transfer has to be caught up. The crystalalloid approach, specifically the modified Parkland formula, is the most common method taught globally. >> Lay out the Parkland formula for us. >> Okay. The Parkland formula uses isotonic crystalloids like Hartman's solution. The calculation is TVSA percentage burn multiplied by the patient's weight in kilogram multiplied by 4. That total volume in milliliters is the target for the first 24 hours. >> And the timing is key. >> The timing is absolutely key. Half of that total volume must be administered in the first 8 hours postburn and the remaining half is given over the subsequent 16 hours. >> And children need that extra boost. >> Yes. Pediatric patients must also

26:12 receive additional maintenance fluid on top of the Parkland requirement following the standard 10020 milligadrial. >> The Parkland formula is the default, but you noted a major disadvantage. The eight-fold volume increase compared to colloid. Is that trade-off truly worth the simplicity, especially when we know excessive edema causes secondary problems? >> That is the major debate in burn care. The disadvantage of crystalalloids is the sheer volume required which significantly increases tissue edema. Historically some centers use the colloid approach like the mirror and barklay formula which uses plasma proteins often human albamin solution to provide that inward encotic pressure >> and that keeps fluid in the vessels. >> It does the mirror and barklay formula estimates the volume over 36 hours based on TBSA percent time weight time.5 to

26:59 equal one portion and six portions are then given over that 36-hour period. And why is the timing of colloid administration so sensitive? >> Because of that initial massive capillary leak. If you give colloid in the first 12 hours, the proteins just leak out along with the water, rendering it useless and potentially worsening odma later. So if you use colloid, it should preferably be given after that initial 12-hour leak phase. >> There's also the strategy using hypertonic saline. What's the advantage of that and why isn't it the standard? Hypertonic saline reduces fluid requirements by leveraging hyperosmolality. Proponents suggest it causes less tissue edema may be reducing the need for espherottomies. But the reason it's not standard is the significant risk of prolonged hyperonetriia and subsequent acute renal dysfunction. It requires

27:45 exceptionally careful monitoring. >> Regardless of the formula, the sources stressed that resuscitation is dynamic, not rigid. What is the key index we use for monitoring? >> Urine output UO is the primary index. We are targeting.5 to 1.0. 0 millm per kilogram of body weight per hour. >> If it drops, >> if the UO drops or we see clinical signs of hypoprofusion, we respond by giving a rapid 10 ml kg fluid bololis. Conversely, we must actively avoid over resuscitation. If the UO consistently exceeds 2 mlghgh, we have to decrease the infusion rate. >> And what role does lactate or acidosis monitoring play? >> Lactate levels and persistent metabolic acidosis are useful indicators of tissue hypoprofusion. A persistently raised lactate despite adequate urine output can indicate that

28:31 we've missed a systemic toxicity like CO or cyanide or that we are failing to adequately peruse critical organs. >> Before we move on, let's circle back to temperature control. Losing the skin means losing the body's thermostat. Why is this so vital? >> Hypothermia is extremely dangerous. It's part of the lethal triad of trauma alongside acidosis and coagulopathy. Allowing the core temperature to drop significantly increases the mortality risk. So the measures are immediate. Infusing only warmed fluids using external warmers like bear huggers and keeping a high ambient room temperature. >> We've addressed the acute life-saving measures. Now we move to section seven, treating the burn wound and the surgical strategy differentiated by our group A and group B burns. Let's start with group A, the superficial dermal burns.

29:17 What's the goal of wound care here? >> The goal is primarily protective. prevent the burn from progressing to a group B injury, which is usually caused by secondary infection, and manage the patient's pain. Since they heal spontaneously, we use dressings that provide a clean, moist environment. >> What are the common dressing options? >> We use simple dressings, Vaseline impregnated gauze or complex antibacterial films. Acticote, which uses silver nano crystals, is a popular choice because it provides effective antimicrobial cover and can stay in place for up to 7 days. and the high-tech choice BioBrain. >> Biobrain is an excellent example of a biosynthetic dressing. It adheres to the superficial burn providing an immediate flexible wound closure. The advantage is that it doesn't need to be changed. As the wound reepithelializes underneath,

