Author : Nikil Naveel Chand (Umanand Prasad School of Medicine & Health Sciences Year 3 Student)
The skin is the largest organ of the body, and is made of the epidermis, the dermis, and the hypodermis. Burns result from exposure of skin cells to an overwhelming amount of energy
in the form of heat, causing cellular necrosis.
The degree of injury depends on the temperature, the duration of exposure, and the baseline structural integrity of the skin; which means younger children and elderly individuals are at higher risk of injury, because their skin is relatively weaker . Burns can be classified based on the cause, or by the depth of injury which corresponds to the severity of the burn.
Burns are most commonly thermal, which can result from scalds, such as hot water, or flames, such as from house-fires . Less commonly, burns can be electrical, like exposure to lightning strike or high-voltage electrical current, or from exposure to chemical substances, which can be acidic or alkaline .
Based on depth, burns can be first, second, or third degree. First degree burns are also called superficial burns, and involve the epidermis only . A prime example would be a simple sunburn from a day on the beach, which appears red, with no blisters. Second degree burns are further sub-classified into superficial partial thickness burns, which involve the epidermis and the superficial dermis, and deep partial-thickness burns, which involve the epidermis and the deep dermis . Superficial partial thickness burns appear red and are often blistered, whereas deep partial thickness burns appear red or white, with no blisters. Third degree burns are full-thickness burns, extending through and destroying the entire dermis. These appear leather-like with a charred appearance and tense feel. Usually, third degree burns are surrounded by a rim of second degree burns [4, 5, 6]. Fourth degree burns extend beyond the dermis, destroying fascia, muscle or bone. Because third and fourth degree burns destroy the entire skin, they destroy the skin nerve endings, and therefore can feel relatively painless .
Due to their strength and velocity, electrical burns have an entrance and an exit wound, similar to a gunshot. But aside from that, the skin actually looks fine. However internally, the muscles are injured and even the heart can be severely damaged [7,4]. Sadly, in children, specific burn patterns raise suspicion for physical abuse. These include burns with a sharply demarcated edge, small circular burns matching a cigarette tip, or burns in the perineal region matching a pattern that could only be explained if the child was dipped into scalding water .
Management of Burns Begins at the Scene.
First, remove the individual from the source, making sure you don’t expose yourself to electrical current or chemicals. Additionally, remove all clothing, accessories or jewelry from the individual, as they may be contributing to injury. On the way to the hospital, cool the injured areas with room-temperature water. It may be intuitive to use ice or iced-water, but this should be avoided because it can worsen the injury .
At the emergency department, management starts with the ABCs; that is airway, breathing and circulation.
Using a fiberoptic or direct laryngoscope, look for edema and obstruction of the airway.
The decision to intubate is based on the presence of oropharyngeal swelling, stridor and
respiratory distress causing hypoxemia. But sometimes, it’s more subtle . Clinical signs like
hoarseness of the voice, facial burns, drooling, soot in the airway, or even singed nasal or facial hairs should encourage you to secure the airway prophylactically, even if the airway isn’t swollen yet or they are not in obvious respiratory distress . Sometimes it’s too late and the airway has closed, and in that case a surgical cricothyroidotomy is performed. Also, If exposure to carbon monoxide is a concern, like in the setting of a closed house-fire, 100 percent oxygen is provided using a non-rebreather mask, and carboxyhemoglobin levels are measured.
Burns cause a tremendous amount of fluid loss, but it’s not as obvious as the fluid loss seen in diarrhea, vomiting or bleeding . Burns increase capillary permeability, causing a tremendous amount of fluid to shift from the plasma to the interstitial space, which is called “third-spacing” . To replace the loss, place two large-bore intravenous lines on an unburnt area of the skin. The amount of fluid to give depends on the total body surface area affected. Importantly, first degree burns are not included in the calculation. To measure this, the “rule of 9s” is used in adults . This method divides the body into eleven areas, each equal to 9 percent. The head is 9, each arm is 9, each leg is 18; that is 9 for the anterior aspect and 9 for the posterior aspect. The chest, abdomen, upper back, and lower back each represent 9 percent [5, 6]. Nine times 11 is 99, so that last 1 percent is the perineum.
Sometimes, the burn areas are patchy, and it can be difficult to ascertain a percentage.
To tackle this issue, the palm can be used to estimate, as the palm approximates 1 percent of a person’s total body surface area . Because children have larger heads and smaller extremities, the “rule of 9s” cannot be applied to them. Instead, the more complex Lund and Browder chart is used, which takes into account the child’s age. This chart may also be applied to adults .
Once you get the percentage, it’s inserted into the Parkland formula, which calculates how
much intravenous Ringer’s lactate the individual should receive. Ringer’s lactate is used
because its composition is closest to the extracellular fluid [5,1].
In the first 24 hours, the amount of Ringer’s lactate to give in milliliters is equal to: 4 multiplied by the weight in kilograms, multiplied by the percentage of the total body surface area involved. Half of the number you get is given in the first 8 hours, and the other half is given over the next 16 hours [1, 5, 6]. The adequacy of fluid resuscitation is determined by inserting a Foley catheter and measuring the urine output hourly. In adults, 0.5 milliliters per kilogram per hour is considered adequate, whereas in children 1 milliliter per kilogram per hour is adequate.
The idea behind this strict fluid regimen is Jackson’s burn model, which states that a burn injury is divided into three zones, a central zone of coagulation, which is dead and unsalvageable, a middle zone of stasis, and an outer zone of hyperemia .
