Anesthesia For Patients With Burns

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Continuing Education Activity

Anesthetic management of the burn patient can be a complex task due to various pathophysiological and hemodynamic changes following burn comprising greater than 20% total body surface area. The severely burned patient poses added challenges of airway management, fluid resuscitation, and vascular access due to direct trauma to the skin and soft tissue structures. This activity reviews and highlights the important components necessary for the anesthetic management of a severely burned patient, emphasizing the inter-professional team in evaluation and treatment.


  • Explain how the pathophysiologic changes associated with burns alter anesthetic management.
  • Identify the ideal approach to an airway complicated by significant thermal injury to supraglottic structures.
  • Review the Parkland formula for fluid resuscitation after a severe burn and the parameters by which fluid resuscitation should be guided.
  • Summarize how interprofessional team dynamics can improve patient outcomes in providing anesthesia for burn patients.


Almost half a million people seek medical care due to burn injuries every year. The anesthesiologist plays a critical role in the management of complicated burn patients in areas of 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. Pathophysiologic changes in the burn patient pose challenges for fluid resuscitation intraoperatively, induction drug selection, as well as special attention to ventilation strategies. The anesthesiologist's role is critical to optimize the care of burn patients.[1][2]

Anatomy and Physiology

Major burns damage tissues directly and result in distortion of the anatomy making traditional airway management, monitoring, and hemodynamic access challenging. Additionally, developing a cytokine-mediated inflammatory response results in pathophysiologic effects both locally and distantly from the injury. This response can be described in two 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 result in edema formation at directly burned areas and unburned sites. Hemoconentration 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 and direct myocardial depression, and increased systemic vascular resistance. In this phase, a rise in systemic vascular resistance occurs due to a surge of catecholamines and antidiuretic hormone constricting blood vessels and inhibiting flow.  Even with aggressive fluid resuscitation, only partial compensation can be obtained due to an imbalance of the cellular transmembrane ionic gradient and reduction of 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 up 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 inhalational 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 hypermetabolic phase is generally characterized by the release of catabolic hormones as well as insulin resistance. The resultant effects of this are protein catabolism (i.e., 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 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


Inhalational Injuries

Inhalational injuries accompanying burns are associated with a significant increase in morbidity and mortality.  Burn patients with inhalational injuries require 30% to 50% more fluid resuscitation compared to their non-inhalational injury counterparts. Chest radiographs may appear benign until further complications develop, such as infection or atelectasis. It may take several days for inhalational injuries to become clinically evident.[1] Inhalational injuries can be divided into three sub-classifications: 

  1. Supraglottic
    • The most common type of inhalational injury to the supraglottic region is typically thermal injury. 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 the development of swelling of various structures (i.e., 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 inhalational injuries can be assessed on 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's innate nature to close, as well as the upper airway's ability to dissipate heat.  Supraglottic swelling typically resolves in 3 to 6 days. The ideal anesthetic approach to a patient with significant supraglottic injuries is to maximize local anesthetic usage and minimize general anesthetics with a fiberoptic approach.  This allows ample time to investigate/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
    • Injury below the glottis is typically caused by the inhalation of noxious chemicals and irritants. These inhaled substances cause direct damage and stimulate inflammation resulting in airway mucosal hyperemia, potential bronchospasm, and mucosal sloughing from inhibiting mucociliary escalator function. Mucociliary impairment contributes to a build-up of bacteria and mucosal debris, increasing the risk of pneumonia in the days following the initial injury. The inflammatory processes inhibit hypoxic pulmonary vasoconstriction resulting in right-to-left shunting of blood, consequently hypoxia. Alveolar collapse occurs because of a loss of surfactant production or plugging by debris. Intermittent bronchospasm and airway edema can further limit oxygenation by inhibiting oxygen delivery to the alveoli. The patient on a ventilator may demonstrate a prolonged expiratory phase and elevated peak inspiratory pressures to suggest these findings. Mucus sloughing resulting in cast formation can obstruct the limited real estate remaining 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 un-obstructed airways resulting in excessive pulmonary pressures to healthy lung tissue propagating barotrauma. This barotrauma can result in acute respiratory distress syndrome (ARDS) and pneumothorax. Acute respiratory distress syndrome 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 to 300 PaO2/FiO2), moderate ARDS (100 to 200 PaO2/FiO2), and severe ARDS (<100 PaO2/FiO2). The primary means of diagnosis of the subglottic injury is clinical by may be supplemented by bronchoscopy. Subglottic inhalational injuries become significant to anesthesiologists due to the necessity of lung-protective ventilation strategies such as low tidal volume (4 to 6 mL/kg) and properly titrated positive end-expiratory pressures to limit barotrauma.[1][6][7]
  3. Systemic
    • The systemic effects of inhalational injuries include hypoxia, acidosis, and systemic inflammation resulting in pulmonary edema. Carbon monoxide and cyanide are soluble in blood, inflicting direct damage to tissues and may inhibit oxygenation. These systemic effects can be checked intraoperatively through arterial blood gas and laboratory studies when clinically indicated. Carbon monoxide inhibits hemoglobin's ability to carry oxygen and has a much higher affinity for hemoglobin than oxygen. Carboxyhemoglobin levels greater than 15% are considered toxic. The burning of nitrogenous materials produces cyanide. Cyanide inhibits oxygen utilization by interacting with the cytochrome system of mitochondria. It blocks the last step of oxidative phosphorylation, preventing the conversion of pyruvate to adenosine triphosphate (ATP); cells may only generate ATP from anaerobic metabolism. Clinical characteristics of cyanide toxicity include an anion gap metabolic acidosis in the presence of ample oxygen delivery. The intraoperative patient with persistent hypoxia and acidosis may be suffering from carbon monoxide or cyanide toxicity.[6]

