Moderator:
Tonight's speaker is Steven Epstein, DVM, DACVECC.
Dr. Steven Epstein attended the University of California at Davis for his Doctorate of Veterinary Medicine and did his residency there, becoming board certified in 2010. Dr. Epstein is now an Associate Professor of Clinical Small Animal Emergency and Critical Care and chief of that service at UC Davis. His research interests are in CPR, diagnostic testing in the emergency room, and antimicrobial resistance patterns as well as chairing the disaster response committee which was engaged in the California wildfires of 2015 and 2017.
Welcome, Dr. Epstein! The floor is yours.
Steven Epstein:
I'm pleased to come and talk to the group about small animal fire-related injuries. My background in this started in 2015. It was actually IVECCS week, and, as you can imagine, most of us are running a little light on staff that week and both the Valley and Butte fires kind of broke out around us. It continued on in 2017 with the Napa/Santa Rosa fires, and then more recently with the Camp Fires in 2018.
All told, I’ve probably been involved in the treatment of about 120 to 130 cats that have been injured in fire-related injuries. I've also had to deal with it from a disaster response, which gives me, I think, a little different perspective in dealing with things on an individual basis.
For an introduction, the way I break up fire-related injuries for myself is I kind of think about them on the most emergent basis, which generally relates to the smoke and the inhalation injury that we see there. That is in the first few hours we really have to worry about those sorts of things.
Then, I think about what are the patient's urgent injuries. These are usually the first day, related mostly to the thermal burns that they’ve suffered and these could be anywhere on the body. Then I have the delayed onset of injuries, which, obviously, we’re still dealing with skin wounds during that period. Then there’s a whole host of other injuries that our experiences in the wildfire has given us some insight that are not really well documented in veterinary medicine. There’s actually relatively zero literature on wildfire-related injuries. I will just briefly cover at the end some of the ocular, cardiac, and coagulation injuries that we can see in these patients as well.
When I think about the emergent wildfire or smoke-related injuries, it’s mostly that smoke inhalation from a variety of gases. In human literature, it would show that this is probably the leading cause of acute death. Oftentimes, these are animals that may not even make it to our clinic, or they are animals that might be in a pretty severe state when they get there from smoke inhalation.
The main smokes that we worry about are carbon monoxide and cyanide. These are definitely gases that can be easily absorbed across the respiratory tract and into the bloodstream and create a variety of different sorts of injuries that relate to them.
There are actually quite a few different types of gases that can be liberated in a fire, and it really is dependent on the material that is burning. We do have a lot more toxic gases that are in house fires where there’s a variety of plastics in that type of burn, versus in a wildfire there’s probably mostly carbon monoxide and cyanide.
The type of smoke inhalation injury that you might see is going to be a little bit different in whether it’s a wildfire versus a house fire. The frequency of it is actually probably going to be different as well.
When we’re dealing with house fires, animals tend to be trapped indoors, and there is a higher proportion of gases that they breathe in versus when they’re out in a wildfire situation. Outside, the atmosphere being much more open, tends to bring those gases into the higher atmosphere and they are in less concentration.
I can say that in the three wildfires that we’ve been involved in, I’ve only had two or three cats and zero dogs that have actually had a smoke inhalation type of injury that’s not related to actually the heat of injury. I dealt with lots of dogs that have had smoke inhalation from house fires.
Looking at carbon monoxide first – it is a gas as you can see there. It’s just made of one molecule of carbon and one molecule of oxygen. It’s produced by the burning of any carbon-based material that is liberated pretty easily from things like wood, cotton, and paper. Even some of the plastics as well will liberate carbon monoxide when they’re burned.
This particular gas itself is not an irritant as opposed to many of the other plastics that are burned and create irritant-type gases.
The toxicity that comes with this is after it’s been absorbed into the bloodstream. If you remember back in vet school, we all know that carbon monoxide reversibly binds to hemoglobin molecules. It also does this with a much higher affinity than oxygen can bind to hemoglobin. The reports are that it has anywhere from about 220 to 250 times the affinity for hemoglobin than an oxygen molecule has. This will definitely displace oxygen off that hemoglobin.
When we see carbon monoxide poisoning, we know that once that carbon monoxide binds to the hemoglobin, about 50% of the oxygen molecules will be removed from it, so two of the four heme groups are bound. That markedly the left shifts the oxyhemoglobin curve that you can see here.
The blue line is the normal oxygen dissociation curve that we’re used to seeing. Once you have carbon monoxide that is bound to those heme groups, it’s so far shifted to the left there.
What this does is it prevents the offloading of oxygen to the tissues. That creates tissue hypoxia, so our actual oxygen content in the blood is low, and it can’t dissolve them through to the cells that need it. This then creates CNS dysfunction. We know oxygen is needed for the brain to function, so that lack of actual oxygen at the level of the brain is what creates the direct CNS dysfunction effects.
There are also a large number of indirect toxicities that carbon monoxide can create as well. Some of these include actual cellular toxicities, the mitochondrial dysfunction that occurs in this disease. It also increases nitric oxide production. One of its more toxic effects that can occur later and it starts early, is it causes white cells to migrate into the brain, and this creates kind of a leukoencephalopathy among some other things in the brain.
Where we actually start to see this occurring is probably at about a carboxyhemoglobin level of about 15%. Less than that and we’re unlikely to see clinical signs. Levels upwards above 70% and 80% are highly associated with death.
