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Smoke inhalation

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Smoke inhalation

  1. 1. Considerations in the Management of Acute Smoke Inhalation Injury<br />Mike Mesisca, M.S., D.O.<br />Department of Emergency Medicine<br />Arrowhead Regional Medical Center<br />Colton, CA<br />February 11, 2010<br />
  2. 2. Lecture Outline<br /><ul><li> Epidemiology of Smoke Inhalation Injury (SII)
  3. 3. Patho-physiology of Injury
  4. 4. Clinical presentation, considerations
  5. 5. Treatment
  6. 6. Stabilization/Rescusitation
  7. 7. Long-term
  8. 8. Other considerations:
  9. 9. Carboxyhemoglobinemia
  10. 10. Cyanide</li></li></ul><li>Epidemiology<br /><ul><li> 35% of hospitalized burn patients have smoke inhalation injury
  11. 11. Can triple the length of stay
  12. 12. Compared to burns alone, there is a 60% increase in mortality if inhalation injury and PNA are also present
  13. 13. When ARDs develops from burn inhalation injury, mortality rate up to 66%.
  14. 14. 60% TBSA burns with inhalation injury & ARDS, almost 100% fatal.</li></li></ul><li>Epidemiology<br />National Burn Repository (1999-2008): <br /><ul><li> Deaths from burns increased with advancing age and burn size, and the presence of inhalation injury.
  15. 15. For patients under 50, TBSA 0.1% to 19.9% burn, inhalation injury increases death rate 15 times.</li></li></ul><li>If AGE + TBSA Burn = 100, then 50% mortality<br />
  16. 16.
  17. 17. Historical Features<br /><ul><li> Type of substances burnt
  18. 18. Closed versus Open Space
  19. 19. Degree of lung ventilation
  20. 20. Victim:
  21. 21. Age
  22. 22. Comorbidities: lung or cardiovascular disease
  23. 23. Intoxication</li></li></ul><li>Patho-physiology of Injury<br /><ul><li> Thermal Injury: Heat Burns
  24. 24. Hypoxic Hypoxemia: Fire steals your oxygen
  25. 25. Toxic Exposure & Asphyxiants:
  26. 26. Fire releases poison</li></li></ul><li>Thermal Injury<br />Direct heat injury, typically supraglottic<br /><ul><li> Facial-oral burns create anatomic obstruction
  27. 27. Laryngospasm (rare) & bronchoconstriction
  28. 28. Local erythema, edema, ulceration
  29. 29. cellular necrosis of ciliated epithelium and capillary leakage
  30. 30. Edema, maximal within 24-48 hours
  31. 31. Causes airflow obstruction, therefore stridor
  32. 32. Resolves after 3-5 days</li></ul>Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. <br />2006. Pediatric Respiratory Reviews. 7, 123-128.<br />
  33. 33. Thermal Injury: Direct Heat<br /><ul><li> Heat dissipates on inhalation and damage occurs above the carina
  34. 34. Steam or prolonged exposure or particles 5-10 microns in diameter of less can damage airway below the cords</li></ul>Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. <br />2006. Pediatric Respiratory Reviews. 7, 123-128.<br />
  35. 35. Hypoxic Hypoxemia<br />Fire consumes the ambient oxygen  lower the environmental FIO2 below 0.21 <br /> Fuel dependent<br /><ul><li> Gasoline: 0.15
  36. 36. Oxygen containing compounds: 0.10</li></ul> Exacerbates CO and HCN toxicity<br /> Increases ventilation <br />Mandel, J. Hales, C. Smoke Inhalation. Uptodate.com 09/30/2009.<br />
  37. 37. Toxic Exposure<br />Smoke: visible, small particulate matter in hot air and toxic gas<br /><ul><li> Local, Bronchopulmonary Toxins
  38. 38. Asphyxiants: Inhaled combustible products cause injury to the lower airway
  39. 39. From synthetic substances
  40. 40. Carbon monoxide and hydrogen cyanide</li></li></ul><li>Toxic Exposure<br /><ul><li>Low molecular weight toxins in smoke alter the pH and create free radicals in distal airways causing tissue destruction, mainly nitrous oxide
