• Share
  • Email
  • Embed
  • Like
  • Save
  • Private Content
Smoke inhalation
 

Smoke inhalation

on

  • 3,345 views

 

Statistics

Views

Total Views
3,345
Views on SlideShare
3,233
Embed Views
112

Actions

Likes
0
Downloads
104
Comments
1

3 Embeds 112

http://onscene1097.com 95
http://www.onscene1097.com 15
http://www.slideshare.net 2

Accessibility

Categories

Upload Details

Uploaded via as Microsoft PowerPoint

Usage Rights

© All Rights Reserved

Report content

Flagged as inappropriate Flag as inappropriate
Flag as inappropriate

Select your reason for flagging this presentation as inappropriate.

Cancel

11 of 1 previous next

  • Full Name Full Name Comment goes here.
    Are you sure you want to
    Your message goes here
    Processing…
Post Comment
Edit your comment
  • Schwartz’s Principles of Surgery, Ch 8. Burns
  • Schwartz’s Principles of Surgery, Ch 8. Burns; American Burn Association: Burn Incidence Fact Sheet. Accessed at www.ameriburn,org, January 11, 2010.
  • Schwartz’s Principles of Surgery, Ch 8. Burns; American Burn Association: Burn Incidence Fact Sheet. Accessed at www.ameriburn,org, January 11, 2010.
  • American Burn Association: Burn Incidence Fact Sheet. Accessed at www.ameriburn,org, January 11, 2010.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.
  • Mandel, J. Hales, C. Smoke Inhalation. Uptodate.com 09/30/2009.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128. Insert photo from Tintinalli.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128. Insert photo from Tintinalli.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128. Insert photo from Tintinalli.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128. Insert photo from Tintinalli.
  • Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128. Insert photo from Tintinalli.
  • Tintinalli
  • Tintinalli
  • Tintinalli
  • Tintinalli
  • Tintinalli
  • Tintinalli
  • Tintinalli
  • Tintinalli