We have our first poll here. The question is: What is the gold standard to identify carbon monoxide poisoning in a dog or a cat?
What is the gold standard to identify carbon monoxide poisoning in a dog or cat?
26 (67%) Arterial blood gas
0 (0%) Standard pulse oximetery
9 (23%) Co-oximetry
4 (10%) Physical examination
Steven Epstein:
We have a large number of answers here.
How do we diagnose carbon monoxide? There are a couple of different ways. Arterial blood gases are actually not ideal. This can reflect a smoke inhalation injury and a decreased ability for oxygen to be reabsorbed across the respiratory epithelium. Since the main mechanism of toxicity or carbon monoxide is a dyshemoglobinemia, it doesn’t generally show up on just arterial blood gases.
With venous blood gases, we might find a low venous oxygen tension, and that’s because more is being absorbed by the tissue, but, on the arterial side, our PaO2 is typically normal. The lack of oxygen delivery might be associated with increased lactate or hyperventilation on an arterial blood gas.
I notice that very few people chose pulse oximetry, which is good. We know that when we’re doing standard pulse oximetry, which uses the two wavelengths of light and infrared spectrum, it does not actually tell us if there’s carboxyhemoglobin present. One of the things to note though, is Masimo now makes something called the Rainbow Pulse Co-oximeter. This is a device that has a different probe. It has more than just the two-standard sensors of light, and then a special machine that can look at that and integrate the data. If you have this information, you could actually get a measurement for carboxyhemoglobin in the blood. It could also measure methemoglobin.
Unfortunately, if you have this technology but you don’t have the correct probe, the machine will give you a number if you set it to do so for carboxyhemoglobin. We had one of our house officers in the middle of the night trying to use this, and they were getting 12% to 15% on the patient. However, we don’t actually have the software in the machine to run it, so it is a device that will give you a reading even if you don’t have the standard equipment for it. If you do have the appropriate probe and the appropriate machine, it is actually a validated method to measure carboxyhemoglobin.
The gold standard, however, is co-oximetry. This is measured off the sample of arterial blood where you could directly measure things like the percent of carboxyhemoglobin, it’ll measure methemoglobin as well, and it will measure the amount of oxygen saturated in arterial blood or SaO2. The downside of these machines is they are human based only and that there’s not a commercially available veterinary co-oximetry device out there. There used to be one that was made that would measure both cat and dog and a variety of large animal species. That is not supported any more. Human co-oximeters probably will accurately measure carbon monoxide and methemoglobin as well, however, but they’re not as good for measuring the SaO2.
If we were to look at a physical exam, the one thing we might see is bright red gums but it is not a very reliable finding.
We know that once our patients are suffering from carbon monoxide, we will potentially see CNS dysfunction. The mainstay of therapy is actually just oxygen. The way this works is you increase the PaO2 in the blood, and then this competes with the carbon monoxide molecule. Then theoretically you will have less carbon monoxide on our hemoglobin and more dissolved in the blood, which can be breathed out once that patient is not having inspired carbon monoxide.
Half-life of carbon monoxide bound to hemoglobin is four to six hours if the patient is breathing room air. We know that if you can put that patient in a 100% oxygen environment, the half-life is reduced to 40 to 80 minutes. This is one of those things that I think is important for those of us who also train first responders in the field – one of the biggest things they could do if they come across a pet in a field is administer oxygen while they’re waiting to get that pet transported to a veterinary clinic. Early oxygen therapy is probably more efficacious at getting that carbon monoxide off and preventing secondary injuries and those indirect effects that we talked about.
There’s been a fair amount of research that goes into looking at hyperbaric oxygen as well. There’s been some evidence that it can actually delay some our delayed onset signs, or alleviate our delayed onset neurologic signs that could occur. It definitely will reduce the half-life of carbon monoxide as well. However, the time it takes to get a patient into that and the treatment is probably not recommended for routine cases as well as not being available for most of us.
One of the things that is interesting about carbon monoxide is that once you do get them through this initial hypoxemic event, they can develop, days or weeks later, this delayed onset neurologic effect. This is very variable in its manifestation. This could be anything for humans where they report cognitive effects. In veterinary medicine, what we’re more likely to see are gait deficits or ataxia. In humans, they report sensory deficiencies as well.
In a large scale analysis, anywhere between 10% to 30% of humans that do experience carbon monoxide poisoning will show effects of these delayed onset neurologic signs. There’s only one retrospective that looked at this in dogs, and it’s not really been documented in cats, but there’s no reason to think it wouldn’t occur. Five of the 11 dogs in that retrospective showed delayed onset neurologic sequelae, and some of those were permanent where those animals never had normal gaits for the rest of their life. It’s something that if I do believe I have a patient that has carbon monoxide, I do warn the owners about this so they can be prepared in the future to look for it, and then they’re not unhappy with me later when that does occur.
Some of the respiratory injuries that can occur in the emergent phase could be actually thermal related. You can see a picture here of this cat that was involved in a wildfire. In addition to the facial and ear burns, you can see burns around the nasal planum, and the upper respiratory tract itself might be affected. This is either from toxic gases that they might breathe (that could affect the respiratory tract) or actually due to the heat injury itself.