  41. 41. Soot (elemental carbon) itself is nontoxic, enhances delivery of toxins
  42. 42. Acute neutrophilic airway inflammation occurs, but symptoms may be delayed 12-36 hours
  43. 43. Progression to pulmonary edema, bronchopulmonary PNA, and/or ARDs</li></li></ul><li>Toxic Exposure: Physiologic Changes<br /><ul><li>Destruction of ciliated epithelium in trachea and bronchial tree
  44. 44. Increased vascular permeability causing pulmonary edema
  45. 45. Alveolar hemorrhage & hyaline membrane formation
  46. 46. Airway obstruction facilitates surfactant consumption, distal airway collapse and atelectasis</li></ul>Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. <br /> Pediatric Respiratory Reviews. 7, 123-128.<br />
  47. 47. CLINICAL ISSUES<br />Making the Diagnosis!<br />Who needs intubation?<br />Who needs admission?<br />Who needs a workup?<br />What tests should be included?<br />How helpful are the tests?<br />
  48. 48. CLINICAL FEATURES OF INHALATION INJURY<br /><ul><li> Classic signs:
  49. 49. Stridor, hoarseness, drooling, dysphagia
  50. 50. Predictive Signs:
  51. 51. Singed nares, body burns
  52. 52. Hard signs:
  53. 53. Soot in the oral cavity
  54. 54. Facial burns
  55. 55. Absolute
  56. 56. True or false vocal cord edema</li></li></ul><li>CLINICAL FEATURES OF INHALATION INJURY<br />When in doubt, <br />secure the airway!<br />Consider:<br />Early Intubation<br />Transport Time<br />Most Experienced Person<br />Get as much Medical History as Possible<br />
  57. 57. Retrospective chart review of patients presenting with smoke inhalation to identify predictors <br />of respiratory distress<br /><ul><li> 41 patients, treated in ER (Burn Center), with an ENT consult for fiberoptic laryngoscopy
  58. 58. 8 required intubation
  59. 59. Intubation correlated with:
  60. 60. soot in the oral cavity (p <0.001)
  61. 61. facial burns (p = 0.025)
  62. 62. body burns (p = 0.025)
  63. 63. Intubation did not correlate with:
  64. 64. stridor, hoarseness, drooling, dysphagia (all p = 1.0)</li></ul>Madani, et al. Factors that predict the need for intubation in patients with smoke inhalation injury. ENT Journal, Jan, 2004.<br />
  65. 65. Retrospective chart review of patients presenting with smoke inhalation to identify predictors <br />of respiratory distress<br /><ul><li> Facial burns correlated with true cord edema (p = 0.01)
  66. 66. Body burns correlated with true (p = 0.047) and false (p = 0.003) </li></ul> cord edema<br />Madani, et al. Factors that predict the need for intubation in patients with smoke inhalation injury. ENT Journal, Jan, 2004.<br />
  67. 67. Indicators of inhalation injury <br />in patients without burns<br />64 patients without burns following household fires, 5 day ICU data collection<br /><ul><li> 35 patients were intubated, mean 101.2 hrs
  68. 68. 27 smokers, no correlation with longer ICU stay or time on vent
  69. 69. 18 intubated in the field and 17 intubated in the hospital
  70. 70. Higher positive bacteriologic analysis from field intubations & significantly more time on the Vent</li></ul>Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.<br />
  71. 71. Indicators of inhalation injury <br />in patients without burns<br /><ul><li> Dysphonia correlated with a longer ICU stay (p=0.05) and a greater likelihood to develop positive sputum culture (p=0.02)
  72. 72. Patients with rhonchi had longer ICU stays (p=0.004) and more days on MV than those without (p=0.003), and more positive sputum cultures (p=0.04)
  73. 73. No correlation found in patients that were wheezing.