30:03 the biobrain naturally lifts and peels off. We call it one-stop management. >> Now to group B, the deep dermal and full thickness burns. These require active surgical management. We need to circle back to that critical surgical emergency, the circumferential burn. >> Circumferential full thickness burns to the limbs or torso are non-negotiable surgical emergencies. The rigidity of the usher means it acts as a tourniquate, compromising peripheral circulation in the limbs or ventilation across the chest. >> How is the incision placed to perform this emergency escarottomy? >> The incisions must score the full length of the constricting cher. For the chest, we do two longitudinal cuts and two horizontal cuts to allow for maximum expansion. For the limbs, the incision runs the full length of the burn in the

30:49 mid- axial line, but the surgeon has to take extreme care to avoid major nerves and vessels. >> And cutting through this tissue isn't without risk. >> No, significant blood loss is possible. We must have cutting diiaothermia available and adequate blood products cross-matched and ready. >> Once the patient is stabilized, we move to the excision. The debate is often early versus staged excision. The strategic advantage lies with early excision. Why do surgeons rush to remove the entire burn? >> The goal of early excision, removing the entire cher within the first few days, is to exploit three critical physiological windows before the systemic inflammatory response becomes overwhelming. >> Let's define those three windows. >> First, the anesthetic window. Doing the major surgery before the lower airway injury decompensates, usually after 48

31:34 hours. Second, the hemodynamic window. Excising the burn early before the peak inflammatory vasoddilation and coagulopathy. Early removal reduces the release of inflammatory mediators >> which means less bleeding. >> Less blood loss during surgery and lower total fluid requirements posttop. Third, the bacterial window. Removing the necrotic deadsher dramatically reduces the bacterial load and the overall risk of systemic infection or sepsis. >> That makes a compelling case for early surgery. But not all units can handle massive immediate excision. What about the staged approach? >> The staged approach involves serial debridement over several shorter operating sessions in the first week. Maybe focusing on one limb at a time. This requires less immediate massive blood transfusion capacity. In between

32:20 the remaining cher has to be managed meticulously with antimicrobial dressings. >> What are some of those silverbased dressings used for temporizing deep burns? >> Silver is the primary antimicrobial agent. Silver sulfidine cream is common. Mapan acetate cream is also highly effective but can be painful and cause metabolic acidosis. And of course the act nanory barrier dressing remains a powerful tool. >> Regardless of the timing, the core principle of burn surgery is control. Hemodnamic control. >> Control is everything. These patients are often labile. Large excisions require meticulous monitoring arterial line central venus access. We have to maintain the core temperature strictly above 36° to prevent compounding clotting irregularities. >> And how do surgeons minimize blood loss

33:06 during the actual excision? >> We use a technique called tumissence. A dilute solution of adrenaline usually 1 to 1 million is injected subcutaneously into the tissues. This induces temporary vasoc constriction dramatically reducing bleeding. >> And then you excise down to bleeding tissue. For deep dermal burns, we do a tangential excision until we see punctate bleeding, confirming we've reached viable tissue. For full thickness burns, excision is deeper down to viable fat or fascia, followed by immediate application of a skin graft or substitute. >> Let's discuss the workhorse of burn coverage, the splitskin graft. >> Splitskin grafts are thin sheets of skin harvested using a dermatome. They consist of the entire epidermis and a variable proportion of the superficial dermis. The key advantage is that the

33:52 donor site because the deep dermal elements remain heals spontaneously. >> But there's a trade-off with thickness. >> There is the thinner the harvested graft, the greater the degree of secondary contraction post application, which is a major concern for function and cosmosis in joints and hands. >> How do surgeons maximize that finite resource of donor skin, especially in massive burns? >> We use meshing. The graft is passed through a measure a roller system that creates offset incisions allowing the sheet of skin to be expanded. Ratios can range from 1:3 up to 1:9 for the most extensive burns >> which gives more coverage and allows drainage. >> Exactly. It prevents hematoma formation beneath the graft which is the enemy of successful take. The trade-off however is the characteristic mesh pattern scarring. >> For burns over 50% TBSA, the problem of

34:41 coverage becomes acute. What are the specialized techniques used when you run out of donor sites? >> When donor site availability is exhausted, surgeons rely on techniques like harvesting very thin graphs to allow the donor sites to re-epithelialize faster for reh harvesting. We also maximize expansion through wide meshing or the highly specialized meek wall technique. >> What's that? >> This involves cutting the graft into numerous tiny 3x3 mm squares that are then spaced out on a carrier. This technique achieves maximum expansion ratios, minimizing waste and maximizing coverage. >> And what role do skin substitutes play in this massive coverage strategy? >> They primarily serve as temporizing measures. We distinguish between passive and active temporization. Passive is using temporary biological