We know that a lot of the heat is dissipated in the upper airways, and this then is either in the nasal cavity, the oropharynx, the larynx or the proximal trachea. By the time these gases make it down to the lower airways and at the level of the alveoli, that heat has generally been dissipated.
The way these injuries manifest is often with nasal passageway obstructions; this could be from mucus plugging within the nasal cavity to actually swelling of the mucosa so that the animal can’t breathe through its nose. Occasionally, we’ll run into thermal injuries at the level of the larynx where they actually have a severe amount of laryngeal edema that could prevent them from breathing completely. This is a rare occurrence but can actually necessitate a tracheostomy in the worst-case scenario.
We know that cats don’t like to breathe through the mouth, but, occasionally, when you get that smart cat with a nasal obstruction, they will just open their mouth and breathe through there. One of the things with cats being very odor driven for feeding, is their ability to eat will be compromised. Supportive care when we see animals with these upper airway injuries is to really closely monitor their food intake and consider feeding tubes early in them. Quite a few of these cats themselves will decide they don’t want to eat just because of their nasal cavity disease. There’s not a lot you can do for them other than nebulization. This is something that is really a lesson learned, that to do intense care here where we will nebulize q 2 hours and really clean any crust that comes off their nose. This really helps those cats breathe easier and heal better, and I think it is more likely they will eat in those situations.
In the lower airways, we may actually see a pulmonary injury. This is generally not thought to be due to heat but toxic substances.
Classically with smoke, you would see a non-cardiogenic pulmonary edema that’s formed. This could be severe and a cause of acute lung injury. It could a cause of an ARDS-like syndrome, and this could cause a massive amount of pulmonary dysfunction, either needing oxygen therapy or mechanical ventilation.
Occasionally, you will see airway sloughing and cast formation. These could cause plugging of some of the large airways. This could be a mainstem bronchus that’s plugged or a single lower airway, so it creates a lot of V/Q mismatch. In its most severe case, it could cause necrosis of the airway, and then that in itself could lead to collapse of those lower airways, leading to inability to ventilate.
Depending on what chemicals are actually liberated, there could be a chemical pneumonitis. This is something that generally is thought of as kind of a ventral alveolar dependent situation similar to what you think you would see with an aspiration pneumonia but generally more diffuse.
At presentation, these animals generally do not have a bacterial pneumonia; however, when you compromise the upper airway defenses or you have this chemical pneumonitis, there could be a secondary bacterial pneumonia that develops. Initially, we generally don’t cover them with antimicrobials. However, if they show secondary signs of inflammation and pneumonia that may develop, that’s when we’d cover them with antimicrobials.
This is a recent house fire victim that we dealt with. This is a 4-year-old Keeshond that was rescued from a house fire. They think the dog probably actually inadvertently started the fire by knocking a lamp off the table. The fire was mainly confined to one room in which the dog was stuck in. Firefighters came on the scene and found this dog to be unconscious, and they gave him oxygen therapy. Initially, he responded quite well in that we went from an unconscious to a conscious state. These radiographs were taken probably about six hours after the initial injury when he was found. You can see that there’s this patchy, ventrally dependent alveolar pattern that is kind of diffuse throughout all lung fields. This is consistent with a chemical pneumonitis.
This dog was hospitalized initially on oxygen therapy as his pulse oximeter was mildly low. Over the next 48 hours, he started to show signs of airway collapse. If you notice, we have some early signs here. There is a redundant dorsal tracheal membrane but its overall tracheal lumen is quite narrow. His bronchi were okay, but he had a lot of signs of what we would say was collapsing airway disease. Ultimately, he was placed on a mechanical ventilator because of his airway collapse. We were unable to ventilate him. We had large positive pressures but we could not actually get gas down to his lower airways.
When we did a postmortem (this is kind of a striking image), you can see in his lungs that we have – the more reddish looking lungs here, but his lower airways showed in the parenchyma a lot of infiltrate, which was probably worsening with time. The most striking airway here is in the trachea. We know airways should never be black, but if you could appreciate that there is this kind of necrotic airway that has complete collapse of it. Unfortunately, with an endotracheal tube, there was absolutely no way that we could put enough pressure in to get air into his lower airways. It was amazing that this dog was doing as well as he was prior to his intubation.
Ultimately, what the path report showed was a severe, diffuse, acute mucosal necrosis of the dorsal tracheal membrane, and then in the lower airways and bronchi, there was a lot of intraluminal mucosal sloughing and obstruction.
I think this was a combination of both a thermal injury and a chemical pneumonitis where the lower respiratory tract just basically died, and there was zero chance for his recovery. This is just, unfortunately, an example of worst-case scenario.
Moving on then to the thermal injuries that are going to be more related to the skin, remember that our injuries that we can get from burns could either be electrical burns, chemical burns, or radiation burns. Primarily, when we’re talking about fires, we’re going to be talking a thermal injury. Where you find them on the body is going to be dependent on the situation. Whether this was a house fire or a wildfire versus that heating pad where an animal has had a heating pad under them at the time of surgery might present quite differently.
With wildfires, what we typically see are injuries to the feet, the face, and then the dorsum as ash may rain down on them, but, far and away, feet and face are the most common.
From our different experiences with wildfire, we actually had kind of what I would say is a socioeconomic distribution to burns. The cats that were in Napa generally were more well cared for. They had higher body condition scores and so that meant they had higher fat content on their abdomens. We actually found a significant number of burns to the ventrum in those cats, versus in our Valley and Butte fires where we had animals that tend to be thinner, we didn’t see the burns to the abdomens just probably because they didn’t hang down enough to reach the ash that the animals were going through.
