Inhalation Injury Workup

  • Author: Denise Serebrisky, MD; Chief Editor: Michael R Bye, MD   more...
 
Updated: Mar 22, 2012
 

Laboratory Studies

Various studies are indicated in patients with inhalation injury.

Pulse oximetry

Cutaneous pulse oximetry uses a 2-wavelength technique of light refractance to measure hemoglobin saturation that is falsely elevated by CO-bound hemoglobin. Obtain direct measures of carboxyhemoglobin and oxyhemoglobin.

To monitor oxygen saturation, recognizing that cutaneous pulse oximetry is falsely elevated by CO is imperative. One must not rely on pulse oximetry until the carboxyhemoglobin level has reached the reference range.

Cooximetry (arterial blood) uses a 4-wavelength technique of light refractance to accurately measure carboxyhemoglobin and oxyhemoglobin, in addition to deoxyhemoglobin and methemoglobin. The percent oxyhemoglobin measured by cooximetry is an accurate measure of the arterial oxygen saturation.

Arterial blood gas

Arterial oxygen tension (partial pressure arterial oxygen [PaO2]) also does not accurately reflect the degree of CO poisoning or cellular hypoxia. The PaO2 level reflects the oxygen dissolved in blood that is not altered by the hemoglobin-bound CO. Because dissolved oxygen makes up only a small fraction of arterial oxygen content, a PaO2 level within the reference range may lead to serious underestimation of the decrement in tissue oxygen delivery and the degree of hypoxia at the cellular level that occurs when CO blocks the delivery of oxygen to the tissues. With most blood gas machines, the oxygen saturation is calculated, based on the PaO2 level. Thus, such a reading does not give an accurate determination of oxygen saturation, which must come from cooximatry.

ABG measurements are nonetheless useful to assess the adequacy of pulmonary gas exchange. Although the presence of a PaO2 level that is within the reference range may not exclude significant tissue hypoxia due to the effects of CO, the presence of a low PaO2 (< 60 mm Hg in room air) or hypercarbia (alveolar [arterial] carbon dioxide pressure [PaCO2] level of 55 mm Hg) are indicative of significant respiratory insufficiency. Metabolic acidosis suggests inadequate oxygen delivery to the tissues.

The alveolar gas equation can be used to estimate the efficiency of pulmonary oxygen delivery to the arterial circulation in the presence of supplemental oxygen administration. This formula determines the alveolar oxygen pressure.

The difference between the partial pressure of oxygen in the alveolus and that measured on an ABG is the alveolar-arterial (A-a) gradient. This value, usually less than 5-10 mm Hg, may be several hundred mm Hg in the setting of significant pulmonary injury and can be used to assess improvement or deterioration in lung function when measured at a stable fraction of inspired oxygen (FiO2).

The alveolar gas equation can be used to estimate the efficiency of pulmonary oxygen delivery to the arterial circulation in the presence of supplemental oxygen administration.

The formula is as follows: PaO2 = (FiO2)(PB - PH2 O) - (PaCO2/RQ). PB represents barometric pressure, PH2 0 represents partial pressure of water vapor (47 mm Hg at body temperature, ambient pressure), and RQ represents respiratory quotient (estimated at 0.8).

Carboxyhemoglobin level

Provide supplemental oxygen therapy to all patients with suspected CO intoxication. Smokers may have baseline levels up to 5-10% and may experience more significant CO poisoning for the same level of exposure as nonsmokers.