35:27 cover like cadaavver skin which buys time. But cadaavver skin is scarce and is only effective if the patient is imunosuppressed enough to prevent rejection. Contrast that with the dermal matrix strategy active temporization. >> The dermal matrix strategy uses synthetic scaffolds like a biodegradable temporizing matrix or BTM. This matrix is applied to the excised wound and encourages the ingrowth of the patient's own fiber blast and vascular structures establishing a robust neodymises over several weeks. >> And then you graft on top of that. Once the matrix is fully integrated, the outer sealing layer is removed and a final much thinner split skin graft is applied on top of the newly formed dermis. The goal here is significantly better long-term scar quality and function. >> We've covered the acute management and

36:12 surgical phases. Now, we must look at post-accute care, which is essential for survival and long-term quality of life. Starting with pain and nutrition. Pain management is often complex and must be continuous using IV infusions transitioning to oral tablets. Critically, patients need powerful short acting medication right before painful procedures like dressing changes and physiootherapy. >> And the catabolic state of a major burn patient is a massive metabolic challenge. >> It is the body in extreme overdrive. Major burns are profoundly catabolic. For any adult burn over 15% TBSA or any child over 10%, nutritional requirements are massively increased. >> And for big burns, >> for burns 20% TBSA or greater, high

36:57 calorie, high protein tube feeding NG or NJ must start within 6 hours of injury to reduce gut mucosal damage and infection risk. Critically, the hyper metabolic catabolic drive persists as long as the wound remains open. So the single most significant factor in reversing it >> is the rapid excision and stable coverage of the burn wound. That's the off switch. >> Infection control is the everpresent threat once that barrier is gone. >> The challenges are immense. The patient is immunosuppressed and there are large portals of entry. Control relies on strict institutional policies, rigorous handwashing, regular bacteriological surveillance of the wound and central lines and a close liaison with microbiology for guided antibiotic selection. And fever is a less reliable sign. >> It is a major burn resets the body's

37:42 core temperature, often slightly above 37. Therefore, a fever is only clinically significant if it exceeds 38.5° C. You have to look for secondary signs of sepsis. >> And rehabilitation physical and psychological must start immediately. >> Day one, physio and occupational therapy are vital. We emphasize elevation to reduce swelling and spintage to prevent contractions in key functional areas. Keeping the hand in a position of function, the knees and extension and the axel and abduction. Supervised movement usually begins after about 5 days. >> And beyond the physical scarring, we have to address the psychological impact. >> A major burn is an overwhelming terrifying event. Patients commonly suffer normal post-traumatic reactions. Intrusive memories, heightened arousal,

38:28 avoidance behaviors, early psychological intervention in developing coping strategies are vitally important. >> Finally, delayed reconstruction and scar management. The long game. When we talk about this, we have to pause and reflect on pioneers like Sir Archbald Macko and Sir Herald Delg Gillies. Their work with the Battle of Britain pilots defined this entire field. They moved burn care from immediate survival to long-term quality of life. They pioneered the meticulous staged reconstructive effort necessary for maximizing function and appearance. They taught us that early focus areas must be prioritized specifically around the eyes. >> To prevent blindness, >> eyelids must be grafted at the first sign of difficulty in closing to prevent exposure keratitis and loss of the cornea. Later the focus shifts to

39:13 establish contraurs causing loss of movement particularly in the hand and axilla. And what are the modern surgical techniques used to release those contracted scars? >> For releasing a single linear band, we use local tissue rearrangements like zlasty. For wider bands, we may transpose local flaps. Tissue expansion is a fantastic technique for treating specific areas like burn alopecia. For very broad or circumferential contraurs, the definitive treatment is incision and replacement with robust vascularized tissue >> and managing scar hypertrophy. the raised red itchy scars. >> Hypertrophy responds to sustained pressure. So pressure garments must be fitted and worn continuously for anywhere from six to 18 months. Silicone patches and intralegional steroid

