Back To Search Results

Anesthesia for Patients With Burns

Editor: Sohail K. Mahboobi Updated: 7/20/2023 1:53:53 PM


Almost half a million people seek medical care annually due to burn injuries. The anesthesiologist plays a critical role in managing complicated cases involving airway management, hemodynamic support, intravascular access, thermoregulation, and pulmonary support. The airway of a severely burned patient can quickly become compromised with traditional means of anesthesia and requires special attention to ensure adequate ventilation. When treating patients with burns, the complex pathophysiologic changes pose challenges in performing intraoperative fluid resuscitation, selecting appropriate induction drugs, and determining optimal ventilation strategies. The anesthesiologist plays a critical role in optimizing the care of these patients.[1][2]

Anatomy and Physiology

Register For Free And Read The Full Article
Get the answers you need instantly with the StatPearls Clinical Decision Support tool. StatPearls spent the last decade developing the largest and most updated Point-of Care resource ever developed. Earn CME/CE by searching and reading articles.
  • Dropdown arrow Search engine and full access to all medical articles
  • Dropdown arrow 10 free questions in your specialty
  • Dropdown arrow Free CME/CE Activities
  • Dropdown arrow Free daily question in your email
  • Dropdown arrow Save favorite articles to your dashboard
  • Dropdown arrow Emails offering discounts

Learn more about a Subscription to StatPearls Point-of-Care

Anatomy and Physiology

Major burns damage tissues directly and distort the anatomy making traditional airway management, monitoring, and hemodynamic access challenging. Developing a cytokine-mediated inflammatory response also results in pathophysiologic effects both locally and distantly from the injury. This response can be described in 2 distinct phases: burn shock (ebb) followed by a hypermetabolic (flow) phase. The inflammatory response begins minutes after tissue destruction resulting in sensitization and irritation of the pain fibers.[1][3]

The burn shock or ebb phase occurs during the first 24 to 48 hours of a severe (or major) burn; a severe burn is defined as a collection of second- and third-degree burns comprising equal to or greater than 20% total body surface area (TBSA). Burn shock is characterized by reduced end-organ perfusion and diminished cardiac output, mainly due to losses in intravascular volume. Essentially, this is a distributive shock state. Intravascular volume losses form edema at directly burned areas and unburned sites. Hemoconcentration of red blood cells occurs due to significant volume extravasation into adjacent tissue. This edematous state can obscure views of the glottic opening during direct laryngoscopy. Reduction in cardiac output is a complication of intravascular volume loss, direct myocardial depression, and increased systemic vascular resistance. During this phase, there is an increase in systemic vascular resistance caused by a surge of catecholamines and antidiuretic hormone. This leads to the constriction of blood vessels and a reduction in blood flow. Even with aggressive fluid resuscitation, only partial compensation can be obtained due to an imbalance of the cellular transmembrane ionic gradient and reduced sodium ATPase activity, which may persist for days after the initial burn injury.[1][2][4]

The hypermetabolic or flow phase of a severe burn develops 48 to 72 hours after the initial injury and is characterized by increased oxygen consumption and carbon dioxide production. Cardiac output improves compared to the burn shock phase resulting in better end-organ perfusion. Cardiac output may increase to 2 to 3 times the normal range due to tachycardia and decreased systemic vascular resistance during this phase, further mimicking sepsis. As a result of decreased vascular resistance, blood flow subsequently improves to all organs. Arteriovenous shunting may occur, resulting in increased venous oxygen saturation. Resorption of edema may result in pulmonary edema, further compounding the damage from inhalation injuries from smoke. If excessive fluid resuscitation is given during the burn shock phase, the consequences of such actions would be observed during the hypermetabolic phase as fluid is resorbed, potentially making weaning from the ventilator intraoperatively troublesome. The release of catabolic hormones and insulin resistance generally characterizes the hypermetabolic phase. This results in protein catabolism (ie, muscle wasting) and hyperglycemia. Glucocorticoid and inflammatory cytokines increase during this phase, thus increasing the caloric needs of a severely burned patient. The hypermetabolic phase can last up to 2 years.[1][2][4]

