EM Critical Care - EB Medicine

EM Critical Care UNDERSTANDING AND CARING FOR CRITICAL ILLNESS IN EMERGENCY MEDICINE

Critical Care Of Severe Thermal Burn Injury Abstract

Robert Preston, MD

Assistant Professor, Division of Burn, Trauma, and Critical Care, Division of Emergency Medicine, Department of Surgery, University of Utah, Salt Lake City, UT

Jeremiah Ray, MD

Severe thermal burn injury is a subset of trauma that necessitates an approach that initially focuses on the airway, breathing, and circulation of the injured patient. Specific features of burn injury, such as direct oropharyngeal injury, inhalation injury, and edema that may result from either the burn itself or as a consequence of iatrogenic fluid administration, render these patients prone to rapid airway deterioration. Clinicians must appreciate that a patient with an initial presentation appearing to be relatively benign may rapidly decompensate and require mechanical ventilation. Altered mental status should not be trivialized and should be assumed to be the consequence of inhalation of poison gas from the burned environment or associated trauma until proven otherwise. Once initial stabilization efforts are successful, local wound care soothes injury and optimizes outcome. During the ensuing 72 hours, patients may ultimately suffer more morbidity and mortality not from the burn injury per se but from the development of burn shock secondary to a profound systemic inflammatory response. Emergency physicians play a key role in ameliorating this response by initiating early and aggressive fluid resuscitation while constantly monitoring volume status to make any necessary adjustments in fluid administration rate. Additionally, familiarity with the criteria for patient transfer ensures appropriate and timely referral to a specialty burn center where dedicated burn teams provide supportive care and surgical intervention, as indicated.

Editor-in-Chief

Volume 2, Number 6 Authors

Division of Emergency Medicine, University of Utah, Salt Lake City, UT Peer Reviewers

Robert Cooney, MD, RDMS, FACEP, FAAEM

Associate Program Director, Emergency Medicine Residency Program, Conemaugh Memorial Medical Center, Johnstown, PA

Julia E. Martin, MD, FACEP

Associate Professor, Department of Emergency Medicine, University of Kentucky College of Medicine, Lexington, KY CME Objectives Upon completion of this article, you should be able to:     1. 2.

3. 4.

Accurately classify burn injury based on depth (degree of injury) and discuss how this informs management, disposition, and prognosis.

Calculate an initial fluid resuscitation prescription and acknowledge the necessity of continually monitoring the various indices of volume status to permit appropriate adjustments.  Provide adequate wound care, including initial cleaning and debridement, the possible application of topical antimicrobials, and an appropriate dressing. Recall the criteria for specialty burn center referral.

Prior to beginning this activity, see “CME Information” on the back page.

Andy Jagoda, MD, FACEP Julie Mayglothling, MD Professor and Chair, Department Assistant Professor, Department of Emergency Medicine, Mount of Emergency Medicine, Sinai School of Medicine; Medical Department of Surgery, Division Lillian L. Emlet, MD, MS, FACEP Director, Mount Sinai Hospital, New of Trauma/Critical Care, Virginia Assistant Professor, Department of York, NY Commonwealth University, Critical Care Medicine, Department Richmond, VA of Emergency Medicine, University of Pittsburgh Medical Center; William A. Knight, IV, MD Program Director, EM-CCM Assistant Professor of Emergency Christopher P. Nickson, MBChB, Fellowship of the Multidisciplinary Medicine, Assistant Professor MClinEpid, FACEM Associate Editor Critical Care Training Program, of Neurosurgery, Emergency Senior Registrar, Intensive Care Pittsburgh, PA Medicine Mid-Level Program Scott Weingart, MD, FACEP Unit, Royal Darwin Hospital, Medical Director, University of Associate Professor, Department of Darwin, Australia Cincinnati College of Medicine, Emergency Medicine, Mount Sinai Michael A. Gibbs, MD, FACEP Cincinnati, OH School of Medicine; Director of Professor and Chair, Department Jon Rittenberger, MD, MS, FACEP Emergency Critical Care, Elmhurst of Emergency Medicine, Carolinas Assistant Professor, Department Hospital Center, New York, NY Medical Center, University of North Haney Mallemat, MD of Emergency Medicine, Carolina School of Medicine, Assistant Professor, Department University of Pittsburgh School Chapel Hill, NC of Emergency Medicine, University of Medicine; Attending Physician, Editorial Board of Maryland School of Medicine, Emergency Medicine and Post Benjamin S. Abella, MD, MPhil, Baltimore, MD Robert Green, MD, DABEM, Cardiac Arrest Services, UPMC FACEP Presbyterian Hospital, Pittsburgh, FRCPC Assistant Professor, Department Evie Marcolini, MD, FAAEM PA Associate Professor, Department of Emergency Medicine and of Anaesthesia, Division of Critical Assistant Professor, Department of Department of Medicine / Emergency Medicine and Critical Care Medicine, Department of Section of Pulmonary Allergy Care, Yale School of Medicine, Emergency Medicine, Dalhousie and Critical Care, University of New Haven, CT University, Halifax, Nova Scotia, Pennsylvania School of Medicine; Canada Clinical Research Director, Robert T. Arntfield, MD, FRCPC, FCCP Assistant Professor, Division of Critical Care, Division of Emergency Medicine, Western University, London, Ontario, Canada

Center for Resuscitation Science, Philadelphia, PA

Emanuel P. Rivers, MD, MPH, IOM Vice Chairman and Director of Research, Department of Emergency Medicine, Senior Staff Attending, Departments of Emergency Medicine and Surgery (Surgical Critical Care), Henry Ford Hospital, Clinical Professor, Department of Emergency Medicine and Surgery, Wayne State University School of Medicine, Detroit, MI Isaac Tawil, MD Assistant Professor, Department of Surgery, Department of Emergency Medicine, University of New Mexico Health Science Center, Albuquerque, NM

Research Editor Amy Sanghvi, MD Department of Emergency Medicine, Mount Sinai School of Medicine, New York, NY

Case Presentations A 44-year-old male presents to the ED via ambulance after a concerned neighbor activated EMS after observing smoke rising from a home roof. The patient was pulled from the front entry at the bottom of a staircase by firefighters who surmise that he fell down the stairs while fleeing from a second-story fire. It is evident that he has left-thigh compartment swelling and burn injury to this extremity as well as to the head, face, and neck. He is mumbling incoherently, and his respiratory rate is 6 breaths per minute. His pulse is rapid and thready, with an SBP of 80 mm Hg. He does not open his eyes but maintains the ability to withdraw without localization to noxious stimuli. A short time later, your ED receives a 26-year-old female by private vehicle who sustained burns to the neck, shoulders, and upper arms and chest secondary to an explosion in a private residence. (See Figure 1.) She admitted that she was cooking methamphetamine and lost control of the process. Her vital signs are: blood pressure of 124/78 mm Hg, heart rate of 120 beats per minute, respiratory rate of 14 breaths per minute, and oxygen saturation of 98% on room air. Her GCS score is 15, and she is able to give a full account of the accident details.

Introduction Since the 1930s, advances in the understanding and treatment of burn injury have resulted in less morbidity, lower mortality, and shorter hospital and intensive care unit stays for survivors of the 450,000 burn injuries that require medical treatment every year in the United States.1 Familiarity with burn injury assessment (including the initial consideration that burn-injured patients are a subset of trauma patients) is a key concept for the emergency physician. If performed well, approximately 90% of burn-injured patients can be safely discharged from the emergency department (ED), which facilitates optimal inpatient resource utilization. (See the Clinical Pathway, page 8.) More importantly, skilled and accurate assessments of the remaining 10% of burn-injured patients form the foundation for initiating fluid resuscitation and timely and appropriate specialty burn consult. The majority of patients hospitalized for burn injury in the United States now receive their definitive care in specialty burn centers, where > 95% of admitted patients survive to discharge.1 Emergency physicians, intensivists, and burn specialists have collectively played important roles in optimizing outcomes by implementing formal resuscitation strategies, following best practices for airway management and ventilator support, initiating early surgical intervention and skin grafting, and undertaking improved infection control and surveillance. Evolving therapies aimed at attenuating the inflammatory response portend even better

EMCC © 2012 2

outcomes. This issue of EMCC focuses on early care of the patient sustaining severe thermal burn injury.

Critical Appraisal Of The Literature A literature search of Ovid MEDLINE® and PubMed for articles related to the management of acute severe burns was performed. The search was narrowed to include only English-language publications and primarily focused on adult human studies, but it did not specifically exclude applicable animal studies. Key words used in the search included critical care burn management, emergency medicine burn management, acute burn management, fluid management in burn injury, infection in burn injury, and wound management in burn injury. Clinical guidelines relevant to the management of burn injury from the American Burn Association, the Cochrane Database of Systematic Reviews, and the National Guideline Clearinghouse were also consulted. Additional articles were identified via bibliography review of the articles found in the primary search described above. This search strategy returned over 5500 articles and reports (as of January 2012). The most weight was given to randomized controlled trials, prospective cohort studies, and aggregate studies including meta-analyses of clinical trials. Other evidence was obtained from retrospective studies, case-controlled studies, and other meta-analyses. Panel consensus, cross-sectional studies, and case reports were also considered in areas lacking stronger evidence.

Burn Injury As A Member Of The Profound Inflammatory Family Burn injury can be conceptualized as 2 distinct temporal processes. Acutely, the primary burn causes variable structural damage to exposed tissues with severity dependent on the type, duration, and intensity of exposure. Of far graver concern, however, is the potential development of a secondary, multifactorial inflammatory response – burn shock – as a consequence of

Figure 1. Female Patient With Third-Degree (Full-Thickness) Burns

Image courtesy of Robert Preston, MD

www.ebmedicine.net • Volume 2, Number 6

the release of various local and systemic vasoactive mediators that compromise capillary integrity and facilitate fluid extravasation into the extravascular space. This process shares many commonalities with other pathologic processes (such as pancreatitis or fulminant sepsis) that incite the inflammatory cascade, including the frequent presence of a superimposed cardiogenic shock component that develops due to direct cardiodepressant effects of circulating cytokines such as tumor necrosis factor-alpha (TNF-alpha).2 The inflammatory cascade further compromises the immune system (which is already challenged by a break in the physical barrier to infection), and tissues far removed from the site of initial exposure can become involved, leading to multiple-organ dysfunction syndrome and death.

arm, and ears – are prone to deeper injury despite what might appear to be a relatively benign appearance on initial evaluation.