We have our second poll here. The question is: What is the definition of a first-degree burn?
What is the definition of a first-degree burn?
38 (86%) A superficial injury limited to the epidermis
6 (14%) A partial thickness injury only superficially affecting the dermis
0 (0%) A full thickness injury affecting all layers of the skin
0 (0%) An injury affecting the tissue down to muscle and bone
Steven Epstein:
It looks like most people have this correct. It is indeed a superficial injury to the epidermis.
When we classify burn injuries, they are to the skin. Our least affected one is the first degree, and this is just the epidermis affected only. You can see a diagram here where we have just the layer of epidermis and cells here. Then the normal skin has dermis with collagen, fibroblasts, and all of those mediators, subcutaneous tissue, and then muscle below it. A partial thickness burn (just the epidermis) is first degree.
I actually struggled to find a picture of that because this is not too common in fire-related injuries. The area right here above the cat’s right eye where you can notice is just a first-degree burn, and it’s characterized by reddened skin and is generally considered painful to the touch. This would be an example of a first-degree burn.
When we have second-degree burns, these are generally superficial or partial thickness wounds that do actually get to the dermis, so now our entire epidermis has been affected. Part of the thickness of the dermis is there but it’s not down to the subcutaneous.
This is charring of the skin which generally will slough. This is when they’re getting more painful. Now we’re going to start to see plasma leakage and hair follicles, or, if it’s feet, the very bottom of the pads will be spared.
When we’re looking at a paw pad, which is where we very commonly see our burn injuries, this area right here in these digits are probably partial thickness, versus right down on this carpal pad of the right pelvic limb. We’re starting to get complete thickness there. This might be a third-degree burn, but, overall, most of these feet that are shown here would just be second-degree burns and that partial thickness.
When we get to our third-degree burns, this is where we have full thickness of the dermis. That entire epithelial and dermal lining is burned. Generally, we have black or yellow skin. All of the hair follicles have been destroyed. The pad has been destroyed, and those nerve roots actually have been destroyed as well, so these might not actually be painful, where first- and second-degree burns tend to be more painful.
What this looks like in a foot is kind of this charred pad. These brown pads are completely affected. We can kind of see some yellow necrotic skin developing around the pad. Very far back at the edge of the pinkness there might be just a little bit of first-degree burns here. There are some second-degree burns as well and then over the paw pads themselves in this cat. This is kind of a classic third-degree burn.
Fourth-degree burns occur as well. This would be kind of a classic example here. It’s when you have a full thickness burn. Remember that dermis and epidermis are burned, but we’re also affecting the subq and then the underlying muscle or bone. The red arrow here is pointing at the process in P3. We’ve actually burned all through the soft tissues and we could find that that bone is sticking out. We know that this is going to be a much more severe case, and we are going to have to be considering more aggressive debridement. We’re going to have to consider removing bone or, potentially, if this is muscle that’s involved, removing muscle.
Other terminology that is talked about in burn injury is eschar. Eschar is dead tissue that results from a full thickness burn. This is different than a scab. Eschars are considered bad and dead tissue versus scabs, which are what can form when you have crusting over an open wound from either serum or blood that’s hardened over an injury.
There’s a little bit of crust here in this kind of pink tissue that’s located at the top of it, versus all of the black tissue and 90% of what you’re seeing on the ventral part of this cat’s abdomen is eschar.
Why does classifying wounds as far as burns go helpful? Well, part of it is expectant healing times. A plain, first-degree burn is probably going to require less care and, generally, will completely heal in about one week’s time.
When we’re dealing with second-degree burns, these generally are going to take between two and three weeks to heal depending on how large they are. Sometimes they will take more than three weeks, but average healing time is going to be in the two- to three-week range.
When we’re dealing with third- and fourth-degree burns, these could be anywhere from classically three to eight weeks to, potentially, a months long process. We have a couple of animals in our hospital that we are still treating, and we’re coming up on the eight- to nine-week period. Just because of the huge amount of surface area that’s affected, we’re projecting out another two to three months for them in order to completely heal.
I think when we’re dealing with client-owned animals, setting up these expectations ahead of time is really important so that they don’t think this is going to be a short process when we’re dealing with third- and fourth-degree burns.
When we have second- and third-degree burns (this is probably not as important in first-degree burns because we’re not exuding a lot of plasma, and we’re not dealing with huge fluid losses that can go with that disease), calculating the total body surface area affected is useful because this is going to help us then later think about how much fluid the patient needs in that first 24 hours.
There’s the Rule of 9’s, which has been around for quite a while where the body is broken up into one-ninth. The head and neck as a whole count as 9%. Each individual forelimb counts as 9% for a total of 18%. Each back limb on its own counts for 18% or 36% surface area. The thorax on its own is another 18%, and the abdomen on its own is 18%.
Then you estimate the amount of each of these individual areas, and then add them up and come up with a total body surface area. This is probably not the most accurate method, but it is relatively simple.
There is another system that is kind of talked about. This is in some surgery textbooks. This is where you estimate the total body surface area based on a credit card sized template. You have a credit card and then count the number of cards that you think are affected. This is then transmitted into a surface area of 0.45/m2, and then you would calculate based on the weight of the animal and the overall percent surface area that is affected.
