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    Manejo via aerea Manejo via aerea Document Transcript

    • Airway Management and Respiratory Care of the Burn Patient Robert L. Sheridan, MD The outcome, both for survival1 and for quality of life,2 has improveddramatically for burn patients over the past 20 years. However, airway andrespiratory complications remain a common cause of morbidity and mor-tality. Anticipation and skillful management of the airway in both theacute and reconstructive burn patient is required if optimal outcomes areto be regularly achieved. Overall Management Strategy Care of a large burn has four general phases (Table 1).3 The firstphase, the initial evaluation and resuscitation phase, occurs from day 1through day 3 and requires an accurate fluid resuscitation and thoroughevaluation for other injuries and comorbid conditions. The second phase,initial wound excision and biological closure, describes the maneuver thatattempts to change the natural history of the disease. This is typicallyaccomplished by a series of staged operations that are completed duringthe first few days after injury. The third phase, definitive wound closure,involves replacement of temporary wound covers with definitive coversand closure and acute reconstruction of areas of small surface area buthigh complexity, such as the face and hands. The final stage of care isrehabilitation, reconstruction, and reintegration. Although this beginsduring the resuscitation period, it becomes very time consuming andinvolved toward the end of the acute hospital stay. There are uniqueairway and respiratory issues relevant to all four phases of care. Physiology of Burn Injury Wound size and depth have a substantial influence on pulmonaryfunction. Wounds should be evaluated for extent, depth, and circumfer- 129
    • 130 SheridanTable 1. Phases of Burn Care Phase ObjectivesInitial Evaluation and Resuscitation Accurate fluid resuscitation (0–72 hours) and thorough evaluationInitial Wound Excision and Biological Accurately identify and excise Closure (days 1–7) all full thickness wounds and achieve biological closureDefinitive Wound Closure Replace temporary with definitive (days 7–week 6) covers and close small complex woundsRehabilitation, Reconstruction, and Initially to maintain range and reduce Reintegration (entire edema, subsequently to strengthen hospitalization) and prepare for return to communityential components (Table 2). As a general rule, burns are usually under-estimated in depth on initial examination, even by experienced examin-ers. There are predictable physiological changes that occur over thecourse of a burn injury that also impact airway and respiratory manage-Table 2. Evaluation of the Burn WoundExtentLund-Browder Chart: Accounts for the changing body proportions with age and is thepreferred method of determining burn extent.Rule of Nines: A rough estimate that assumes adult body proportions. The head andneck are roughly 9%, the anterior and posterior chest are 9% each, the anteriorand posterior abdomen (including buttocks) are 9% each, each upper extremity is9%, each thigh is 9%, each leg and foot is 9%, and the remaining 1% representsthe genitals.Palmar Surface of the Hand: The palmar surface of the patient’s hand isapproximately 0.5% of the body surface over all age groups.DepthFirst Degree: Red, dry, and painful and are often deeper than they appear.Second Degree: Red, wet, and very painful. There is a great variability in their depth,ability to heal, and propensity to hypertrophic scar formation.Third Degree: Leathery, dry, insensate, and waxy.Fourth Degree: Involve underlying subcutaneous tissue, tendon, or bone.Circumferential ComponentsExtremities: Progressive edema of tissue beneath nonelastic burns will threatenextremity viability. Extremities at risk must be identified, closely monitored, andpromptly decompressed when distal circulation is compromised.Neck: Although rare, deep circumferential neck burns can result in reduced venousoutflow from the head and should be decompressed when noted.Torso: Chest compliance will be sharply reduced by near circumferential burns.Prompt escharotomy in such patients will dramatically improve ventilation.