Using Lund And Browder To Determine The Percentage Of Total-Body Surface Area

The accurate determination of the percentage of total-body surface area (% TBSA) burned is crucial, as it is an input variable in the calculation of initial fluid resuscitation prescriptions (see below) and is an important consideration when referral to a burn center is contemplated. Unfortunately, calculating % TBSA is notoriously inaccurate when performed by inexperienced6 and experienced7 clinicians alike. To minimize error, particularly with larger burns, avoid using the Wallace “rule of nines”8 to estimate burn size, as it does not account for patient size, differences in body type, or sex-related proportion differences. Furthermore, Wallace’s corollary that the examiner’s hand is equivalent to 1% TBSA has been shown to be confusing (at best) and inaccurate (at worst), since no consideration is given to the relative sizes of examiner or patient, nor is there consensus about what constitutes the boundary of the palm. Instead, use the Lund and Browder diagram to determine % TBSA.9 (See Figure 6, page 5.) In brief, the assessor superimposes a graphical depiction of burned areas on the diagram, being careful to exclude areas of first-degree burn. By consulting the accompanying table, which assigns a % TBSA to each body area, based on anthropometric data, the total % TBSA of the burn-injured area may be easily determined. The Lund and Browder diagram is not without criticism, as it is based on decades-old anthropometric data and has not been validated externally. However, no gold standard exists for comparison, and when

Tools And Techniques For Managing Burns Classifying Burns

The authors advocate for classifying burns according to depth of injury, stratified by degree. (See Table 1 and Figures 2-4, page 4.) The act of dividing second-degree (partial-thickness) burns into 2 separate categories (corresponding to superficial and deep injury) denotes who is likely to benefit from early surgical debridement and skin grafting, since deep second-degree (partial-thickness) burns act, clinically, like third-degree (full-thickness) burns and involve some destruction of the blood vessels, hair follicles, and sweat glands rooted in the deep dermis. Note that burn depth is often heterogeneous (see Figure 5, page 4), particularly in the immediate hours after injury, which renders definitive depth determinations unreliable for up to 3 weeks postinjury.3 It is also noteworthy that certain areas – the perineum, medial thigh area, axilla, anterior fore-

Table 1. Burn Depth Classification System4,5 Designation

Characteristics

Approximate Healing Time

Is Skin Grafting Typical?

First-degree (superficial) burn

• • • •

Erythematous Blanches easily No blistering Painful

2-3 d

No

Superficial second-degree (partialthickness) burn

• • • • •

Erythematous Wet appearance Blanches with pressure Blisters typical Painful

14 d

No

Deep second-degree (partialthickness) burn

• • • •

Wet appearance Does not easily blanch Blisters typical Less painful than above

> 21 d

Yes

Third-degree (full-thickness) burn

• Variable erythematous, blanched, or charred appearance • Does not blanch • Insensate

Highly variable

Yes

www.ebmedicine.net • Volume 2, Number 6

3

EMCC © 2012

computerized planimetry (a method by which a computer calculates % TBSA based on the clinician tracing an outline of the burn on a computer-displayed diagram) is used as the de facto gold standard, the Lund and Browder diagram outperforms the rule of nines with regard to interrater variability,10 and it is designed to attempt to take into account the relative % TBSA affected by growth.3

Figure 2. Superficial Second-Degree (PartialThickness) Burn Of Lower Abdomen

Stabilization In The Emergency Department History

Important historical information may be obtained from family members, bystanders, and emergency medical services personnel. Environmental observations, such as a building collapse or explosion may suggest an increased risk of orthopedic trauma or viscera injury secondary to barotrauma. Confirmation that a fire occurred in a closed space or the knowledge that several unconscious victims were involved may heighten the suspicion of associated carbon monoxide poisoning or indicate that other noxious chemicals may have been liberated from

Figure 4. Third-Degree (Full-Thickness) And Second-Degree (Partial-Thickness) Burn Deep second degree (partial thickness)

Note erythematous appearance with blistering. This wound blanched easily with pressure. Image courtesy of Robert Preston, MD

Figure 3. Third-Degree (Full-Thickness) Burn Third degree Third degree

Third degree The lower part of the burn (white area) is a third-degree (full-thickness) burn. The upper parts are mostly deep second-degree (partialthickness) burns and did not blanch with pressure. Image courtesy of Robert Preston, MD

Figure 5. Heterogeneous Mix Of Superficial And Deep Second-Degree (PartialThickness) And Third-Degree (FullThickness) Burns Third degree

Third degree

Deep second degree (partial thickness) Areas of third-degree (full-thickness) burn are evident based on the white appearance and lack of sensation on physical examination. The surrounding erythematous areas are a combination of superficial second-degree (partial-thickness) burns (blanch with pressure) and deep second-degree (partial-thickness) burns (do not blanch with pressure). Image courtesy of Robert Preston, MD

Third degree White areas represent third-degree (full-thickness) burn. Image courtesy of Robert Preston, MD

For color versions of these figures, please visit www.ebmedicine.net/EMCC1212figures

EMCC © 2012 4

www.ebmedicine.net • Volume 2, Number 6

plastics, textiles, or furniture. An accurate social history may be helpful for general management of the patient who is known to use tobacco, alcohol, or drugs, and it may even provide important prognostic details. For example, victims injured in the production of methamphetamine have deeper burns,11 routinely requiring double or triple the amount of fluid predicted by resuscitation formulas,11,12 and are prone to developing nosocomial pneumonia, respiratory failure, and sepsis,11,12 though this may be related to the fact that these patients have a significantly higher incidence of inhalation injury.11,12

secondary survey should be a conscientious attempt to uncover other injuries (such as inhalation injury, head trauma, bone fractures, or lacerations) and to appreciate subtle injury features that might suggest child or elder abuse. It must be emphasized that the presence of altered mental status should prompt a thorough search for the etiology, as the cutaneous burn would not be expected to be the root cause. The presence of circumferential burn injury to the neck, abdomen, chest, or limbs must be noted and closely monitored in the event that limb- or life-saving escharotomy becomes indicated. Any evidence of hypothermia, drug overdose, or poisoning from carbon monoxide or cyanide should be actively sought.

Physical Examination

A recent review estimated that approximately 10% of burn-injured patients have associated traumatic injuries,5 illustrating that burn injury is an important subset of trauma. Thus, the initial approach should follow Advanced Trauma Life Support® (ATLS®) practices and focus on airway, breathing, circulation, and disability. The patient should be fully exposed, in order to avoid missing burns in hidden areas such as the perineum and axilla, and care should be exercised to remove any hot or burned clothing, dirt, or debris. A low threshold to consider cervical spine injury in the unconscious patient mandates the use of a cervical collar until such injury is excluded. The

Laboratory Studies And Diagnostic Tests

While no evidence in the form of improved clinical endpoints supports specific laboratory or radiologic testing, we advocate a pragmatic approach aimed mainly at establishing baseline indices for comparison as clinical status evolves as well as screening for occult conditions. A complete blood count screens for anemia, and trends in hematocrit can be useful to elucidate hemoconcentration, which is a common phenomenon due to third spacing of fluid. A chemistry panel can establish baseline renal and electrolyte levels, which may become perturbed during the course of a large fluid resuscitation. Coagulation studies are not mandated but could prove prescient should the patient require emergent surgery, need escharotomy, or have signs of disseminated intravascular coagulation. An arterial blood gas with direct measurement (ie, not calculated) of the carboxyhemoglobin level must be performed. Serum lactate is prognostic13,14 and may be a clue to cyanide poisoning, which can present as an otherwise unexplained lactic acidosis. A plain film chest x-ray can assess for aspiration, air trapping, pneumothorax, or other respiratory processes, though it is unhelpful in the early diagnosis of inhalation injury. Peak expiratory flow rate (PEFR), even in relatively benign-appearing cases, should be performed; negatively trending PEFR measurements in the setting of clinical decline in other respiratory parameters (such as oxygen saturation) can portend impending respiratory failure. An electrocardiogram is recommended only in cases of known preexisting coronary artery disease, with evidence of cardiac arrhythmia, or when high-voltage current was a component of the trauma. A noncontrast head computed tomography scan is indicated in comatose patients, as noxious inhalation should not be assumed.

Figure 6. The Lund And Browder Diagram

Fluid Resuscitation

Over 80 years ago, Underhill recognized the key role of fluid resuscitation in the recovery and survival of burn-injury patients,15 and subsequent work linked

Used with permission from the University of Utah Burn Center.

www.ebmedicine.net • Volume 2, Number 6

5

EMCC © 2012

fluid requirements to patient weight and % TBSA burned.16 Like other illnesses characterized by a profound inflammatory response, it is preferable to anticipate and prevent shock rather than to wait to initiate treatment only after it is recognized. Shock develops rapidly if burns involve more than 15% to 20% of TBSA,6 underpinning the American Burn Association recommendation that a formal fluid resuscitation strategy should be implemented for nonsuperficial burns affecting > 20% TBSA.17 What is not known is precisely what the resuscitation strategy should comprise in terms of amount and type of fluid, since no study definitively answers this clinical quandary and a great degree of provider and regional practice variation exists.14 The most common formula used to calculate an initial fluid resuscitation prescription is the Parkland Formula, named for the Dallas hospital where Baxter and colleagues determined that adequate resuscitation was achieved in the majority of patients by using 3.7 to 4.3 mL/kg/% TBSA of crystalloid.18,19 These seminal works serve as the basis for the current formula that decrees the use of 4 mL/kg/% TBSA of crystalloid fluid during the first 24 hours following burn injury. Half the volume is infused in the first 8 hours postinjury (not from the time the patient sought medical treatment), with the remaining aliquot given over the subsequent 16 hours. Lactated Ringer’s solution was originally recommended, based on a belief that this crystalloid most closely approximates human body fluids. Since no evidence directly supports the choice of lactated Ringer’s over other crystalloid solutions, the authors recommend that an appropriate crystalloid be chosen based on prevailing electrolyte levels to avoid sodium perturbations and hyperchloremic acidosis. Though its simplicity renders the Parkland Formula attractive, it has been criticized because of observations that modern physicians are using more fluid compared to historical averages, a phenomenon coined “fluid creep.”20 Whereas, in Baxter’s original work, only 12% of patients required more fluid than the formula predicted, recent studies suggest that up to 84% of patients significantly exceed their Parkland Formula prediction,21-24 and a report comparing patients from the 1970s to an agematched and %-TBSA-burn-matched cohort 30 years later found that the modern group received roughly double the amount of fluid.25 However, “fluid creep” might reflect an appropriate shift in management as the understanding of burn injury has evolved. For instance, it may be that modern patients require more fluid owing to a vasodilatory effect secondary to increased usage of narcotics as clinicians have placed appropriate emphasis on pain control.26,27 If true, then modern cohorts of burn-injured patients may require further study in order to revise the Parkland Formula or to discard it altogether for an