Once the burn has reached a total body surface area (TBSA) of approximately 25% to 30%, the inflammatory response produces systemic effects altering the physiology of a burn patient.[1][5]

The initial pathophysiologic alterations/complications during the burn shock (ebb phase) can be summarized by the organ system as follows:[1][5]

  • Cardiovascular
    • Increased capillary membrane permeability (loss of intravascular proteins to the interstitial compartment)
    • Vasoconstriction (increased systemic vascular resistance)
    • Decreased myocardial contractility (decreased cardiac index, stroke volume, and blood pressure)
    • Metabolic acidosis (decreased kidney perfusion)
    • Overall result: systemic hypotension with reduced end-organ perfusion
  • Pulmonary
    • Pulmonary edema
    • Increased susceptibility to bronchospasm due to bronchorrhea
    • Overall result: Potential adult respiratory distress syndrome development
  • Integumentary 
    • Fluid loss through compromised skin
    • Generalized edema when BSA of burn exceeds 25%
    • Circumferential burn of the chest/abdomen/limb may result in compartment syndrome.
    • Impaired ability to regulate temperature
    • Overall result: Need for aggressive fluid resuscitation and special attention to circumferential burns
  • Immunologic 
    • Downregulated immune response
    • Overall result: Increased susceptibility to infection


Inhalation Injuries

Inhalation injuries accompanying burns are associated with a significant increase in morbidity and mortality. Patients with serious burns and inhalation injuries require 30% to 50% more fluid resuscitation than their non-inhalation injury counterparts. Chest radiographs may appear benign until complications such as infection or atelectasis develop. Inhalation injuries may take several days to become clinically evident.[1] Inhalation injuries can be divided into 3 subclassifications: 

  1. Supraglottic
    • Thermal injury is the most common inhalation injury to the supraglottic region. The main anesthetic concern related to injury to the supraglottic region is upper airway edema which can obstruct the airway and create difficulties with intubation. Exposure to direct heat and steam may result in swelling of various structures (ie, face, tongue, epiglottis, glottis), making mask ventilation and visualization of the glottis more difficult. As the burn shock phase progresses, this problem may be compounded.
    • Supraglottic inhalation injuries can be assessed by physical examination and using tools such as fiberoptic bronchoscopy to directly examine the oropharynx and vocal cords for edema. Those with upper airway edema exhibiting mental status changes, stridor, hoarseness, or mucosal edema should be treated with early intubation to prevent further airway complications and impending respiratory arrest. The subglottic structures are generally protected from thermal injuries due to the glottis' innate nature to close and the upper airway's ability to dissipate heat. Supraglottic swelling typically resolves in 3 to 6 days.
    • The ideal anesthetic approach for patients with significant supraglottic injuries is to maximize local anesthetic usage and minimize general anesthetics with a fiberoptic approach. This allows ample time to investigate and then navigate a difficult airway while maintaining spontaneous patient respiration, thus reducing the risk of patient harm and manipulation of the airway.[1][6]
  2. Subglottic
    • Inhalation of noxious chemicals and irritants often causes injury below the glottis. This can lead to direct damage and inflammation, resulting in airway mucosal hyperemia, potential bronchospasm, and mucosal sloughing. Consequently, mucociliary escalator function may be inhibited, leading to a buildup of bacteria and mucosal debris, increasing the risk of pneumonia in the days following the injury. Inflammatory processes can also inhibit hypoxic pulmonary vasoconstriction, leading to right-to-left shunting of blood and hypoxia. Alveolar collapse may occur due to a loss of surfactant production or plugging by debris. Intermittent bronchospasm and airway edema may further limit oxygenation by inhibiting oxygen delivery to the alveoli. These findings may be evident in a patient on a ventilator with a prolonged expiratory phase and elevated peak inspiratory pressures.
    • Cast formation due to mucus sloughing can also obstruct the already limited space in the airways. Bronchoscopy can be utilized intraoperatively to remove casts and improve airway pressures and oxygenation. Widespread cast formation in airways redistributes tidal volumes to unobstructed airways resulting in excessive pulmonary pressures to healthy lung tissue, propagating barotrauma.
    • This barotrauma can result in acute respiratory distress syndrome (ARDS) and pneumothorax. ARDS occurs within a week of inciting events and cannot be explained by congestive heart failure or hypervolemia. ARDS can be further classified as PaO2/FiO2 ratios; mild ARDS (200-300 PaO2/FiO2), moderate ARDS (100-200 PaO2/FiO2), and severe ARDS (<100 PaO2/FiO2). The primary means of diagnosis of the subglottic injury is clinical but can be supplemented by bronchoscopy. Subglottic inhalation injuries become significant to anesthesiologists due to the necessity of lung-protective ventilation strategies such as low tidal volume (4-6 mL/kg) and properly titrated positive end-expiratory pressures to limit barotrauma.[1][6][7]
  3. Systemic
    • Inhalation injuries can have systemic effects, causing hypoxia, acidosis, and systemic inflammation, resulting in pulmonary edema. Tissues can be directly damaged by carbon monoxide and cyanide, which are soluble in blood and can inhibit oxygenation. Intraoperative checks can be performed to monitor these systemic effects through arterial blood gas and laboratory studies when necessary.
    • Carbon monoxide can hinder hemoglobin's ability to carry oxygen and has a higher affinity for hemoglobin than oxygen. Toxicity is considered when carboxyhemoglobin levels exceed 15%. When nitrogenous materials burn, they produce cyanide which interacts with the cytochrome system of mitochondria, inhibiting oxygen utilization. This can block the last step of oxidative phosphorylation, preventing the conversion of pyruvate to adenosine triphosphate (ATP), resulting in cells generating ATP from anaerobic metabolism.
    • Cyanide toxicity is characterized by an anion gap metabolic acidosis in the presence of ample oxygen delivery. If an intraoperative patient experiences persistent hypoxia and acidosis, it may be due to carbon monoxide or cyanide toxicity.