This, again, is not terribly difficult to do and is potentially more accurate and might be more helpful for us when we’re dealing with burns that are in that second- to third-degree nature.
We have this cat here. I have a poll. Based on this picture, what percent of surface area do you think will be burned?
The cat pictured in this photo will have a calculated TBSA burned of XX?
4 (10%) <9%
29 (69%) 18-36%
8 (19%) 36-54%
2 (5%) >54%
Steven Epstein:
I think that probably most people chose the correct answer here.
If we go by our Rules of 9, we have part of all limbs affected. Our bandages are hiding things here, so we have probably at least half of each of our thoracic limbs affected, which counts for then probably 4.5% each since they’re 9% total. That gets around 9%. Then we have a small amount affected of each of our back legs as well as a little bit of our head affected.
The reality is this cat is probably going to be somewhere around that 18% to 20% affected. We’re a little limited by that bandaging, but that would probably be the correct amount.
Again, why do we want to calculate this? There are two aspects of this disease. Why? One is it helps us predict if there are going to be future metabolic derangements in this animal. Once we hit more than about 20% of the body surface area that’s affected by a second- or third-degree burn, it’s more likely that animal is going to have metabolic derangements that are associated with it. The higher the percent of body surface area affected, the more likely and severe those metabolic derangements might be.
The other part, again, is fluid needs. Remember those burn wounds that are affected have a lot of plasma. That’s the fluid that is high in albumin and high in electrolytes that they’re going to lose. Traditionally, we replace that fluid loss with an isotonic crystalloid. There are cons of using albumin-containing fluids like plasma or synthetic colloids in the first 24 hours. Almost all of what you give is going to be lost back out through the skin. It’s better to save those products for later.
The way the fluid anticipated needs are done is we would calculate 4 mL/kg per percentage of surface area that has a second- or third-degree burn in the first 24 hours. Generally, half of that total amount would be administered over the first eight hours when fluid loss is at its highest. The remainder of that fluid is administered over the next 16 hours, so that total of 24-hour period.
This in all the human studies is shown to be a good indicator for the amount of fluid that they’re going to need and then prevent that patient from becoming hypovolemic.
In the initial phase, again, so in our urgent phases of this, pain control is going to be key. As I talked about earlier, with third-degree burns, you may actually burn the nerve roots themselves, so they’re not painful, versus when you have extensive first- and second-degree burns, the animal might be quite painful, and it could be quite severe in nature.
In the first 24 hours, generally, we’d be recommending full mu agonists. There are some animals, however, that may not be that severe where you would consider using a partial mu agonist, but, in general, our recommendations are to treat them in the initial phase with full use of morphine, fentanyl CRIs, or methadone – whatever might be available at your clinic.
Other things that can be helpful will be topical analgesic creams. These are probably going to depend on the species, but these can be made up with things like ketamine, they can be made up with lidocaine, they could be made up with NSAIDs. We do know that these burn creams that could be made up often are absorbed through the skin, and they reach systemic levels. There are some concerns in, say, cats about using things with lidocaine because we’re worried about toxicity, or, if you were to put a non-steroidal in it, could that potentially result in a renal injury.
In cats, I typically have not used any of these burn creams. We rely on systemic analgesia, but, in dogs and other species in our clinics, they are commonly being used.
In the long term for pain control, we rely on partial mu agonists. Part of this is, when we’re dealing with a disaster situation we’re doing large volumes, and to help reduce our nursing care time, we’ve used Simbadol. We found this to be a pretty effective analgesic in cats with burns to both their face and their feet. Generally we’re transitioning them kind of in the 48- to 72-hour period to the Simbadol off our full mu agonist.
The way we go about this, since this is a 24-hour drug, is we time it to be after their bandage changes. The Simbadol itself is waning, and we’ll use a full mu agonist as part of their sedation plan for their bandage change, and then give them the Simbadol after we are done with that. That will then take care of the analgesia for another 20 to 24 hours until our full mu agonist is then again needed for bandaging. We give them one dose of a full mu agonist a day and then Simbadol to follow for that remaining 24-hour pain control.
Once we’re out of the first few days and we have a good handle on their fluid needs, and they’re hopefully eating and drinking well, we’ll consider doing non-steroidals in cats and dogs at that point. Onsior in cats or things like carprofen in dogs could be very useful analgesics as well.
Oftentimes, these animals do need weeks long of analgesia depending on the severity of the burns. Some of the cats now that we currently have, our eight-week outs are not on any analgesics, but they seem to be doing quite well without them. They were on and off them for a four- to five-week period, which does introduce the concept of opioid dependency. Those animals do probably need to be weaned off their opioids so that they don’t get withdrawal symptoms. It’s not something that’s been well studied but something to consider in those cats that are on long-term opioid analgesics that need some tapering of those medications.
When we talk about the principles of wound care for these types of burns, the way I think about it is initially they need to have daily evaluation of those tissues. Once we get into a more static phase, they could be evaluated every other day or every third day as the wounds progress in a more reliable fashion.
Debridement of dead tissue as needed is really, really important. What we found is people tend to not want to do a lot to these wounds as far as removing the dead tissue with surgeries. Once we get into the first couple days, it is really important to remove the dead tissue because that will help the patient heal faster.