    • Airway Management of the Burn Patient 131ment (Table 3). Those patients with burns over about 15% of the bodysurface have a clinically important diffuse capillary leak that is felt to becaused by wound-released mediators and is unique to burn-injured pa-tients in its magnitude. This results in the extravasation of fluids, electro-lytes, and moderate-sized colloid molecules into tissues adjacent to anddistant from the wound. A variety of formulas have been developed topredict resuscitation volume requirements. However, there are multiplevariables that impact resuscitation requirements, including delay in ini-tiation of resuscitation, inhalation injury, and the depth and vapor trans-mission characteristics of the wound itself. No two injuries are exactlyalike, and no formula has yet been developed that can predict with ac-ceptable accuracy the volume requirements necessary. Inaccurate volumeadministration is associated with substantial airway, respiratory, and othermorbidity, and it is therefore essential that burn resuscitations be guidedby the hourly evaluation of resuscitation end-points, the formula servingonly to help determine initial volume infusion rate and to roughly predictoverall requirements. Circumferential, or near circumferential, burn wounds of the torsoshould be noted because they represent areas in which special monitor-ing, and sometimes escharotomy, are essential. Constricting torso woundscan reduce chest wall compliance as soft tissues swell beneath the inelasticeschar. It is important that the need for escharotomy is recognized in atimely way so effective intervention can follow. Dramatic improvement inventilation is common after needed escharotomy of the chest and abdo-men (Fig. 1). In exceptional situations, bowel edema may result in ab-dominal compartment syndrome in burn patients in the absence of ab-dominal trauma. 4 This should be suspected based on physicalexamination and clinical course and treated by abdominal decompres-sion.5 After successful resuscitation, there is an abrupt decline in volumerequirements 18 to 24 hours after injury, as the diffuse capillary leakTable 3. Predictable Physiologic Changes in Burn Patients Time Predictable Changes ImplicationsResuscitation Period Massive diffuse Fluid resuscitation is (from day 0 to day 3) capillary leak required and airway edema is pronouncedPost Resuscitation Hyperdynamic and Early wound closure Period (from day 3 until hypercatabolic state with will reduce risk of bulk of wound is relative sepsis; nutritional definitively closed) immunosuppressed support is status essentialRecovery Period Ongoing catabolic state Nutritional support (from wound closure to remains essential; about 1 year after anticipate and manage injury) septic complications
    • 132 SheridanFigure 1. Improvement in chest wall compliance and ventilation can be dramatic afterescharotomy of the chest wall.predictably abates. Subsequently, a systemic inflammatory state evolves,characterized clinically by a hyperdynamic circulation, fever, and mas-sively increased protein catabolism. These changes are thought to beeffected by a combination of wound colonization with release of bacteriaand their byproducts, translocation of similar substances through a com-promised gastrointestinal barrier, foci of infection, and augmented re-lease of the counter regulatory hormones cortisol, catecholamines, andglucagon. Serious burns are associated with severe and protracted metabolicstress, and an important part of burn critical care involves support of thisphysiology through accurate fluid and electrolyte repletion, nutritionalsupport, control of environmental temperature, prompt removal of non-viable tissue with physiological wound closure, support of the gastrointes-tinal barrier, and proper management of pain and anxiety. Techniques toaddress all of these issues have evolved substantially. However, at present,airway and respiratory complications associated with burn injury remain amajor source of morbidity and mortality. Inhalation Injury Inhalation injury is defined as the sequelae of aspiration of super-heated gases, steam, or noxious products of incomplete combustion. Ap-