Carbon Monoxide Poisoning

Pulse oximetry may not accurately measure oxygenation levels in cases of carbon monoxide poisoning. This is because pulse oximetry cannot differentiate between oxyhemoglobin and carboxyhemoglobin. To determine the severity of carbon monoxide poisoning, laboratory tests can measure the levels of carboxyhemoglobin present in the blood. In cases where time is crucial, one can consider using a carbon monoxide oximeter. Unfortunately, such devices are not commonly found in modern hospitals.

Carbon monoxide has a higher affinity for hemoglobin than oxygen (about 230 to 270 times higher), leading to a shift in the oxygen-hemoglobin dissociation curve towards the left. This results in reduced oxygen delivery to the body's tissues, which can manifest as mental confusion, agitation, nausea, dizziness, and headaches—all indicative of carbon monoxide poisoning. Any patient with suspected carbon monoxide poisoning should immediately receive 100% oxygen. Administration of normobaric 100% oxygen can reduce the half-life of carbon monoxide to 40 to 80 minutes from 240 to 320 minutes, thus expediting recovery.

After the carboxyhemoglobin level falls below 10%, stopping administering 100% oxygen is safe. However, monitoring the patient for roughly 24 hours is crucial to ensure they're not experiencing any respiratory issues. Patients with a carboxyhemoglobin level >20% should be considered for intubation and mechanical ventilation to expedite carbon monoxide elimination further and improve tissue oxygenation. Patients requiring mechanical ventilation with accompanying carbon monoxide poisoning should receive 100% FiO2 until carboxyhemoglobin levels normalize to expedite dissociation with hemoglobin. Hyperbaric oxygen therapy should also be considered in severe cases of carbon monoxide poisoning.[1][6][7][8]


Airway Management

When dealing with a burn patient requiring anesthesia in an acute setting, conducting a thorough airway assessment is crucial to detect any indications of airway edema that could lead to a complex airway challenge. Decreased mandibular mobility from burn contractures or glottic edema from airway swelling may make laryngoscopy difficult. When faced with a suspected difficult airway due to thermal injury to supraglottic structures, the most widely accepted and safe approach is to use fiberoptic intubation. This technique involves the application of topical anesthetic and minimal general anesthetics.