Infection prevention is important. Most of these wounds could be handled with topical therapy, and they don’t need systemic antimicrobials. Before there is a good granulation bed, which we know is very resistant to infection, there may need to be systemic antimicrobials present. Those could be broad spectrum or considering antipseudomonals as pseudomonas is a bacteria that we commonly find when we’re dealing with burn injuries.
Thinking about their nutritional requirements is also really important. As I said, we can lose a lot of albumin and so that could cause decreased wound healing. Not only do we lose albumin, but we lose a lot of other factors that promote wound healing. That albumin is just a marker of such, so making sure they’re in a good nutritional state is important.
Our nurses play a huge role in this, so just general nursing care. Sometimes these animals don’t want to get up and get out of their feces or their urine and so they need frequent cleaning, just paying attention to their overall haircoat and cleaning them and a little bit of pampering. As you can see, this cat here is on his royal bed. He was one of our long-time visitors from our fire last year in which case he just sat in our ICU on his bed and made sure we were doing a good job with everyone else, so every night he’d come in and spend a few hours getting some attention.
With our initial evaluation on day 1 (I'm going to show you the same foot every day so that you have an example of how things can progress), one of the most important things is shaving and removing surrounding hair coat so that it doesn’t get matted into the scabs that form. Initially, I think, people are a little reluctant to keep an animal heavily sedated or anesthetized because shaving four feet can take upwards of an hour, but I think is really, really important to get this done on day one and remove all that dirt that you can.
On day one, I do conservative debridement and I'm not doing a lot surgically with the scalpel blade. Wounds do need time to declare themselves, and this could take upwards of three or four days. Sometimes, as in that fourth-degree wound I showed you earlier on, it’s very clear that there’s dead tissue there. On day one I generally will do conservative debridement. To me that means if the tissue comes off easily, remove it, but don’t remove things with a scalpel blade.
Hydrotherapy – Flushing the wounds thoroughly with isotonic crystalloids. Get all of that dirt and debris off.
Generally, if the wound is looking like this, I would start with a wet to dry bandage to get some extra debridement. If it’s a second or a first-degree wound, we obviously would not want to do a debriding type of bandage, and there you would just do a non-adherent dressing and things that we’ll talk about later. These wounds do need to be covered in their entirety.
When we’re talking about topical dressings, the two mainstays in veterinary medicine are either silver sulfadiazine (SSD for short) or honey. SSD has some really good antimicrobial effects. It’s great against pseudomonas and is probably the most widely used topical dressing for a burn injury both in human and veterinary medicine initially.
One of the downsides of SSD, however, is that when you start to have wounds that are starting in the epithelialization phase, so it has good granulation tissue, and the epithelium is trying to migrate across it, it could actually decrease the rate of healing in that phase, so it’s only used in the early phases. One of the goals is to sterilize the wound topically.
Honey has some extra benefits. It is an antimicrobial as well. Remember, this is medical grade honey that we’re using, so Manuka honey or honey-impregnated bandages that you can buy, not just topical honey from the store. This can actually decrease inflammatory mediators within the wound and decrease edema formation. Also, it’s been shown to accentuate the sloughing of dead necrotic tissue, whereas SSD does not do that.
When we looked at human literature, this is a meta-analysis looking at all the randomized controlled trials of silver sulfadiazine versus honey. What they didn’t show is that honey did result in shorter healing times, and, when they cultured the surface of those wounds, there was an increased number of wounds that achieved sterilization, so that was a negative culture.
The summary of all the evidence suggests that honey dressings do promote better wound healing over silver sulfadiazine. However, there are some down sides that honey does create a bit of a more messy wound. When you have to clean it off, you do have to scrub the tissue a bit more, and there is an extra cost in general that goes with it. There isn’t enough high-quality evidence to recommend routine honey in clinical practice. However, it has been shown to show a slight improvement.
We once looked at a cost benefit analysis on this individual patient, it might worthwhile, but, for us in a disaster situation, we generally use SSD.
Here’s that same foot just one day later. You can see with the wet to dry bandage we were able to debride a lot of that necrotic tissue. We have here third-degree burns across all of those surfaces except for our accessory carpal pad. We have nail beds all the way here that are exposed.
One thing to be aware of in the healing of foot pad injuries is that they might slough their toenails, and, as the healing progresses, it could granulate over the nail bed in which case you wind up with a chronic abscessation. We might need to actually do a digit amputation of P3 to prevent that from occurring.
Here is what I would say is a well-debrided wound in just 24 hours.
On day three, you can see this wound is already looking a lot healthier and that we have some granulation tissue forming. We have probably a little more tissue on some of these pads that’s going to slough. Overall, this wound is healing well and undergoing some good debridement.
By day five, we have a healthy-looking wound. We have full granulation tissue across its carpal pad. The third digits are already showing epithelialization, the fourth digit a tiny bit up at the top here of epithelialization, not too much on our metacarpal pad here, but this is a nice clean wound. With all the epithelial or granulation tissue, it’s going to be now pretty resistant to infection. Things like SSD are probably not going to be needed for a wound that looks like this because it’s not going to be prone to infection, and we’d move to probably a non-adhering dressing.
When we’re dealing with these mid-range wounds, kind of four to seven days or five to seven days, this is where we really want to consider aggressive surgical debridement. Theoretically, the wound itself will have fully declared itself over this type of period. Our patient, theoretically, if it’s made it this far, is systemically going to be much healthier, so we can fully anesthetize these patients and remove all the dead tissue with a scalpel blade. If you have fourth-degree burns, removing muscle itself would be indicated and then suturing that closed.