Smoke inhalation Smoke inhalation Presentation Transcript

  • 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
  • Lecture Outline
    • Epidemiology of Smoke Inhalation Injury (SII)
    • Patho-physiology of Injury
    • Clinical presentation, considerations
    • Treatment
    • Stabilization/Rescusitation
    • Long-term
    • Other considerations:
    • Carboxyhemoglobinemia
    • Cyanide
  • Epidemiology
    • 35% of hospitalized burn patients have smoke inhalation injury
    • Can triple the length of stay
    • Compared to burns alone, there is a 60% increase in mortality if inhalation injury and PNA are also present
    • When ARDs develops from burn inhalation injury, mortality rate up to 66%.
    • 60% TBSA burns with inhalation injury & ARDS, almost 100% fatal.
  • Epidemiology
    National Burn Repository (1999-2008):
    • Deaths from burns increased with advancing age and burn size, and the presence of inhalation injury.
    • For patients under 50, TBSA 0.1% to 19.9% burn, inhalation injury increases death rate 15 times.
  • If AGE + TBSA Burn = 100, then 50% mortality
  • Historical Features
    • Type of substances burnt
    • Closed versus Open Space
    • Degree of lung ventilation
    • Victim:
    • Age
    • Comorbidities: lung or cardiovascular disease
    • Intoxication
  • Patho-physiology of Injury
    • Thermal Injury: Heat Burns
    • Hypoxic Hypoxemia: Fire steals your oxygen
    • Toxic Exposure & Asphyxiants:
    • Fire releases poison
  • Thermal Injury
    Direct heat injury, typically supraglottic
    • Facial-oral burns create anatomic obstruction
    • Laryngospasm (rare) & bronchoconstriction
    • Local erythema, edema, ulceration
    • cellular necrosis of ciliated epithelium and capillary leakage
    • Edema, maximal within 24-48 hours
    • Causes airflow obstruction, therefore stridor
    • Resolves after 3-5 days
    Lee, A., Mellins, R. B. Lung Injury from smoke inhalation.
    2006. Pediatric Respiratory Reviews. 7, 123-128.
  • Thermal Injury: Direct Heat
    • Heat dissipates on inhalation and damage occurs above the carina
    • Steam or prolonged exposure or particles 5-10 microns in diameter of less can damage airway below the cords
    Lee, A., Mellins, R. B. Lung Injury from smoke inhalation.
    2006. Pediatric Respiratory Reviews. 7, 123-128.
  • Hypoxic Hypoxemia
    Fire consumes the ambient oxygen  lower the environmental FIO2 below 0.21
    Fuel dependent
    • Gasoline: 0.15
    • Oxygen containing compounds: 0.10
    Exacerbates CO and HCN toxicity
    Increases ventilation
    Mandel, J. Hales, C. Smoke Inhalation. Uptodate.com 09/30/2009.
  • Toxic Exposure
    Smoke: visible, small particulate matter in hot air and toxic gas
    • Local, Bronchopulmonary Toxins
    • Asphyxiants: Inhaled combustible products cause injury to the lower airway
    • From synthetic substances
    • Carbon monoxide and hydrogen cyanide
  • Toxic Exposure
    • Low molecular weight toxins in smoke alter the pH and create free radicals in distal airways causing tissue destruction, mainly nitrous oxide
    • Soot (elemental carbon) itself is nontoxic, enhances delivery of toxins
    • Acute neutrophilic airway inflammation occurs, but symptoms may be delayed 12-36 hours
    • Progression to pulmonary edema, bronchopulmonary PNA, and/or ARDs
  • Toxic Exposure: Physiologic Changes
    • Destruction of ciliated epithelium in trachea and bronchial tree
    • Increased vascular permeability causing pulmonary edema
    • Alveolar hemorrhage & hyaline membrane formation
    • Airway obstruction facilitates surfactant consumption, distal airway collapse and atelectasis
    Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006.
    Pediatric Respiratory Reviews. 7, 123-128.
  • 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?
  • CLINICAL FEATURES OF INHALATION INJURY
    • Classic signs:
    • Stridor, hoarseness, drooling, dysphagia
    • Predictive Signs:
    • Singed nares, body burns
    • Hard signs:
    • Soot in the oral cavity
    • Facial burns
    • Absolute
    • True or false vocal cord edema
  • CLINICAL FEATURES OF INHALATION INJURY
    When in doubt,
    secure the airway!
    Consider:
    Early Intubation
    Transport Time
    Most Experienced Person
    Get as much Medical History as Possible
  • Retrospective chart review of patients presenting with smoke inhalation to identify predictors
    of respiratory distress
    • 41 patients, treated in ER (Burn Center), with an ENT consult for fiberoptic laryngoscopy
    • 8 required intubation
    • Intubation correlated with:
    • soot in the oral cavity (p <0.001)
    • facial burns (p = 0.025)
    • body burns (p = 0.025)
    • Intubation did not correlate with:
    • 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.
  • Retrospective chart review of patients presenting with smoke inhalation to identify predictors
    of respiratory distress
    • Facial burns correlated with true cord edema (p = 0.01)
    • 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.
  • Indicators of inhalation injury
    in patients without burns
    64 patients without burns following household fires, 5 day ICU data collection
    • 35 patients were intubated, mean 101.2 hrs
    • 27 smokers, no correlation with longer ICU stay or time on vent
    • 18 intubated in the field and 17 intubated in the hospital
    • Higher positive bacteriologic analysis from field intubations & significantly more time on the Vent
    Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.
  • Indicators of inhalation injury
    in patients without burns
    • Dysphonia correlated with a longer ICU stay (p=0.05) and a greater likelihood to develop positive sputum culture (p=0.02)
    • 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)
    • No correlation found in patients that were wheezing.
    • 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.
  • Indicators that no inhalation injury
    occurred after smoke exposure
    • 57 patients with smoke exposure were divided into 5 groups
    • Group 1 (23): normal vitals, normal exam
    • Group 2 (26): no burn, but abnormal vitals and/or abnormal exam
    • Group 3 (5): minor burn (<15% TBSA)
    • Group 4 (2): major burn (>15% TBSA)
    • Group 5 (1): cardiac arrest
    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.
  • Indicators that no inhalation injury
    occurred after smoke exposure
    • 57 patients with smoke exposure were divided into 5 groups
    • Group 1 (23): normal vitals, normal exam
    • 28 studies ordered, mostly CO level (16) and ABG (9)
    • 1 patient, a smoker, after 3 hours of smoke exposure had a CO level 22%
    • All others discharged
    • Group 2 (26): no burn, abnormal vitals and/or exam
    • 81 studies ordered , 14% had abnormal CO or ABG results
    • Recommendation:
    • 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.
  • Diagnostic Studies for Inhalation Injury
    • CXR
    • ABG
    • Labs
    • Xenon
    • Bronchoscopy
    • CT
  • CXR is a Poor Indicator of Inhalation Injury
    • 29 of 56% of patients had normal chest xrays
    • Most frequent abnormal findings is diffuse alveolar infiltrates (35%)
    • Focal abnormalities, consolidation or atelectasis, 12.5% on admission and 25.6% on day 2
    • First CXR not predictive of duration of MV or ICU length of stay, or positive sputum cultures
    Hantson, et al. Early complications and value of initial clinical and paraclinical observations in victims of smoke inhalation without burns. Chest, 111 (3), 2007.
  • CXR is a Poor Indicator of Inhalation Injury
    • Other studies have shown 12/29 (41%) of patients with acute inhalation injury and burns to have normal chest radiographs (Wittram, 1994).
    • In a study of 45 patients from a “major fire disaster”, 33/45 patients had abnormal chest radiographs on admission (Lee, 1988).
    • 29, bronchial wall thickening
    • 13 subglottic edema
    • 7 pulmonary edema
    • 3 patchy consolidation
  • Xenon Scan & Bronchoscopy
    • Xenon ventilation-perfusion scan:
    • ventilation is shunted away from damaged airways
    • nonspecific
    • Bronchoscopy:
    • Invasive, and limited access at some centers
    • Useful in evaluating bacterial contamination and disease progression
    These techniques do not alter therapeutic protocols or outcomes, so many centers still rely on a clinical diagnosis (Heimbach, 1988).
  • ABG & Fluid Requirements
    • A decreased partial pressure of arterial oxygen:fraction of inspired oxygen (PaO2:FIO2 ratio) less than 350 was:
    • Predictive of severe inhalation injury (on broncoscopy)
    • 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.
  • 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.
  • 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.
  • The Utility of Cat Scan in Inhalation Injury
    20 anesthetized sheep underwent graded smoke inhalation injury
    • 4 groups based on degree of smoke exposure
    • (no smoke, 5 smoke units (SU), 10 SU, 16SU)
    • CT scans at 6, 12, 24 hours
    • Radiologist’s score (RADS): normal, interstitial markings, ground
    glass or opacification on all 4 quandrants of each slice
    • Computerized analysis of Hounsefield unit ranges:
    • 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.
  • The Utility of Cat Scan in Inhalation Injury
    Conclusion:
    • Significant changes in PaO2 and cardiac index were not seen until a certain threshold of smoke was reached
    • Expert analysis of CT scan at 24 hours was predictive of the clinical severity of SII
    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.
  • Airway Considerations
    Procedural Considerations
    • Have difficult airway materials available
    • Large ET tube
    • Do NOT change the tube
    • 3-5 days of observation in setting of upper airway edema
    • Larger doses of paralytics may be required
    • Avoid Succinylcholine for delayed burn presentation intubation
  • Airway Considerations
    Always Assume SII is a difficult airway
    • Bougie
    • Glide scope
    • Cric kit
    • Intubating LMA
    • LMA
  • Airway Considerations
  • Airway Considerations: Video
  • ASPHYXIANTS
    CO & CN
  • Carbon Monoxide
    • 40,000 annual emergency department visits
    • 5,000 to 6,000 deaths annually
    • Most common poison related death in the U.S.
    • Case fatality rate is 0 to 30%, 40% morbidity rate among survivors, primarily neurocognitive
  • Carbon Monoxide
    • Colorless, odorless gas
    • Generated by incomplete combustion of carbon-containing materials
    • Associated with 50% of fire related deaths
    • Binds hemoglobin, 230-250 times the affinity of oxygen
    • Shifts the oxygen-hemoglobin curve left
    • Displaces oxygen, impairing oxygen binding to hemoglobin and oxygen utilization
  • Carbon Monoxide
    • Impairs oxidative phosphorylation within the mitochondria
    • Co binds myoglobin, cytochromes, and NADPH reductase