EMCC © 2012 6

alternative strategy. Alternatively, fluid creep may be the consequence of clinician errors in calculating, adhering to, or adjusting Parkland Formula prescriptions based on inaccurate volume assessments or biased approaches to adjusting fluid administration. Urine output has been considered a key indicator of adequate shock therapy in the burn patient since the 1950s28 and persists today among burn specialists as the major index.29 However, taken in isolation as an index of systemic perfusion, urine output is a poor performer,30-32 as it has been demonstrated that a hypovolemic state can exist despite preserved urine output.32,33 No randomized trial has yet identified a single variable that, when taken in isolation, is capable of being an accurate and reproducible indicator of volume status, nor is there a consensus about precisely which combination of variables and tools should be used to best assess systemic perfusion.30,32,34-40 In addition to the error mentioned above, where a true hypovolemic state may be missed if the patient has preserved urine output, the converse is also true: fluid creep may be the consequence of physicians opting to increase fluid rates based solely on observed oliguria in situations where other available indicators suggest that the patient is euvolemic or even hypervolemic. Even if urine output is an accurate index of volume status in a particular patient, fluid creep may be the unintended consequence of a generation of physicians ever ready to increase fluids in the setting of oliguria but disinclined to match this vigilance with corresponding adjustments when urine output is more than adequate.23,41 Saffle et al pointed out that many burn intensive care unit physicians are cross-trained as general intensivists and may have a propensity to resuscitate patients with a liberal fluid strategy, as is recommended in the Surviving Sepsis Campaign (a high-profile initiative to optimize care in a patient population also considered to be marked by a great degree of inflammation).42 Whether the principles governing fluid resuscitation in the patient with fulminant sepsis are generalizable to the burn patient has not been clarified. Alternatives to the Parkland Formula exist, including the modified Brooke formula, which mandates half the volume of fluid for the initial prescription (2 mL/kg/% TBSA) compared to the Parkland Formula. However, no study supports the use of one formula over another in terms of improving meaningful endpoints or outcomes. Rather than perseverating about the virtues of one resuscitation formula relative to another, it is necessary to grasp the concept that any fluid prescription – regardless of which equation was used to derive it – should be considered merely an initial guide to resuscitation and not an infallible, rigid order to be completed regardless of subsequent clinical course. The physician must carefully titrate fluid administration to achieve adequate organ and tissue perfusion (based on consideration of the availwww.ebmedicine.net • Volume 2, Number 6

Pain Management

able spectrum of monitored variables) while striving to avoid the complications of too much fluid, which include pulmonary edema, cardiac failure, abdominal compartment syndrome, and fasciotomies of not only burned limbs but also limbs not involved in the initial bun insult.13,14,35,43 Unfortunately, even if resuscitation prescriptions are accurately calculated and appropriately titrated, victims can have fluid-related complications. Patients with large burns are particularly at risk, as their initial fluid prescriptions commonly exceed 250 to 300 mL/kg in a 24-hour period. This threshold is associated with the development of intra-abdominal hypertension,44,45 orbital compartment syndrome,46 and increased risk of infectious complications, acute respiratory distress syndrome, and death.41 It must be acknowledged, however, that a causal relationship has not been established, since those who received fluid volumes greater than the abovementioned threshold also had worse injury severity scores41 and would be predicted to have worse outcomes independent of fluid administration.

Partial-thickness burns are particularly painful, owing to exposure of raw tissue with preservation of nociceptors in the deep dermis. No definitive agent or strategy has proven effective in all settings. The selected regimen should be structured, be tailored to the patient and the prevailing clinical setting, and involve both pharmacologic and nonpharmacologic therapies.53 The most commonly used pharmacologic agents are opioids, and their prevalent use does not appear to translate into higher incidence of opioid dependency.54 While no head-to-head trials have been performed to compare various narcotic agents, fentanyl (Sublimaze®, Actiq®, Duragesic®) and hydromorphone (Dilaudid®, Palladone®) may be preferable to morphine. Burn injury prolongs morphine’s half-life,55 and its association with histamine release can contribute to hypotension (and thus beget more fluid) as well as pruritus, a particular problem with cutaneous injury and nascent skin grafts. Delivering pain medication via patient-controlled analgesia is a safe option in the alert patient and has the benefit of affording the patient a modicum of control over their management while also being more efficient from a nursing perspective.54 If the sedative, propofol, is used for a synergistic approach to pain control, dosing may be higher than typically administered since burn patients clear it more rapidly.56 Benzodiazepines should be used when anxiety is demonstrably present, as they may be synergistic with pain relievers, particularly in the setting of severe pain.57 Highquality data are absent to guide optimum nonopioid therapy, but ketorolac (Toradol®, Acular®), dexmedetomidine (Precedex®, Dexdor®), and ketamine (Ketalar®) are all potential adjuncts or short-term options for debridement and dressing changes. Dexmedetomidine may be suitable if sedation, anxiolysis, and pain control are all required, as it provides multimodal relief and typically preserves respiratory drive better than other sedative pain-control combinations.58 Local or regional pain blocks can be employed for dressing changes and limited debridement.

Monitoring

Routine vital signs should be monitored, with the caveat that a normal pulse oximeter reading may not be reliable if carbon monoxide poisoning is present because the technology cannot differentiate between carboxyhemoglobin and oxyhemoglobin. Continuous pulse oximetry is reliable once carbon monoxide levels return to normal. Diminished pulse pressure may indicate shock before a fall in systolic blood pressure occurs.13 Invasive blood pressure monitoring with an arterial catheter is more accurate in the setting of tissue edema, as cuff measurements can underestimate blood pressure in this setting.47 Urine output with a goal of 30 to 50 cc/h48 is one index of volume status, and the American Burn Association practice guidelines recommend maintaining at least 0.5 mL/kg/h,17 but sole reliance on this variable should be avoided, as previously discussed. Central venous pressure, though still frequently used, is unsupported by the literature to guide fluid management.49 Resuscitation in well-resourced intensive care units and certain tertiary care EDs may be aided by the ability to monitor cardiac output using systems that utilize arterial pulse wave contour50 or via Swan-Ganz catheter (which also permits trending of central venous oxygen saturation). Trends in serum lactate51 may prove useful to guiding resuscitation and may be more practical in the vast majority of EDs. Distal pulses should be monitored, and physicians should be cognizant that inadequate fluid resuscitation is the most common etiology of loss of distal pulses in fresh burns.52 When adjudicating volume status that might lead to altering fluid infusion rates, physicians are urged to consider all available indices in their particular clinical environment rather than relying on any singular variable. www.ebmedicine.net • Volume 2, Number 6

Blood Products

Burn-injured patients typically become hemoconcentrated in the initial hours after injury, often obviating the need for transfusion. When transfusion is considered for the anemic or actively bleeding burntrauma patient, it is safer to maintain a restrictive transfusion threshold similar to the practice recommended for other critical-care populations.59 In 1 study, administering even 1 unit of packed red blood cells to a burn-injured cohort increased the risk of infection,60 and patients managed with a restrictive transfusion strategy (mean hemoglobin of 7.1) have been found to have less organ dysfunction and lower mortality.61 The use of fresh frozen plasma is discouraged as a volume expander and should in7

EMCC © 2012

Clinical Pathway For Management Of The Burned Patient Initial ATLS® approach (Class I)

NO

Patient stable?

Resuscitate via ATLS® algorithm until stable (Class I)

YES

• • • •

Full history and physical examination Determine burn classification Calculate % TBSA burned Evaluate for concomitant injuries: Inhalation injury Carbon monoxide poisoning Cyanide poisoning Associated trauma (orthopedic, visceral, intracranial, spinal, or blast injury) n

n

n

n

Criteria met for transfer to burn center? 1. Extremes of age 2. Multiple comorbidites 3. > 10% TBSA burned 4. > deep partial-thickness 5. Burn is circumferential or affects face, genitalia, or perineum 6. Electrical or chemical burn 7. Significant concomitant trauma 8. Inhalation injury

ED Management 1. Remove ruptured blisters and devitalized tissue (Class III) 2. Wash burn with mild soap and lukewarm water (Class II) 3. Apply topical ointment and dressing (Class II) 4. Treat pain (Class I) 5. Update tetanus booster, if necessary (Class II)

NO

YES

Admit

• Concern for inhalation injury? • Inability to control pain? • Oral intake intolerable?

YES

Transfer (Class I)

NO

Abbreviations: ATLS®, Advanced Trauma Life Support®; ED, emergency department; TBSA, total-body surface area.

Primary care provider followup (Class Indeterminate)

Class Of Evidence Definitions Each action in the clinical pathways section of EM Critical Care receives a score based on the following definitions. Class I • Always acceptable, safe • Definitely useful • Proven in both efficacy and effectiveness

Level of Evidence: • One or more large prospective studies are present (with rare exceptions) • High-quality meta-analyses • Study results consistently positive and compelling

Class II • Safe, acceptable • Probably useful

Level of Evidence: • Generally higher levels of evidence • Non-randomized or retrospective studies: historic, cohort, or case control studies • Less robust randomized controlled trials • Results consistently positive

Class III • May be acceptable • Possibly useful • Considered optional or alternative treatments

Level of Evidence: • Generally lower or intermediate levels of evidence • Case series, animal studies, consensus panels • Occasionally positive results

Indeterminate • Continuing area of research • No recommendations until further research

Level of Evidence: • Evidence not available • Higher studies in progress • Results inconsistent, contradictory • Results not compelling Significantly modified from: The Emergency Cardiovascular Care Committees of the American Heart Association and represen-

tatives from the resuscitation councils of ILCOR: How to Develop Evidence-Based Guidelines for Emergency Cardiac Care: Quality of Evidence and Classes of Recommendations; also: Anonymous. Guidelines for cardiopulmonary resuscitation and emergency cardiac care. Emergency Cardiac Care Committee and Subcommittees, American Heart Association. Part IX. Ensuring effectiveness of communitywide emergency cardiac care. JAMA. 1992;268(16):2289-2295.

This clinical pathway is intended to supplement, rather than substitute for, professional judgment and may be changed depending upon a patient’s individual needs. Failure to comply with this pathway does not represent a breach of the standard of care. Copyright ©2012 EB Medicine. 1-800-249-5770. No part of this publication may be reproduced in any format without written consent of EB Medicine.

EMCC © 2012 8

www.ebmedicine.net • Volume 2, Number 6

stead be reserved for the truly coagulopathic and/or actively bleeding patient due to the risk of infection as well as the economic and supply dynamics inherent to its use.13,17,62

and quantification of the affected area. The wound should be washed with mild soap and lukewarm water. Cooling the burn and surrounding tissue with gauze soaked in cold saline in hopes of easing pain and staunching the spread of burn injury through tissue planes is practiced by many physicians, but there is a dearth of evidence to support this strategy. In addition, if the saline is too cold, hypothermia could result, especially if the burn affects a large surface area and a prolonged transport is required. Ice should be avoided entirely.5 Firstdegree (superficial) burns and superficial seconddegree (partial-thickness) burns with intact epithelium require no topical agent.66 For all other burns, the application of topical antimicrobial preparations (Table 2) reduces microbial load within the wound and speeds re-epithelialization by maintaining a moist environment.67-70 There is a paucity of quality data comparing topical agents head-to-head,63 so choices are based on empiric knowledge of microbial susceptibility and formulary availability. Silver nitrate 0.5% is associated with electrolyte disturbances and poor wound penetration, so it is rarely used except for cases when the patient’s risk factors suggest a possible benefit from the inherent antifungal properties that this preparation affords.4 Silver sulfadiazine effectively controls colonization, is cheap, and is simple to apply as a thick white cream once or twice per day. It should be avoided in patients with sulfa allergies, in women in the last term of pregnancy (because it can cause kernicterus), and in women who are nursing71 or have children

