A Case of Carbon Monoxide-Induced Delayed Neurological Sequelae Successfully Treated with Hyperbaric Oxygen Therapy, N-Acetylcysteine, and Glucocorticoids: Clinical and Neuroimaging Follow-Up

Abstract

Carbon monoxide (CO) poisoning is a leading cause of intentional and unintentional poisoning worldwide, associated with mortality and severe morbidity. Some survivors of CO poisoning develop, after a lucid interval, a potentially permanent encephalopathy in the form of cognitive impairment and movement disorders, such as Parkinsonism. One of the most frequent neuroimaging findings is a cerebral white matter damage, but so far its precise cause and specific therapy are still debated. We here report the case of a 33-year-old woman with severe carbon monoxide poisoning who, after a period of lucid interval, presented symptoms of declining motor and cognitive functions. She was treated with 40 sessions of Hyperbaric Oxygen Therapy (HBOT). The therapeutic use of oxygen at supraphysiological pressures might either increase systemic oxidative stress or cause an overproduction of oxygen free radicals as drawbacks. Concurrent use of antioxidants and anti-inflammatory drugs may prevent the side effects of oxygen therapy at supraphysiological pressure due to oxidative stress. For this reason, the patient was also treated with high-dose N-Acetylcysteine and glucocorticoids. Here, we describe the longitudinal monitoring of patient’s cognitive abilities and leukoencephalopathy associated with her positive clinical outcome.

Is “delayed” hyperbaric therapy effective for “delayed” encephalopathy after carbon monoxide intoxication?

“…Current literature on DNS treated with delayed HBOT plus ROS-scavenger drugs is scanty. One such report was by Spina et al, who reported the clinical-radiological follow-up of a DNS case treated with HBOT, N-Acetylcysteine and glucocorticoids, who had a progressive and sustained clinical and radiological improvement [6]. This case is strikingly similar to ours, as were the treatment modalities, including late HBOT.…”

Ambient carbon monoxide exposure and elevated risk of mortality in the glioblastoma patients: A double‐cohort retrospective observational study

“…23,24 We speculate that if CO can deteriorate OPCs, 3 the delayed neurological sequelae-associated effects of CO can be exaggerated or accelerated in the OPC-related GBM. 25,26 The limitations include the characteristics of this study, methodology, included patients, behavioral differences, and migration issues. As this is an observational study, our result shows a preliminary example of the association of the air pollutant and not address the causality of the phenomenon.…”

“…it is still uncertain whether the air pollutant affected the nonbiological factors, the baseline patient condition, other organs such as heart, other factor/cells in the bloodstream, cancer‐origin‐related cell (such as oligodendrocyte progenitor cells [OPC]), the tumor cell itself, the necrotic portion of the disease, or its surrounding cells 23,24 . We speculate that if CO can deteriorate OPCs, 3 the delayed neurological sequelae‐associated effects of CO can be exaggerated or accelerated in the OPC‐related GBM 25,26 …”

Effects of intravascular laser phototherapy on delayed neurological sequelae after carbon monoxide intoxication as evaluated by brain perfusion imaging: A case report and review of the literature

“…There is no consensus regarding the treatment of DNS. Several studies have found that HBOT alone or combined with steroids, N-butylphthalide, or N-acetylcysteine seemed to achieve better neurological recovery[ 20 , 21 ]. The anti-inflammatory and anti-oxidative nature of these medications are capable of attaining similar results to those of ILIB therapy[ 8 ].…”