seizure can be result of hyperbaric oxygen therapy

The acute onset of seizure during HBO therapy delivered without air breaks in an individual with moderate severity CO toxicity is most likely secondary to oxygen toxicity. HBO is increasingly used as adjuvant treatment of chronic and acute conditions—from nonhealing wounds secondary to diabetes and postradiation lesions to acute injury from diving accidents or CO toxicity. Typical oxygen delivery protocols call for varying partial pressures applied inside a multiplace or monoplace chamber where inhaled supplemental oxygen is delivered with high alveolar driving pressures that increase PO2 at the alveoli and ultimately raises distal tissue oxygenation. A multiplace chamber comprises a large steel unit with the capacity to house two up to 12 people or more who are provided oxygen via a hood, while a monoplace chamber comprises a unit built with a clear acrylic center in which the patient lies in the cylindrical vessel and breathes the ambient air under pressure without a hood.

In the case of CO toxicity, sequential HBO treatments for a duration of 80 to 90 min each for several sessions are typically provided. Emergent treatment protocols of shorter duration but even higher pressures are used to treat conditions such as arterial gas emboli. Extended exposure to above-normal PO2, including shorter exposures to very high PO2, can cause oxidative damage to cell membranes leading to alveolar injury and may also result in CNS toxicity. Pulmonary effects on a cellular level may present as early as within 24 h of breathing pure oxygen, with symptoms including pleuritic chest pain, substernal heaviness, coughing and dyspnea secondary to tracheobronchitis, and absorptive atelectasis leading to pulmonary edema. CNS effects present with a multitude of potential symptoms, and in rare cases, individuals may experience generalized tonic-clonic seizures from oxygen toxicity. The threshold for seizures and other forms of CNS toxicity is lowered by factors such as hypercarbia, stress, fatigue, and cold.

The prevalence of oxygen toxicity seizures is rare, having been noted in retrospective studies to be less than 0.01%. Inclusion of air breaks, in which room air is used between sessions of HBO delivery, has mitigated seizure risk further.

In this case, however, the patient had received supplemental oxygen at high flows followed by delivery of HBO, making significant hypoxia of high enough severity to induce a seizure unlikely. In fact, seizures secondary to CO toxicity are generally thought to occur only after carboxyhemoglobin levels climb to a range of 40% or greater. With delivery of 100% FIO2, the half-life of CO is less than 90 min. With hyperbaric oxygen at a pressure of 3 ATA, the half-life of CO is decreased to 23 min.

Importantly, patients who develop oxygen toxicity seizures have not been noted to develop epilepsy or have persistent neurological sequelae.1

Footnotes

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