Wound Care

For the burn-injured patient, wound care refers to the initial cleaning and debridement of the wound, the possible application of topical agents, and choosing an appropriate dressing. The principle aims are to protect the wound from further trauma and contamination, ameliorate pain, provide a moist environment to facilitate wound healing, and temper bacterial colonization in an effort to avoid invasive infection. No evidence endorses a single all-encompassing strategy, and considerable variation exists among physicians and between specialty centers.63 After providing adequate pain control, any devitalized tissue (including ruptured blisters) should be gently removed by peeling, cutting, curettage, or gentle brushing/scraping with moistened gauze. The removal of intact blisters remains contentious, with no supporting data to guide physicians.64 Those who favor leaving blisters intact believe that this preserves a mechanical barrier to infection and that the contained fluid hastens wound healing; others believe that the fluid exerts the opposite effect. No data exist to support either claim. The authors recommend removing all but the most trivial blisters, provided that other aspects of wound care are adhered to, so as to provide a clean and moist environment and to permit the most accurate assessment

Table 2. Topical Ointments And Burn Dressings Type

Advantages

Disadvantages

Topical Ointments Topical antimicrobials

• Reduce microbial load • Speed re-epithelialization

Silver nitrate 0.5%

• Has antifungal properties

• Causes electrolyte disturbances • Has poor wound penetration

Silver sulfadiazine

• Controls colonization

• Must be avoided in pregnant, nursing, or infant patients • Can cause hemolysis and leukopenia (rarely)

Mafenide acetate

• Has excellent wound penetration • Has pseudomonal activity

Honey

• Results in faster wound healing (in limited studies)

Dressings Nonadherent fine mesh gauze

• Can remove scab and soiled gauze en bloc • Is inexpensive

• Increases pain due to more-frequent (daily) dressing changes

Hydrocolloid dressings

• Reduce healing time • Improve patient satisfaction due to less frequent dressing change

• Cost

Silver-impregnated dressings

• Has additional antimicrobial coverage • Requires less-frequent dressing changes

• Cost

www.ebmedicine.net • Volume 2, Number 6

9

EMCC © 2012

< 2 months of age. It should also be avoided in areas near the eyes and mouth due to ocular irritation and keratitis,72 and it has been linked to hemolysis and leukopenia.73 Mafenide acetate has superior eschar penetration relative to silver sulfadiazine, so it is a fitting choice if eschar excision is likely to be delayed; additionally, it has activity against Pseudomonas, rendering it well suited for wounds believed to have a high bacteria burden.74 Nonsilver products (including triple antibiotic ointments with broad gram-negative and gram-positive activity such as polymyxin B, neomycin, or mupirocin) can also be used.69 According to 9 randomized or quasirandomized controlled trials conducted by a single author (recently summarized in a review75), a modestly faster wound-healing time may be achieved by applying honey. Burn dressings protect the wound and absorb exudate. Nonadherent fine mesh gauze dressings are typically changed once per day to avoid traumatizing tissue unless obvious contamination, excessive exudate, or infection is apparent. Combining dressings with one of the topical agents above is preferable, as the moist environment can lessen pain when changing dressings and promotes wound healing. If no topical agent is available, fine mesh gauze alone can be used to dress the wound. Fine mesh gauze promotes the formation of scabs; when dressing changes are performed, the scab and gauze can be removed en bloc for wound inspection, antisepsis, and redressing. As an alternative to gauze, hydrocolloid dressings work by forming a gel barrier when the polymer matrix comes in contact with burn exudate. These dressings permit less-frequent dressing changes (every 5 days), reduce healing time, and result in higher patient satisfaction scores relative to fine mesh gauze/silver sulfadiazine combination dressings.63 Silver-impregnated dressings (eg, Mepilex®, Aquacel®, Acticoat®) release silver into the wound to provide antimicrobial coverage and may provide an anti-inflammatory effect76 and result in less-frequent dressing changes,77 but a meta-analysis failed to confirm any positive effect on wound healing or infection rates.78

Consideration For Carbon Monoxide And Cyanide Poisoning

Altered mental status may be due to shock, head injury, drug ingestion, or alcohol intoxication, but it may also be caused by poisoning from carbon monoxide or cyanide. The use of 100% oxygen decreases the half-life of carbon monoxide from an average of 280 minutes to as little as 40 minutes,79 and oxygen should be applied empirically in suspected cases until the carboxyhemoglobin level is confirmed to be normal. Instituting treatment with hyperbaric oxygen in confirmed cases is an option, but evidence-based data to guide initiation triggers, to guide duration of therapy, and to confirm efficacy are lacking.80 In gen-

EMCC © 2012 10

eral, the authors do not recommend this, even in the setting of confirmed carbon monoxide poisoning, owing to the inherent difficulty of managing a massive fluid resuscitation and possibly an unstable airway in the confines of a hyperbaric chamber. With regard to the latter, should it be determined after careful deliberation that hyperbaric therapy is in the interest of the acutely burned patient, it should be considered almost mandatory that the patient be intubated prior to entering the chamber. Cyanide poisoning shunts cellular metabolism to anaerobic pathways as mitochondria shut down. Determination of cyanide blood levels is possible, but an unexplained lactic acidosis in a patient with a history of exposure to incendiaries that might liberate cyanide should prompt empiric treatment. Cyanide poisoning should also be considered when patients present in cardiac arrest or experience a precipitous decline in cardiac function. Treatment for cyanide poisoning in the setting of burn injury diverges from what many consider the standard first-line therapy for cyanide poisoning, namely inhaled amyl nitrite followed by intravenous sodium nitrite. This combination is efficacious because it promotes the formation of methemoglobin, which binds the cyanide ion to form cyanomethemoglobin, leaving cytochrome oxidase unmolested by cyanide and able to continue unabated in its role in aerobic metabolism. In the setting of burn injury, however, coincident carbon monoxide may be present, creating a “double whammy” effect on oxygen-carrying capacity, with potentially dire consequences. Instead, treatment with the sulfur donor sodium thiosulfate (which combines with cyanide to form the much-less-toxic thiocyanate) and/or hydroxocobalamin (which combines with cyanide to form cyanocobalamin, which is readily excreted in urine) is preferred. Nonetheless, some commercially available cyanide antidote kits may leave the physician little option, and the contraindication of amyl nitrite/sodium nitrite is only relative.81,82 If critical iatrogenic methemoglobinemia develops, the application of hyperbaric oxygen therapy may be contemplated, though the concerns raised previously remain valid.

Tetanus Prophylaxis

Based upon case reports of nonimmunized or incompletely immunized patients, tetanus immunization (tetanus toxoid, reduced diphtheria toxoid, and acellular pertussis [Tdap]) should be administered for burn injuries more severe than first-degree (superficial) burns if more than 5 years have elapsed since the last booster.83 Although this review does not specifically address the pediatric population, burn patients who have not received the complete primary immunization series of 3 doses of tetanus toxoid should have human tetanus immune globulin administered.84 www.ebmedicine.net • Volume 2, Number 6

hour.42 If, after 2 hours, these adjustments have failed to get the resuscitation on track, colloid in the form of albumin may be helpful. Whereas empiric colloid resuscitation fails to confer benefit13,93-96 and may cause harm (based on a meta-analysis that reported a 2.4-fold risk of death among those receiving colloid vs crystalloid),62 limited evidence supports the use of colloid as a “rescue therapy” in the subset of patients that appears to be requiring more fluid than predicted by the Parkland Formula. In these patients, the addition of a colloid infusion allowed a return to predicted rates.14,97 Another option, hypertonic saline, diminishes the volume of fluid required, and a small study found a positive impact on rates of abdominal compartment syndrome.44 Nonetheless, in the absence of a robust, well-designed trial, the authors do not recommend using hypertonic saline, based on associations with acute kidney injury and increased mortality.98

Deterioration In The Emergency Department Airway Management

Patients with moderate or severe burns may require definitive airway management, particularly if inhalation injury (a leading cause of death in burned adults85,86) is present. However, even when inhalation injury is absent, massive fluid resuscitation can lead to airway edema, mandating measures to secure the airway. Unfortunately, no clinical factors reliably predict which patients will proceed to near or complete obstruction.87 Since patients with even mild burns with inhalation injury should be admitted for observation due to the hazards of progressive swelling, equivocal inhalation injury should be excluded by direct laryngoscopy or fiberoptic bronchoscopy in the ED. If intubation is required, rapid sequence induction is indicated. Theoretical concerns about precipitating severe hyperkalemia with succinylcholine are unwarranted in acute burns, as this phenomenon requires 5 to 15 days for the proliferation of acetylcholine receptors to occur.88 Similarly, the well-described resistance to nondepolarizing agents takes a similar interval to arise.89 Once intubated, a lung-protective ventilation strategy should be utilized, since the use of low tidal volumes reduces acute lung injury and improves outcome.43 The use of bronchodilators may have utility if bronchospasm is present, but corticosteroids should otherwise be avoided due to an association with increased infection rates.87

Escharotomy

Raised compartment pressures can occur in limbs with circumferential burns as peripheral edema accumulates due to the profound local inflammatory reaction, but the combination of massive fluid resuscitation and conversion of the local inflammatory reaction to a systemic response can result in elevated compartment pressures even in unburned limbs. No study has established a precise value that should prompt escharotomy, but expert guidelines suggest that the procedure should be considered if compartment pressures exceed 25 mm Hg.99 This is in agreement with management strategies for compartment syndrome due to other causes, but given the lack of evidence-based guidelines, the authors advise the physician to consider other factors, such as the presence of hard signs of neurovascular compromise, if ongoing resuscitation needs are expected to remain robust or as the gap between compartment pressure and diastolic pressure narrows to < 30 mm Hg. It is worth noting the distinction between escharotomy and fasciotomy, since the former may be sufficient for limb salvage in a burned extremity but the latter may eventually be required in burned and nonburned limbs alike. In addition to critical limb constriction, mechanical constriction of the neck, chest, or abdomen may interfere with adequate respiratory excursion, necessitating escharotomy of the affected body area.

Fluid Resuscitation Failure: Additional And Alternative Fluids

Certain factors predict a need for higher resuscitation volumes than predicted by the Parkland Formula. Inhalation injury is one such factor,18,90-92 though this has also been refuted.41 The occurrence of deeper burns and delays in resuscitation from the time of injury18,90,91 as well as burns sustained from an electrical source92 render the victim fluid avid. Patients who require mechanical ventilation independent of inhalation injury23,41,91 and patients with injury sustained with evidence of alcohol or drug intoxication91 can have raised fluid requirements. Age41 and the need for escharotomy or fasciotomy92 also predict increased fluid needs. With or without the presence of these factors, when the physician considering all of the imperfect variables used to assess volume status judges that the patient is being underresuscitated despite administering a carefully calculated resuscitation prescription, several options are available. The first option is to increase the crystalloid infusion by 10% to 20% (or 100-200 mL/h, whichever is greater) for 1 hour and reassess. If the clinical parameters that indicated that the patient was failing resuscitation do not improve, the infusion may again be increased by the same proportion for a second www.ebmedicine.net • Volume 2, Number 6

Controversies And Cutting Edge Therapy Systemic Prophylactic Antibiotics

Primary injury from burn insult compromises mechanical immunity and provides ready access to lymph or blood for bacteria that can proliferate in the milieu inherent to the injured, necrotic tissue. As such, burn-injured patients should be considered to be in an immunocompromised state,100-102 lead11

EMCC © 2012

ing some to suggest a role for systemic prophylaxis. The current standard of care is to defer their use,67,103 though no high-quality evidence has been offered to settle the issue definitively. Both the Infectious Diseases Society of America and the Surgical Infection Society endorse the strategy of deferral, but they acknowledge the low-quality evidence supporting this stance.104 A 2010 systematic review and metaanalysis of 17 randomized controlled trials involving 1113 patients concluded that a 4- to 14-day course of systemic prophylactic antibiotics reduced all-cause mortality by nearly one-half but was accompanied by increased microbial resistance; however, the authors had concerns about the poor quality of the individual trials in the analysis.105 Collectively, these studies underscore the need for a robust randomized controlled trial to settle this issue. Until this occurs, it is not recommended that systemic prophylactic antibiotics be employed unless concomitant indications or patient-specific factors favoring their use exist.