39:59 injections also help speed up scar maturation and pharmacological treatment of the chronic itch is an essential part of therapy. >> We must carve out time for non-therrmal burn injuries starting with electrical injuries. The sources divide this into low and high voltage with the threshold at 1,00 volts. What's the fundamental difference? >> Low tension or domestic injuries generally don't cause significant deep conduction damage. They result in small deep contact burns, typically on the fingers. The main danger here is cardiac arrest from the alternating current interfering with the heart's pacing rhythm. >> But high tension injuries are exponentially more destructive. >> They are massive trauma events. Damage comes from three sources. The intense flash, the flame igniting clothing, and the current itself. The current causes massive subcutaneous tissue and deep

40:44 muscle damage along the path between the entry and exit points. >> And this carries severe risks. >> Yes. Rapid onset of compartment syndrome requiring urgent fasciottomies and massive release of myoglobin from destroyed muscle. This myoglobin causes myoglobinura and subsequent acute renal dysfunction. >> So in these specific patients, the fluid monitoring target changes. >> Absolutely critical point. For high attention injuries, the normal UO target is insufficient. We have to push fluids to maintain an unusually high urine output of up to two millibl per kilogram per hour to aggressively flush out the myoglobin and prevent permanent kidney damage. >> Next, chemical injuries damage from corrosion and potential systemic poisoning. What are the crucial initial steps? >> First is rescuer safety. Then identify

41:30 the state of the chemical. If it's a solid powder-like elemental sodium or phosphorus, it must be removed with forceps or brushed off before irrigation >> because water can make it worse. >> Water can cause a further massive exothermic reaction. Most common injuries are liquids, acids or alkalies, which require copious sustained lavage with water. >> Alkali versus acid, which is generally more destructive. >> Alkalies are generally more destructive because they cause liquefosis, which allows deeper tissue penetration. Acids cause coagulation necrosis which creates a protective cher that can limit penetration but both require massive irrigation especially if the eye is involved. >> There is one acid that requires highly specific dedicated management. Hydrofluoric acid. Why is this so

42:17 exceptional? >> Hydrofluoric acid is unique because the acid burn is secondary to the profound systemic toxicity. The fluoride ion rapidly penetrates the skin and tissues chilating calcium and magnesium. This process causes agonizing pain and can lead to systemic hypocalcemia and cardiac arhythmias. >> And the specific treatment >> for mild burns topical calcium gluconate gel is used to chilate the fluoride. For more severe burns, it's treated with regional anesthesia blocks beers blocks containing 10% calcium gluconate. If the concentration is very high, say over 50%, the systemic threat is so immediate that the patient requires acute early surgical excision. And finally, let's briefly touch on radiation and cold injuries. >> Localized radiation damage requires initial conservative management. If deep

43:04 ulceration occurs, excision and coverage with a vascularized flap is necessary. For whole body radiation exposure, acute skin desamation indicates a lethal dose and management is entirely supportive. For cold injuries like frostbite, initial treatment is rapid rewarming and a 42° C bath. Assessing the true depth is difficult early on, so surgery is always delayed until absolute demarcation is visible. >> That was an incredibly thorough guide taking us from the immediate risk factors and the specific pathophysiology right through the entire structured process of burn care. We synthesized the ABCDEF structure, emphasized the critical need for early intubation, detailed the calculation tools like the London Browder chart, and clarified that fundamental distinction between group A and group B management. did and we also

43:51 covered the new directions that are driving the field forward. The sources note that recent advances are focusing intensely on sophisticated skin substitutes and cultured autous FIN essentially taking the patients own cells and growing them into a sheet to improve long-term outcomes. >> So, what does this all mean for you, the clinician, when the acute crisis is over? >> Well, we've established that the most significant factor in reversing the patients catastrophic hyper metabolic and catabolic state is rapid excision and stable wound coverage. That surgical intervention ends the physical leak and the massive inflammatory trigger. However, the patient remains pathologically hyper metabolic until the wound is fully healed. >> So, the fire is out, but the engine is still running red hot. >> That's a great way to put it, and it raises an important question for the future. While fluid resuscitation and

44:37 surgery are crucial, how might future advancements in metabolic control, perhaps specific pharmaceutical interventions targeting the hormonal cascade, further reduce mortality and dramatically improve recovery in the weeks after successful resuscitation? How do we address that persistent destructive catabolic drive? That is the challenge that lingers long after the acute emergency has passed.