    • Airway Management of the Burn Patient 133proximately 20% of patients admitted to regional burn centers have somedegree of inhalation injury. It has adverse effects on both gas exchangeand on hemodynamics, but the severity of individual injuries is onlyroughly predictable based on history, examination, and currently avail-able diagnostic tests. Inhalation injury has been demonstrated to have aprofound effect on mortality in multiple institutional reviews, with thediagnosis as much as doubling mortality from that predicted based on ageand burn size alone.6 As there is no specific treatment for inhalationinjury, management involves providing the degree of support required tocompensate for decrements in gas exchange while the injured endobron-chial and alveolar mucosa regenerate. Physiology of Inhalation Injury Inhalation injury involves the entire respiratory system, from the up-per airway to the alveoli, to a variable and unpredictable degree. Super-heated gas and liquid cause direct burning of the upper airway with re-sultant mucosal edema and airway obstruction. This swelling isexacerbated by the diffuse capillary leak associated with a cutaneous burn.More distal injury is caused by chemicals adherent to fine particles(smoke) that deposit in various parts of the respiratory system based onthe size of the particulate. Irritating gasses trigger bronchospasm. Themajor airways are denuded of their normal mucosal layer and the ciliarytransport mechanism is therefore impaired. Small airways become ob-structed with sloughed endobronchial debris and accumulated secretionsin the days after injury, as necrotic endobronchial mucosa sloughs. Pneu-monia and tracheobronchitis frequently occur in partially obstructed lungsegments. The alveolar epithelium is disrupted by toxic products releasedby burning synthetic products, resulting in alveolar flooding. The clini-cally important problems that predictably occur include (1) loss of airwaypatency secondary to mucosal edema, (2) bronchospasm, (3) intrapulmo-nary shunting from small airway occlusion, (4) diminished compliancesecondary to alveolar flooding and collapse, (5) pneumonia secondary toloss of ciliary clearance, (6) respiratory failure secondary to a combinationof the above factors, and (7) bronchiectasis and variable degrees of ob-structive and restrictive defects in those who survive, particularly in seriousinhalation injuries.7 Diagnosis of Inhalation Injury Most patients, even those with severe inhalation injuries, will havelittle or no pulmonary dysfunction at initial presentation.8 The initialchest radiograph is routinely normal. The noxious substances in structuralsmokes are legion and generally unknown. Although there are a host ofdiagnostic adjuncts reported for inhalation injury, none can reliably pre-
    • 134 Sheridandict injury severity or subsequent clinical course.9 Available diagnosticsinclude history, physical examination, chest radiograph, bronchoscopy,admission arterial oxygen tension/inspired oxygen concentration ratio,and radioisotope scanning. Inhalation injuries evolve over time and in-volve the respiratory system from the upper airway to the alveoli to avariable degree. Although nonspecific, most authors have based the diag-nosis of inhalation injury on history and physical examination supple-mented by bronchoscopy. The pertinent points of history include burnssustained in a closed space or aspiration of hot steam or liquid. Physicalfindings suggesting the diagnosis have included the presence of carbona-ceous debris in the mouth or the sputum, singed nasal hairs, and facialburns. Chest radiographs are generally normal initially, consistent withthe evolution of these injuries over time. Invasive measures sometimes used to supplement history and physicalexamination in the diagnosis of inhalation injury include bronchoscopy,radioisotope scanning, and determination of serum carboxyhemoglobinpercentage. Despite its inability to determine parenchymal injury, mostclinicians use bronchoscopy as the gold standard for diagnosis of inhala-tion injury. Bronchoscopic findings consistent with this diagnosis includecarbonaceous endobronchial debris, mucosal pallor, and mucosal ulcer-ation (Fig. 2).10 Radioisotope imaging has been used to diagnose inhala-tion injury in two forms: xenon-133 (administered intravenously) or tech-Figure 2. Bronchoscopic findings consistent with inhalation injury include carbonaceousendobronchial debris, mucosal pallor, and mucosal ulceration.