Vitamin Therapy

Burn injury can prompt the release of free radical oxygen species that promote fluid shifts into the interstitium. Ascorbic acid (vitamin C) is an antioxidant thought to ameliorate the inflammatory response by scavenging free radicals, and patients receiving high-dose ascorbic acid (66 mg/kg/h for 24 h) within the first 48 hours of burn injury have been shown to have lower fluid requirements and fewer ventilator days.106,107 A large randomized controlled trial is still required for this to become standard of care, but it is currently a treatment option with seemingly little downside and is now being used sporadically in the United States, including at the authors’ own institution. Animal studies of supplementation with vitamin A108 or pentoxifylline109 and replenishment of trace elements such as zinc are other promising therapies aimed at attenuating the immune response that await investigation in humans.

Plasmapheresis

Circulating inflammatory mediators play a key role in developing and sustaining burn shock, leading to the possibility that plasmapheresis could be a therapeutic candidate by removing inflammatory agents from the circulation. A small retrospective review of patients with large burns requiring significantly more fluid than predicted by the Parkland Formula found that plasmapheresis resulted in improved hemodynamic status and urine output, with overall reductions in fluid requirement and serum lactate.110 However, a subsequent trial by the same group in which 22 adults were randomized to a treatment group receiving plasmapheresis found no difference in the amount of fluid required for resuscitation (nor was the course of burn shock attenuated) but did find that resuscitation was completed earlier.111

EMCC © 2012 12

The largest study, to date, was recently completed in which 21 patients requiring total resuscitation volumes exceeding 120% of Parkland Formula predictions underwent plasmapheresis and were retrospectively compared to 19 matched controls. The treatment group had better mean arterial pressure and greater urine output with concomitant reductions in fluid requirements and serum lactate.112 A strong recommendation for plasmapheresis cannot be given until prospective randomized trials confirm efficacy, but it should be regarded as a treatment option for those with elevated admission lactates who appear to be failing resuscitation despite using more than 120% of an appropriately derived Parkland Formula fluid prescription.

Beta Blockers

Beta blockade improves glucose control and helps patients resist sepsis.113 Preinjury beta-blocker use is associated with faster healing and improved mortality,114 and 1 randomized controlled trial in which patients received propranolol confirmed a benefit on healing time, resulting in shorter hospital stays.115 On this basis, propranolol is recommended, though current practice is to begin therapy after the initial resuscitation is complete. Future studies will be required to clarify the utility of other beta blockers.

Oxandrolone

Anabolic agents have mechanistic appeal; in the pediatric population, they have been shown to restore lean body mass, improve nutritional status and wound healing, and result in shorter hospital stays.116 Several small single-center adult trials failed to uncover much of an effect, but a large multicenter trial was stopped early when length of hospital stay plummeted 28% among those with large burns (20%-60% TBSA) who received oxandrolone 10 mg twice daily from the point at which enteral nutrition was tolerated until discharge.117 A subsequent multicenter observational study demonstrated reductions in mortality.118 At the authors’ institution, intensivists managing patients with large burns consider oxandrolone as soon as the patient is tolerating enteral nutrition.

Disposition Approximately 60% to 70% of burns seen in EDs affect < 10% TBSA119 and are suitable for outpatient management after minor debridement and topical wound management, provided the patient can tolerate oral intake and outpatient follow-up is assured. Patients with moderate burns may be admitted to a nonspecialty center hospital bed for hydration, pain control, and observation. For other patients, the optimum inpatient care is delivered in a burn specialty center.7 Transfer guidelines broadly encompass patients at the extremes of www.ebmedicine.net • Volume 2, Number 6

age, those with significant comorbidities, or those with burns that are particularly large or affecting delicate anatomical areas.120,121 (See Table 3.) Deep second-degree (partial-thickness) burns and thirddegree (full-thickness) burns tend to scar badly compared to shallower burns; thus, they usually undergo surgical excision of necrotic and nonviable tissue followed by skin grafting or the application of cultured skin substitutes at the specialty center. Burn surgeons increasingly choose to operate early, based on data indicating attenuated inflammatory response and lower rates of sepsis.122,123 A comprehensive review on the timing of operative intervention is beyond the scope of this review, and the burn community has not yet reached consensus on this aspect of burn care. However, 1 report of a small cohort of patients under the age of 30 suggested that operation within the first 72 hours improved mortality and shortened length of stay,124 so timely transfer of appropriate individuals is prudent.

ing for the duration of the resuscitation allows the emergency physician to make global assessments of volume status and adjust the fluid prescription accordingly so as to balance end-organ perfusion against the complications of overresuscitation. Local wound care involves cleansing and limited debridement with the application of topical antibiotics and a clean, dry dressing. When stabilized patients meet transfer criteria, they should be expeditiously referred to a specialty burn center, where early eschar excision and skin grafting is increasingly utilized.

Case Conclusions Prior to the first patient’s arrival, he was designated as a Level I trauma. ATLS® procedures were followed in the trauma bay, and recognizing that the patient was unstable from a hemodynamic and respiratory perspective, rapid sequence induction and intubation were performed. Then, 100% oxygen was empirically administered for carbon monoxide poisoning, and a cervical spine collar was applied. Using the Lund and Browder diagram to determine the % TBSA of second- and third-degree burns, an initial fluid resuscitation prescription was begun based on the Parkland Formula. The patient’s left lower extremity, neurovascularly intact, was splinted. Notable initial lab values included a carboxyhemoglobin of 21%. Initial imaging confirmed a left femur fracture, but computed tomography imaging revealed no intracranial or associated traumatic injury to the spine, chest, or abdomen. The patient was admitted to the burn unit for further resuscitation with trauma and orthopedic consult for probable interval repair of the femur fracture. After a primary and secondary survey were performed to exclude nonburn injury, the second patient was given hydromorphone for pain and started on a 2-L bolus of normal saline while the % TBSA of the burn was determined and a fluid prescription was calculated with the Parkland Formula. As it was now 90 minutes since the initial burn, the maintenance rate was recalibrated to account for normal patient management fluid requirements and half of the calculated prescription volume – minus the initial 2 L that was administered as an empiric bolus – to be infused over the next 6.5 hours. An arterial blood gas returned a normal value for carboxyhemoglobin. Her wounds were cleaned, and blisters were debrided. Topical antibiotics and fine mesh gauze were applied to the wounds. After 2 hourly intervals of relative hypotension, tachycardia, and oliguria despite having increased fluid administration by 10% each hour, the patient began to desaturate and develop crackles bilaterally. She was intubated with rapid sequence induction. Her fluids were again increased 10% per hour; over the next 2 hours, with her respiratory status supported by the ventilator, her hemodynamics improved. Phone consultation with a burn surgeon was done, and arrangements for transfer to a regional burn center were made.

Summary The collective efforts of emergency physicians, intensivists, and burn surgeons have significantly decreased morbidity and mortality in burn-injured patients over recent decades. After applying ATLS® principles to the acutely burned patient, emergency physicians should rapidly and accurately assess the extent of the burn with an appropriate tool, such as the Lund and Browder diagram. This permits the emergency physician to derive and initiate an initial fluid prescription in anticipation of the development of burn shock. Continued real-time monitor-

Table 3. Adult Patient Criteria For Burn Center Referral120,121 • Second-degree (partial-thickness) burns or third-degree (full-thickness) burns totaling > 20% TBSA (if patient between ages of 10 and 50) or > 10% (if patient outside this age range) • Third-degree (full-thickness) burns > 5% TBSA (any age) • Second-degree (partial-thickness) burns or third-degree (full-thickness) burns that involve face, hands, feet, genitalia, perineum, or skin overlying major joints • Electrical burns, including lightning injury • Chemical burns • Inhalation injury • Burn injury in patients with sufficient preexisting medical disorders that could complicate management, prolong recovery, or affect mortality • Presence of concomitant trauma in which burn injury is the greatest threat. If the trauma is judged to be more serious, the patient may be initially stabilized in a trauma center prior to transfer to a burn specialty center • Burn injury in patients who will require special social, emotional, or rehabilitative intervention Abbreviation: TBSA, total-body surface area.

www.ebmedicine.net • Volume 2, Number 6

13

EMCC © 2012

Must-Do Markers Of Quality Care • Apply appropriate ATLS® algorithms with due consideration of associated injuries exclusive of burn. • Assign burn classification based on depth of injury. • Use a precise quantification of % TBSA affected. • Perform an arterial blood gas analysis with direct measurement of lactate and carboxyhemoglobin. • Promptly initiate an accurately determined fluid resuscitation prescription. • Use real-time assessment of global volume status to inform proper adjustments to fluid prescription as indicated. • Cleanse and debride the wound and apply an appropriate topical antibiotic and dressing. • Refer patients to a specialty burn center in a timely manner, based on application of transfer criteria.

Acknowledgements The authors wish to thank Drs. Amalia Cochran, Stephen Morris, and Jeffrey Saffle at the University of Utah Burn Center.

References Evidence-based medicine requires a critical appraisal of the literature based upon study methodology and number of subjects. Not all references are equally robust. The findings of a large, prospective, random­ized, and blinded trial should carry more weight than a case report. To help the reader judge the strength of each reference, pertinent information about the study, such as the type of study and the number of patients in the study, will be included in bold type following the ref­erence, where available. In addition, the most infor­mative references cited in this paper, as determined by the authors, will be noted by an asterisk (*) next to the number of the reference. 1.

2.

3. 4. 5.

American Burn Association. Burn incidence and treatment in the United States: 2011 Fact Sheet. 2012. Available at: http:// www.ameriburn.org/resources_factsheet.php. (Retrospective registry review) Willis MS, Carlson DL, Dimaio JM, et al. Macrophage migration inhibitory factor mediates late cardiac dysfunction after burn injury. Am J Physiol Heart Circ Physiol. 2005;288(2):H795H804. (Animal study) Mertens DM, Jenkins ME, Warden GD. Outpatient burn management. Nurs Clin North Am. 1997;32(2):343-364. (Review) Kasten KR, Makley AT, Kagan RJ. Update on the critical care management of severe burns. J Intensive Care Med. 2011;26(4):223-236. (Review) Grunwald TB, Garner WL. Acute burns. Plast Reconstr Surg. 2008;121(5):311e-319e. (Review)

EMCC © 2012 14

6. 7.* 8. 9. 10.

11. 12.

13.

14. 15. 16. 17. 18. 19. 20. 21.

22. 23.

