Oxygen Toxicity

The primary risk of HBOT is oxygen toxicity, also known as oxygen toxicity syndrome, oxygen intoxication, and oxygen poisoning.  It is a condition resulting from the harmful effects of breathing molecular oxygen (O2) at elevated pressure.  Oxygen toxicity results in cell damage and death and is mostly seen in the central nervous system (CNS), lungs, and eyes.  It is due to an excess of 02 in the body tissues and is called hyperoxia.

Normal atmospheric pressure is expressed as 1 bar or 100KPA.  Exposures to partial pressures of oxygen above1.6 bars (160 KPA), about eight times the atmospheric concentration, are usually associated with CNS O2 toxicity.  CNS toxicity occurs only under hyperbaric conditions (where ambient pressure is above normal).

Effects of O2 toxicity are called the “Paul Bert” syndrome when seen in the central nervous system (CNS).  Symptoms include the following:  visual changes, especially tunnel vision; tinnitus (ringing in the ears); nausea, twitching, especially of the face; personality changes including irritability, anxiety and confusion; dizziness; and tonic-clonic seizure (intense muscle contraction for several seconds followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking and ending with a period of unconsciousness called the postictal state).

The onset of seizures is unpredictable and dependent on several factors.  There is a wide variation among individuals and even in the same individual from day to day.  Factors include individual sensitivity, treatment protocol and therapy indications as well as the type of equipment used.  The presence of a fever or a history of seizures are relative contraindications for HBOT. Steroids at high doses can increase the risk of seizures from oxygen toxicity.

Generally narcotics decrease respiration.  Administering oxygen can further decrease respiration.  Elevated CO2 can dilate cerebral blood vessels and cause increased diffusion of oxygen into the brain leading to an oxygen toxic seizure.

Care must be given not to over-sedate the patient with pain or anti-anxiety medications.  This can happen if intramuscular medication is given.  During and immediately after hyperbaric sessions generalized vasoconstriction is present and the effect on medication delivered in this manner is a decrease in drug absorbency that may lead to more injections.

Sedation can be used to increase the seizure threshold at risk of oxygen toxicity and also to treat anxiety.  Xanax, Ativan, or Valium may be prescribed and taken 30-60 minutes before treatment.  The normal advice applies for the patient not to drive or operate machinery.

The patient should be closely monitored for signs of CNS oxygen toxicity including anxiety, behavioral changes, sweating, nausea, twitching of the lips and face, visual field and auditory changes, vertigo, syncope (fainting or temporary loss of consciousness caused by insufficient blood flow to the brain), and tonic-clonic seizures, which also may occur without warning.  Preventive measures include air breaks of a longer than usual length (e.g., 10 minutes instead of 5 minutes).

Seizure–prone patients should receive preventative anti-convulsant therapy before HBOT treatment.  Depending on the need for HBOT, the physician may continue treatments at a lower atmospheric pressure. The use of anticonvulsants may be used to prevent or treat seizures that continue when oxygen inhalation is terminated. In treating necrotizing infections, air embolism, or decompression sickness where exposures above 2.0 ATA are needed, the risk of oxygen –induced seizures may be decreased by allowing air breaks.

CNS oxygen toxicity is very rare:  Welslaw in 1996 reported 16 incidents out of 107,264 patients (0.015%).  Hampson and Atik in 2003 found a 0.03% incidence and Yildiz, Ay, and Qyrdedi reported a rate of 0.008%.  A later review of 80,000 patients showed an even lower rate of 0.0024%.