  74. 74. Soot in oral pharynx on bronchoscopy correlated with longer ICU stay (p=0.02)</li></ul>Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.<br />
  75. 75. Indicators that no inhalation injury <br />occurred after smoke exposure<br /><ul><li> 57 patients with smoke exposure were divided into 5 groups
  76. 76. Group 1 (23): normal vitals, normal exam
  77. 77. Group 2 (26): no burn, but abnormal vitals and/or abnormal exam
  78. 78. Group 3 (5): minor burn (<15% TBSA)
  79. 79. Group 4 (2): major burn (>15% TBSA)
  80. 80. Group 5 (1): cardiac arrest</li></ul>Mushtaq, F., Graham, C. A. Dischargefrom the accident and emergency department after smoke inhalation: influence of clinical factors and emergency investigations. European Journal of Emergency Medicine. 2004, 11;141-144.<br />
  81. 81. Indicators that no inhalation injury <br />occurred after smoke exposure<br /><ul><li> 57 patients with smoke exposure were divided into 5 groups
  82. 82. Group 1 (23): normal vitals, normal exam
  83. 83. 28 studies ordered, mostly CO level (16) and ABG (9)
  84. 84. 1 patient, a smoker, after 3 hours of smoke exposure had a CO level 22%
  85. 85. All others discharged
  86. 86. Group 2 (26): no burn, abnormal vitals and/or exam
  87. 87. 81 studies ordered , 14% had abnormal CO or ABG results
  88. 88. Recommendation:
  89. 89. Patients with normal vitals and exam and limited exposure (less than 30 min.) need no testing </li></ul>Mushtaq, F., Graham, C. A. Discharge from the accident and emergency department after smoke inhalation: influence of clinical factors and emergency investigations. European Journal of Emergency Medicine. 2004, 11;141-144.<br />
  90. 90. Diagnostic Studies for Inhalation Injury<br /><ul><li> CXR
  91. 91. ABG
  92. 92. Labs
  93. 93. Xenon
  94. 94. Bronchoscopy
  95. 95. CT</li></li></ul><li>CXR is a Poor Indicator of Inhalation Injury<br /><ul><li> 29 of 56% of patients had normal chest xrays
  96. 96. Most frequent abnormal findings is diffuse alveolar infiltrates (35%)
  97. 97. Focal abnormalities, consolidation or atelectasis, 12.5% on admission and 25.6% on day 2
  98. 98. First CXR not predictive of duration of MV or ICU length of stay, or positive sputum cultures</li></ul>Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.<br />
  99. 99. CXR is a Poor Indicator of Inhalation Injury<br /><ul><li> Other studies have shown 12/29 (41%) of patients with acute inhalation injury and burns to have normal chest radiographs (Wittram, 1994).
  100. 100. In a study of 45 patients from a “major fire disaster”, 33/45 patients had abnormal chest radiographs on admission (Lee, 1988).
  101. 101. 29, bronchial wall thickening
  102. 102. 13 subglottic edema
  103. 103. 7 pulmonary edema
  104. 104. 3 patchy consolidation</li></li></ul><li>Xenon Scan & Bronchoscopy <br /><ul><li> Xenon ventilation-perfusion scan:
  105. 105. ventilation is shunted away from damaged airways
  106. 106. nonspecific
  107. 107. Bronchoscopy:
  108. 108. Invasive, and limited access at some centers
  109. 109. Useful in evaluating bacterial contamination and disease progression</li></ul>These techniques do not alter therapeutic protocols or outcomes, so many centers still rely on a clinical diagnosis (Heimbach, 1988).<br />