24.* 25. 26. 27.

28.

Mitra B, Fitzgerald M, Cameron P, et al. Fluid resuscitation in major burns. ANZ J Surg. 2006;76(1-2):35-38. (Retrospective; 127 patients) Latenser BA. Critical care of the burn patient: the first 48 hours. Crit Care Med. 2009;37(10):2819-2826. (Review) Wallace AB. The exposure treatment of burns. Lancet. 1951;1(6653):501-504. (Historical reference) Lund CC, Browder NC. The estimation of areas of burns. Sug Gynecol Obstet. 1944;79:352-358. (Historical reference) Wachtel TL, Berry CC, Wachtel EE, et al. The inter-rater reliability of estimating the size of burns from various burn area chart drawings. Burns. 2000;26(2):156-170. (Comparative; simulation cases) Burke BA, Lewis RW 2nd, Latenser BA, et al. Methamphetamine-related burns in the cornbelt. J Burn Care Res. 2008;29(4):574-579. (Retrospective; 410 patients) Santos AP, Wilson AK, Hornung CA, et al. Methamphetamine laboratory explosions: a new and emerging burn injury. J Burn Care Rehabil. 2005;26(3):228-232. (Retrospective; 60 patients) Ahrns KS. Trends in burn resuscitation: shifting the focus from fluids to adequate endpoint monitoring, edema control, and adjuvant therapies. Crit Care Nurs Clin North Am. 2004;16(1):75-98. (Review) Cochran A, Morris SE, Edelman LS, et al. Burn patient characteristics and outcomes following resuscitation with albumin. Burns. 2007;33(1):25-30. (Retrospective; 101 patients) Underhill FP. The significance of anhydremia in extensive surface burn. JAMA. 1930;95:852-857. (Historical reference) Cope O, Moore FD. The redistribution of body water and the fluid therapy of the burned patient. Ann Surg. 1947;126(6):1010-1045. (Case series; 19 patients) Pham TN, Cancio LC, Gibran NS, et al. American Burn Association practice guidelines burn shock resuscitation. J Burn Care Res. 2008;29(1):257-266. (Practice guideline) Baxter CR, Shires T. Physiological response to crystalloid resuscitation of severe burns. Ann NY Acad Sci. 1968;150(3):874-894. (Animal study) Baxter CR. Fluid volume and electrolyte changes of the early postburn period. Clin Plast Surg. 1974;1(4):693-703. (Retrospective) Pruitt BA Jr. Protection from excessive resuscitation: “pushing the pendulum back.” J Trauma. 2000;49(3):567-568. (Review) Engrav LH, Colescott PL, Kemalyan N, et al. A biopsy of the use of the Baxter formula to resuscitate burns or do we do it like Charlie did it? J Burn Care Rehabil. 2000;21(2):91-95. (Retrospective; 50 patients) Blumetti J, Hunt JL, Arnoldo BD, et al. The Parkland formula under fire: is the criticism justified? J Burn Care Res. 2008;29(1):180-186. (Retrospective; 487 patients) Cancio LC, Chavez S, Alvarado-Ortega M, et al. Predicting increased fluid requirements during the resuscitation of thermally injured patients. J Trauma. 2004;56(2):404-413; discussion 413-404. (Retrospective; 104 patients) Cartotto R, Zhou A. Fluid creep: the pendulum hasn’t swung back yet! J Burn Care Res. 2010;31(4):551-558. (Retrospective; 196 patients) Friedrich JB, Sullivan SR, Engrav LH, et al. Is supra-Baxter resuscitation in burn patients a new phenomenon? Burns. 2004;30(5):464-466. (Retrospective; 22 patients) Sullivan SR, Friedrich JB, Engrav LH, et al. “Opioid creep” is real and may be the cause of “fluid creep.” Burns. 2004;30(6):583-590. (Retrospective; 22 patients) Wibbenmeyer L, Sevier A, Liao J, et al. The impact of opioid administration on resuscitation volumes in thermally injured patients. J Burn Care Res. 2010;31(1):48-56. (Retrospective; 154 patients) Evans EI. The early management of the severely burned patient. Surg Gynecol Obstet. 1952;94(3):273-282. (Historical)

www.ebmedicine.net • Volume 2, Number 6

29. Greenhalgh DG. Burn resuscitation: the results of the ISBI/ ABA survey. Burns. 2010;36(2):176-182. (Multicenter survey; 101 respondents) 30. Agarwal N, Petro J, Salisbury RE. Physiologic profile monitoring in burned patients. J Trauma. 1983;23(7):577-583. (Prospective observational; 18 patients) 31. Cartotto RC, Innes M, Musgrave MA, et al. How well does the Parkland formula estimate actual fluid resuscitation volumes? J Burn Care Rehabil. 2002;23(4):258-265. (Retrospective; 31 patients) 32. Dries DJ, Waxman K. Adequate resuscitation of burn patients may not be measured by urine output and vital signs. Crit Care Med. 1991;19(3):327-329. (Retrospective; 14 patients) 33. Jeng JC, Lee K, Jablonski K, et al. Serum lactate and base deficit suggest inadequate resuscitation of patients with burn injuries: application of a point-of-care laboratory instrument. J Burn Care Rehabil. 1997;18(5):402-405. (Prospective; 53 patients) 34. Holm C. Resuscitation in shock associated with burns. Tradition or evidence-based medicine? Resuscitation. 2000;44(3):157-164. (Review) 35. Holm C, Mayr M, Tegeler J, et al. A clinical randomized study on the effects of invasive monitoring on burn shock resuscitation. Burns. 2004;30(8):798-807. (Randomized controlled trial; 50 patients) 36. Bernard F, Gueugniaud PY, Bertin-Maghit M, et al. Prognostic significance of early cardiac index measurements in severely burned patients. Burns. 1994;20(6):529-531. (Retrospective; 38 patients) 37. Aikawa N, Ishibiki K, Naito C, et al. Individualized fluid resuscitation based on haemodynamic monitoring in the management of extensive burns. Burns Incl Therm Inj. 1982;8(4):249-255. (Case series; 21 patients) 38. Aikawa N, Martyn JA, Burke JF. Pulmonary artery catheterization and thermodilution cardiac output determination in the management of critically burned patients. Am J Surg. 1978;135(6):811-817. (Retrospective; 39 patients) 39. Barton RG, Saffle JR, Morris SE, et al. Resuscitation of thermally injured patients with oxygen transport criteria as goals of therapy. J Burn Care Rehabil. 1997;18(1 Pt 1):1-9. (Prospective observational; 9 patients) 40. Miller JG, Bunting P, Burd DA, et al. Early cardiorespiratory patterns in patients with major burns and pulmonary insufficiency. Burns. 1994;20(6):542-546. (Retrospective; 50 patients) 41. Klein MB, Hayden D, Elson C, et al. The association between fluid administration and outcome following major burn: a multicenter study. Ann Surg. 2007;245(4):622-628. (Retrospective; 72 patients) 42.* Saffle JI. The phenomenon of “fluid creep” in acute burn resuscitation. J Burn Care Res. 2007;28(3):382-395. (Review) 43. Ipaktchi K, Arbabi S. Advances in burn critical care. Crit Care Med. 2006;34(9 Suppl):S239-S244. (Review) 44. Oda J, Ueyama M, Yamashita K, et al. Hypertonic lactated saline resuscitation reduces the risk of abdominal compartment syndrome in severely burned patients. J Trauma. 2006;60(1):64-71. (Prospective comparative; 36 patients) 45. Oda J, Yamashita K, Inoue T, et al. Resuscitation fluid volume and abdominal compartment syndrome in patients with major burns. Burns. 2006;32(2):151-154. (Prospective comparative; 48 patients) 46. Sullivan SR, Ahmadi AJ, Singh CN, et al. Elevated orbital pressure: another untoward effect of massive resuscitation after burn injury. J Trauma. 2006;60(1):72-76. (Retrospective; 13 patients) 47. Ahrns KS, Harkins DR. Initial resuscitation after burn injury: therapies, strategies, and controversies. AACN Clin Issues. 1999;10(1):46-60. (Review) 48. Chung KK, Wolf SE, Cancio LC, et al. Resuscitation of severely burned military casualties: fluid begets more fluid. J Trauma. 2009;67(2):231-237. (Retrospective; 58 patients)

www.ebmedicine.net • Volume 2, Number 6

49. Marik PE, Baram M, Vahid B. Does central venous pressure predict fluid responsiveness? A systematic review of the literature and the tale of seven mares. Chest. 2008;134(1):172178. (Review) 50. Reid RD, Jayamaha J. The use of a cardiac output monitor to guide the initial fluid resuscitation in a patient with burns. Emerg Med J. 2007;24(5):e32. (Case report) 51. Holm C, Melcer B, Horbrand F, et al. Haemodynamic and oxygen transport responses in survivors and non-survivors following thermal injury. Burns. 2000;26(1):25-33. (Retrospective; 21 patients) 52. Ramzy PI, Barret JP, Herndon DN. Thermal injury. Crit Care Clin. 1999;15(2):333-352. (Review) 53. Faucher L, Furukawa K. Practice guidelines for the management of pain. J Burn Care Res. 2006;27(5):659-668. (Practice guideline) 54. Abdi S, Zhou Y. Management of pain after burn injury. Curr Opin Anaesthesiol. 2002;15(5):563-567. (Review) 55. Furman WR, Munster AM, Cone EJ. Morphine pharmacokinetics during anesthesia and surgery in patients with burns. J Burn Care Rehabil. 1990;11(5):391-394. (Retrospective; 14 patients) 56. Yamashita S, Kaneda K, Han TH. Population pharmacokinetics of a propofol bolus administered in patients with major burns. Burns. 2010;36(8):1215-1221. (Retrospective; 36 patients) 57. Patterson DR, Ptacek JT, Carrougher GJ, et al. Lorazepam as an adjunct to opioid analgesics in the treatment of burn pain. Pain. 1997;72(3):367-374. (Randomized controlled trial; 79 patients) 58. Lin H, Faraklas I, Sampson C, et al. Use of dexmedetomidine for sedation in critically ill mechanically ventilated pediatric burn patients. J Burn Care Res. 2011;32(1):98-103. (Retrospective; 11 patients) 59. Hebert PC, Wells G, Blajchman MA, et al. A multicenter, randomized, controlled clinical trial of transfusion requirements in critical care. N Engl J Med. 1999;340(6):409-417. (Randomized controlled trial; 838 patients) 60. Palmieri TL, Caruso DM, Foster KN, et al. Effect of blood transfusion on outcome after major burn injury: a multicenter study. Crit Care Med. 2006;34(6):1602-1607. (Retrospective; 661 patients) 61. Kwan P, Gomez M, Cartotto R. Safe and successful restriction of transfusion in burn patients. J Burn Care Res. 2006;27(6):826-834. (Retrospective; 172 patients) 62. Berger MM, Bernath MA, Chiolero RL. Resuscitation, anaesthesia and analgesia of the burned patient. Curr Opin Anaesthesiol. 2001;14(4):431-435. (Review) 63.* Wasiak J, Cleland H, Campbell F. Dressings for superficial and partial thickness burns. Cochrane Database Syst Rev. 2008(4):CD002106. (Systematic literature review) 64. Sargent RL. Management of blisters in the partial-thickness burn: an integrative research review. J Burn Care Res. 2006;27(1):66-81. (Practice guideline) 65. Sawada Y, Urushidate S, Yotsuyanagi T, et al. Is prolonged and excessive cooling of a scalded wound effective? Burns. 1997;23(1):55-58. (Animal study) 66. Hunter GR, Chang FC. Outpatient burns: a prospective study. J Trauma. 1976;16(3):191-195. (Retrospective) 67. Brown TP, Cancio LC, McManus AT, et al. Survival benefit conferred by topical antimicrobial preparations in burn patients: a historical perspective. J Trauma. 2004;56(4):863-866. (Review) 68.* D’Avignon LC, Chung KK, Saffle JR, et al. Prevention of infections associated with combat-related burn injuries. J Trauma. 2011;71(2 Suppl 2):S282-S289. (Review) 69. Dai T, Huang YY, Sharma SK, et al. Topical antimicrobials for burn wound infections. Recent Pat Antiinfect Drug Discov. 2010;5(2):124-151. (Review) 70. Woodley DT, O’Keefe EJ, Prunieras M. Cutaneous wound

15

EMCC © 2012

71. 72.