    • Airway Management of the Burn Patient 135netium-99 (administered by inhalation). Both radioisotopes are rapidlycleared by normal lungs,11 and asymmetric or delayed clearance is con-sistent with the diagnosis of inhalation injury.12 Although physiologicallysound, xenon and technetium scanning have not been widely used be-cause of logistic difficulty and expense. Tracheobronchial cytology andbiopsy have been reported to facilitate the diagnosis of inhalation injuryin small clinical series, but because of logistic difficulties and potentialcomplications, they have not been widely employed.13 In practical terms,a clinical suspicion of inhalation injury, based on history and physicalexamination and supplemented with bronchoscopy in selected patients, isadequate information upon which to base transfer decisions and carefulmonitoring for respiratory complications. Management of the Airway in the Burn Patient There are a few unique aspects of airway management in burn pa-tients. These are detailed as they are typically encountered through thecourse of the illness. Initial Evaluation and Resuscitation Phase The most important points of airway management in this phase areassessment of current (and prediction of subsequent) airway patency anddocumentation of the presence or absence of inhalation injury. Evenpatients with incipient loss of airway patency from mucosal edema willhave open airways if they present to the hospital promptly after injury.Loss of airway patency from mucosal edema usually only occurs after timehas passed and resuscitation fluid has been administered. The risk ofsubsequent loss of airway patency is particularly acute in small children, inwhom moderate mucosal edema can lead to complete airway occlusion.The use of heliox has been proposed as a way to avoid intubation in suchchildren.14 However, as subsequent intubation in those who fail on helioxmay be even more difficult, it seems wiser in most circumstances to pro-ceed directly to careful intubation in burned small children with progres-sive stridor. Airway assessment is best done clinically, based on history and physicalexamination and supplemented with laryngoscopy and bronchoscopy inselected patients. Physical signs of particular importance are singed nasalhairs, facial burns, and soot in the mouth and between the teeth (Fig. 3).Stridor mandates intubation. In questionable cases, direct laryngoscopyand fiberoptic bronchoscopy can be very useful; the bonchoscope can beused as a stylet and intubation effected at the end of the diagnostic ex-amination if indicated. Patients at risk for progressive edema should be
    • 136 SheridanFigure 3. Physical signs of particular importance in initial airway assessment are singed nasalhairs, facial burns, and soot in the mouth and between the teeth.admitted to the hospital and closely observed so that intubation can bedone in a timely fashion. If one waits until edema is advanced, intubationcan be very difficult. On occasion, hot liquids are aspirated by youngchildren and can lead to rapid and massive upper airway edema. If sus-pected, immediate visualization of the airway and intubation is important(Fig. 4). Such situations should be treated as thermal epiglottitis.15 Initial Wound Excision and Biological Closure Phase During this phase of care, the principal burn-specific airway issue isprevention of unplanned extubation. Unplanned extubation in the gen-eral critical care setting is hazardous but not usually a cause of death orpermanent neurological injury. However, in the setting of massive face,neck, and airway edema associated with burn resuscitation, reintubationafter unplanned extubation can be incredibly difficult, if not impossible.The need for urgent reintubation is best avoided by compulsive attentionto adequate sedation and endotracheal tube security. Securing endotra-cheal tubes in those with facial burns can be a challenge, but it can bereliably done using umbilical tie harnesses (Fig. 5). Despite all properprecautions, unplanned extubation will occur in some patients. Althoughmost can be reintubated using standard techniques, adjunctive techniquesmay, on occasion, be lifesaving. These include laryngeal mask airway(LMA) placement (with subsequent endotracheal intubation through theLMA), fiberoptic intubation, needle cricothyroidotomy, and open crico-
    • Airway Management of the Burn Patient 137Figure 4. On occasion, hotliquids are aspirated by youngchildren and can lead to rapid andmassive upper airway edema. Ifsuspected, based on history orexamination of the burn pattern,immediate visualization of theairway and intubation isimportant.thyroidotomy. These techniques are detailed in other sections of this work.Despite the most compulsive attention to this matter, deaths and adverseevents will occur because of the difficult nature of the clinical problem. In selected patients, tracheostomy may be properly performed in thisphase of care, particularly if prolonged intubation is anticipated. It is idealif neck edema has subsided such that the procedure is not so technicallydifficult and that there are no neck burns overlying the planned trache-ostomy site.16,17 Tracheostomy in burned children is associated with ahigh incidence of serious structural problems requiring airway reconstruc-tion and is best avoided if possible. Definitive Wound Closure Phase In this phase of protracted intensive care, the issue of airway securityremains, although airway and facial edema are usually much reduced.However, as facial edema subsides, pulmonary function often worsens inthose who have sustained significant parenchymal inhalation injury. Aunique problem that is seen in such patients is acute endotracheal tube