If fiberoptic intubation is chosen, ketamine-induced sedation/anesthesia can create ideal intubation conditions due to the maintenance of pharyngeal muscle tone. Ketamine is associated with preserving hemodynamic stability, hypercapnia responses, and decreased airway resistance, making it an ideal agent for individuals with supraglottic swelling. Utilizing anesthetic agents that disrupt airway tones, such as propofol and paralytic agents, may further obstruct the airway creating much more difficult intubating conditions.[1][3]

Intravascular Access

Individuals who have suffered severe burns may face challenges when receiving intravenous treatment due to the damage caused to common access areas such as the neck, limbs, and groin. Additionally, edema resulting from the burn shock phase or fluid creep from the overcompensation of fluid infusion to address intravascular loss can further complicate the process. Delay of fluid resuscitation for more than 2 hours after the initial injury is associated with an increased risk of mortality, making vascular access an essential and critical component of burn management. When intravascular access proves too difficult via conventional means, peripheral intravenous or central venous access, intraosseous access can be overly beneficial. Intraosseous access is typically faster than peripheral intravenous and central venous line placement, with a much higher chance of first-time attempt success. 

The caveat of intraosseous access is that it is more likely to cause insertion and infusion pain than conventional methods. Despite its faster and easier placement, it is still not as common an access tool as one would surmise. To prevent intraosseous access failure, it is crucial to familiarize the device beforehand, as improper placement is the most common cause of failure. The proximal tibia is the most common location for placing an intraosseous needle, but the proximal humerus is equally effective. The proximal tibia is advantageous as it does not interfere with cardiopulmonary resuscitation.[2][9][10]


Patients suffering from severe burns lose their principal barrier to preventing heat loss. Thus, hypothermia becomes a primary anesthetic consideration. Evaporative heat and water loss from burn wounds create a direct means of heat loss. The cerebral mechanisms that combat hypothermia become dysregulated in severe burns. The critical temperature is the temperature at which a physiologic response to hypothermia occurs to produce heat-generating and conserving activity, ie, shivering, teeth chattering, vasoconstriction, cellular non-shivering thermogenesis. 

With severe burns, the critical temperature is decreased. When the innate mechanisms of combating hypothermia are combined with a general anesthetic, patients are significantly predisposed to hypothermia. General anesthesia is associated with both redistribution of heat from the core to the periphery and inhibiting the central thermoregulatory control making even healthy patients prone to hypothermia from the subsequent vasodilation. The critical means to ensure optimal thermoregulation for all burn patients include forced-air warming, fluid warming, and raising the operating room temperature. An accurate means of temperature measurement, such as a distal esophageal or rectal temperature probe, becomes essential for the perioperative management of severely burned patients.[4][11][12]

Technique or Treatment

Fluid Resuscitation

Proper fluid resuscitation is recommended for burns involving >15% TBSA to prevent complications associated with the burn shock phase. A lack of early and aggressive fluid resuscitation in severe burns (>15% TBSA) will result in hypovolemic shock. The intravascular volume becomes depleted due to fluid shifts and increased capillary permeability. Delaying fluid resuscitation for more than 2 hours after the initial severe burn is associated with an appreciable increase in mortality. Of note, when calculating TBSA, only second- and third-degree burns are factored into the calculation of TBSA; first-degree burns are excluded from TBSA estimation. Intravascular volume repletion helps mitigate the resultant hypovolemia complications, such as tissue hypoperfusion and the associated reflexive vasoconstriction. Burns less than 15% TBSA can be appropriately managed with oral fluids or a maintenance intravenous fluid rate of 1.5 times normal.[1][2]

The accepted crystalloid for fluid resuscitation is lactated Ringer solution due to the worsening metabolic acidosis associated with a large volume of normal saline (0.9%) infusions required for severe burns. Patients with severe burns are predisposed to metabolic acidosis due to decreased kidney perfusion during burn shock. Although several formulas exist for calculating the recommended amount of volume needed for fluid resuscitation, the clinician should not lose focus of the clinical markers of appropriate resuscitation and taper fluid resuscitation to feedback from objective findings such as:[1][2]