    • Can cause myocardial stunning
    • Generates free radicals causing lipid peroxidation that facilitates delayed neurologic sequlae (DNS)
  • Sources of Carbon Monoxide
    • Heating systems
    • Fuel burning devices
    • kerosene heaters, charcoal grills, camping stoves
    • Motor vehicles
    • Motorboat exhaust
    • Underground electrical cable fires
    • Methyl chloride, industrial solvent and paint remover
    • Inhaled or ingested is converted to CO by the liver
  • Carbon Monoxide
    Clinical Presentation: Variable & Non-specific
    • Smoke or exhaust in an enclosed area
    • HA, nausea, malaise, altered cognition, dyspnea, angina, seizures, cardiac arrhythmias, CHF, coma
    • Neurologic signs, syncope impart poor prognosis
    • Cherry red lips and skin (insensitive)
  • Non-pulmonary Consequences of Carbon Monoxide
    Cardiac Sequelae:
    • 30% of patients with moderate to severe CO poisoning developed cardiac ischemia, in patients without cardiac risk factors or disease
    • Cardiac ischemia doubled the mortality rate
    Neurologic Sequelae:
    • Occurs in 40% of patients with significant CO exposure
    • Occurs 3 to 240 days after recovery, typically 20 days
    • Correlates with LOC with exposure, but not with levels
  • Carbon Monoxide Diagnosis
    • The partial pressure of arterial oxygen (PaO2) is normal as it reflects the amount of oxygen dissolved in the blood, which is unchanged.
    • Hemoglobin bound O2 is profounding reduced.
    • Pulse oximetry does not differentiate between carboxyhemoglobin and oxyhemoglobin
    • Carotid body senses PaO2, ventilation may not increase until tissue hypoxia and lactic acidosis begin
    • Co-oximetry is helpful** but not specific for severity
  • Carbon Monoxide Levels
    • Non-smokers: 3 percent CO level
    • Smokers: 10 to 15 percent CO level
  • Carbon Monoxide Treatment
    • Containment of exposure
    • High-flow oxygen
    • COHb half life is 300 min, but reduced to 90 minutes with high flow NRB
    • Consider transfer if CO not available
    • Hyperbaric Oxygen
  • Hyperbaric Oxygen
    • Reduces the half-life of CO from 90 minutes (on 100% NRB) to 30 minutes
    • Conflicting data regarding immediate and long term benefit
    • Contra-indication:
    • PTX
    • General recommendations:
    • CO level above 25
    • CO level above 20 in a pregnant patient
    • Evidence of fetal distress
    • Evidence of ongoing ischemia or end organ damage
    • Loss of consciousness
  • Physiology of Hydrogen Cyanide
    • High affinity for metal containing enzymes
    • Inhibits the final stage of oxidative phosphorylation
    • Prevents cytochrome aa3 from reducing oxygen to water
    • Forces anaerobic reduction of pyruvate to lactate
  • Sources of Hydrogen Cyanide
    • Combustion products of:
    • wool, nylon, polyurethane, malemine, polyacrylonitrite, polamidepastics
    • Fumigants, fertilizers
    • Chemistry labs
    • Pharmaceuticals:
    • Laetrile (an apricot derivative, no longer available in U.S.)
    • Sodium nitroprusside
    • Plants:
    • Prunus species: apricots, cherries, plums, peaches
    • PCP manufacturing
    • Cigarette smoke & Vehicles
  • Clinical Effects of Hydrogen Cyanide
    • Dose dependent, immediate effects
    • Less than 50 ppm:
    • restless, anxious, palpitations, dyspnea and headache
    • Above 50 ppm:
    • severe dyspnea, loss of consciousness, seizures, cardiac arrythmias
    • Lethal dose estimated at:
    • 200 ppm, at 30 minutes of exposure
    • 600 to 700 ppm at 5 minutes exposure
  • Clinical Effects of Hydrogen Cyanide
    • Dose dependent, immediate effects
    • Less than 50 ppm:
    • restless, anxious, palpitations, dyspnea and headache
    • Above 50 ppm:
    • severe dyspnea, loss of consciousness, seizures, cardiac arrythmias
    • Lethal dose estimated at:
    • 200 ppm, at 30 minutes of exposure
    • 600 to 700 ppm at 5 minutes exposure
  • Clinical Indicators of Hydrogen Cyanide
    • Anxious appearing or seizures in a patient after smoke exposure
    • Functional hypoxemia in the absence of cyanosis or abnormal pulse oximetry
    • Normal PaO2 and high lactate
    • Typical presentation:
    • Comatose, hyperventilating, hypotensive and bradycardic, with severe metabolic acidosis (lactate above 10 is predictive)
    • Cyanide levels:
    • Toxic > 0.5 micrograms/mL
    • Fatal > 2.5 micrograms/ml
  • Treatmentof Hydrogen Cyanide
    • 100% Oxygen
    • Amyl nitrite inhaler
    • only if an IV line is not in place
    • Sodium nitrite 10 mL IV
    • Sodium thiosulfate 50 mL IV
    • safer, use in empiric
    therapy when CO is present
    • Nitrates
    • Nitrates cause methemoglobinemia
    • Hypotension is NOT a contraindication
    • Caution with CO present
  • Treatmentof Hydrogen Cyanide
    • Hydroxycobalamin (B12) in combination with sodium thiosulfate
    • Used in France
    • Hyberbaric oxygen when CO toxicity is present
    • Synergistic effect
  • SUMMARY
    When in doubt, secure the airway!
    Consider:
    Burns anywhere, particularly the face, suggest SLI
    Look for:
    dysphagia, dysarthria, voice changes, soot in nares/throat
    The exposed environment is important
    Get PMHx when available
    Consider Transport Time
    Most Experienced Person
    Adjunctive Equipment
    Avoid Succs in delayed burns, crush injury
    Higher doses of paralytics may be needed
  • 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.
  • Contact:
    mmesisca@westernu.edu