    • 138 Sheridan Figure 5. In the setting of the massive edema associated with burn resuscitation, reintubation after unplanned extubation can be incredibly difficult and is best prevented by compulsive attention to endotracheal tube security.obstruction from inspissated endobronchial debris (Fig. 6). Acute tubeocclusions or near occlusions are caused by wads of debris or even casts ofsmall airways lodging in the endotracheal tube. This problem is mini-mized by the use of good humidification and frequent pulmonary toilet.When it occurs, it is managed by prompt recognition and an initial at-tempt to clear the tube with a relatively stiff suction catheter (especially iffacial edema predicts a difficult reintubation); extubation, mask ventila-tion, and reintubation are used in those patients in whom the tube simplycannot be cleared. Reconstruction and Rehabilitation Phase In this phase of care, there are two airway issues that occur with somefrequency: difficult elective intubations for reconstructive surgery and un-suspected tracheal and subglottic stenosis.16,18 There are common con-tractures that occur in burn patients that will predictably hinder safemanagement of the airway on induction of anesthesia. Most notable areflexion neck contractures and microstomia (Fig. 7). Adjuncts, such as
    • Airway Management of the Burn Patient 139Figure 6. (A) A unique problemthat is seen in patients with severeinhalation injury is acuteendotracheal tube obstruction frominspissated endobronchial debris.(B) Occasionally, total tubeobstruction is caused by the passageof large endobronchial casts,particularly in young children withsmall tubes and severe inhalationinjury, as in this case in whichemergent extubation andreintubation was required.fiberoptic intubation or LMA can be useful in these patients. On occasion,emergent sharp release is needed immediately after induction to allow formask ventilation and intubation. The surgeon should be in the operatingroom prior to induction of anesthesia in patients with contractures of themouth or neck. Any contracture that precludes safe access to the airwayassumes a very high priority and should be addressed as soon as identified.Patients are ideally not sent into rehabilitation settings until these areaddressed. Patients who have required prolonged intubation or tracheostomyhave a low but important incidence of subglottic stenosis.19 This oftenpresents after discharge, either in the rehabilitation setting or at the timeof planned reconstructive operations. It should be suspected if slowlyprogressive stridor develops or if a properly sized tube will not fit into thetrachea. Optimal diagnostic techniques are endoscopic, and managementis surgical.20
    • 140 SheridanFigure 7. There are common contractures that occur in burn patients that will predictably hindersafe management of the airway on induction of anesthesia. Most notable are flexion neckcontractures and microstomia. On occasion, emergent sharp release is needed immediately afterinduction to allow for mask ventilation and intubation. The surgeon should be in the operatingroom prior to induction of anesthesia in patients with significant contractures of the mouth or neck. Management of Inhalation Injury in the Burn Patient Clinical management of inhalation injury is supportive only. Interest-ingly, it is very typical that pulmonary function is relatively normal for thefirst few days following the injury, with impaired gas exchange and com-pliance occurring toward the end of the first week after injury. During thisinterval, it is ideal to complete interfacility transfers and needed surgicalprocedures. Prophylactic antibiotics and steroids are of no value.21,22 Af-ter the airway has been secured (see above), there are five predictableclinical problems that may need to be addressed in patients with inhala-tion injury: bronchospasm, small airway obstruction, infection, respiratoryfailure, and carbon monoxide (CO) poisoning. Bronchospasm In some patients, intense bronchospasm from aerosolized irritantsoccurs during the first 24 to 48 hours, especially in young children. Thisis well managed with in-line beta agonists in most patients, although somewill require intravenous bronchodilators such as terbutaline, low-dose
    • Airway Management of the Burn Patient 141epinephrine infusions, or even parenteral steroids. Ventilatory strategiesshould be designed to minimize intrinsic positive end-expiratory pressurein this setting, much as one would do to ventilate a patient with statusasthmaticus. Small Airway Obstruction As necrotic endobronchial debris slough, increasing difficulty withpulmonary toilet routinely occurs. An aggressive program of chest phys-iotherapy and pulmonary toilet is an important component of care. Toiletbronchoscopy can greatly facilitate clearance of the airways. Vigilant pul-monary toilet is an essential component of the management of patientswith inhalation injury. Nebulized heparin and acetylcysteine has beenproposed as an adjunct to improve pulmonary toilet in patients with in-halation injury,23 but available data do not seem adequate to recommendthe general use of this therapy as yet. Pulmonary Infection Approximately half of those with inhalation injury can be expected todevelop pulmonary infection, either pneumonia or purulent tracheobron-chitis. Differentiating between these two entities can be difficult, but thedifference is of little practical importance. Infection typically occurs towardthe end of the first week following injury, and it is common to see patientswith serious inhalation injuries deteriorate at this time. A patient with a newlypurulent sputum, fever, and perhaps diminished gas exchange should betreated with antibiotics based on sputum culture. The physiology of inha-lation injury, involving injury to endobronchial mucosa with hamperedmucociliary clearance, makes good pulmonary toilet essential. Respiratory Failure Respiratory failure in burn patients is caused as often by sepsis as it isby inhalation injury. Overly vigorous attempts to force high or even nor-mal tidal volumes into such lungs will exacerbate the underlying injury.24These patients do well with a pressure-limited ventilation strategy basedon permissive hypercapnia (Table 4).25 Burn patients who fail this ap-proach are potential candidates for extracorporeal membrane oxygen-ation26 or inhaled nitric oxide.27,28 Although weaning and extubation of burn patients follows the generalguidance presented elsewhere in this issue, there are some unique aspectsin this patient group that are important to know (Table 5). Of particularimportance is balancing the pain medication needs of those with largewounds and donor sites with the need for an alert sensorium to protectthe airway and the frequent occurrence of severe upper airway edema inthose with inhalation injury.
