Hyperbaric oxygen treatment in delayed post-hypoxic encephalopathy following inhalation of liquefied petroleum gas: a case report.

Delayed post-hypoxic encephalopathy can occur after an episode of anoxia or hypoxia. Symptoms include apathy, confusion, and neurological deficits. We describe a 47-year-old male patient who inhaled gas from a kitchen stove liquid petroleum gas cylinder. He was diagnosed with hypoxic ischaemic encephalopathy 12 hours after his emergency department admission. He received six sessions of hyperbaric oxygen treatment (HBOT) and was discharged in a healthy state after six days. Fifteen days later, he experienced weakness, loss of appetite, forgetfulness, depression, balance problems, and inability to perform self-care. One week later, he developed urinary and fecal incontinence and was diagnosed with post-hypoxic encephalopathy. After 45 days from the onset of symptoms, he was referred to the Underwater and Hyperbaric Medicine Department for HBOT. The patient exhibited poor self-care and slow speech rate, as well as ataxic gait and dysdiadochokinesia. Hyperbaric oxygen was administered for twenty-four sessions, which significantly improved the patient's neurological status with only hypoesthesia in the left hand remaining at the end of treatment. Hyperbaric oxygen has been reported as successful in treating some cases of delayed neurological sequelae following CO intoxication. It is possible that HBO therapy may also be effective in delayed post-hypoxic encephalopathy from other causes. This may be achieved through mechanisms such as transfer of functional mitochondria to the injury site, remyelination of damaged neurons, angiogenesis and neurogenesis, production of anti-inflammatory cytokines, and balancing of inflammatory and anti-inflammatory cytokines.

Analysis of the cardiovascular effects of hyperbaric oxygen therapy in diabetic patients.

During hyperbaric oxygen (HBO2) therapy in humans, there are changes in cardiovascular physiology due to high pressure and hyperoxygenation. Peripheral vasoconstriction, bradycardia, and a decrease in cardiac output are observed during HBO2 therapy. These physiological effects of HBO2 therapy on the cardiovascular system are tolerated in healthy people. However, patients with underlying cardiac disease may experience severe problems during HBO2 therapy, such as pulmonary edema and death. In addition, cardiac complications may occur in patients with diabetes mellitus (DM). Therefore, HBO2 therapy may negatively affect cardiovascular physiology in patients with DM. The present study aimed to examine the cardiovascular effects of HBO2 therapy in diabetic patients. The findings of NT-ProBNP, troponin I, and electrocardiography (ECG) of diabetic patients who applied to the Ministry of Health University Gülhane Training Research Underwater and Hyperbaric Medicine Clinic were compared before and after the first HBO2 therapy session. When ECG findings were analyzed at the end of a session of HBO2 exposure, a statistically significant increase was observed in the QTc and QTc dispersion measurements (p≺0.001 and p = 0.02, respectively). In cardiac enzymes, there was a statistically significant increase in troponin I values after an HBO2 therapy session, but no statistically significant change was observed in Pro-BNP (p = 0.009, p = 0.3, respectively). Short-term exposure to HBO2 therapy had statistically significant changes in troponin I, QT, and QTc in patients with DM, which did not reach clinical significance. Despite very little evidence of cardiac dysfunction, we recommend caution in using HBO2 therapy in patients with DM and emphasize the need for further investigation of these measurements.

Hemiplegia resulting from acute carbon monoxide poisoning.

Carbon monoxide (CO) poisoning can cause neurological complications such as movement disorders and cognitive impairment through hypoxic brain damage. Although peripheral neuropathy of the lower extremities is a known complication of CO poisoning, hemiplegia is very rare. In our case, a patient who developed left hemiplegia due to acute CO poisoning received early hyperbaric oxygen treatment (HBOT). The patient had left hemiplegia and anisocoria at the beginning of HBOT. Her Glasgow coma score was 8. A total of five sessions of HBOT at 243.2 kPa for 120 minutes were provided. At the end of the 5th session, the patient's hemiplegia and anisocoria were completely resolved. Her Glasgow coma score was 15. After nine months of follow-up, she continues to live independently with no sequelae, including delayed neurological sequelae. Clinicians should be aware that CO poisoning can (rarely) present with hemiplegia.