  110. 110. ABG & Fluid Requirements<br /><ul><li> A decreased partial pressure of arterial oxygen:fraction of inspired oxygen (PaO2:FIO2 ratio) less than 350 was:
  111. 111. Predictive of severe inhalation injury (on broncoscopy)
  112. 112. Indicates increased fluid needs more accurately than bronchoscopic grading of the severity of inhalation.</li></ul>Endorf, F.W., Gamelli, R.L. Inhalation Injury, pulmonary perturbations, and fluid rescusitation.Journal of Burn Care Research. 2007; 28 (1): 80-83.<br />
  113. 113. The Utility of Cat Scan in Inhalation Injury<br />Case Report: 22 y.o. indoor <br />industrial fire, 22% TBSA burns, <br />face, left arm, thorax<br />Reske, A., Bak, Z., Samuelson, A., Morales, O., Seiwerts, M., Sjoberg, F. Computer Tomography – a possible aid in the diagnosis of smoke inhalation injury. Acta Anesthesiol Scand 2005; 49; 257-260.<br />
  114. 114. The Utility of Cat Scan in Inhalation Injury<br />Reske, A., Bak, Z., Samuelson, A., Morales, O., Seiwerts, M., Sjoberg, F. Computer Tomography – a possible aid in the diagnosis of smoke inhalation injury. Acta Anesthesiol Scand 2005; 49; 257-260.<br />
  115. 115. The Utility of Cat Scan in Inhalation Injury<br />20 anesthetized sheep underwent graded smoke inhalation injury<br /><ul><li> 4 groups based on degree of smoke exposure
  116. 116. (no smoke, 5 smoke units (SU), 10 SU, 16SU)
  117. 117. CT scans at 6, 12, 24 hours
  118. 118. Radiologist’s score (RADS): normal, interstitial markings, ground </li></ul>glass or opacification on all 4 quandrants of each slice<br /><ul><li> Computerized analysis of Hounsefield unit ranges:
  119. 119. Hyperinflated, normal, poorly aerated and nonaerated and a computation of the fraction of abnormal lung tissue was calculated (FALT)</li></ul>Park, S., et. al. Assessment of severity of ovine smoke inhalation injury by analysis of computed tomographic scans. Journal of Trauma Injury, Infection, and Critical Care. 2003; 55:417-429.<br />
  120. 120. The Utility of Cat Scan in Inhalation Injury<br />Conclusion:<br /><ul><li> Significant changes in PaO2 and cardiac index were not seen until a certain threshold of smoke was reached
  121. 121. Expert analysis of CT scan at 24 hours was predictive of the clinical severity of SII</li></ul>Park, S., et. al. Assessment of severity of ovine smoke inhalation injury by analysis of computed tomographic scans. Journal of Trauma Injury, Infection, and Critical Care. 2003; 55:417-429.<br />
  122. 122. Airway Considerations<br />Procedural Considerations<br /><ul><li> Have difficult airway materials available
  123. 123. Large ET tube
  124. 124. Do NOT change the tube
  125. 125. 3-5 days of observation in setting of upper airway edema
  126. 126. Larger doses of paralytics may be required
  127. 127. Avoid Succinylcholine for delayed burn presentation intubation </li></li></ul><li>Airway Considerations<br />Always Assume SII is a difficult airway<br /><ul><li>Bougie
  128. 128. Glide scope
  129. 129. Cric kit
  130. 130. Intubating LMA
  131. 131. LMA</li></li></ul><li>Airway Considerations<br />
  132. 132. Airway Considerations: Video<br />
  133. 133. ASPHYXIANTS<br />CO & CN<br />
  134. 134. Carbon Monoxide<br /><ul><li> 40,000 annual emergency department visits
  135. 135. 5,000 to 6,000 deaths annually
  136. 136. Most common poison related death in the U.S.