  • Urine output goal: 0.5 to 0.1 mL/kg/h
  • Fractional excretion of sodium: <1% suggests hypovolemia
  • BUN-to-creatinine ratio: >20 suggests hypovolemia
  • Echocardiogram: assessment of stroke volume and ejection fraction
  • Arterial blood gas: base deficit <5 suggests hypoperfusion in the absence of carbon monoxide poisoning

When medical professionals fail to pay enough attention to the physiological indicators of adequate fluid resuscitation, especially urine output, a phenomenon known as "fluid creep" can occur. This refers to the excessive administration of fluids to burn patients beyond what is necessary for their clinical condition. This can cause excessive tissue and pulmonary edema, further complicating the patient's condition. Pulmonary edema can lead to breathing difficulties and may require tracheal intubation or cause pneumonia. Fluid creep can also exacerbate airway edema, resulting in the need for intubation. Typically, fluid creep occurs due to a miscalculation of fluid resuscitation volumes in the first 24 hours after an initial burn.

Clinicians may fail to consider the multiple intravenous medications a patient may receive, such as antibiotics, analgesics, and sedatives, which should be included when considering fluid resuscitation. The most crucial objective finding to taper fluid replacement is urine output, which can result in fluid creep when not considered. The role of colloids has not yet been defined but could be considered an adjunct therapy to prevent hypervolemia.[2]

The most common formula for estimating the amount of fluid resuscitation needed for a patient is the Parkland formula. The Parkland formula estimates the amount of fluid to be administered over the first 24 hours, with half of the calculated volume recommended to be administered over the first 8 hours. The patient's percentage of TBSA that is burned is expressed as a whole number.[1]

Parkland Formula: 4 mL x kg x percentage of TBSA burned

Example: A 75 kg male has a burn comprising 30% TBSA 

  1. Calculate the total amount of lactated Ringer solution to give in the first 24 hours
    • 4 mL x 75 kg x 30 = 9,000 mL for the first 24 hours
  2. Calculate the amount of fluid to give in the first 8 hours
    • Half of the total volume should be administered in the first 24 hours
    • 9,000 mL /2 = 4,500 mL of lactated Ringer solution in the first 8 hours
  3. Administer the remaining amount of fluid in the last 16 hours
    • 4,500 mL in the last 16 hours 

Estimation of TBSA

The Wallace Rule of Nines is a standard method to estimate the TBSA of the burn. The Rule of Nines is valued for its simplicity and practicality in clinical scenarios. For more minor burns, clinical providers may use the Rule of Palms, which involves estimating the size of a burn by using the patient's palm size to indicate 1% of TBSA. When calculating TBSA for fluid resuscitation or clinical diagnosis criteria, first-degree burns are not included, only second- and third-degree burns. Despite these tools, enormous amounts of variability in body surface area due to gender, age, and body mass index can make it challenging to provide a standardized method for estimating TBSA. Those with a larger body mass index often have an overestimated calculation of their burn TBSA.

Advances in technology may allow for 3D body scanning to determine the TBSA of burns more accurately. Accurate estimation of TBSA is important for transfer to appropriate burn centers and to help dictate fluid resuscitation goals. The anesthesiologist needs to communicate openly with other healthcare professionals when accepting the care of a severely burned patient in the operating room to understand better the patient's fluid goals in the perioperative period. With the prevalence of miscalculations and the ill consequences of fluid creep, the astute anesthesiologist should be able to estimate the TBSA of a burn upon initial assessment to administer fluids accurately.[13][14]

Neuromuscular Blockade

A major concern with burn patients is the upregulation of acetylcholine receptors after a burn resulting in life-threatening hyperkalemia after using succinylcholine. In healthy patients, succinylcholine use is associated with only 0.5 mEq/L, but in the burn patient, this response is exaggerated. The increased susceptibility to hyperkalemia is likely associated with changes in the nicotinic acetylcholine receptor (nAChR) subunits. Recent evidence suggests that burn patients have upregulated alpha7 and gamma subunit genes producing more acetylcholine receptors spread throughout the body and slightly altered receptors. These altered receptors likely have abnormal electrophysiological interactions with succinylcholine producing more significant hyperkalemia.

