Carbon monoxide poisoning and phototherapy.

Carbon monoxide (CO) poisoning is a leading cause of poison-related morbidity and mortality worldwide. By binding to hemoglobin and other heme-containing proteins, CO reduces oxygen delivery and produces tissue damage. Prompt treatment of CO-poisoned patients is necessary to prevent acute and long-term complications. Oxygen therapy is the only available treatment. Visible light has been shown to selectively dissociate CO from hemoglobin with high efficiency without affecting oxygen affinity. Pulmonary phototherapy has been shown to accelerate the rate of CO elimination in CO poisoned mice and rats when applied directly to the lungs or via intra-esophageal or intra-pleural optical fibers. The extracorporeal removal of CO using a membrane oxygenator with optimal characteristic for blood exposure to light has been shown to accelerate the rate of CO illumination in rats with or without lung injury and in pigs. The development of non-invasive techniques to apply pulmonary phototherapy and the development of a compact, highly efficient membrane oxygenator for the extracorporeal removal of CO in humans may provide a significant advance in the treatment of CO poisoning.

Clinical features and predictors of delayed neurological syndrome in carbon monoxide poisoning: the AMICO study. / Caracterización clínica y factores predictivos de desarrollo de síndrome neurológico tardío en la intoxicación por monóxido de carbono: estudio AMICO.

OBJECTIVES: To identify predictors for developing delayed neurological syndrome (DNS) after an initial episode of carbon monoxide (CO) poisoning in the interest of detecting patients most likely to develop DNS so that they can be followed. MATERIAL AND METHODS: Retrospective review of cases of CO poisoning treated in the past 10 years in the emergency departments of 4 hospitals in the AMICO study (Spanish acronym for the multicenter analysis of CO poisoning). We analyzed demographic characteristics of the patients and the clinical characteristics of the initial episode. The records of the cohort of patients with available follow-up information were reviewed to find cases of DNS. Data were analyzed by multivariant analysis to determine the relationship to characteristics of the initial exposure to CO. RESULTS: A total of 240 cases were identified. The median (interquartile range) age of the patients was 36.2 years (17.6-49.6 years); 108 patients (45.0%) were men, and the poisoning was accidental in 223 cases (92.9%). The median carboxyhemoglobin concentration on presentation was 12.7% (6.2%-18.7%). Follow-up details were available for 44 patients (18.3%). Eleven of those patients (25%) developed DNS. A low initial Glasgow Coma Scale score predicted the development of DNS with an odds ratio (OR) of 0.61 (95% CI, 0.41-0.92) and an area under the receiver operating characteristic curve of 0.876 (95% CI, 0.761-0.990) (P .001). CONCLUSION: The initial Glasgow Coma Scale score seems to be a clinical predictor of DNS after CO poisoning. We consider it important to establish follow-up protocols for patients with CO poisoning treated in hospital EDs.

OBJETIVO: Identificar factores pronósticos de desarrollo de síndrome neurológico tardío (SNT) después de un episodio inicial de intoxicación por monóxido de carbono (ICO), con el fin detectar precozmente a la población más susceptible y facilitar su acceso a un seguimiento específico. METODO: Revisión retrospectiva de todos los casos de ICO que acudieron a los servicios de urgencias (SU) de 4 hospitales durante los últimos 10 años. Se analizaron datos demográficos y características clínicas en el momento del episodio. En la cohorte de pacientes con datos de seguimiento disponibles, se evaluó la aparición de SNT y su relación con diferentes variables en la exposición inicial al CO a través de técnicas de análisis multivariante. RESULTADOS: Se identificaron 240 pacientes. La mediana de edad fue de 36,2 años (17,6-49,6). De ellos 108 (45,0%) eran hombres y 223 casos (92,9%) fueron accidentales. El nivel medio de COHb fue del 12,7% (6,2-18,7). En 44 (18,3%) episodios se disponía de datos de un seguimiento específico. En esta cohorte, 11 (25%) pacientes desarrollaron SNT. Una puntuación inicial más baja en la Escala Coma de Glasgow (GCS) (OR: 0,61, IC 95%: 0,41-0,92) fue predictor independiente del desarrollo del SNT, con un ABC en la curva COR de 0,876 (IC 95%: 0,761-0,990, p 0,001). CONCLUSIONES: Una puntuación inicial baja en la GCS parece ser un predictor clínico de desarrollo de SNT en la ICO. Dada la incidencia de SNT, consideramos fundamental establecer protocolos de seguimiento específico de estos pacientes tras su asistencia inicial en los SU.

