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.

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.

Iodine-Induced Retinopathy: A Case Report

Potassium iodide is used as an iodine supplement in salt as part of a national program in Turkey. An overdose of iodine has a toxic effect on the retinal pigment epithelium and photoreceptors. The case presented here is a patient who developed retinopathy following consumption of an excessive dose of iodine.

Levels of circulating homocysteine, vitamin B6, vitamin B12, and folate in different types of open-angle glaucoma.

OBJECTIVE: To compare the levels of plasma homocysteine (Hcy), vitamin B6 (vit-B6), serum vitamin B12 (vit-B12), and folate in healthy individuals and in patients with normal tension glaucoma (NTG), pseudoexfoliative glaucoma (PXG), or primary open-angle glaucoma (POAG). STUDY DESIGN: A prospective controlled trial. PARTICIPANTS AND METHODS: Forty healthy subjects, 48 patients with NTG, 38 patients with PXG, and 34 patients with POAG were included in the study. Those who used vitamin supplements or medications affecting Hcy and vitamin levels were excluded from the study. The levels of Hcy and vit-B6 were measured by High Performance Liquid Chromatography (HPLC). The levels of serum vit-B12 and folic acid were measured by competitive chemiluminescent enzyme immunoassay (CEI). One-way analysis if variance (ANOVA), analysis of covariance (ANCOVA), and the Tukey honestly significant difference test were used for statistical analysis. RESULTS: The mean Hcy level of the PXG group was 15.46+/-9.27 micromol/L which was significantly higher (P=0.03) than that of the control group. There were no statistical differences in serum vit-B12 and folate levels among control subjects and NTG, PXG and POAG groups (P>0.05). It was found that the mean plasma vit-B6 level was significantly higher in subjects with NTG (P=0.03) and POAG (P=0.025) versus controls. Mean vit-B6 levels in NTG and POAG were 30.50+/-11.29 microg/L and 30+/-12.15 microg/L, respectively. CONCLUSIONS: The plasma level of Hcy was found to be increased only in PXG patients and the plasma levels of vit-B6 were found to increase in the NTG and POAG sample groups. Using homocysteine and vit-B6 levels as the determinants of hyperhomocysteinemia still needs further research.