73.

74. 75. 76.

77. 78. 79.

80. 81. 82. 83. 84. 85.

86. 87. 88. 89.

90. 91.

92. 93.

healing: a model for cell-matrix interactions. J Am Acad Dermatol. 1985;12(2 Pt 2):420-433. (Basic science investigation) Schonfeld N. Outpatient management of burns in children. Pediatr Emerg Care. 1990;6(3):249-253. (Review) Kulick MI, Wong R, Okarma TB, et al. Prospective study of side effects associated with the use of silver sulfadiazine in severely burned patients. Ann Plast Surg. 1985;14(5):407-419. (Retrospective; 45 patients) Thomson PD, Moore NP, Rice TL, et al. Leukopenia in acute thermal injury: evidence against topical silver sulfadiazine as the causative agent. J Burn Care Rehabil. 1989;10(5):418-420. (Retrospective; 70 patients) Kucan JO, Smoot EC. Five percent mafenide acetate solution in the treatment of thermal injuries. J Burn Care Rehabil. 1993;14(2 Pt 1):158-163. (Retrospective; 669 patients) Subrahmanyam M. Honey dressing for burns. Indian J Plast Surg. 2010;43(2):231-232. (Review) Nadworny PL, Wang J, Tredget EE, et al. Anti-inflammatory activity of nanocrystalline silver-derived solutions in porcine contact dermatitis. J Inflamm (Lond). 2010;7:13. (Animal study) Dunn K, Edwards-Jones V. The role of Acticoat with nanocrystalline silver in the management of burns. Burns. 2004;(30 Suppl 1):S1-S9. (Review) Storm-Versloot MN, Vos CG, Ubbink DT, et al. Topical silver for preventing wound infection. Cochrane Database Syst Rev. 2010(3):CD006478. (Systematic literature review) Weaver LK, Howe S, Hopkins R, et al. Carboxyhemoglobin half-life in carbon monoxide-poisoned patients treated with 100% oxygen at atmospheric pressure. Chest. 2000;117(3):801808. (Review) Kealey GP. Carbon monoxide toxicity. J Burn Care Res. 2009;30(1):146-147. (Review) Baud FJ, Barriot P, Toffis V, et al. Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med. 1991;325(25):1761-1766. (Retrospective; 223 patients) Barillo DJ. Diagnosis and treatment of cyanide toxicity. J Burn Care Res. 2009;30(1):148-152. (Review) Karyoute SM, Badran IZ. Tetanus following a burn injury. Burns Incl Therm Inj. 1988;14(3):241-243. (Case report) Padmakumar B, Date AR. Tetanus in an unvaccinated child in the United Kingdom: case report. J Public Health (Oxf). 2005;27(1):118-119. (Case report) Gomez R, Murray CK, Hospenthal DR, et al. Causes of mortality by autopsy findings of combat casualties and civilian patients admitted to a burn unit. J Am Coll Surg. 2009;208(3):348-354. (Autopsy review; 74 autopsies) Bloemsma GC, Dokter J, Boxma H, et al. Mortality and causes of death in a burn centre. Burns. 2008;34(8):1103-1107. (Retrospective registry review) Miller K, Chang A. Acute inhalation injury. Emerg Med Clin North Am. 2003;21(2):533-557. (Review) Gronert GA, Theye RA. Pathophysiology of hyperkalemia induced by succinylcholine. Anesthesiology. 1975;43(1):89-99. (Animal study) Marathe PH, Dwersteg JF, Pavlin EG, et al. Effect of thermal injury on the pharmacokinetics and pharmacodynamics of atracurium in humans. Anesthesiology. 1989;70(5):752-755. (Retrospective; 8 patients) Baxter CR, Marvin JA, Curreri PW. Early management of thermal burns. Postgrad Med. 1974;55(1):131-139. (Review) Cancio LC, Reifenberg L, Barillo DJ, et al. Standard variables fail to identify patients who will not respond to fluid resuscitation following thermal injury: brief report. Burns. 2005;31(3):358-365. (Retrospective; 3807 patients) Greenhalgh DG. Burn resuscitation. J Burn Care Res. 2007;28(4):555-565. (Review) Fodor L, Fodor A, Ramon Y, et al. Controversies in fluid resuscitation for burn management: literature review and our experience. Injury. 2006;37(5):374-379. (Review)

EMCC © 2012 16

94. Gore DC, Dalton JM, Gehr TW. Colloid infusions reduce glomerular filtration in resuscitated burn victims. J Trauma. 1996;40(3):356-360. (Prospective comparative; 6 patients) 95. Goodwin CW, Dorethy J, Lam V, et al. Randomized trial of efficacy of crystalloid and colloid resuscitation on hemodynamic response and lung water following thermal injury. Ann Surg. 1983;197(5):520-531. (Randomized controlled trial; 79 patients) 96. Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2011(3):CD000567. (Systematic literature review) 97.* Lawrence A, Faraklas I, Watkins H, et al. Colloid administration normalizes resuscitation ratio and ameliorates “fluid creep.” J Burn Care Res. 2010;31(1):40-47. (Retrospective; 52 patients) 98. Huang PP, Stucky FS, Dimick AR, et al. Hypertonic sodium resuscitation is associated with renal failure and death. Ann Surg. 1995;221(5):543-554; discussion 554-547. (Retrospective; 174 patients) 99. Saffle J. Practice guidelines for burn care. J Burn Care. 2001;22(Suppl):i. (Practice guideline) 100. Bjerknes R, Vindenes H, Laerum OD. Altered neutrophil functions in patients with large burns. Blood cells. 1990;16(1):127-141; discussion 142-143. (Prospective; 116 patients) 101. Schwacha MG, Ayala A, Chaudry IH. Insights into the role of gammadelta T lymphocytes in the immunopathogenic response to thermal injury. J Leukoc Biol. 2000;67(5):644-650. (Animal study) 102. Peter FW, Schuschke DA, Barker JH, et al. The effect of severe burn injury on proinflammatory cytokines and leukocyte behavior: its modulation with granulocyte colonystimulating factor. Burns. 1999;25(6):477-486. (Animal study) 103. Ugburo AO, Atoyebi OA, Oyeneyin JO, et al. An evaluation of the role of systemic antibiotic prophylaxis in the control of burn wound infection at the Lagos University Teaching Hospital. Burns. 2004;30(1):43-48. (Randomized controlled trial; 61 patients) 104. Hospenthal DR, Murray CK, Andersen RC, et al. Guidelines for the prevention of infections associated with combat-related injuries: 2011 update: endorsed by the Infectious Diseases Society of America and the Surgical Infection Society. J Trauma. 2011;71(2 Suppl 2):S210-S234. (Practice guideline) 105.* Avni T, Levcovich A, Ad-El DD, et al. Prophylactic antibiotics for burns patients: systematic review and meta-analysis. BMJ. 2010;340:c241. (Systematic literature review) 106. Tanaka H, Matsuda T, Miyagantani Y, et al. Reduction of resuscitation fluid volumes in severely burned patients using ascorbic acid administration: a randomized, prospective study. Arch Surg. 2000;135(3):326-331. (Randomized controlled trial; 37 patients) 107. Kahn SA, Beers RJ, Lentz CW. Resuscitation after severe burn injury using high-dose ascorbic acid: a retrospective review. J Burn Care Res. 2011;32(1):110-117. (Retrospective; 40 patients) 108. Aida T, Murata J, Asano G, et al. Effects of polyprenoic acid on thermal injury. Br J Exp Pathol. 1987;68(3):351-358. (Animal study) 109. Costantini TW, Loomis WH, Putnam JG, et al. Pentoxifylline modulates intestinal tight junction signaling after burn injury: effects on myosin light chain kinase. J Trauma. 2009;66(1):17-24; discussion 24-25. (Animal study) 110. Warden GD, Stratta RJ, Saffle JR, et al. Plasma exchange therapy in patients failing to resuscitate from burn shock. J Trauma. 1983;23(10):945-951. (Retrospective; 22 patients) 111. Kravitz M, Warden GD, Sullivan JJ, et al. A randomized trial of plasma exchange in the treatment of burn shock. J Burn Care Rehabil. 1989;10(1):17-26. (Randomized controlled trial; 22 patients) 112. Neff LP, Allman JM, Holmes JH. The use of theraputic

www.ebmedicine.net • Volume 2, Number 6

1. “Burn shock,” as described in this article, is: a. Airway compromise secondary to airway edema b. A consequence of capillary integrity compromise that causes fluid extravasation into the extravascular space c. Cardiac dysrhythmias secondary to burns d. Respiratory collapse secondary to smoke inhalation

plasma exchange (TPE) in the setting of refractory burn shock. Burns. 2010;36(3):372-378. (Retrospective; 40 patients) 113. Norbury WB, Jeschke MG, Herndon DN. Metabolism modulators in sepsis: propranolol. Crit Care Med. 2007;35(9 Suppl):S616-S620. (Review) 114. Arbabi S, Ahrns KS, Wahl WL, et al. Beta-blocker use is associated with improved outcomes in adult burn patients. J Trauma. 2004;56(2):265-269; discussion 269-271. (Retrospective; 107 patients) 115. Mohammadi AA, Bakhshaeekia A, Alibeigi P, et al. Efficacy of propranolol in wound healing for hospitalized burn patients. J Burn Care Res. 2009;30(6):1013-1017. (Randomized controlled trial; 79 patients) 116. Jeschke MG, Finnerty CC, Suman OE, et al. The effect of oxandrolone on the endocrinologic, inflammatory, and hypermetabolic responses during the acute phase postburn. Ann Surg. 2007;246(3):351-360; discussion 360-362. (Randomized controlled trial; 235 patients) 117. Wolf SE, Edelman LS, Kemalyan N, et al. Effects of oxandrolone on outcome measures in the severely burned: a multicenter prospective randomized double-blind trial. J Burn Care Res. 2006;27(2):131-139; discussion 140-141. (Multicenter randomized controlled trial; 81 patients) 118. Pham TN, Klein MB, Gibran NS, et al. Impact of oxandrolone treatment on acute outcomes after severe burn injury. J Burn Care Res. 2008;29(6):902-906. (Retrospective; 117 patients) 119. Latenser BA, Miller SF, Bessey PQ, et al. National Burn Repository 2006: a ten-year review. J Burn Care Res. 2007;28(5):635-658. (Retrospective registry review) 120. American Burn Association. Guidelines for the operation of burn centers. From: Resources for optimal care of the injured patient. 2006:79-86. (Practice guideline) 121. Edlich RF, Haynes BW, Larkham N, et al. Emergency department treatment, triage and transfer protocols for the burn patient. JACEP. 1978;7(4):152-158. (Review) 122. Hart DW, Wolf SE, Chinkes DL, et al. Effects of early excision and aggressive enteral feeding on hypermetabolism, catabolism, and sepsis after severe burn. J Trauma. 2003;54(4):755761; discussion 761-764. (Retrospective; 46 patients) 123. Barret JP, Herndon DN. Effects of burn wound excision on bacterial colonization and invasion. Plast Reconstr Surg. 2003;111(2):744-750; discussion 751-752. (Retrospective; 12 patients) 124. Muangman P, Sullivan SR, Honari S, et al. The optimal time for early excision in major burn injury. J Med Assoc Thai. 2006;89(1):29-36. (Retrospective; 75 patients)