This upregulation of acetylcholine receptors does not happen fast enough for significant hyperkalemia to develop until approximately 24 to 48 hours after the initial burn injury. Resistance to non-depolarizing neuromuscular blockade happens much faster than the sensitivity to succinylcholine (within the 24-48 hour window). Thus, the presenting burn patient may require higher than usual doses of a non-depolarizing neuromuscular blockade than expected. An increased dose can partially overcome resistance to the neuromuscular blockade produced by rocuronium. Rocuronium can provide reasonably good intubating conditions with a 1.2 mg/kg dose after a significant burn injury.[15][16][17]



Severe burns can weaken the immune system due to increased cytokine inflammatory markers, leading to a greater risk of infection. Wounds quickly become colonized with gram-positive organisms like Staphylococcus aureus and Staphylococcus epidermis. Over several days, intestinal microbes such as Pseudomonas aeruginosa and Escherichia coli colonize the wounds.

Systemic antibiotic therapy is not necessarily warranted for these microbe colonizations perioperatively, although thorough wound cleansing with soap, water, normal saline, and/or chlorhexidine is advisable. Topical antibiotic therapy should be suitable for the perioperative period in the early phases of a burn. A conversation between the surgeon and anesthesiologist can minimize the overuse of antibiotics in this subset of patients.[18][19][20]

Clinical Significance

Anesthesia for patients with burns is a challenging subspecialty that requires a cautious approach and an understanding of the pathophysiology of burns to optimize clinical outcomes. Understanding the airway difficulties one could encounter when managing severe head and neck burns is essential to prevent the dreaded "can't ventilate, can't intubate" scenario. The most conservative approach involves just enough anesthetic to make the patient comfortable while maintaining spontaneous ventilation and performing fiberoptic intubation.

Understanding the pathophysiology of burns is essential to anticipate hemodynamic changes in burn patients and how to adequately fluid resuscitate the patient intraoperatively before transferring to an intensive care setting. Intraoperative intervention related to the thermoregulatory changes in burn patients undergoing anesthesia can help to prevent wound infection, impaired coagulation, and perioperative shivering. Anesthesiologists play a critical role in the perioperative care of burn patients, and a better understanding of the hazards in treating patients with burns patients can reduce perioperative morbidity and mortality.

Enhancing Healthcare Team Outcomes

Approximately 500,000 people present to the emergency department each year with a burn, but most of these patients do not require critical care.[1] When critical care is required, minutes count as a difficult airway can quickly advance to a "can't ventilate, can't intubate" situation with the swelling that occurs during the hours after a severe burn injury. The anesthesiologist can play an important role in managing these cases with their vast knowledge of physiology, pharmacology, airway management skills, and critical care skills. However, it is only through effective communication and coordination among all patient's interprofessional care team members that the patient can have the best chance at a favorable outcome.

Severely burned patients are a complex population that requires a multidisciplinary approach to their medical care. This population of patients can have multifaceted problems, including complicated airways, smoke inhalation injuries, and a unique approach to hemodynamic optimization considering the pathophysiology of burns. Optimizing the care of this complex population may require interdisciplinary collaboration and a myriad of services.

A retrospective study involving a Difficult Airway Response Team (DART) composed of anesthesiologists, otolaryngologists, and trauma surgeons as a multidisciplinary approach to difficult airways found that a team-based approach was able to secure the airway more often without the need for an emergency cricothyrotomy in a statistically significant manner.[21] Applying a multidisciplinary approach to a burn patient with a difficult airway can lead to a safer and less harmful method of securing the airway. 

