eMedicine Specialties > Pediatrics: General Medicine > Pulmonology

Inhalation Injury: Differential Diagnoses & Workup

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
Coauthor(s): Emily B Nazarian, MD, Fellow, Department of Pediatrics, Division of Critical Care, University of Rochester Medical Center; Heidi Connolly, MD, Associate Professor of Pediatrics and Psychiatry, University of Rochester; Director, Pediatric Sleep Medicine Services, Strong Sleep Disorders Center
Contributor Information and Disclosures

Updated: Jun 6, 2008

Workup

Laboratory Studies

  • 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 level
    • 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.
  • Electrolytes
    • 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.

Imaging Studies

  • C-spine radiography: Test for 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).
  • Chest radiography
    • 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.

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
    • 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.4
    • 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.

More on Inhalation Injury

Overview: Inhalation Injury
Differential Diagnoses & Workup: Inhalation Injury
Treatment & Medication: Inhalation Injury
Follow-up: Inhalation Injury
References

References

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Further Reading

Keywords

inhalation injury, smoke inhalation, smoke, carbon monoxide, CO, hydrogen cyanide, reflex bronchoconstriction, hydrocarbon inhalation, hypoxemia, bacterial pneumonia, airway obstruction, residual reactive airway disease, bronchiectasis, bronchiolitis obliterans, interstitial fibrosis, asthma, respiratory distress, obtundation, hyperinflation, atelectasis, air trapping, lung injury, alveolar edema, ventilation-perfusion mismatch, hypoxia, lactic acidosis, hypotension, renal tubular acidosis, hepatitis, bone marrow insufficiency, thermal burns, conjunctivitis, corneal edema, rhinitis, pharyngitis, laryngitis, tracheitis, bronchitis, alveolitis, respiratory insufficiency

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, Fellow, Department of Pediatrics, Division of Critical Care, University of Rochester Medical Center
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; 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.

Medical Editor

Girish D Sharma, MD, Associate Professor, Department of Pediatrics, Rush University Medical Center, Rush Children's Hospital; Director of Pediatric Pulmonary Section and Rush Cystic Fibrosis 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.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine.com, Inc
Disclosure: Pfizer Inc Stock Investment from broker recommendation; Avanir Pharma Stock Investment from broker recommendation

Managing Editor

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.

CME Editor

Mary E Cataletto, MD, Associate Director, Division of Pediatric Pulmonology, Winthrop University Hospital; Associate Professor, Department 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, American Heart Association, and American Thoracic Society
Disclosure: Nothing to disclose.

Chief Editor

Michael R Bye, MD, Attending Physician, Pediatric Pulmonary Medicine, Columbia University Medical Center; Professor of Clinical Pediatrics, Division of Pulmonary Medicine, Columbia University College of Physicians and Surgeons
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: Merck Honoraria Speaking and teaching

 
 
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