Oxygen toxicity: Difference between revisions

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**Generally, FiO2 of 40% or less (0.40 ATA) can be tolerated indefinitely<ref name="Hedley">Hedley-Whyte J. Pulmonary Oxygen Toxicity: Investigation and Mentoring. The Ulster Medical Journal. 2008;77(1):39-42.</ref>
**Generally, FiO2 of 40% or less (0.40 ATA) can be tolerated indefinitely<ref name="Hedley">Hedley-Whyte J. Pulmonary Oxygen Toxicity: Investigation and Mentoring. The Ulster Medical Journal. 2008;77(1):39-42.</ref>
**Most common in hyperbaric oxygen therapy and prolonged administration of normobaric supplemental oxygen
**Most common in hyperbaric oxygen therapy and prolonged administration of normobaric supplemental oxygen
**Pulmonary toxicity occurs sooner and at lower partial pressures than CNS toxicity<ref name="Hedley" />
**Pulmonary toxicity occurs sooner and at lower partial pressures than CNS toxicity<ref name="Hedley" />, however there is no predictable pattern or sequence of symptoms for CNS toxicity (initial symptom may be seizure/coma)<ref name="Bitterman" />


==Clinical Features==
==Clinical Features==
===Pulmonary===
===Pulmonary===
*Tracheobronchial irritation → pleuritic chest pain, dyspnea and coughing<ref name="Thomson">Thomson L, Paton J. Oxygen toxicity. Paediatr Respir Rev. 2014 Jun;15(2):120-3.</ref>
*Tracheobronchial irritation (initial manifestation) → pleuritic chest pain, dyspnea and coughing<ref name="Thomson">Thomson L, Paton J. Oxygen toxicity. Paediatr Respir Rev. 2014 Jun;15(2):120-3.</ref><ref name="Bitterman">Bitterman H. Bench-to-bedside review: Oxygen as a drug. Critical Care. 2009;13(1):205. doi:10.1186/cc7151.</ref>
*Atelectasis
*Atelectasis
*Diffuse alveolar damage → [[Pulmonary edema]]/[[ARDS]]
*Diffuse alveolar damage → [[Pulmonary edema]]/[[ARDS]]

Revision as of 04:09, 5 March 2016

Background

  • The harmful effects of breathing oxygen at higher partial pressures than normal
    • Partial pressure of O2 at sea level = 0.21 ATA
  • Toxicity based on both time and partial pressure of oxygen
    • Generally, FiO2 of 40% or less (0.40 ATA) can be tolerated indefinitely[1]
    • Most common in hyperbaric oxygen therapy and prolonged administration of normobaric supplemental oxygen
    • Pulmonary toxicity occurs sooner and at lower partial pressures than CNS toxicity[1], however there is no predictable pattern or sequence of symptoms for CNS toxicity (initial symptom may be seizure/coma)[2]

Clinical Features

Pulmonary

  • Tracheobronchial irritation (initial manifestation) → pleuritic chest pain, dyspnea and coughing[3][2]
  • Atelectasis
  • Diffuse alveolar damage → Pulmonary edema/ARDS

Central nervous system

  • Tunnel vision
  • Tinnitus
  • Nausea
  • Facial twitching
  • Irritability (personality changes, anxiety, confusion, etc.)
  • Seizure

Ocular

  • Retinopathy of prematurity (retrolentar fibroplasia)
    • Seen in premature infants
  • In adults exposed to repeated toxic levels of oxygen, can get hyperoxic myopia[4]
    • Resolves spontaneously over several weeks

Differential Diagnosis

Diving Emergencies

Diagnosis

  • Clinical diagnosis

Management

  • Lower inhaled partial pressure of oxygen to as low as tolerated while maintaining tissue perfusion[5]

Disposition

  • Admit

See Also

External Links

References

  1. 1.0 1.1 Hedley-Whyte J. Pulmonary Oxygen Toxicity: Investigation and Mentoring. The Ulster Medical Journal. 2008;77(1):39-42.
  2. 2.0 2.1 Bitterman H. Bench-to-bedside review: Oxygen as a drug. Critical Care. 2009;13(1):205. doi:10.1186/cc7151.
  3. Thomson L, Paton J. Oxygen toxicity. Paediatr Respir Rev. 2014 Jun;15(2):120-3.
  4. Anderson B, Farmer JC. Hyperoxic myopia. Transactions of the American Ophthalmological Society. 1978;76:116-124.
  5. Deutschman, C. S., & Neligan, P. J. (2010). Evidence-based practice of critical care. Philadelphia, PA: Saunders/Elsevier.