The Parkland Formula is a valuable tool for estimating the necessary amount of fluid resuscitation for a burn patient. However, relying solely on this number for calculating the administration of isotonic fluid can be prone to human errors. Accidentally forgetting to include fluid volumes from intravenous medications is a common issue. Burn patients must receive the correct amount of fluid resuscitation as too little fluid is associated with increased morbidity and mortality. Too much fluid is associated with fluid creep, which can lead to higher rates of infection and intubation.[1][2] A retrospective review of burn patients found that patients actually receive much higher volumes of fluid than estimated by the Parkland Formula to properly fluid resuscitate a burn patient.[22] 

Effective team communication can help prevent fluid creep and its associated issues. Nursing staff plays a crucial role in ensuring accurate intake and output recording and can provide essential feedback to physicians and advanced practice clinicians when significant volumes of medications, such as antibiotics, sedation, and electrolyte replacement, are being infused. These fluid volumes are often overlooked when calculating fluid resuscitation goals, making the nursing staff's vigilance and communication vital for effective patient care. 

The anesthesiologist and critical care physician collaborate with the surgeons to make adjustments in fluid delivery so surgical sites or respiratory function are not compromised. Effective communication among team members is key to improving outcomes for this complex subset of patients without the need to alter the currently available therapies.



Bittner EA, Shank E, Woodson L, Martyn JA. Acute and perioperative care of the burn-injured patient. Anesthesiology. 2015 Feb:122(2):448-64. doi: 10.1097/ALN.0000000000000559. Epub     [PubMed PMID: 25485468]


Snell JA, Loh NH, Mahambrey T, Shokrollahi K. Clinical review: the critical care management of the burn patient. Critical care (London, England). 2013 Oct 7:17(5):241. doi: 10.1186/cc12706. Epub 2013 Oct 7     [PubMed PMID: 24093225]


Griggs C, Goverman J, Bittner EA, Levi B. Sedation and Pain Management in Burn Patients. Clinics in plastic surgery. 2017 Jul:44(3):535-540. doi: 10.1016/j.cps.2017.02.026. Epub 2017 Apr 18     [PubMed PMID: 28576242]


Sommerhalder C, Blears E, Murton AJ, Porter C, Finnerty C, Herndon DN. Current problems in burn hypermetabolism. Current problems in surgery. 2020 Jan:57(1):100709. doi: 10.1016/j.cpsurg.2019.100709. Epub 2019 Nov 11     [PubMed PMID: 32033707]


Hettiaratchy S, Dziewulski P. ABC of burns: pathophysiology and types of burns. BMJ (Clinical research ed.). 2004 Jun 12:328(7453):1427-9     [PubMed PMID: 15191982]


Foncerrada G, Culnan DM, Capek KD, González-Trejo S, Cambiaso-Daniel J, Woodson LC, Herndon DN, Finnerty CC, Lee JO. Inhalation Injury in the Burned Patient. Annals of plastic surgery. 2018 Mar:80(3 Suppl 2):S98-S105. doi: 10.1097/SAP.0000000000001377. Epub     [PubMed PMID: 29461292]


Gigengack RK, Cleffken BI, Loer SA. Advances in airway management and mechanical ventilation in inhalation injury. Current opinion in anaesthesiology. 2020 Dec:33(6):774-780. doi: 10.1097/ACO.0000000000000929. Epub     [PubMed PMID: 33060384]

Level 3 (low-level) evidence


Kinoshita H, Türkan H, Vucinic S, Naqvi S, Bedair R, Rezaee R, Tsatsakis A. Carbon monoxide poisoning. Toxicology reports. 2020:7():169-173. doi: 10.1016/j.toxrep.2020.01.005. Epub 2020 Jan 20     [PubMed PMID: 32015960]


Paxton JH, Knuth TE, Klausner HA. Proximal humerus intraosseous infusion: a preferred emergency venous access. The Journal of trauma. 2009 Sep:67(3):606-11. doi: 10.1097/TA.0b013e3181b16f42. Epub     [PubMed PMID: 19741408]

Level 2 (mid-level) evidence


Sunde GA, Heradstveit BE, Vikenes BH, Heltne JK. Emergency intraosseous access in a helicopter emergency medical service: a retrospective study. Scandinavian journal of trauma, resuscitation and emergency medicine. 2010 Oct 7:18():52. doi: 10.1186/1757-7241-18-52. Epub 2010 Oct 7     [PubMed PMID: 20929544]

