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

Smoke inhalation

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Page 1: Smoke inhalation

Considerations in the Management of Acute Smoke Inhalation Injury

Mike Mesisca, M.S., D.O.Department of Emergency MedicineArrowhead Regional Medical Center

Colton, CAFebruary 11, 2010

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• Epidemiology of Smoke Inhalation Injury (SII)• Patho-physiology of Injury• Clinical presentation, considerations• Treatment

• Stabilization/Rescusitation • Long-term

• Other considerations:• Carboxyhemoglobinemia• Cyanide

Lecture Outline

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• 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

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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.

Epidemiology

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If AGE + TBSA Burn = 100, then 50% mortality

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• Type of substances burnt• Closed versus Open Space• Degree of lung ventilation• Victim:

• Age• Comorbidities: lung or cardiovascular disease• Intoxication

Historical Features

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• Thermal Injury: Heat Burns• Hypoxic Hypoxemia: Fire steals your oxygen• Toxic Exposure & Asphyxiants:

• Fire releases poison

Patho-physiology of Injury

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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

Thermal Injury

Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.

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• 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

Thermal Injury: Direct Heat

Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.

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• 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

Hypoxic Hypoxemia

Mandel, J. Hales, C. Smoke Inhalation. Uptodate.com 09/30/2009.

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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

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• 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

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• 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

Toxic Exposure: Physiologic Changes

Lee, A., Mellins, R. B. Lung Injury from smoke inhalation. 2006. Pediatric Respiratory Reviews. 7, 123-128.

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

CLINICAL ISSUES

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• 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

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When in doubt, secure the airway!

Consider:Early IntubationTransport Time

Most Experienced PersonGet as much Medical History as Possible

CLINICAL FEATURES OF INHALATION INJURY

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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.

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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.

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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.

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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.

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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.

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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.

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• CXR• ABG• Labs• Xenon• Bronchoscopy• CT

Diagnostic Studies for Inhalation Injury

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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.

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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

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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).

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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.

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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.

Case Report: 22 y.o. indoor industrial fire, 22% TBSA burns, face, left arm, thorax

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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.

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The Utility of Cat Scan in Inhalation Injury

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.

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)

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The Utility of Cat Scan in Inhalation Injury

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.

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

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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

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Always Assume SII is a difficult airway• Bougie• Glide scope • Cric kit• Intubating LMA• LMA

Airway Considerations

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Airway Considerations

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Airway Considerations: Video

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ASPHYXIANTS

CO & CN

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• 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

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• 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

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• 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)

Carbon Monoxide

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• 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

Sources of Carbon Monoxide

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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)

Carbon Monoxide

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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

Non-pulmonary Consequences of Carbon Monoxide

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• 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 Diagnosis

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• Non-smokers: 3 percent CO level• Smokers: 10 to 15 percent CO level

Carbon Monoxide Levels

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• 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

Carbon Monoxide Treatment

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• 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

Hyperbaric Oxygen

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• 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

Physiology of Hydrogen Cyanide

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• Combustion products of:• wool, nylon, polyurethane, malemine, polyacrylonitrite, polamide pastics

• 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

Sources of Hydrogen Cyanide

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• 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

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• 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

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• 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

Clinical Indicators of Hydrogen Cyanide

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• 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

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• Hydroxycobalamin (B12) in combination with sodium thiosulfate

• Used in France

• Hyberbaric oxygen when CO toxicity is present • Synergistic effect

Treatmentof Hydrogen Cyanide

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When in doubt, secure the airway!Consider:

Burns anywhere, particularly the face, suggest SLILook for:

dysphagia, dysarthria, voice changes, soot in nares/throatThe exposed environment is important

Get PMHx when availableConsider Transport TimeMost Experienced Person

Adjunctive Equipment Avoid Succs in delayed burns, crush injuryHigher doses of paralytics may be needed

SUMMARY

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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.

References