Surviving cardiac arrest after carbon monoxide poisoning treated with hyperbaric oxygen therapy.

Carbon monoxide (CO) and cyanide poisoning are frequent causes of morbidity and mortality in cases of house and industrial fires. The 14th edition of guidelines from the Undersea and Hyperbaric Medical Society does not recommend hyperbaric oxygen (HBO2) treatment in those patients who have suffered a cardiac arrest and had to receive cardiopulmonary resuscitation. In this paper, we describe the case of a 31-year-old patient who received HBO2 treatment in the setting of cardiac arrest and survived.

Hyperbaric oxygen for the treatment of carbon monoxide-induced delayed neurological sequelae: a case report and review of the literature.

Introduction: Hyperbaric oxygen treatment (HBOT) remains a recognised treatment for acute carbon monoxide (CO) poisoning, but the utility of HBOT in treating CO-induced delayed neurological sequelae (DNS) is not yet established. Case description: A 26-year old woman presented with reduced consciousness secondary to CO exposure from burning charcoal. She underwent a single session of HBOT with US Navy Treatment Table 5 within six hours of presentation, with full neurological recovery. Eight weeks later, she represented with progressive, debilitating neurological symptoms mimicking Parkinsonism. Magnetic resonance imaging of her brain demonstrated changes consistent with hypoxic ischaemic encephalopathy. The patient underwent 20 sessions of HBOT at 203 kPa (2 atmospheres absolute) for 115 minutes, and received intravenous methylprednisolone 1 g per day for three days. The patient's neurological symptoms completely resolved, and she returned to full-time professional work with no further recurrence. Discussion: Delayed neurological sequelae is a well-described complication of CO poisoning. In this case, the patient's debilitating neurocognitive symptoms resolved following HBOT. Existing literature on treatment of CO-induced DNS with HBOT consists mainly of small-scale studies and case reports, many of which similarly suggest that HBOT is effective in treating this complication. However, a large, randomised trial is required to adequately determine the effectiveness of HBOT in the treatment of CO-induced DNS, and an optimal treatment protocol.

Effect and molecular mechanism of Sulforaphane alleviates brain damage caused by acute carbon monoxide poisoning:Network pharmacology analysis, molecular docking, and experimental evidence.

Sulforaphane (SFN) has attracted much attention due to its ability on antioxidant, anti-inflammatory, and anti-apoptotic properties, while its functional targets and underlying mechanism of action on brain injury caused by acute carbon monoxide poisoning (ACOP) have not been fully elucidated. Herein, we used a systematic network pharmacology approach to explore the mechanism of SFN in the treatment of brain damage after ACOP. In this study, the results of network pharmacology demonstrated that there were a total of 81 effective target genes of SFN and 36 drug-disease targets, which were strongly in connection with autophagy-animal signaling pathway, drug metabolism, and transcription disorders in cancer. Upon the further biological function and KEGG signaling pathway enrichment analysis, a large number of them were involved in neuronal death, reactive oxygen metabolic processes and immune functions. Moreover, based on the results of bioinformatics prediction associated with multiple potential targets and pathways, the AMP-activated protein kinase (AMPK) signaling pathway was selected to elucidate the molecular mechanism of SFN in the treatment of brain injury caused by ACOP. The following molecular docking analysis also confirmed that SFN can bind to AMPKα well through chemical bonds. In addition, an animal model of ACOP was established by exposure to carbon monoxide in a hyperbaric oxygen chamber to verify the predicted results of network pharmacology. We found that the mitochondrial ultrastructure of neurons in rats with ACOP was seriously damaged, and apoptotic cells increased significantly. The histopathological changes were obviously alleviated, apoptosis of cortical neurons was inhibited, and the number of Nissl bodies was increased in the SFN group as compared with the ACOP group (p < .05). Besides, the administration of SFN could increase the expressions of phosphorylated P-AMPK and MFN2 proteins and decrease the levels of DRP1, Caspase3, and Casapase9 proteins in the brain tissue of ACOP rats. These findings suggest that network pharmacology is a useful tool for traditional Chinese medicine (TCM) research, SFN can effectively inhibit apoptosis, protect cortical neurons from the toxicity of carbon monoxide through activating the AMPK pathway and may become a potential therapeutic strategy for brain injury after ACOP.