When we’re dealing with foot injuries, we often actually have to remove the digits of P3, so P3 of those digits. For me, when it is indicated is if you’re still seeing exposed bone at day 5 to 7. If that bone itself is brown or looking dead, those would be times where we’d want to remove it.
Could you potentially if you had healthy bone allow it to granulate over there? Absolutely, but what we found is we could accentuate the healing of those cats probably by 10 to 14 days if we remove that digit. We typically will recommend it as long as we know those cats in the future could be kept indoors and not the outdoor cats where they would need to have their claws. We recommend the amputation of P3 for those.
At this point, we’re looking to see if there’s healthy granulation tissue developing. Once you have a wound that fully has granulation tissue, we’ll stop honey, we’ll stop SSD generally although it would be okay to continue honey in this situation, and then we’d want a good, non-adherent dressing at that point. At this point, you could use things like Vaseline to keep the wound moist. There are a lot of gels that are out there that actually promote wound healing. I think part of what you’re going to use is dependent on if this is an individual patient or a disaster situation and looking at things like expense. There are a lot of good wound dressings out there that could promote the wound healing.
In this mid-range to late healing, we get what we call the epithelialization phase. This is where the epithelium migrates cell to cell and will completely cover the wound. At this point, for sure they don’t need daily bandaging; they could have every-other-day bandaging, they could have potentially every-three-day bandaging. When things start looking like this is when you want to have gentle cleaning only. If you really scrub the wounds at this point, you’re killing the epithelial cells that are trying to migrate, and then, when you re-bandage, they have to regrow over where you knocked them off, so we have just light cleaning of the foot at this point or our wound elsewhere.
Often at this point, the patients can stop their analgesics. When we have monitored behavior they have shown us that they don’t truly need analgesics at this point.
Then we get to what I call the late stage healing effects. This is where most of epithelialization has occurred. We’re really unlikely to get any sort of infection. This is where you might choose to let a scab stay.
See here, at day 16 that these pads are mostly healed, but there’s a small amount of scab that’s formed. At this point, we let the patient get out of bandages, and then the epithelial layer itself can migrate under that scab and fix itself. In general, then you don’t have the patient in a bandage and it might be more comfortable for them.
This is kind of an example of a late stage. This is a photo that was taken eight weeks in of treating the cat. We have a mixture of epithelial growth. This cat actually had a circumferential wound going all the way up its leg, so this is looking great right now. You can see nice, healthy granulation tissue, but because of the amount of granulation tissues present, we still have to keep this cat in bandages. However, if it was a smaller area, we wouldn’t.
This cat, as you can see, has no claws, so we did have to have P3 amputated on each digit. What may happen (this is a severe case) is all the pads can fuse into one, but you can see there’s a little bit of distinction right here at the center where there’s epithelial tissue. We often get a lot of paw pad fusion in these cats. Clinically, it doesn’t seem to affect them. They go on to live their lives. Normally, they run around on it, so, although it may look very different, it does not tend to affect them when that occurs. This cat probably has another two or three weeks ahead of him, but he’s got a family that comes and visits and is excited for him for when he may be able to go home and clinically is doing great walking on this foot.
Another thing that is very important in the late stage is nutrition. Throughout the hospitalization period, I think having a daily body weight and actually measuring accurately assessment of food is important. This is because we know hypoalbuminemia is very common, and all those other wound-healing factors are lost through the plasma, so we consider early on enteric nutrition. Probably within two to four days if our patients are not eating, we’re providing either nasogastric tubes or esophagostomy tubes.
The place of feeding tube is probably dependent on the facial injuries. If you have a cat with no burns around its nose or its mouth, we typically would just place a nasogastric tube in them because we can avoid full anesthesia. If the pet is not eating at day five to seven and is still getting NG feedings, that’s when we place an esophagostomy tube. For a patient with very severe nasal or pharyngeal burns, then we would go ahead and place the feeding tube right away and that allows us to make sure they get the calories that they need that we think are so important for their healing.
Finally, I just want to share a few lessons from wildfires that we learned that we definitely didn’t know about when we had our first set of fires.
This is ocular disease. A decrease in ability to make tear film is quite common, and we see that in probably upwards of 25% to 50% of the cats that have been exposed to wildfires. This may happen even if they look like they have a completely normal head and no burns around their face. We do supplement their tear film with lubricant generally twice a day to four times and sometimes even six times a day, even if their eyes look normal, and we’re monitoring their tear film production and looking for evidence of conjunctivitis to form.
For a patient with completely normal eyes on day one we will start with twice a day tear film. If they start to show any signs of dry eye, that’s when we will step it up. We’re fortunate enough that we have an ophthalmologist who is interested in looking at this, so they will look for evaluation of all these cats’ eyes, but, when we didn’t supplement their tear film with lubrication frequently, we found a lot of corneal ulceration. Cats that present like this with kind of a burn injury above their eyelids, we also have to consider monitoring for their ability to blink because as that wound starts to contract, it may inhibit their ability to blink.
This is a sequential set of photos of that cat where you can see as it’s healing over its left eye, this cat developed an inability to completely close its eye. He developed some ulceration. He also got conjunctivitis.