However, blood carboxyhemoglobin levels may underestimate the degree of CO intoxication because of oxygen administration before arrival to the hospital. The use of nomograms to extrapolate levels to the time of rescue has been shown to have greater prognostic value. Symptoms vary with peak carboxyhemoglobin levels, but correlation between carboxyhemoglobin levels and eventual neurologic outcome is poor. The symptoms in relation to carboxyhemoglobin in the blood are as follows:[2]

  • Carboxyhemoglobin level of 0-10% - Usually no symptoms
  • Carboxyhemoglobin level of 10-20% - Mild headache, atypical dyspnea
  • Carboxyhemoglobin level of 20-30% - Throbbing headache, impaired concentration
  • Carboxyhemoglobin level of 30-40% - Severe headache, impaired thinking
  • Carboxyhemoglobin level of 40-50% - Confusion, lethargy, syncope
  • Carboxyhemoglobin level of 50-60% - Respiratory failure, seizures
  • Carboxyhemoglobin level of more than 70% - Coma, death

Cyanide levels

Levels correlate closely with the level of exposure and toxicity but may not be readily available. Many hospitals send out tests for cyanide levels; therefore, laboratory confirmation may take several days to a week. Persistent neurologic dysfunction unresponsive to use of supplemental oxygen, cardiac dysfunction, and severe lactic acidosis, particularly in the presence of high mixed venous oxygen saturation, are indicative of cyanide intoxication. In a setting consistent with potential cyanide exposure, institute specific empiric therapy while waiting for laboratory confirmation of the diagnosis.

Electrolyte levels

Obtain tests at regular and frequent intervals to monitor for electrolyte abnormalities that result from large-volume fluid resuscitation. Use results to adjust both fluid and electrolyte replacement.

CBC count, type, and cross

Hemoconcentration resulting from fluid losses is common immediately following injury. Adequate restoration of intravascular volume results in a progressive fall in hematocrit. Severe anemia may require blood replacement, particularly in the presence of significant hypoxia or hemodynamic instability. A baseline WBC count can also be used for comparison when concerns arise about infection.

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Imaging Studies

C-spine radiography is indicated to investigate neck injury in all unconscious patients and in those in whom a potential mechanism of injury cannot be excluded (eg, jumped from window to escape fire, fell down stairs).

Roentgenographic abnormalities are frequently delayed and may not manifest on the initial chest radiograph. Radiographic evidence of pulmonary injury typically appears 24-36 hours after the inhalation. Obtain a chest radiograph at the baseline examination for subsequent comparison in cases of significant injury. Radiographic studies are also useful to establish correct placement of the endotracheal tube and central venous catheters.

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Other Tests

Direct laryngoscopy and fiberoptic bronchoscopy

Both have diagnostic and therapeutic use. Visualization of erythema, edema, ulceration, and soot deposition make bronchoscopy useful in evaluating the extent of injury to the tracheobronchial tree, although severe vasoconstriction from hypovolemia may mask significant injury.

Fiberoptic bronchoscopy can also be used to facilitate endotracheal tube placement, even in the technically difficult airway.

Bronchoscopy is more sensitive and accurate than clinical examination alone in diagnosing inhalation injury and is, therefore, particularly useful in cases in which the decision to perform endotracheal intubation is unclear.

Serial bronchoscopy can help remove debris and necrotic cells in cases with aggressive pulmonary toilet or when suctioning and positive pressure ventilation are insufficient

The use of bronchoscopy among patients with inhalation injury complicated by pneumonia is associated with a decreased duration of mechanical ventilation, length of intensive care unit stay, and decreased overall hospital cost.[4]

Because of their small size, a child's airway can only accommodate a relatively small diameter bronchoscope. Extremely small diameter fiberoptic bronchoscopes with a suction port (capable of entering an endotracheal tube sized for a small toddler or infant) are only recently available, and whether these limit the ability to remove heavy particulate matter is unclear.

Radionucleotide scintigraphy

Delayed or inhomogeneous clearance of 133Xenon can be used to detect small airway parenchymal injury but adds little to the clinical management and is not known to have any particular therapeutic advantage.[5]

Likewise, increased clearance of aerosolized technetium-99m–labeled diethylenetriaminepentaacetate (99mTcDTPA) is a sensitive indicator of injury to the alveolar capillary membrane; however, its clinical use is not yet established.

Pulmonary function tests

With an inhalation injury, a decrease in pulmonary compliance, vital capacity, and functional residual capacity occurs. Airway obstruction causes a decrease in FEV1 and peak flow. Although this helps determine lower airway disease and injury, similar to radionucleotide scintigraphy, it has little clinical use in the initial stages of treatment.