    • 142 SheridanTable 4. Responses to Progressive Respiratory Failure in the Burn Patient1. Address bronchospasm with nebulized beta-agonist agents.2. Address poor chest wall compliance secondary to overlying eschar with escharotomies.3. Ensure ventilator synchrony with adequate opiate and benzodiazepine infusions. Neuromuscular blockade may be required on occasion.4. Reset end-point of ventilation to a physiological pH (7.2 or more). Allow gradual onset hypercapnia as long as there is no head injury.5. Reset end-point of oxygenation to an arterial saturation of at least 90%, typically associated with an arterial oxygen partial pressure of 60 torr or greater.6. Optimize inflating pressures. A. Choose optimal positive end-expiratory pressure (PEEP). This is best done by creating a pressure-volume curve with a graduated inflation and setting PEEP just above the inflection point. B. Choose optimal peak inflating pressure (PIP). This is best done by using pressure controlled ventilation and targeting a tidal volume of 10–15 ml/kg, as long as total inflating pressures (PIP + PEEP) can be kept under 40 cm H2O. If this is inconsistent with meeting the reset end-points of oxygenation and ventilation, then the pressure cap should be violated. C. Choose optimal mean airway pressure (Pmaw). Lengthen expiratory time to a target of 20 to 25 cm H2O, as long as intrinsic PEEP is not detectable.7. In those few patients in whom these measures are not sufficient, consider the use of innovative adjuncts, such as nitric oxide, partial liquid ventilation, or extracorporeal support. Carbon Monoxide Exposure Carbon monoxide poisoning commonly occurs in conjunction withinhalation injury. The obtunded state seen in many of these patients ismultifactorial, involving a combination of CO, anoxia, drugs, alcohol, andTable 5. Important Considerations in Weaning and Extubation of Burn PatientsSensorium: The patient must be awake and alert enough to guard their airway.Airway patency: Upper airway edema must be resolved to the degree that there isan audible airleak around the endotracheal tube (with cuff deflated if tube iscuffed) at a moderate inflating pressure (20 to 30 cm H2O). A short course ofsteroids (24 hours) may be useful in selected patients to reduce airway edema.Muscle strength: Strength must be adequate for ventilation. An indirect measure ofthis is a tidal volume (6 to 10 ml/kg) with continuous positive airway pressure of5 cm H2O and a negative inspiratory force less than −20 cm H2O.Compliance: Combined chest wall and lung compliance must be high enough thatthe work of spontaneous breathing is not excessive. Indirect measures of this are ameasured static compliance of at least 50 ml/cm H2O and tidal volumes of at least10 ml/kg with moderate inflating pressures (less than about 25 cm H2O).Gas Exchange: An intrapulmonary shunt less than 20%, indicated by a PaO2/FIO2ratio greater than 200, should be documented.PaO2/FIO2 = arterial oxygen tension/inspired oxygen concentration.