By the third image here, this is the cat healed, but he developed a complete inability to close his eye on the left and was getting chronic ulcerations at the midpoint of his eye, so our ophthalmologist actually did a releasing incision, so he actually would be able to go ahead and blink again.
This is a six-week followup from the surgery that you can see in the picture on the far right where everything is completely healed. He does have a little bit of conjunctivitis there that ultimately went away, but it’s something to just be aware of that may develop when you get burn injuries periorbitally.
Another interesting manifestation with smoke inhalation is cardiac disease that could happen. This has been shown in people with smoke inhalation. It’s something that we did not see in the 2015 fires but definitely saw in the 2017 and 2018 fires. It might be because we didn’t know to look for it, but, upon looking at these cats on echocardiography, we see a lot of myocardial thickening and endomyocardium brightness. We’ve seen a lot of spontaneous contrast as well that shows up on echo from abnormal flow. We’ve seen third-degree heart block develop and a variety of other conduction disturbances. Probably most commonly we’ve seen a decrease in systolic function and multiple patients have gone into congestive heart failure, some of them without fluid therapy but some with.
I think, luckily, this tends to be a transient thing, so we’re less pessimistic about this than when we first started seeing this. We’re able to medically treat these cats with symptomatic care, so furosemide or pimobendan and treat as needed. It’s something I think to be very aware of that when you have a patient with smoke inhalation that they’re probably going to be more likely to be fluid overloaded and have pulmonary edema from it, and then that is transient in nature.
The other thing that was an unexpected thing is a coagulopathy that develops. This is actually a prothrombotic state. We’ve documented quite a few arterial and aortic thrombi in these animals, and it’s something that now we can assess for with platelet function, and we have some evidence that this might be due to a platelet hyper-reactivity.
As I mentioned before, we’ve kind of seen a lot of smoke when we looked at echo on these animals, so we’re considering antithrombotics. If smoke is seen on our echo, or if we have the ability to do platelet testing and we’re showing platelet hyper reactivity, we’ll consider starting these animals on Clopidogrel or aspirin. You have to balance this, however, against the amount of wound care that they’re going to need because potentially starting those drugs will cause them to bleed more. We always take the overwhelming evidence or we worry that they’re more likely going to need surgery and bleed or versus are more likely they’re going to throw a clot that could be life-ending thing for them, and then make that decision overall on whether we start an antithrombotic.
Definitely the ocular, the cardiac, and thrombotic areas are something we need to look at more evidence for, but, ultimately they are areas we would like to do more research on in order to move forward and have some more answers from them.
Q: Do you ever consider short-acting anticoagulants such as fractionated heparin?
Steven Epstein: We definitely have considered the heparins for them. Unfortunately, the evidence shows that this probably is a platelet hyper-reactive thing, so it’s probably going to be more effective to use things like the Clopidogrel or aspirin than use fractionated heparin, but that definitely would be a consideration, or potentially things like rivaroxaban. That would go away as well if you had a dog or some bigger animal.
This is just a picture of one of our burn cats that was adopted by one of our surgeons. You can see how they can go on to look so much better if you give them enough time.
I just wanted to open up the floor for any questions now because that’s what I have for our presentation. We’re at our 60-minute mark.
Moderator:
While people are typing their questions, I just want to say thank you so much for such a great informative rounds session, Dr. Epstein. I think I can say that on behalf of everybody. Thank you. Thank you for all you do.
Q: Do the fluid requirements vary with degree of burns?
Steven Epstein: Yes it does. It’s primarily if you have second- and third-degree burns. First-degree burns don’t exude the plasma loss that the second- and third-degree burns do, so it’s going to be only for those. That’s where we use one of those burn indexes whether it’s the card system or estimated on the Rules of 9 and then our estimate of the 24-hour needs. This is just the first 24 hours of care and this is the 4 mL/kg/percent surface area. Then you make that calculation. If there’s a 20% burn, that would be 80 mL/kg that you expect them to need, and you would give half of that, so 40 mL/kg, over the first eight hours, and then the remainder, 40 mL/kg, of say LRS plus/minus potassium depending on the rate, you might need to run separate fluid for the potassium needs over that final 16 hours.
Q: What do you use for nebulization?
Steven Epstein: We’re just nebulizing saline for their nares and their upper airways. We’re not really doing any drugs.
Q: What is your preferred antibiotic to start while awaiting culture?
Steven Epstein: The question there is kind of twofold. One, if there’s a small amount of burns, we actually don’t start any systemic antibiotics, and we just try topical ones. If you have a large degree of burns, then we probably would start systemic antimicrobials, and in that situation, I would probably just start with something like ampicillin sulbactam knowing that that’s not going to be great for pseudomonas and rely on our topical for the pseudomonas.
The other caveat to that that I will say is when we are dealing with a disaster situation, we’re practicing a little bit of different type of medicine. We will often use Convenia when we have 30 or 40 cats in the hospital just because that dramatically reduces our nursing time to give antibiotics. Something simple like that that we can do on day one versus having to do it three times a day makes it so much easier when we’re caring for 40 patients at a time. I would say it appears that that drug has an equal effect to when I’ve used something like Unasyn on a clinical patient. Whether that speaks to just killing common skin bacteria or the fact that they probably don’t need a systemic antimicrobial, I'm not sure what the right answer there is.
Thank you everyone for being here.