Carbon Monoxide Poisoning

Pulse oximetry can create a false reassurance of appropriate oxygenation in the setting of carbon monoxide poisoning. Pulse oximetry cannot distinguish between oxyhemoglobin and carboxyhemoglobin. Measurement of carboxyhemoglobin through laboratory studies can be used to quantify the degree of carbon monoxide poisoning. If time is of the essence, a carbon monoxide-oximeter can be utilized. However, these are typically not readily available in modern hospitals. Carbon monoxide has a greater affinity for hemoglobin (about 230 to 270 times more affinity than oxygen) which causes the oxygen-hemoglobin dissociation curve to shift to the left resulting in impairment of delivery of oxygen to the tissues. Indications of carbon monoxide poisoning may include alterations in mental statuses (such as confusion and agitation), nausea, dizziness, and headaches. Any patient with suspected carbon monoxide poisoning should receive 100% oxygen without hesitation. 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.  When the carboxyhemoglobin level drops below 10%, 100% oxygen can be discontinued, but the patient should still be observed for approximately 24 hours to ensure the patient is not advancing towards respiratory compromise. Patients with a carboxyhemoglobin >20% should be considered for intubation and mechanical ventilation to further expedite carbon monoxide elimination 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 can also be considered in severe cases of carbon monoxide poisoning.[1][6][7][8]


Airway Management

Examination of the burn patient presenting for anesthesia in the acute setting should involve proper airway assessment to look for any signs of airway edema that could pose the challenge of a difficult airway.  Decreased mandibular mobility from burn contractures or glottic edema from airway swelling may make laryngoscopy difficult.  The most accepted and safest way to handle a suspected difficult airway after thermal injury to supraglottic structures is fiberoptic intubation using 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 the preservation of 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

Patients with severe burns can have difficult intravenous access due to direct damage to the most common areas for intravenous access (i.e., limbs, neck, groin, etc.) and edema from the burn shock phase or fluid creep from excessive fluid infusion overcompensate for intravascular loss. Delay of fluid resuscitation for more than 2 hours after the initial injury is associated with an increased risk of mortality, therefore, making vascular access an essential and critical component of burn management. When intravascular access proves to be too difficult via conventional means, peripheral intravenous or central venous access, intraosseous access can prove to 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 compared to conventional methods. Despite its faster and easier placement, it is still not as common of an access tool as one would surmise. The most common cause of failure for intraosseous access is placement failure, so familiarizing oneself with the device before critical times is paramount. The most common placement location of an intraosseous needle is typically the proximal tibia, but the proximal humerus is just as effective of a location. The proximal tibia is an advantageous location 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 major anesthetic consideration. Evaporative heat and water loss from the 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/conserving activity (i.e., 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 as well as inhibiting the central thermoregulatory control making even healthy patients prone to hypothermia from the subsequent vasodilation. The critical means to ensure optimal thermoregulation for burn patients include forced-air warming, fluid warming, and raising the operating room temperature for all burn patients. An accurate means of temperature measurement such as a distal esophageal or rectal temperature probe becomes an essential tool for the peri-operative management of severely burned patients.[4][11][12]