Level 2 (mid-level) evidence


Ikeda T, Sessler DI, Kikura M, Kazama T, Ikeda K, Sato S. Less core hypothermia when anesthesia is induced with inhaled sevoflurane than with intravenous propofol. Anesthesia and analgesia. 1999 Apr:88(4):921-4     [PubMed PMID: 10195549]

Level 1 (high-level) evidence


Díaz M, Becker DE. Thermoregulation: physiological and clinical considerations during sedation and general anesthesia. Anesthesia progress. 2010 Spring:57(1):25-32; quiz 33-4. doi: 10.2344/0003-3006-57.1.25. Epub     [PubMed PMID: 20331336]


Retrouvey H, Chan J, Shahrokhi S. Comparison of two-dimensional methods versus three-dimensional scanning systems in the assessment of total body surface area estimation in burn patients. Burns : journal of the International Society for Burn Injuries. 2018 Feb:44(1):195-200. doi: 10.1016/j.burns.2017.07.003. Epub 2017 Aug 7     [PubMed PMID: 28797577]


Giretzlehner M, Ganitzer I, Haller H. Technical and Medical Aspects of Burn Size Assessment and Documentation. Medicina (Kaunas, Lithuania). 2021 Mar 5:57(3):. doi: 10.3390/medicina57030242. Epub 2021 Mar 5     [PubMed PMID: 33807630]


Han T, Kim H, Bae J, Kim K, Martyn JA. Neuromuscular pharmacodynamics of rocuronium in patients with major burns. Anesthesia and analgesia. 2004 Aug:99(2):386-92, table of contents     [PubMed PMID: 15271712]


Osta WA, El-Osta MA, Pezhman EA, Raad RA, Ferguson K, McKelvey GM, Marsh HM, White M, Perov S. Nicotinic acetylcholine receptor gene expression is altered in burn patients. Anesthesia and analgesia. 2010 May 1:110(5):1355-9. doi: 10.1213/ANE.0b013e3181d41512. Epub 2010 Mar 19     [PubMed PMID: 20304984]

Level 1 (high-level) evidence


Nosek MT, Martyn JA. Na+ channel and acetylcholine receptor changes in muscle at sites distant from burns do not simulate denervation. Journal of applied physiology (Bethesda, Md. : 1985). 1997 Apr:82(4):1333-9     [PubMed PMID: 9104873]

Level 3 (low-level) evidence


Rowan MP, Cancio LC, Elster EA, Burmeister DM, Rose LF, Natesan S, Chan RK, Christy RJ, Chung KK. Burn wound healing and treatment: review and advancements. Critical care (London, England). 2015 Jun 12:19():243. doi: 10.1186/s13054-015-0961-2. Epub 2015 Jun 12     [PubMed PMID: 26067660]


Alebachew T, Yismaw G, Derabe A, Sisay Z. Staphylococcus aureus burn wound infection among patients attending yekatit 12 hospital burn unit, addis ababa, ethiopia. Ethiopian journal of health sciences. 2012 Nov:22(3):209-13     [PubMed PMID: 23209356]


Church D, Elsayed S, Reid O, Winston B, Lindsay R. Burn wound infections. Clinical microbiology reviews. 2006 Apr:19(2):403-34     [PubMed PMID: 16614255]


Hillel AT, Pandian V, Mark LJ, Clark J, Miller CR, Haut ER, Cover R, Berkow LC, Agrawal Y, Bhatti N. A novel role for otolaryngologists in the multidisciplinary Difficult Airway Response Team. The Laryngoscope. 2015 Mar:125(3):640-4. doi: 10.1002/lary.24949. Epub 2014 Sep 24     [PubMed PMID: 25251732]

Level 2 (mid-level) evidence


Mitra B, Fitzgerald M, Cameron P, Cleland H. Fluid resuscitation in major burns. ANZ journal of surgery. 2006 Jan-Feb:76(1-2):35-8     [PubMed PMID: 16483293]

Level 2 (mid-level) evidence