    • Airway Management of the Burn Patient 143hypotension. Hyperbaric oxygen has been proposed as a means of im-proving the prognosis of those suffering serious CO exposures, but its useremains controversial.29 To treat with 100% normobaric oxygen or withhyperbaric oxygen is a decision that must be made if serious CO poisoningis suspected or documented. Unfortunately, available data conflict, andthe efficacy of this therapy remains an open question.30–32 CO binds to iron-containing enzymes, particularly hemoglobin andthe cytochromes, which it thereby inactivates. The formation of carboxy-hemoglobin results in an acute physiological anemia. The occurrence ofunconsciousness at a carboxyhemoglobin concentration of 50% impliesthat other mechanisms are involved in the pathophysiology of CO injury.It is likely that CO binding to the cytochrome system in the mitochondria,interfering with oxygen utilization, is more toxic than CO binding tohemoglobin. For unknown reasons, between 5% and 25% of patients withserious CO exposures have been reported to develop delayed neurologi-cal sequelae.32 These patients can be managed with 100% isobaric oxygenor with hyperbaric oxygen. If serious exposure has occurred, manifestedby overt neurological impairment or a high carboxyhemoglobin level, thenhyperbaric oxygen treatment is probably warranted if it can be safely admin-istered. Many patients with severe carbon monoxide exposure have also beenexposed to cyanide, which is released from burning synthetics. However, thedegree of exposure is rarely such that specific treatment is required.33 Most patients treated with hyperbaric oxygen receive their exposurein a monoplace hyperbaric chamber. Treatment regimens vary, but thetypical regimens is 2 or 3 atmospheres for 90 minutes, with 3 10-minute“air breaks” to decrease the incidence of oxygen toxicity seizures. Becausepatient access is compromised in a monoplace chamber, unstable patientsare poor candidates. Other relative contraindications are wheezing or airtrapping, which increase the risk of pneumothorax, and high fever, whichincreases the risk of seizures. Prior to placement in the chamber, endo-tracheal tube balloons should be filled with saline to avoid balloon com-pression–associated air leaks, and upper body central venous cannulationshould be avoided if possible to avoid sudden enlargement of an occultpneumothorax during decompression. The decision whether to treat withhyperbaric oxygen or 100% normobaric oxygen can be difficult to makebut is grounded in these considerations. Conclusion Airway and respiratory issues remain important sources of morbidityand mortality in the burn unit. With fewer patients now succumbing towound sepsis, those with concomitant inhalation injury find airway andrespiratory issues the biggest threat to their life. Fortunately, the problemsassociated with the injuries are predictable and can usually be successfullymanaged by an informed burn care team.
    • 144 Sheridan References 1. Sheridan RL, Remensnyder JP, Schnitzer JJ, et al. Current expectations for survival in pediatric burns. Arch Pediatr Adolesc Med 2000;154:245–249 2. Sheridan RL, Hinson MM, Liang MM, Tompkin RG. Long term outcomes of children surviving massive burns. JAMA 2000;283:69–73 3. Sheridan RL. The seriously burned child: resuscitation through reintegration—Part One. Curr Problems Pediatr 1998;28:105–127 4. Greenhalgh DG, Warden GD. The importance of intra-abdominal pressure measure- ments in burned children. J Trauma 1994;36:685–690 5. Sheridan R, Driscoll D, Felsen R. Packing and temporary closure in a liver injury. Injury 1997;28:711–712 6. Shirani KZ, Pruitt BA, Jr, Mason AD, Jr. The influence of inhalation injury and pneu- monia on burn mortality. Ann Surg 1987;205:82–87 7. McElroy K, Alvarado MI, Hayward PG, et al. Exercise stress testing for the pediatric patient with burns: a preliminary report. J Burn Care