In patients with cutaneous burns, the reduction in vital capacity and FEV1 correlates closely with the extent of surface burns. Full resolution of pulmonary function test result abnormalities may take several months.

Some agents, particularly chlorine gas, may result in reactive airways syndrome, with subsequent development of airflow obstruction.

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Contributor Information and Disclosures
Author

Denise Serebrisky, MD  Assistant Professor, Department of Pediatrics, Albert Einstein College of Medicine; Director, Division of Pulmonary Medicine, Lewis M Fraad Department of Pediatrics, Jacobi Medical Center; Director, Jacobi Asthma and Allergy Center for Children

Denise Serebrisky, MD is a member of the following medical societies: American Thoracic Society

Disclosure: Nothing to disclose.

Coauthor(s)

Emily B Nazarian, MD  MD, Assistant Professor of Pediatrics, Fellowship Director, Pediatric Critical Care, Golisano Children's Hospital at Strong

Emily B Nazarian, MD is a member of the following medical societies: American Academy of Pediatrics

Disclosure: Nothing to disclose.

Heidi Connolly, MD  Associate Professor of Pediatrics and Psychiatry, University of Rochester School of Medicine and Dentistry; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center

Heidi Connolly, MD is a member of the following medical societies: American Academy of Pediatrics, American Thoracic Society, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Girish D Sharma, MD  Professor of Pediatrics, Rush Medical College; Senior Attending, Department of Pediatrics, Director, Section of Pediatric Pulmonology and Rush Cystic Fibrosis Center, Rush University Medical Center

Girish D Sharma, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American Thoracic Society, and Royal College of Physicians of Ireland

Disclosure: Nothing to disclose.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Charles Callahan, DO  Professor, Deputy Chief of Clinical Services, Walter Reed Army Medical Center

Charles Callahan, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, American College of Osteopathic Pediatricians, American Thoracic Society, Association of Military Surgeons of the US, and Christian Medical & Dental Society

Disclosure: Nothing to disclose.

Mary E Cataletto, MD  Director of Children's Sleep Services, Winthrop Sleep Disorders Center; Professor of Clinical Pediatrics, State University of New York at Stony Brook

Mary E Cataletto, MD is a member of the following medical societies: American Academy of Pediatrics and American College of Chest Physicians

Disclosure: Shering Plough Pharmaceuticals Honoraria Consulting

Chief Editor

Michael R Bye, MD  Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons; Attending Physician, Pediatric Pulmonary Medicine, Morgan Stanley Children's Hospital of New York Presbyterian, Columbia University Medical Center

Michael R Bye, MD is a member of the following medical societies: American Academy of Pediatrics, American College of Chest Physicians, and American Thoracic Society

Disclosure: Nothing to disclose.

References
  1. Whitelock-Jones L, Bass DH, Millar AJ, Rode H. Inhalation burns in children. Pediatr Surg Int. 1999;15(1):50-5. [Medline].

  2. Rorison DG, McPherson SJ. Acute toxic inhalations. Emerg Med Clin North Am. May 1992;10(2):409-35. [Medline].

  3. Weiss SM, Lakshminarayan S. Acute inhalation injury. Clin Chest Med. Mar 1994;15(1):103-16. [Medline].

  4. Carr JA, Phillips BD, Bowling WM. The utility of bronchoscopy after inhalation injury complicated by pneumonia in burn patients: results from the National Burn Repository. J Burn Care Res. Nov-Dec 2009;30(6):967-74. [Medline].

  5. Agee RN, Long JM 3rd, Hunt JL, Petroff PA, Lull RJ, Mason AD Jr, et al. Use of 133xenon in early diagnosis of inhalation injury. J Trauma. Mar 1976;16(3):218-24. [Medline].