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% BSA 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's due to the worsening of metabolic acidosis associated with a large volume of normal saline (0.9%) infusions required for severe burns. Patients with severe burns are already 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 0.1ml/kg/hr
  • 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 clinicians lose focus on the physiologic parameters (particularly urine output) of adequate fluid resuscitation, the phenomenon of "fluid creep" occurs. Fluid creep can be described as excessive volume administration to burn patients past what is appropriate resuscitation for their clinical condition. Fluid creep can result in excessive tissue and pulmonary edema, further complicating the clinical picture. Pulmonary edema can result in worsening respiratory status leading to tracheal intubation or pneumonia.  Airway edema can be worsened by fluid creep, producing a clinical scenario requiring 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 be receiving (i.e., antibiotics, analgesics, sedatives, etc.), which should be included when considering fluid resuscitation. The most important objective finding to taper fluid replacement is urine output which, when not considered, can also result in fluid creep.  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 eight hours. The percentage of the burn's body surface area (BSA) is expressed as a whole number.[1]

Parkland Formula: 4mL x kg x Percentage of burn BSA 

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

  1. Calculate the total amount of Lactated Ringer's to give in the first 24 hours
    • 4mL x 75kg 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
    • 9.000mL/2 = 4,500 of Lactated Ringer's in the first 8 hours
  3. Administer the remaining amount of fluid in the last 16 hours
    • 4,500mL in the last 16 hours 

Estimation of TBSA

The Wallace Rule of Nines is a common method to estimate the TBSA of the burn.  The Rule of Nines is valued for its simplicity and practicality in clinical scenarios.  For smaller burns, clinical providers may use the Rule of Palms, which involves estimating the size of a burn by using the patient's palm to indicate 1% of TBSA. When calculating TBSA for fluid resuscitation or clinical diagnosis criteria, first-degree burns are generally not included (just 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 difficult 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 more accurately determine the TBSA of burns. Accurate estimation of TBSA is important for transfer to appropriate burn centers and to help dictate fluid resuscitation goals. The anesthesiologist needs to have open communication with other health care professionals when accepting the care of a severely burned patient in the operating room to better understand the fluid goals of the patient in the perioperative period. With the prevalence of miscalculations and the ill consequences of fluid creep, the astute anesthesiologist should be able to estimate 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 subsequent to 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 not only more acetylcholine receptors spread throughout the body but also slightly altered receptors. These altered receptors likely have abnormal electrophysiological interactions with succinylcholine producing greater 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. Resistance to the neuromuscular blockade produced by rocuronium can be partially overcome through an increased dose. Rocuronium can provide reasonably good intubating conditions with a dose of 1.2mg/kg after a significant burn injury.[15][16][17]



Severe burn injuries result in impaired immune response related to a surge of cytokine inflammatory markers increasing the risk of infection. Wounds quickly become colonized with gram-positive organisms like Staphylococcus aureus and Staphylococcus epidermis. Over the course of 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 peri-operatively, 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 burn patients is a challenging subspecialty that requires a cautious approach and an understanding of the pathophysiology of burns to optimize clinical outcomes. An understanding of 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 still maintaining spontaneous ventilation and performing fiberoptic intubation.

An understanding of the pathophysiology of burns is essential to anticipate hemodynamic changes in burn patients and the means by which to properly 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 managing burn 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 patients with their vast knowledge of physiology, pharmacology, airway management skills, and critical care skills.  However, it is only through effective communication and coordination between 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. Interdisciplinary work between a myriad of services may be necessary to optimize the care of this complex population.

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] [Level 3] The same multidisciplinary approach to a burn patient with a difficult airway can help to secure the airway in a safer and less harmful way. 

The Parkland Formula can provide a valuable means of estimating the required amount of fluid resuscitation for a burn patient but is subject to human error when providers use this number as the sole number for calculating how much isotonic fluid to administer to the patient. Often, volumes of fluid from intravenous medications are accidentally forgotten to be included. 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 the phenomenon of 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] [Level III[22] 

Effective team communication can help prevent fluid creep and its associated issues. Nursing can ensure accurate intake and output recording and comment to physicians when a large volume of medications are being infused (i.e., antibiotics, sedation, electrolyte replacement, etc.), which are typically forgotten when clinicians calculate fluid resuscitation goals. It is the role of the anesthesiologist and critical care physician to work with the surgeons to make adjustments in the delivery of these fluids so surgical sites or respiratory function are not compromised. It is only through effective communication between team members that outcomes for this complex subset of patients can be improved without changing the current therapies available at hand.

Article Details

Article Author

Nicholas E. Hill

Article Editor:

Sohail K. Mahboobi


7/29/2022 2:09:36 PM



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