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Oxygen Toxicity

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Other Names

  • Oxygen Toxicity
  • Paul Bert effect
  • Pulmonary oxygen toxicity

Background

  • This page refers to oxygen toxicity associated with breathing oxygen at higher partial pressures than normal
    • Primarily referencing diving and other sports and recreational activities

History

  • Named after Paul Bert, the French physiologist who first described it in 1878[1]

Epidemiology

  • Incidence in closed circuit oxygen rebreather
    • Estimates range from 1 in 157,930 CCR dives to approximately 3.5% of the CCR dives [2][3]

Pathophysiology

  • General
    • Characterized by breathing oxygen at higher partial pressures than normal
    • Heavily correlates with dive depth, exposure time
    • Patients tend to have traciobronchial symptoms initially, CNS symptoms in more severe cases
  • Causes
  • Oxygen partial pressure ranges
    • "Green Light" region is 1.4 ATA or less (about 82 feet/ 25 m on 40% oxygen mix)
      • For open circuit scuba, CNS toxicity is unlikely
    • "Yellow Light" is between 1.4 and 1.6 ATA (about 99 feet/ 30 m on 40% oxygen mix)
      • Risk is low, but slim margin of error for developing oxygen toxicity
      • Increasing depth, strenuous exercise or other emergencies increase the risk
    • "Red Light" is above 1.6 ATA
      • Recreational divers should not exceed this level
      • Even mild exercise breathing high-density nitrox increases risk

Etiology

  • General
    • Exact mechanism of toxicity is not fully understood
    • Directly related to duration of exposure, partial pressure of oxygen
  • Depth/ ATM
    • Partial pressure of O2 at sea level is 0.21 ATM
    • FiO2 of 40% or less, equivalent to 0.40 ATM, can be tolerated indefinitely[4]
    • Occurs faster, at lower partial pressure than CNS toxicity
    • No predictable pattern or sequence of symptoms

Hyperoxia

  • Hyperoxia: an excess of oxygen in body tissues
  • Physical effects
    • Drying of the respiratory mucosa
    • Adverse affects on the respiratory mucous blanket and the activity of cilia may result
    • For these reasons, oxygen is typically humidified
  • Physiological effects
    • Vasodilatation of the pulmonary vasculature and vasoconstriction of the systemic circulation.
    • High oxygen concentrations may indirectly ameliorate the inflammatory response by reducing tissue hypoxia
      • This occurs as a consequence the levels of hypoxic inducible factor-1a (HIF-1a), a key regulatory molecule of both hypoxia and the inflammatory response[5]
    • In patients with COPD, they may develop hypercapnic respiratory failure
  • Reactive Oxygen Species (ROS)
    • Most probably mechanism related to an overflow of reactive oxygen species (ROS) in the brain after an increase of cerebral blood flow[6]

Consequences of Hyperoxia

  • Pulmonary
    • Latent period is inversely proportional to the level and duration of inspired oxygen
    • First manifestation of pulmonary toxicity is tracheobronchial irritation (substernal chest pain, pleuritic pain, cough, progressive dyspnea)
    • May occur as fast as 14 hours at 100% oxygen[7]
    • Decrease in forced vital capacity is the most widely applied index of oxygen toxicity[8]
      • This has been shown to occur as early as 24 hours after continuous exposure to 100% oxygen[9]
    • Late findings include pulmonary edema, ARDS
  • CNS
    • Start with visual changes such as tunnel vision, tinnitus, nausea, facial twitching, dizziness and confusion.
    • Followed by tonic clonic seizures and subsequent unconsciousness.
    • There appears to be no consistent pattern in the appearance of minor signs before the development of seizures.
  • Ocular
    • Prolonged exposure to high, inspired fractions of oxygen damages the retina
    • In infants, risk factor for retinopathy of prematurity[10]
    • Hyperoxic myopia tends to be seen in adults
  • Other organs have been implicated
    • Heme: red cell destruction[11]
    • Cardiovascular: myocardial[12]
    • Endocrine: adrenal, gonads and thyroid[13]
    • Renal damage[14]

Risk Factors

  • Diving
    • Oxygen Concentration
    • Duration of exposure

Differential Diagnosis

Differential Diagnosis Dive Medicine


Clinical Features

  • History
    • Initial symptoms are typically trachobronchial including pleuritic chest pain, dypsnea, coughing
    • CNS symptoms include tunnel vision, tinnitis, nausea, twitiching, irritability, seizure
    • Patients may complain of flashing lights, tunnel vision
    • Tinnitus (loud ringing or roaring in ears)
    • Change in mental status including confusion, lethargy
    • Nausea, vertigo
    • Numbness or tingling
    • Muscular twitching, especially at the lips
    • Grand mall convulsion
    • Visual disturbances generally precede convulsions[15]
  • Physical Exam
    • Important to perform a thorough neurological exam
    • CNS symptoms may include irritability, cold shivering, twitching, tonic-clonic activity
    • Lung exam may reveal rales, uncontrollable coughing, hiccups
    • ENT exam can reveal hyperemia of nasal mucosa

Evaluation

  • Diagnosis is primarily clinical

Radiographs

Pulmonary Function Testing

  • Strongly consider to assess status or establish baseline
    • Trending helps guide clinical picture

Classification

  • Not applicable

Management

Nonoperative

  • Reduce exposure to increased oxygen levels
    • Reduce partial pressure of inhaled oxygen
    • As low as tolerated while still maintaining tissue perfusion[16]
  • For patients who require Hyperbaric Oxygen Therapy
    • Consider anti-epileptic medications, prolonged air breaks, limited treatment pressure
    • "Air breaks": allow intermittent air-breathing while in the hyperbaric environment, may decrease oxygen toxicity by a factor of 10[17]
  • Deep diving
    • May require breathing mixtures that contain less than 21% oxygen to reduce toxicity risk
  • Disposition
    • Patients typically require admission to the hospital