  137. 137. Case fatality rate is 0 to 30%, 40% morbidity rate among survivors, primarily neurocognitive</li></li></ul><li>Carbon Monoxide<br /><ul><li> Colorless, odorless gas
  138. 138. Generated by incomplete combustion of carbon-containing materials
  139. 139. Associated with 50% of fire related deaths
  140. 140. Binds hemoglobin, 230-250 times the affinity of oxygen
  141. 141. Shifts the oxygen-hemoglobin curve left
  142. 142. Displaces oxygen, impairing oxygen binding to hemoglobin and oxygen utilization</li></li></ul><li>Carbon Monoxide<br /><ul><li> Impairs oxidative phosphorylation within the mitochondria
  143. 143. Co binds myoglobin, cytochromes, and NADPH reductase
  144. 144. Can cause myocardial stunning
  145. 145. Generates free radicals causing lipid peroxidation that facilitates delayed neurologic sequlae (DNS)</li></li></ul><li>Sources of Carbon Monoxide<br /><ul><li> Heating systems
  146. 146. Fuel burning devices
  147. 147. kerosene heaters, charcoal grills, camping stoves
  148. 148. Motor vehicles
  149. 149. Motorboat exhaust
  150. 150. Underground electrical cable fires
  151. 151. Methyl chloride, industrial solvent and paint remover
  152. 152. Inhaled or ingested is converted to CO by the liver</li></li></ul><li>Carbon Monoxide<br />Clinical Presentation: Variable & Non-specific<br /><ul><li> Smoke or exhaust in an enclosed area
  153. 153. HA, nausea, malaise, altered cognition, dyspnea, angina, seizures, cardiac arrhythmias, CHF, coma
  154. 154. Neurologic signs, syncope impart poor prognosis
  155. 155. Cherry red lips and skin (insensitive)</li></li></ul><li>Non-pulmonary Consequences of Carbon Monoxide<br />Cardiac Sequelae:<br /><ul><li> 30% of patients with moderate to severe CO poisoning developed cardiac ischemia, in patients without cardiac risk factors or disease
  156. 156. Cardiac ischemia doubled the mortality rate</li></ul>Neurologic Sequelae:<br /><ul><li> Occurs in 40% of patients with significant CO exposure
  157. 157. Occurs 3 to 240 days after recovery, typically 20 days
  158. 158. Correlates with LOC with exposure, but not with levels</li></li></ul><li>Carbon Monoxide Diagnosis<br /><ul><li> The partial pressure of arterial oxygen (PaO2) is normal as it reflects the amount of oxygen dissolved in the blood, which is unchanged.
  159. 159. Hemoglobin bound O2 is profounding reduced.
  160. 160. Pulse oximetry does not differentiate between carboxyhemoglobin and oxyhemoglobin
  161. 161. Carotid body senses PaO2, ventilation may not increase until tissue hypoxia and lactic acidosis begin
  162. 162. Co-oximetry is helpful** but not specific for severity</li></li></ul><li>Carbon Monoxide Levels<br /><ul><li> Non-smokers: 3 percent CO level
  163. 163. Smokers: 10 to 15 percent CO level</li></li></ul><li>Carbon Monoxide Treatment<br /><ul><li> Containment of exposure
  164. 164. High-flow oxygen
  165. 165. COHb half life is 300 min, but reduced to 90 minutes with high flow NRB
  166. 166. Consider transfer if CO not available
  167. 167. Hyperbaric Oxygen</li></li></ul><li>Hyperbaric Oxygen<br /><ul><li> Reduces the half-life of CO from 90 minutes (on 100% NRB) to 30 minutes
  168. 168. Conflicting data regarding immediate and long term benefit
  169. 169. Contra-indication:
  170. 170. PTX
  171. 171. General recommendations:
  172. 172. CO level above 25
  173. 173. CO level above 20 in a pregnant patient
  174. 174. Evidence of fetal distress
  175. 175. Evidence of ongoing ischemia or end organ damage
  176. 176. Loss of consciousness</li></li></ul><li> Physiology of Hydrogen Cyanide<br /><ul><li> High affinity for metal containing enzymes
  177. 177. Inhibits the final stage of oxidative phosphorylation
  178. 178. Prevents cytochrome aa3 from reducing oxygen to water
  179. 179. Forces anaerobic reduction of pyruvate to lactate</li></li></ul><li> Sources of Hydrogen Cyanide<br /><ul><li> Combustion products of:
  180. 180. wool, nylon, polyurethane, malemine, polyacrylonitrite, polamidepastics
  181. 181. Fumigants, fertilizers
  182. 182. Chemistry labs
  183. 183. Pharmaceuticals:
  184. 184. Laetrile (an apricot derivative, no longer available in U.S.)
