Abstract:Carbon monoxide (CO) inhalation is nowadays the most common cause of fatal poisoning worldwide. CO binds to haemoglobin 230-270 times more avidly than oxygen, thus leading to formation of carboxyhaemoglobin with subsequent reduction of tissue oxygenation. Brain is mainly affected due to its high oxygen requirement. Up to two-thirds of patients who survive the acute phase of this pathology present a delayed leukoencephalopathy, usually in a period ranging from two to 40 days. White matter damage closely relates… Show more
“…Occult glymphatic dysfunction is speculated to be the basis for a variety of demyelinating diseases ( Barz et al., 2017 ). MRI changes common to CO poisoning are often seen in those with glymphatic dysfunction ( Jeon et al., 2018 ; Varrassi et al., 2017 ). It remains to be determined whether such changes relate to the elevation of MBP-containing MPs seen 1–4 weeks following CO exposure ( Fig.…”
We hypothesized that carbon monoxide (CO) establishes an inflammatory cycle mediated by microparticles (MPs). Mice exposed to a CO protocol (1000 ppm for 40 min and then 3000 ppm for 20 min) that causes neuroinflammation exhibit NF-κB activation in astrocytes leading to generation of MPs expressing thrombospondin-1(TSP-1) that collect in deep cervical lymph nodes draining the brain glymphatic system. TSP-1 bearing MPs gain access to the blood stream where they activate neutrophils to generate a new family of MPs, and also stimulate endothelial cells as documented by leakage of intravenous 2000 kDa dextran. At the brain microvasculature, neutrophil and MPs sequestration, and myeloperoxidase activity result in elevations of the p65 subunit of NF-κB, serine 536 phosphorylated p65, CD36, and loss of astrocyte aquaporin-4 that persist for at least 7 days. Knock-out mice lacking the CD36 membrane receptor are resistant to all CO inflammatory changes. Events triggered by CO are recapitulated in naïve wild type mice injected with cervical node MPs from CO-exposed mice, but not control mice. All MPs-mediated events are inhibited with a NF-κB inhibitor, a myeloperoxidase inhibitor, or anti-TSP-1 antibodies. We conclude that astrocyte-derived MPs expressing TSP-1 establish a feed-forward neuroinflammatory cycle involving endothelial CD36-to-astrocyte NF-κB crosstalk. As there is currently no treatment for CO-induced neurological sequelae, these findings pose several possible sites for therapeutic interventions.
“…Occult glymphatic dysfunction is speculated to be the basis for a variety of demyelinating diseases ( Barz et al., 2017 ). MRI changes common to CO poisoning are often seen in those with glymphatic dysfunction ( Jeon et al., 2018 ; Varrassi et al., 2017 ). It remains to be determined whether such changes relate to the elevation of MBP-containing MPs seen 1–4 weeks following CO exposure ( Fig.…”
We hypothesized that carbon monoxide (CO) establishes an inflammatory cycle mediated by microparticles (MPs). Mice exposed to a CO protocol (1000 ppm for 40 min and then 3000 ppm for 20 min) that causes neuroinflammation exhibit NF-κB activation in astrocytes leading to generation of MPs expressing thrombospondin-1(TSP-1) that collect in deep cervical lymph nodes draining the brain glymphatic system. TSP-1 bearing MPs gain access to the blood stream where they activate neutrophils to generate a new family of MPs, and also stimulate endothelial cells as documented by leakage of intravenous 2000 kDa dextran. At the brain microvasculature, neutrophil and MPs sequestration, and myeloperoxidase activity result in elevations of the p65 subunit of NF-κB, serine 536 phosphorylated p65, CD36, and loss of astrocyte aquaporin-4 that persist for at least 7 days. Knock-out mice lacking the CD36 membrane receptor are resistant to all CO inflammatory changes. Events triggered by CO are recapitulated in naïve wild type mice injected with cervical node MPs from CO-exposed mice, but not control mice. All MPs-mediated events are inhibited with a NF-κB inhibitor, a myeloperoxidase inhibitor, or anti-TSP-1 antibodies. We conclude that astrocyte-derived MPs expressing TSP-1 establish a feed-forward neuroinflammatory cycle involving endothelial CD36-to-astrocyte NF-κB crosstalk. As there is currently no treatment for CO-induced neurological sequelae, these findings pose several possible sites for therapeutic interventions.
“…This brain magnetic resonance imaging (MRI) finding is typical of carbon monoxide poisoning on MRI. ), which is a typical finding of CO poisoning on MRI 2 ) . His family then informed us that he had spent the daytime in his living room, where he had a kotatsu with briquettes ( Figure 2 Figure 2 Kotatsu with briquettes (left) and briquette braziers (right).…”
Objective: Although much is known about acute carbon monoxide (CO) poisoning, little is known about chronic CO poisoning. Chronic CO poisoning is often diagnosed based on the patient's living environment and medical history. Herein, we report the case of an older patient who presented with repeated unconsciousness due to chronic CO poisoning. Case presentation: A 90-year-old man was brought to the emergency department after being found at home with a disturbance of consciousness. Arterial blood gas measurements in room air revealed a carboxyhemoglobin level of 18.0%. Impaired consciousness was caused by chronic CO poisoning. The patient received high-flow oxygen therapy, which promptly improved his condition. According to his family, briquette kotatsu was the cause of chronic CO poisoning.
Conclusion:Although high-flow oxygen therapy has been said to be less effective than hyperbaric oxygen therapy in CO poisoning treatment, recent studies have demonstrated that high-flow oxygen has similar effects and benefits. Thus, in institutions that do not have hyperbaric oxygen, high-flow oxygen may be sufficient to treat patients with CO poisoning, as seen in the present case. It should be noted that briquette kotatsu can lead to CO poisoning. This case highlights the need for clinicians to consider patients' living conditions.
“…5.51 and 5.52), which lacks anastomotic vascular supply. The heme iron of the globus pallidus is the most abundant, which is the most easily taken away by CO, causing hypoxia and cytotoxic edema [43]. In addition to the globus pallidus, the white matter in centrum semiovale (Fig.…”
CT is the first tool for the diagnosis of acute infarction, but CT is not sensitive to detect early infarction. Several signs of early stages of MCA infarction are noted, including loss of insular ribbon sign, obscuration of lentiform nucleus sign, loss of gray-white matter contrast sign, effacement of cortical sulci sign, and bright MCA sign. The DWI of MRI can accurately diagnose large and small infarctions at a very early stage because the infarct area is cytotoxic edema with diffusion restriction, showing bright (hyperintense) in DWI. CT perfusion is a method to determine whether the infarction is in golden 6 h. Using parameters, such as CBF, CBV, MTT, and DT, can determine the core and penumbra of the hypoperfusion area to determine whether to perform IV thrombolysis and IA thrombectomy. Cerebral vein and venous sinus thrombosis may cause venous infarction edema similar to arterial infarction edema on CT. CT can identify the thrombus as an "empty delta sign." MRI reveals that the venous infarction edema is cytotoxic edema in the middle and combines with peripheral vasogenic edema. The brain damage caused by CO poisoning is primarily in the bilateral globus pallidus, and severe poisoning may involve the centrum semiovale. These brain injuries are also bright in DWI. Moyamoya disease is stenosis and occlusion of the distal ICA with smoke-like collateral circulation vessels in the brain. In adults, it may present ICH and IVH and in children it may present ischemic infarction. Small vessel diseases include leukoaraiosis, microbleeds, and dilated Virchow-Robin spaces. Using variable pulse sequences, MRI is more sensitive than CT in diagnosing small vessel diseases.
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