Prevention

  • See: Dive Medicine Prevention
  • Oxygen Toxicity[18]
    • Pay close attention to partial pressure, exposure time
    • The U.S. Navy uses 1.3 ATA as the maximum limit in its closed-circuit rebreathers
    • National Oceanic and Atmospheric Administration (NOAA) recommends a more conservative 180 minutes at 1.3 ATA for normal exposures and 240 minutes only for exceptional exposures
    • Professional Association of Diving Instructors (PADI) has proposed a limit of 1.4 ATA for open-circuit nitrox scuba diving
    • Shallow exposure times in the 1.3 to 1.4 ATA range are mainly to avoid lung oxygen toxicity
    • The NOAA limit for nitrox diving at 1.6 ATA is 45 minutes for normal diving and 120 minutes for exceptional exposure diving
    • Breathing 100 percent oxygen during a decompression stop at 20 feet (6.1 meters) is a common practice

Rehab and Return to Play

Rehabilitation

  • No clear rehab guidelines

Return to Play/ Work

  • Needs to be updated

Complications and Prognosis

Prognosis

  • CNS Toxicity
    • With removal of the inciting agent; no long term neurological damage typically occurs[19]
  • Pulmonary Toxicity
    • Damage due to oxygen-induced pulmonary toxicity is reversible in most adults.

Complications

  • Pulmonary
    • Pulmonary Edema
    • Acute Respiratory Distress Syndrome (ARDS)
  • Ocular
    • Retinopathy of prematurity can be seen in infants
    • Hyperoxic myopia
    • Delayed cataract formation
  • CNS
    • Tonic-clonic activity
    • Amnesia

See Also


References

  1. Bert P. (1878). La Pression Barométrique: Recherches de Physiologie Expérimentale. Paris: Masson.
  2. Harabin A. L., Survanshi S. S., Homer L. D. (1995). A model for predicting central nervous system oxygen toxicity from hyperbaric oxygen exposures in humans. Toxicol. Appl. Pharmacol. 132, 19–26. 10.1006/taap.1995.1082
  3. Walters K. C., Gould M. T., Bachrach E. A., Butler F. K. (2000). Screening for oxygen sensitivity in U.S. Navy combat swimmers. Undersea Hyperb. Med. 27, 21–26.
  4. Hedley-Whyte J. Pulmonary Oxygen Toxicity: Investigation and Mentoring. The Ulster Medical Journal. 2008;77(1):39-42.
  5. Nathan, Carl. "Oxygen and the inflammatory cell." Nature 422.6933 (2003): 675-676.
  6. Visser G. H., Van Hulst R. A., Wieneke G. H., Van Huffelen A. C. (1996a). Transcranial doppler sonographic measurements of middle cerebral artery flow velocity during hyperbaric oxygen exposures. Undersea Hyperb. Med. 23, 157–165.
  7. COMROE, JULIUS H., et al. "Oxygen toxicity: the effect of inhalation of high concentrations of oxygen for twenty-four hours on normal men at sea level and at a simulated altitude of 18,000 feet." Journal of the American Medical Association 128.10 (1945): 710-717.
  8. Caldwell, P. R., et al. "Changes in lung volume, diffusing capacity, and blood gases in men breathing oxygen." Journal of applied physiology 21.5 (1966): 1477-1483.
  9. Bitterman, Haim. "Bench-to-bedside review: oxygen as a drug." Critical Care 13.1 (2009): 1-8.
  10. Drack, Arlene V. "Preventing blindness in premature infants." New England Journal of Medicine 338.22 (1998): 1620-1621.
  11. Larkin, EDWARD C., et al. "Hematologic responses to hypobaric hyperoxia." American Journal of Physiology-Legacy Content 223.2 (1972): 431-437.
  12. Caulfield, J. B., R. W. Shelton, and J. F. Burke. "Cytotoxic effects of oxygen on striated muscle." Archives of pathology 94.2 (1972): 127-132.
  13. Bean, John W., and Paul C. Johnson. "Adrenocortical response to single and repeated exposure to oxygen at high pressure." American Journal of Physiology-Legacy Content 179.3 (1954): 410-414.
  14. Hess, R. T., and D. B. Menzel. "Effect of dietary antioxidant level and oxygen exposure on the fine structure of the proximal convoluted tubules." Aerospace medicine 42.6 (1971): 646-649.
  15. Arieli R., Arieli Y., Daskalovic Y., Eynan M., Abramovich A. (2006a). CNS oxygen toxicity in closed-circuit diving: signs and symptoms before loss of consciousness. Aviat. Space Environ. Med. 77, 1153–1157
  16. Deutschman, C. S., & Neligan, P. J. (2010). Evidence-based practice of critical care. Philadelphia, PA: Saunders/Elsevier.
  17. Domachevsky L, Rachmany L, Barak Y, Rubovitch V, Abramovich A, Pick CG. Hyperbaric oxygen-induced seizures cause a transient decrement in cognitive function. Neuroscience. 2013 Sep 05;247:328-34.
  18. Dan.org, "Oxygen toxicity"
  19. Xiao Y, Xiong T, Meng X, Yu D, Xiao Z, Song L. Different influences on mitochondrial function, oxidative stress and cytotoxicity of antibiotics on primary human neuron and cell lines. J Biochem Mol Toxicol. 2019 Apr;33(4):e22277.
Created by:
John Kiel on 2 July 2022 06:49:16
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Last edited:
25 July 2022 19:59:11
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