  185. 185. Sodium nitroprusside
  186. 186. Plants:
  187. 187. Prunus species: apricots, cherries, plums, peaches
  188. 188. PCP manufacturing
  189. 189. Cigarette smoke & Vehicles </li></li></ul><li> Clinical Effects of Hydrogen Cyanide<br /><ul><li> Dose dependent, immediate effects
  190. 190. Less than 50 ppm:
  191. 191. restless, anxious, palpitations, dyspnea and headache
  192. 192. Above 50 ppm:
  193. 193. severe dyspnea, loss of consciousness, seizures, cardiac arrythmias
  194. 194. Lethal dose estimated at:
  195. 195. 200 ppm, at 30 minutes of exposure
  196. 196. 600 to 700 ppm at 5 minutes exposure</li></li></ul><li> Clinical Effects of Hydrogen Cyanide<br /><ul><li> Dose dependent, immediate effects
  197. 197. Less than 50 ppm:
  198. 198. restless, anxious, palpitations, dyspnea and headache
  199. 199. Above 50 ppm:
  200. 200. severe dyspnea, loss of consciousness, seizures, cardiac arrythmias
  201. 201. Lethal dose estimated at:
  202. 202. 200 ppm, at 30 minutes of exposure
  203. 203. 600 to 700 ppm at 5 minutes exposure</li></li></ul><li> Clinical Indicators of Hydrogen Cyanide<br /><ul><li> Anxious appearing or seizures in a patient after smoke exposure
  204. 204. Functional hypoxemia in the absence of cyanosis or abnormal pulse oximetry
  205. 205. Normal PaO2 and high lactate
  206. 206. Typical presentation:
  207. 207. Comatose, hyperventilating, hypotensive and bradycardic, with severe metabolic acidosis (lactate above 10 is predictive)
  208. 208. Cyanide levels:
  209. 209. Toxic > 0.5 micrograms/mL
  210. 210. Fatal > 2.5 micrograms/ml</li></li></ul><li>Treatmentof Hydrogen Cyanide<br /><ul><li> 100% Oxygen
  211. 211. Amyl nitrite inhaler
  212. 212. only if an IV line is not in place
  213. 213. Sodium nitrite 10 mL IV
  214. 214. Sodium thiosulfate 50 mL IV
  215. 215. safer, use in empiric </li></ul>therapy when CO is present<br /><ul><li>Nitrates
  216. 216. Nitrates cause methemoglobinemia
  217. 217. Hypotension is NOT a contraindication
  218. 218. Caution with CO present</li></li></ul><li>Treatmentof Hydrogen Cyanide<br /><ul><li>Hydroxycobalamin (B12) in combination with sodium thiosulfate
  219. 219. Used in France
  220. 220. Hyberbaric oxygen when CO toxicity is present
  221. 221. Synergistic effect</li></li></ul><li>SUMMARY<br />When in doubt, secure the airway!<br />Consider:<br />Burns anywhere, particularly the face, suggest SLI<br />Look for: <br />dysphagia, dysarthria, voice changes, soot in nares/throat<br />The exposed environment is important<br />Get PMHx when available<br />Consider Transport Time<br />Most Experienced Person<br />Adjunctive Equipment <br />Avoid Succs in delayed burns, crush injury<br />Higher doses of paralytics may be needed<br />
  222. 222. References<br />American Burn Association: Burn Incidence Fact Sheet. Accessed at www.ameriburn,org, January 11, 2010.<br />Endorf, F.W., Gamelli, R.L. Inhalation Injury, pulmonary perturbations, and fluid rescusitation. Journal of Burn Care Research. 2007; 28 (1): 80-83.<br />Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.<br />Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.<br />Madani, et al. Factors that predict the need for intubation in patients with smoke inhalation injury. ENT Journal, Jan, 2004.<br />Mandel, J. Hales, C. Smoke Inhalation. Uptodate.com 09/30/2009.<br />Park, S., et. al. Assessment of severity of ovine smoke inhalation injury by analysis of computed tomographic scans. Journal of Trauma Injury, Infection, and Critical Care. 2003; 55:417-429.<br />Reske, A., Bak, Z., Samuelson, A., Morales, O., Seiwerts, M., Sjoberg, F. Computer Tomography – a possible aid in the diagnosis of smoke inhalation injury. Acta Anesthesiol Scand 2005; 49; 257-260.<br />Schwartz’s Principles of Surgery, Ch 8. Burns.<br />
  223. 223. Contact: <br />mmesisca@westernu.edu<br />

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