Adequate fluid resuscitation may potentially save the zones of stasis and hyperemia from
irreversible injury . Under- or over-resuscitation may result in more tissue injury. Also, under-resuscitation may cause acute kidney injury, while over-resuscitation may worsen compartment syndrome or cause pulmonary edema. Also, tetanus toxoid should be given if the individual had not received it in the past 5 years . Tetanus immunoglobulin is added if they haven’t received the primary series during childhood.
In addition to fluid resuscitation, individuals with electrical burns should be placed on a continuous cardiac monitor, because they might have cardiac arrhythmias. Electrical burns and burns that damage muscle tissue may cause rhabdomyolysis, which releases myoglobin into the circulation [2, 3]. Myoglobin is toxic to the renal tubular epithelial cells, causing acute tubular necrosis. In addition to fluids, alkalization of the urine with the osmotic diuretic mannitol is recommended .
In addition, extensive tissue necrosis releases potassium, causing hyperkalemia. Full-thickness burns appear as a leathery, necrotic eschar. If that eschar circumferentially covers and pressures the neck, chest or an extremity, it can impair perfusion, and this is called compartment syndrome[5, 6].
Also, an eschar around the neck can compress the trachea, and an eschar around the chest can impair breathing mechanics . To prevent tissue necrosis and hypoventilation, an escharotomy is performed. This involves making an incision through the eschar, relieving the pressure. Anesthesia is usually not needed because eschars are usually painless, since all the nerve endings in the dermis have been destroyed .
A crucial aspect of burn management is analgesia. In minor burns, acetaminophen or non-steroidal anti-inflammatory drugs (NSAIDs) can be given. However, in more severe burns, IV opioids like morphine can help especially if they’re given early on . However, a challenging balance should be maintained, because opioids also cause hypotension and respiratory depressions; side effects that we don’t want in burns. Additionally, sedation with benzodiazepines or ketamine may be initiated, to ease taking care of the wounds .
Because burns increase the risk of stress peptic ulcers, or Curling ulcers, intravenous proton pump inhibitors are given .
The risk of venous thromboembolism such as deep venous thrombosis or pulmonary embolism is also increased in the setting of burns, and therefore prophylaxis is instituted using unfractionated or low-molecular weight heparin [2, 4].
Burns cause a hypermetabolic state, and individuals often cannot feed themselves. Therefore nutritional support is important. Enteral feeding using a nasogastric tube is preferred, but if they can’t tolerate it, total parenteral nutrition or TPN may be required [4, 5].
Next, is local wound management. The skin is the most important barrier to infection, so if that barrier is damaged, the skin needs help preventing infection and augmenting healing.
The wound should be cleaned with soap and water or sterile saline .
Povidone-iodine solutions on the other hand have been shown to delay wound healing and should be avoided .
Acidic chemical burns should be irrigated continuously with water only for 20 to 30 minutes, and alkaline burns should be irrigated for hours, since they are far worse. And it’s actually not a good idea to neutralize an acid with a base and vice versa - in fact it’s contraindicated, because this results in the release of thermal energy, which further damages the tissue .
Any eschar or necrotic tissue should be debrided, because dead tissue serves as a habitable environment for bacteria. Debridement is done in a tangential method, meaning that thin layers of the necrotic tissue should be removed until there’s uniform capillary bleeding throughout the wound . This indicates that you’ve reached viable tissue. An important aspect of preventing infection is giving antibiotics, but because blood flow is often compromised at the necrotic burn area, systemic antibiotics may not adequately reach it. Therefore, topical antibiotics are usually preferred, with a large number of options to choose from.
Silver sulfadiazine covers most gram positive and gram negative bacterial organisms as well as fungi, and it’s application is not painful. It’s downsides however are that it doesn’t cover Pseudomonas aeruginosa, which is the most common cause of sepsis from burns, and it’s not conducive to wound healing . Mafenide acetate covers Pseudomonas, but it is painful to apply.
Silver nitrate is a good option for individuals with sulfa allergies, who cannot be given silver sulfadiazine. However, it leaves a blackish stain, making it difficult to assess the wound.
If a wound infection is suspected, a tissue biopsy is obtained, and topical as well as systemic antibiotics are tailored to the offending organism. Sterile dressings should be applied daily, as they aid in wound healing .
1. Burns: Video, Anatomy, Definition & Function. (2018, November 08). Retrieved from https://www.osmosis.org/learn/burns
2. Dale, M. M., & Haylett, D. G. (2009). Pharmacology condensed. Elsevier.
3. Hall, J. E. (2015). Guyton and hall textbook of medical physiology, international edition. Elsevier Saunders.
4. Harrison, T. R., Longo, D. L., Kasper, D. L., Jameson, J. L., Fauci, A. S., Hauser, S. L., & Loscalzo, J. (2012). Harrison's principles of internal medicine: Editors, Dan L. Longo ... McGraw-Hill.
5. Kumar, P., & Clark, M. (2017). Kumar and Clark's clinical medicine: International edition. Elsevier.
6. Ralston, S., Penman, I. D., Strachan, M. W., Hobson, R. P., Britton, R., & Davidson, S. (2018). Davidson's principles and practice of medicine. Elsevier.
7. Robbins, S. L., Cotran, R. S., Kumar, V., Abbas, A. K., & Aster, J. C. (2015). Pathologic basis of disease. Saunders Elsevier.