Despite growing attention to the prevention of DNS following CO poisoning, no standardised treatment protocols have been established. HBOT remains the only widely accepted intervention for acute management and DNS prevention [2].
In this case, HBOT was initiated promptly after the patient’s transfer to our hospital. However, due to hypothermia and severe lactic acidosis at the referring facility, a broader differential diagnosis for the impaired consciousness was likely considered. HBOT was also unavailable at the referral hospital. Although the CO-Hb level and clinical presentation would have warranted urgent HBOT, these factors might have contributed to the prolonged work-up. This highlights the importance of early HBOT initiation, widely supported in the literature as critical for improving neurological outcomes in cases involving unconsciousness and elevated COHb levels [3].
Pathophysiologically, CO exposure induces immune-mediated demyelination through oxidative damage to the myelin basic protein (MBP) [4]. Animal studies and clinical reports suggest that corticosteroids may mitigate this process by reducing inflammation and preventing CD4 + cell apoptosis [4, 5]. Elevated MBP levels in the cerebrospinal fluid (CSF) have been associated with DNS, and steroid therapy has been shown to reduce MBP levels and improve outcomes [6].
For example, Xiang et al. demonstrated that patients receiving HBOT plus dexamethasone had significantly lower CSF MBP levels and improved cognitive scores compared to those receiving HBOT only [7]. Another prospective study reported a lower incidence of DNS among patients treated with intravenous dexamethasone [8].
However, the referenced study was retrospective in nature and involved a shift in treatment strategies, introducing potential biases such as selection and temporal confounding [8]. The reduced DNS incidence may have been influenced by other factors, including increased HBOT use or improved overall care. As with all retrospective studies, the findings should be interpreted with caution, and prospective randomised trials are needed to confirm the results.
SPT may also benefit CO-related encephalopathy through dual mechanisms: suppressing cytokine-mediated inflammation and reducing vasogenic oedema by stabilising the endothelial tight junctions [9]. These effects are also relevant to other inflammatory brain conditions such as encephalitis and autoimmune encephalopathy [10,11,12].
Nevertheless, corticosteroids may, in some cases, induce or exacerbate encephalopathy [10]. This dual nature underscores the complexity of their role in neurological disorders and highlights the need for careful patient selection and close monitoring when using steroids in CO poisoning.
CO toxicity involves the high-affinity binding of CO to haemoglobin and inhibition of mitochondrial cytochrome oxidase, leading to cellular hypoxia and cerebral oedema [13, 14]. In this context, SPT may help reduce inflammation and brain oedema, potentially improving outcomes [15].
This case presentation suggests that SPT, as an adjunct to HBOT, may reduce the risk of DNS following CO poisoning. These therapies target key mechanisms of injury-impaired oxygen delivery, mitochondrial dysfunction, inflammation, and oedema. While this case is suggestive, causality cannot be established due to its single-patient nature. Further prospective studies are required to confirm therapeutic efficacy and define optimal protocols.