2. Which of the following areas may be prone to deeper injury despite a relatively benign initial appearance? a. Fingertips and skin over palm b. Skin over scalp and back c. Neck and shoulders d. Axilla, anterior forearm, medial thigh e. Abdomen and chest 3. Although no gold standard exists, the authors suggest using the Lund and Browder diagram instead of the Wallace “rule of nines” to estimate burn size because: a. The Wallace “rule of nines” does not account for patient size, differences in body type, sex-related proportion differences, or the size of the examiner’s hand. b. The Wallace “rule of nines” is more laborious. c. The Lund and Browder diagram takes body mass index into account. d. The Wallace “rule of nines” is not as universally used. 4. The authors suggest that all of the following studies be performed initially on burn injury patients EXCEPT: a. Serum lactate b. Chest x-ray c. Complete blood count d. Chemistry panel e. Methemoglobin level

CME Questions Take This Test Online!

5. The Parkland Formula guide for fluid resuscitation is: a. 4 mL/kg/% TBSA over 24 hours with the first half over the first 16 hours and the second half over the next 8 hours b. 6 mL/kg/% TBSA over 24 hours with the first half over the first 8 hours and the second half over the next 16 hours c. 4 mL/kg/% TBSA over 24 hours with the first half over the first 8 hours and the second half over the next 16 hours d. 2 mL/kg/% TBSA over 24 hours with the first half over the first 16 hours and the second half over the next 8 hours

Current subscribers can receive CME credit absolutely free by completing the following test. This issue includes 3 AMA PRA Category 1 CreditsTM. Online testing is now available for current and Take This Test Online! archived issues. To receive your free CME credits for this issue, scan the QR code below or visit www.ebmedicine.net/C1212

www.ebmedicine.net • Volume 2, Number 6

17

EMCC © 2012

EMCC Has Gone Mobile! You can now view all EMCC content on your iPhone or Android smartphone. Simply visit www.ebmedicine.net from your mobile device, and you’ll automatically be directed to our mobile site. On our mobile site, you can: • View all issues of EMCC since inception, including issues on NIV, blunt trauma, ACS, and more • Take CME tests for all issues – that’s over 20 AMA Category 1 CreditsTM! • View your CME records, including scores, dates of completion, and certificates • Comment on EMCC’s What’s Your Diagnosis blog, by visiting http://www.ebmedicine.net/emccblog/ • Renew your subscription or purchase additional content Check out our mobile site, and give us your feedback! Simply click the link at the bottom of the mobile site to complete a short survey to tell us what features you’d like us to add or change.

EMCC © 2012 18

www.ebmedicine.net • Volume 2, Number 6

Just Released, Exclusively For EMCC Subscribers: Walking The Tightrope: Pain Management And Sedation In The Hypotensive Patient Authors: JOHN SAUCIER, MD, FACEP Attending Physician, Emergency Department, Maine Medical Center, Portland, ME; Clinical Assistant Professor in Emergency Medicine, Tufts University School of Medicine, Boston, MA TREVOR EIDE, MD Emergency Department, Maine Medical Center, Portland, ME EXCERPT FROM THE ARTICLE: It’s the beginning of your evening shift, and it’s a busy one. Upon entering the critical care room, you find your patient to be profusely diaphoretic and writhing in pain while holding his left chest. His vital signs show a blood pressure of 90/50 mm Hg and a pulse of 56 beats per minute. He is afebrile, with a respiratory rate of 20 breaths per minute and an oxygen saturation of 96%. A stat ECG confirms sinus bradycardia and reveals mild diffuse ST depressions. The nurse attempts to establish an IV line as the patient continues to cry out in pain on the stretcher. You quickly weigh your options for analgesia and perhaps sedation given the current differential of (at least) acute myocardial infarction, pulmonary embolus, and thoracic dissection. Meanwhile, several questions come to mind: Should you attend to the blood pressure first with fluids or pressors? Should you try to narrow your potential diagnoses with further testing? Since the patient keeps trying to sit up, should you sedate, paralyze, and intubate him? What rapid sequence induction method is the safest yet most effective? You begin to mull over these questions as you consider your next steps… Get your copy of this article to find out: • • • •

Practical considerations for the above case (as well as two additional case studies) The above patient’s clinical course – and his final outcome What evidence-based recommendations might change the management of this patient And more!

Get your free copy today by scanning the QR code below or visiting www.ebmedicine.net/RCCAX.

Or, purchase your copy today, including 3 AMA PRA Category 1 CreditsTM, for just $49 at www.ebmedicine.net/WTTstore www.ebmedicine.net • Volume 2, Number 6

19

EMCC © 2012

Upcoming EMCC Topics

CME Information

•

Severe Sepsis And Septic Shock

Date of Original Release: December 1, 2012. Date of most recent review: November 1, 2012. Termination date: December 1, 2015.

•

Massive Gastrointestinal Bleeding

Accreditation: EB Medicine is accredited by the ACCME to provide continuing medical education for physicians.

•

Massive Transfusion

•

Status Epilepticus

Credit Designation: EB Medicine designates this enduring material for a maximum of 3 AMA PRA Category 1 Credits™. Physicians should claim only the credit commensurate with the extent of their participation in the activity.

•

Dying In The Emergency Department

AOA Accreditation: EMCC is eligible for up to 18 American Osteopathic Association Category 2A or 2B credit hours per year.

•

High-Risk Scenarios In Penetrating Trauma

Needs Assessment: The need for this educational activity was determined by a survey of medical staff, including the editorial board of this publication; review of morbidity and mortality data from the CDC, AHA, NCHS, and ACEP; and evaluation of prior activities for emergency physicians. Target Audience: This enduring material is designed for emergency medicine physicians, physician assistants, nurse practitioners, and residents as well as intensivists and hospitalists.

Now Available: The Latest Research On ECMO

Goals: Upon completion of this article, you should be able to: (1) demonstrate medical decision-making based on the strongest clinical evidence; (2) cost-effectively diagnose and treat the most critical ED presentations; and (3) describe the most common medicolegal pitfalls for each topic covered.

Dr. Joe Bellezzo and Dr. Zack Shinar have pioneered an ED ECPR (ECMO) service at Sharp Memorial Hospital in San Diego. This groundbreaking program — and the research behind it — are discussed in detail in their latest article: Extracorporeal Cardiopulmonary Resuscitation In The Emergency Department.

Discussion of Investigational Information: As part of the newsletter, faculty may be presenting investigational information about pharmaceutical products that is outside Food and Drug Administrationapproved labeling. Information presented as part of this activity is intended solely as continuing medical education and is not intended to promote off-label use of any pharmaceutical product. Faculty Disclosure: It is the policy of EB Medicine to ensure objectivity, balance, independence, transparency, and scientific rigor in all CME-sponsored educational activities. All faculty participating in the planning or implementation of a sponsored activity are expected to disclose to the audience any relevant financial relationships and to assist in resolving any conflict of interest that may arise from the relationship. In compliance with all ACCME Essentials, Standards, and Guidelines, all faculty for this CME activity were asked to complete a full disclosure statement. The information received is as follows: Dr. Preston, Dr. Ray, Dr. Cooney, Dr. Martin, Dr. Arntfield, and their related parties report no significant financial interest or other relationship with the manufacturer(s) of any commercial product(s) discussed in this educational presentation.

To learn how you can get a free copy of this article, visit www.ebmedicine.net/EDECPR

Send Us Your Feedback

Earning Credit: Two Convenient Methods: (1) Go online to www. ebmedicine.net/CME and click on the title of this article. (2) Mail or fax the Answer and Evaluation form included with your December issue to EB Medicine. Hardware/Software Requirements: You will need a Macintosh or PC to access the online archived articles and CME testing. Adobe Reader is required to view the PDFs of the archived articles.

Please send us your feedback so we can improve the quality and content of EMCC. To take a quick survey, visit http://www.surveymonkey.com/s/EMCCsurvey.

Additional Policies: For additional policies, including our statement of conflict of interest, source of funding, statement of informed consent, and statement of human and animal rights, visit www.ebmedicine.net/policies.

CEO & Publisher: Stephanie Williford Managing Editor: Dorothy Whisenhunt Managing Editor & CME Director: Jennifer Pai Director of Member Services: Liz Alvarez Director of Marketing: Robin Williford

EB Medicine

1-800-249-5770 or 1-678-366-7933 Fax: 1-770-500-1316 5550 Triangle Parkway, Suite 150, Norcross, GA 30092 E-mail: [email protected] Website: www.ebmedicine.net To write a letter to the editor, please email: [email protected]

EMCC Subscription Information: 6 print issues per year, 18 AMA PRA Category 1 CreditsTM, and full online access to searchable archives and additional CME: $299 (Call 1-800-249-5770 or go to www.ebmedicine.net/EMCCinfo to order)

EM Critical Care (EMCC) (ISSN Print: 2162-3031, ISSN Online: 2162-3074, ACID-FREE) is published 6 times per year by EB Medicine (5550 Triangle Parkway, Suite 150, Norcross, GA 30092). Opinions expressed are not necessarily those of this publication. Mention of products or services does not constitute endorsement. This publication is intended as a general guide and is intended to supplement, rather than substitute, professional judgment. It covers a highly technical and complex subject and should not be used for making specific medical decisions. The materials contained herein are not intended to establish policy, procedure, or standard of care. EM Critical Care and EMCC are trademarks of EB Medicine. Copyright © 2011 EB Medicine. All rights reserved. No part of this publication may be reproduced in any format without written consent of EB Medicine. This publication is intended for the use of the individual subscriber only and may not be copied in whole or part or redistributed in any way without the publisher’s prior written permission -- including reproduction for educational purposes or for internal distribution within a hospital, library, group practice, or other entity.

EMCC © 2012 20

www.ebmedicine.net • Volume 2, Number 6