  6. Oremus M, Hanson MD, Whitlock R, Young E, Archer C, Dal Cin A, et al. A systematic review of heparin to treat burn injury. J Burn Care Res. Nov-Dec 2007;28(6):794-804. [Medline].

  7. Jones WG, Madden M, Finkelstein J, Yurt RW, Goodwin CW. Tracheostomies in burn patients. Ann Surg. Apr 1989;209(4):471-4. [Medline]. [Full Text].

  8. Bartlett RH. Critical Care Physiology. Little, Brown and Company: Boston, Mass; 1996:68-69.

  9. Blanc PD, Galbo M, Hiatt P, Olson KR, Balmes JR. Symptoms, lung function, and airway responsiveness following irritant inhalation. Chest. Jun 1993;103(6):1699-705. [Medline].

  10. Chou KJ, Fisher JL, Silver EJ. Characteristics and outcome of children with carbon monoxide poisoning with and without smoke exposure referred for hyperbaric oxygen therapy. Pediatr Emerg Care. Jun 2000;16(3):151-5. [Medline].

  11. Clark CJ, Campbell D, Reid WH. Blood carboxyhaemoglobin and cyanide levels in fire survivors. Lancet. Jun 20 1981;1(8234):1332-5. [Medline].

  12. Cohen MA, Guzzardi LJ. Inhalation of products of combustion. Ann Emerg Med. Oct 1983;12(10):628-32. [Medline].

  13. Demarest GB, Hudson LD, Altman LC. Impaired alveolar macrophage chemotaxis in patients with acute smoke inhalation. Am Rev Respir Dis. Feb 1979;119(2):279-86. [Medline].

  14. DiVincenti FC, Pruitt BA Jr, Reckler JM. Inhalation injuries. J Trauma. Feb 1971;11(2):109-17. [Medline].

  15. Haponik EF, Crapo RO, Herndon DN, Traber DL, Hudson L, Moylan J. Smoke inhalation. Am Rev Respir Dis. Oct 1988;138(4):1060-3. [Medline].

  16. Heimbach DM, Waeckerle JF. Inhalation injuries. Ann Emerg Med. Dec 1988;17(12):1316-20. [Medline].

  17. Jackson MP, Philp B, Murdoch LJ, Powell BW. High frequency oscillatory ventilation successfully used to treat a severe paediatric inhalation injury. Burns. Aug 2002;28(5):509-11. [Medline].

  18. Juurlink DN, Buckley NA, Stanbrook MB, Isbister GK, Bennett M, McGuigan MA. Hyperbaric oxygen for carbon monoxide poisoning. Cochrane Database Syst Rev. Jan 25 2005;CD002041. [Medline].

  19. Kipen HM, Rab S, Mohr S. Incidence of persistent symptoms and morbidity after inhalation exposure. American Review of Respiratory Disease. 1993;147:A113.

  20. Madnani DD, Steele NP, de Vries E. Factors that predict the need for intubation in patients with smoke inhalation injury. Ear Nose Throat J. Apr 2006;85(4):278-80. [Medline].

  21. Moritz AR, Henriques FC, McLean R. The effects of inhaled heat on the air passages and lungs: an experimental investigation. American Journal of Pathology. 1945;21:311-325.

  22. Peterson JE, Stewart RD. Absorption and elimination of carbon monoxide by inactive young men. Arch Environ Health. Aug 1970;21(2):165-71. [Medline].

  23. Pruitt BA Jr, Cioffi WG, Shimazu T, Ikeuchi H, Mason AD Jr. Evaluation and management of patients with inhalation injury. J Trauma. Dec 1990;30(12 Suppl):S63-8. [Medline].

  24. Pruitt BA Jr, Erickson DR, Morris A. Progressive pulmonary insufficiency and other pulmonary complications of thermal injury. J Trauma. May 1975;15(5):369-79. [Medline].

  25. Rossignol AM, Boyle CM, Locke JA, Burke JF. Hospitalized burn injuries in Massachusetts: an assessment of incidence and product involvement. Am J Public Health. Nov 1986;76(11):1341-3. [Medline].

