Complications

Complication
Timeframe
Likelihood
short term
high

Otic barotrauma is the most common adverse effect of hyperbaric oxygen therapy. A pressure gradient develops across the tympanic membrane, followed by hemorrhage or serous effusion.

Pulmonary barotrauma (pneumothorax, arterial gas embolism) is rare.[79]

Prevention of ear barotraumas may include instruction on autoinflation techniques, topical and oral decongestants, and use of an autoinflation device.[80] Myringotomy can be useful in patients with depressed mentation or unconsciousness. A chest tube is required for monoplace chamber treatment of a patient with pneumothorax.

short term
low

ECG, cardiac biomarkers, and cardiac monitoring may detect acute cardiac damage in patients with moderate or severe CO poisoning.[77]

Overview of acute coronary syndrome

short term
low

A feature of severe carbon monoxide poisoning.[78]

Acute kidney injury

short term
low

The risk of seizures is 1 in 2000-3000 patient treatments with hyperbaric oxygen. Patients with acidosis, sepsis, or hypercapnia are at a higher risk for seizures.[79]

Seizures should be managed by temporarily discontinuing the oxygen. Administration of an anticonvulsant is an option.

Overview of seizure disorder

short term
low

Excessive or inappropriate oxygen supplemental therapy can result in cellular injury through formation of reactive oxygen species.

Pulmonary complications of oxygen toxicity include reduced vital capacity, pulmonary fibrosis, acute respiratory distress syndrome, and impaired gas exchange.[79]

Pulmonary complications are rare with standard treatment protocols.

short term
low

Fire accidents can occur if a source of fire or ignition is placed in the hyperbaric oxygen chamber. Hyperbaric chambers should be operated according to official protocols, to maximize safety including taking precautions against the risk of fire.[81][82]

long term
medium

Neurologic sequelae can occur immediately (PNS) or may occur after a lucid interval of several days (DNS). Reported rates vary due to heterogeneous exposures, inconsistencies in the definition of DNS, and whether patients received treatment. Risk factors for neurologic sequelae include prolonged exposure to CO, seizures, hypotension, elevated creatine phosphokinase, leukocytosis, older age, higher body mass index, hypertension, loss of consciousness, lower Glasgow Coma Scale on-site/at emergency room, elevation of lactate, and CO-Hb ≥25%.[83][84]​ The reported benefits of hyperbaric oxygen therapy in reducing the incidence of DNS vary; however, the preponderance of evidence supports the efficacy of hyperbaric oxygen when administered at 2.5 to 2.8 atmospheres absolute (ATA).[59][83][85][86][87][88][89][90]

variable
medium

One third of patients may have subtle memory deficits after CO poisoning.

Evaluation of memory deficit

variable
medium

One third of patients may have personality changes after CO poisoning.

variable
medium

Caused by muscle cell injury. Muscular pain or discomfort is common, but it can have no symptoms or physical signs. Diagnosis is confirmed with an elevated creatine kinase level. Fluid hydration is the mainstay of therapy.

Rhabdomyolysis

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