Rehabil 1992;13:236–238 8. Pruitt BA, Jr, Erickson DR, Morris A. Progressive pulmonary insufficiency and other pulmonary complications of thermal injury. J Trauma 1975;15:369–379 9. Ryan CM, Schoenfeld DA, Thorpe WP, et al. Objective estimates of the probability of death from burn injuries. N Engl J Med 1998;338:362–36610. Moylan JA, Adib K, Birnbaum M. Fiberoptic bronchoscopy following thermal injury. Surg Gynecol Obstet 1975;140:541–54311. Lull RJ, Anderson JH, Telepak RJ, Brown JM, Utz JA. Radionuclide imaging in the assessment of lung injury. Semin Nuclear Med 1980;10:302–31012. Lull RJ, Tatum JL, Sugerman HJ, et al. Radionuclide evaluation of lung trauma. Semin Nuclear Med 1983;13:223–23713. Masanes MJ, Legendre C, Lioret N, et al. Using bronchoscopy and biopsy to diagnose early inhalation injury. Macroscopic and histologic findings. Chest 1995;107:1365–136914. Rodeberg DA, Easter AJ, Washam MA, et al. Use of a helium-oxygen mixture in the treatment of postextubation stridor in pediatric patients with burns. J Burn Care Re- habil 1995;16:476–48015. Sheridan RL. Recognition and management of hot liquid aspiration in children. Ann Emerg Med 1996;27:89–9116. Hunt JL, Purdue GF, Gunning T. Is tracheostomy warranted in the burn patient? Indications and complications. J Burn Care Rehabil 1986;7:492–49517. Jones WG, Madden M, Finkelstein J, et al. Tracheostomies in burn patients. Ann Surg 1989;209:471–47418. Colice GL, Munster AM, Haponik EF. Tracheal stenosis complicating cutaneous burns: an underestimated problem. Am Rev Respir Dis 1986;134:1315–131819. Lund T, Goodwin CW, McManus WF, et al. Upper airway sequelae in burn patients requiring endotracheal intubation or tracheostomy. Ann Surg 1985;201:374–38220. Eliachar I, Moscona R, Joachims HZ, et al. The management of laryngotracheal stenosis in burned patients. Plast Reconstr Surg 1981;68:11–1721. Levine BA, Petroff PA, Slade CL, Pruitt BA, Jr. Prospective trials of dexamethasone and aerosolized gentamicin in the treatment of inhalation injury in the burned patient. J Trauma 1978;18:188–19322. Robinson NB, Hudson LD, Riem M, et al. Steroid therapy following isolated smoke inhalation injury. J Trauma 1982;22:876–87923. Desai MH, Mlcak R, Richardson J, et al. Reduction in mortality in pediatric patients with inhalation injury with aerosolized heparin/acetylcysteine therapy. J Burn Care Rehabil 1998;19:210–21224. Parker JC, Hernandez LA, Peevy KJ. Mechanisms of ventilator-induced lung injury. Crit Care Med 1993;21:131–143
    • Airway Management of the Burn Patient 14525. Sheridan RL, Kacmarek RM, McEttrick MM, et al. Permissive hypercapnia as a venti- latory strategy in burned children: effect on barotrauma, pneumonia, and mortality. J Trauma 1995;39:854–85926. Goretsky MJ, Greenhalgh DG, Warden GD, et al. The use of extracorporeal life support in pediatric burn patients with respiratory failure. J Pediatr Surg 1995;30:620–62327. Sheridan RL, Hurford WE, Kacmarek RM, et al. Inhaled nitric oxide in burn patients with respiratory failure. J Trauma 1997;42:641–64628. Sheridan RL, Zapol WM, Ritz RH, Tompkins RG. Low-dose inhaled nitric oxide in acutely burned children with profound respiratory failure. Surgery 1999;126:856–86229. Sheridan RL, Shank ES. Hyperbaric oxygen treatment: a brief overview of a controver- sial topic. J Trauma 1999;47:426–43530. Scheinkestel CD, Bailey M, Myles PS, et al. Hyperbaric or normobaric oxygen for acute carbon monoxide poisoning: a randomised controlled clinical trial. Med J Aust 1999; 170:203–21031. Moon RE, DeLong E. Hyperbaric oxygen for carbon monoxide poisoning. Med J Aust 1999;170:197–19932. Thom SR, Taber RL, Mendiguren II, et al. Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen. Ann Emerg Med 1995;25:474–48033. Barillo DJ, Goode R, Esch V. Cyanide poisoning in victims of fire: analysis of 364 cases and review of the literature. J Burn Care Rehabil 1994;15:46–57