This document provides an overview of considerations in the management of acute smoke inhalation injury. It discusses the epidemiology of smoke inhalation injury, including increased mortality when it occurs alongside burns or ARDS. The pathophysiology of inhalation injury involves thermal injury from heat, hypoxic hypoxemia from fire consuming oxygen, and toxic exposure to combustion byproducts like carbon monoxide and hydrogen cyanide. Clinical presentation may include stridor, hoarseness, or soot in the oral cavity. Diagnostic studies like CXRs and ABGs have limitations, while bronchoscopy can directly evaluate airway injury but access may be limited. Care should focus on stabilization, treatment of complications, and managing long-term effects

1. Considerations in the Management of Acute Smoke Inhalation Injury Mike Mesisca, M.S., D.O. Department of Emergency Medicine Arrowhead Regional Medical Center Colton, CA February 11, 2010

3. Patho-physiology of Injury

4. Clinical presentation, considerations

5. Treatment

6. Stabilization/Rescusitation

7. Long-term

8. Other considerations:

9. Carboxyhemoglobinemia

11. Can triple the length of stay

12. Compared to burns alone, there is a 60% increase in mortality if inhalation injury and PNA are also present

13. When ARDs develops from burn inhalation injury, mortality rate up to 66%.

18. Closed versus Open Space

19. Degree of lung ventilation

20. Victim:

21. Age

22. Comorbidities: lung or cardiovascular disease

24. Hypoxic Hypoxemia: Fire steals your oxygen

25. Toxic Exposure & Asphyxiants:

27. Laryngospasm (rare) & bronchoconstriction

28. Local erythema, edema, ulceration

29. cellular necrosis of ciliated epithelium and capillary leakage

30. Edema, maximal within 24-48 hours

31. Causes airflow obstruction, therefore stridor

32. Resolves after 3-5 daysLee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.

34. Steam or prolonged exposure or particles 5-10 microns in diameter of less can damage airway below the cordsLee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.

36. Oxygen containing compounds: 0.10 Exacerbates CO and HCN toxicity Increases ventilation Mandel, J. Hales, C. Smoke Inhalation. Uptodate.com 09/30/2009.

38. Asphyxiants: Inhaled combustible products cause injury to the lower airway

39. From synthetic substances

41. Soot (elemental carbon) itself is nontoxic, enhances delivery of toxins

42. Acute neutrophilic airway inflammation occurs, but symptoms may be delayed 12-36 hours

44. Increased vascular permeability causing pulmonary edema

45. Alveolar hemorrhage & hyaline membrane formation

46. Airway obstruction facilitates surfactant consumption, distal airway collapse and atelectasisLee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.

47. CLINICAL ISSUES Making the Diagnosis! Who needs intubation? Who needs admission? Who needs a workup? What tests should be included? How helpful are the tests?

49. Stridor, hoarseness, drooling, dysphagia

50. Predictive Signs:

51. Singed nares, body burns

52. Hard signs:

53. Soot in the oral cavity

54. Facial burns

55. Absolute

58. 8 required intubation

59. Intubation correlated with:

60. soot in the oral cavity (p <0.001)

61. facial burns (p = 0.025)

62. body burns (p = 0.025)

63. Intubation did not correlate with:

64. stridor, hoarseness, drooling, dysphagia (all p = 1.0)Madani, et al. Factors that predict the need for intubation in patients with smoke inhalation injury. ENT Journal, Jan, 2004.

66. Body burns correlated with true (p = 0.047) and false (p = 0.003) cord edema Madani, et al. Factors that predict the need for intubation in patients with smoke inhalation injury. ENT Journal, Jan, 2004.

68. 27 smokers, no correlation with longer ICU stay or time on vent

69. 18 intubated in the field and 17 intubated in the hospital

70. Higher positive bacteriologic analysis from field intubations & significantly more time on the VentHantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.

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. No correlation found in patients that were wheezing.

74. Soot in oral pharynx on bronchoscopy correlated with longer ICU stay (p=0.02)Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.

76. Group 1 (23): normal vitals, normal exam

77. Group 2 (26): no burn, but abnormal vitals and/or abnormal exam

78. Group 3 (5): minor burn (<15% TBSA)

79. Group 4 (2): major burn (>15% TBSA)

80. Group 5 (1): cardiac arrestMushtaq, 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.

82. Group 1 (23): normal vitals, normal exam

83. 28 studies ordered, mostly CO level (16) and ABG (9)

84. 1 patient, a smoker, after 3 hours of smoke exposure had a CO level 22%

85. All others discharged

86. Group 2 (26): no burn, abnormal vitals and/or exam

87. 81 studies ordered , 14% had abnormal CO or ABG results

88. Recommendation:

89. Patients with normal vitals and exam and limited exposure (less than 30 min.) need no testing 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.

91. ABG

92. Labs

93. Xenon

94. Bronchoscopy

96. Most frequent abnormal findings is diffuse alveolar infiltrates (35%)

97. Focal abnormalities, consolidation or atelectasis, 12.5% on admission and 25.6% on day 2

98. First CXR not predictive of duration of MV or ICU length of stay, or positive sputum culturesHantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.

100. In a study of 45 patients from a “major fire disaster”, 33/45 patients had abnormal chest radiographs on admission (Lee, 1988).