  26. Ruddy RM. Smoke inhalation injury. Pediatr Clin North Am. Apr 1994;41(2):317-36. [Medline].

  27. Stone JP, Hazlett RN, Johnson JE. The transport of hydrogen chloride by soot from burning polyvinyl chloride. J of Fire Flammability. 1973;4:42.

  28. Thom SR, Keim LW. Carbon monoxide poisoning: a review epidemiology, pathophysiology, clinical findings, and treatment options including hyperbaric oxygen therapy. J Toxicol Clin Toxicol. 1989;27(3):141-56. [Medline].

  29. Vogel SN, Sultan TR, Ten Eyck RP. Cyanide poisoning. Clin Toxicol. Mar 1981;18(3):367-83. [Medline].

  30. Weaver LK, Hopkins RO, Chan KJ, Churchill S, Elliott CG, Clemmer TP, et al. Hyperbaric oxygen for acute carbon monoxide poisoning. N Engl J Med. Oct 3 2002;347(14):1057-67. [Medline].

  31. Whitener DR, Whitener LM, Robertson KJ, Baxter CR, Pierce AK. Pulmonary function measurements in patients with thermal injury and smoke inhalation. Am Rev Respir Dis. Nov 1980;122(5):731-9. [Medline].

  32. Witten ML, Quan SF, Sobonya RE, Lemen RJ. New developments in the pathogenesis of smoke inhalation-induced pulmonary edema. West J Med. Jan 1988;148(1):33-6. [Medline]. [Full Text].

  33. Wright MJ, Murphy JT. Smoke inhalation enhances early alveolar leukocyte responsiveness to endotoxin. J Trauma. Jul 2005;59(1):64-70. [Medline].

  34. Zikria BA, Weston GC, Chodoff M, Ferrer JM. Smoke and carbon monoxide poisoning in fire victims. J Trauma. Aug 1972;12(8):641-5. [Medline].

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Table. Inhalants[2, 3]
TypeInhalantSourceInjury/Mechanism
Irritant gasesAmmoniaFertilizer, refrigerant, manufacturing of dyes, plastics, nylonUpper airway epithelial damage
ChlorineBleaching agent, sewage and water disinfectant, cleansing productsLower airway epithelial damage
Sulfur dioxideCombustion of coal, oil, cooking fuel, smeltingUpper airway epithelial damage
Nitrogen dioxideCombustion of diesel, welding, manufacturing of dyes, lacquers, wall paperTerminal airway epithelial damage
AsphyxiantsCarbon monoxide*Combustion of weeds, coal, gas, heatersCompetes for oxygen sites on hemoglobin, myoglobin, heme-containing intracellular proteins
Hydrogen cyanideBurning of polyurethane, nitrocellulose (silk, nylon, wool)Tissue asphyxiation by inhibiting intracellular cytochrome oxidase activity, inhibits ATP production, leads to cellular anoxia
Hydrogen sulfideSewage treatment facility, volcanic gases, coal mines, natural hot springsSimilar to cyanide, tissue asphyxiant by inhibition of cytochrome oxidase, leads to disruption of electron transport chain, results in anaerobic metabolism
Systemic toxinsHydrocarbonsInhalant abuse (toluene, benzene, Freon); aerosols; glue; gasoline; nail polish remover; typewriter correction fluid; ingestion of petroleum solvents, kerosene, liquid polishes CNS narcosis, anesthetic stats, diffuse GI symptoms, peripheral neuropathy with weakness, coma, sudden death, chemical pneumonitis, CNS abnormalities, GI irritation, cardiomyopathy, renal toxicity
OrganophosphatesInsecticides, nerve gasesBlocks acetylcholinesterase, cholinergic crisis with increased acetylcholine
Metal fumesMetal oxides of zinc, copper, magnesium, jewelry makingFlulike symptoms, fever, myalgia, weakness
* Major component of smoke



† Smells like almonds, component of smoke from fires



‡ Smells like rotten eggs



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