101. 29, bronchial wall thickening

102. 13 subglottic edema

103. 7 pulmonary edema

105. ventilation is shunted away from damaged airways

106. nonspecific

107. Bronchoscopy:

108. Invasive, and limited access at some centers

109. Useful in evaluating bacterial contamination and disease progressionThese techniques do not alter therapeutic protocols or outcomes, so many centers still rely on a clinical diagnosis (Heimbach, 1988).

111. Predictive of severe inhalation injury (on broncoscopy)

112. Indicates increased fluid needs more accurately than bronchoscopic grading of the severity of inhalation.Endorf, F.W., Gamelli, R.L. Inhalation Injury, pulmonary perturbations, and fluid rescusitation.Journal of Burn Care Research. 2007; 28 (1): 80-83.

113. The Utility of Cat Scan in Inhalation Injury Case Report: 22 y.o. indoor industrial fire, 22% TBSA burns, face, left arm, thorax 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.

114. The Utility of Cat Scan in Inhalation Injury 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.

116. (no smoke, 5 smoke units (SU), 10 SU, 16SU)

117. CT scans at 6, 12, 24 hours

119. Hyperinflated, normal, poorly aerated and nonaerated and a computation of the fraction of abnormal lung tissue was calculated (FALT)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.

121. Expert analysis of CT scan at 24 hours was predictive of the clinical severity of SIIPark, 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.

123. Large ET tube

124. Do NOT change the tube

125. 3-5 days of observation in setting of upper airway edema

126. Larger doses of paralytics may be required

128. Glide scope

129. Cric kit

130. Intubating LMA

132. Airway Considerations: Video

133. ASPHYXIANTS CO & CN

135. 5,000 to 6,000 deaths annually

136. Most common poison related death in the U.S.

138. Generated by incomplete combustion of carbon-containing materials

139. Associated with 50% of fire related deaths

140. Binds hemoglobin, 230-250 times the affinity of oxygen

141. Shifts the oxygen-hemoglobin curve left

143. Co binds myoglobin, cytochromes, and NADPH reductase

144. Can cause myocardial stunning

146. Fuel burning devices

147. kerosene heaters, charcoal grills, camping stoves

148. Motor vehicles

149. Motorboat exhaust

150. Underground electrical cable fires

151. Methyl chloride, industrial solvent and paint remover

153. HA, nausea, malaise, altered cognition, dyspnea, angina, seizures, cardiac arrhythmias, CHF, coma

154. Neurologic signs, syncope impart poor prognosis

157. Occurs 3 to 240 days after recovery, typically 20 days

159. Hemoglobin bound O2 is profounding reduced.

160. Pulse oximetry does not differentiate between carboxyhemoglobin and oxyhemoglobin

161. Carotid body senses PaO2, ventilation may not increase until tissue hypoxia and lactic acidosis begin

164. High-flow oxygen

165. COHb half life is 300 min, but reduced to 90 minutes with high flow NRB

166. Consider transfer if CO not available

168. Conflicting data regarding immediate and long term benefit

169. Contra-indication:

170. PTX

171. General recommendations:

172. CO level above 25

173. CO level above 20 in a pregnant patient

174. Evidence of fetal distress

175. Evidence of ongoing ischemia or end organ damage

177. Inhibits the final stage of oxidative phosphorylation

178. Prevents cytochrome aa3 from reducing oxygen to water

180. wool, nylon, polyurethane, malemine, polyacrylonitrite, polamidepastics

181. Fumigants, fertilizers

182. Chemistry labs

183. Pharmaceuticals:

184. Laetrile (an apricot derivative, no longer available in U.S.)

185. Sodium nitroprusside

186. Plants:

187. Prunus species: apricots, cherries, plums, peaches

188. PCP manufacturing

190. Less than 50 ppm:

191. restless, anxious, palpitations, dyspnea and headache

192. Above 50 ppm:

193. severe dyspnea, loss of consciousness, seizures, cardiac arrythmias

194. Lethal dose estimated at:

195. 200 ppm, at 30 minutes of exposure

197. Less than 50 ppm:

198. restless, anxious, palpitations, dyspnea and headache

199. Above 50 ppm:

200. severe dyspnea, loss of consciousness, seizures, cardiac arrythmias

201. Lethal dose estimated at:

202. 200 ppm, at 30 minutes of exposure

204. Functional hypoxemia in the absence of cyanosis or abnormal pulse oximetry

205. Normal PaO2 and high lactate

206. Typical presentation:

207. Comatose, hyperventilating, hypotensive and bradycardic, with severe metabolic acidosis (lactate above 10 is predictive)

208. Cyanide levels:

209. Toxic > 0.5 micrograms/mL

211. Amyl nitrite inhaler

212. only if an IV line is not in place

213. Sodium nitrite 10 mL IV

214. Sodium thiosulfate 50 mL IV

216. Nitrates cause methemoglobinemia

217. Hypotension is NOT a contraindication

219. Used in France

220. Hyberbaric oxygen when CO toxicity is present

222. References American Burn Association: Burn Incidence Fact Sheet. Accessed at www.ameriburn,org, January 11, 2010. Endorf, F.W., Gamelli, R.L. Inhalation Injury, pulmonary perturbations, and fluid rescusitation. Journal of Burn Care Research. 2007; 28 (1): 80-83. Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007. Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128. Madani, et al. Factors that predict the need for intubation in patients with smoke inhalation injury. ENT Journal, Jan, 2004. Mandel, J. Hales, C. Smoke Inhalation. Uptodate.com 09/30/2009. 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. 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. Schwartz’s Principles of Surgery, Ch 8. Burns.

223. Contact: mmesisca@westernu.edu