Sensorineural Hearing Loss due to Acute Carbon Monoxide Poisoning.

Carbon monoxide (CO) can cause "irreversible" severe-to-profound sensorineural hearing loss. However, there are few reports of detailed hearing test results. Here, we report a case of acute sensorineural hearing loss caused by acute CO poisoning with partial hearing recovery, evaluated by a detailed hearing examination. A 25-year-old woman was brought to the emergency department for attempted suicide. On admission, her consciousness was impaired, and she was treated for severe CO poisoning, including using hyperbaric-oxygen therapy. After regaining consciousness, symptoms of hearing loss and tinnitus were discovered, and a detailed audiological examination revealed bilateral hearing loss, suggesting cochlear damage. Steroids were systemically administered, and her hearing impairment was partially resolved. Sensorineural hearing loss caused by acute CO poisoning includes cochlear pathology and may be partially treatable. The early evaluation of hearing in patients with severe CO poisoning is advisable for early treatment.

Meta-analysis of the effectiveness and safety of Xingnaojing and naloxone in the treatment of carbon monoxide poisoning.

BACKGROUND: To evaluate the effectiveness and safety of Xingnaojing combined with naloxone in the treatment of carbon monoxide poisoning. METHODS: By retrieving the literatures published in the databases of PubMed, Cochrane Library, Web of Science, Embase, Wanfang Database, Weipu Database, and China National Knowledge Infrastructure from January 2010 to September 2021, the data of randomized controlled trials (RCTs) of Xingnaojing combined with naloxone in the treatment of carbon monoxide poisoning were extracted. The methodological quality of the included RCTs was evaluated by using the tools of bias risk evaluation of Cochrane Collaboration, and the data were statistically analyzed by using RevMan 5.3 software. RESULTS: A total of 20 literatures were included, involving in 771 cases treated by Xingnaojing combined with naloxone and 761 cases in the control group. The effective rate of the experimental group is higher than that of the control group [risk ratio (RR) = 1.20, 95% confidence interval (CI) (1.14, 1.26)]. The average awake time (STD mean difference = -2.08, 95% CI [-2.60, -1.56]), physical recovery time (STD mean difference = -2.94, 95% CI [-3.59, -2.28]), delayed encephalopathy (RR = 0.44, 95% CI [0.31, 0.62]), and adverse reactions (RR = 0.23, 95% CI [0.10, 0.54]) was lower than that of the control group. CONCLUSION: Xingnaojing combined with naloxone in the treatment of carbon monoxide poisoning is significantly superior to naloxone, but it still needs to be further verified by high-quality large samples of RCTs.

Hyperbaric oxygen treatment in carbon monoxide poisoning - Does it really matter?

Carbon monoxide (CO) is an odorless and colorless gas that can lead to fulminant and life-threatening intoxications. Besides an early diagnosis, an appropriate treatment of the intoxication is important. In this context the reduction of CO concentration in blood and tissues is crucial revealing hyperbaric oxygen treatment (HBO) as a highly promising tool. However, the benefit of HBO in CO intoxications is still considered controversial. In this review, we discuss the evidence of the role of HBO treatment in isolated CO intoxication.

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.

Hydranencephaly following carbon monoxide poisoning during pregnancy: An uncommon and potentially fatal complication in infant.

BACKGROUND: Hydranencephaly is a rare malformation of the brain system with an incidence of 0.5 per 1000 births. Its principal etiologies are bilateral occlusion of the internal carotid arteries and congenital infections. CASE: We reported an uncommon case of hydranencephaly diagnosed in 50-day old infant and attributable to carbon monoxide (CO) poisoning during the first trimester of pregnancy. CONCLUSIONS: We recommend a prompt diagnosis and management of CO poisoning in pregnant women since it can dramatically affect both the fetus and mother.

Extracorporeal membrane oxygenators with light-diffusing fibers for treatment of carbon monoxide poisoning: Experiments, mathematical modeling, and performance assessment with unit cells.

BACKGROUND AND OBJECTIVES: Approximately 50,000 emergency department visits per year due to carbon monoxide (CO) poisoning occur in the United States alone. Tissue hypoxia can occur at very low CO concentration exposures because CO binds with a 250-fold higher affinity than oxygen to hemoglobin. The most effective therapy is 100% hyperbaric oxygen (HBO) respiration. However, there are only a limited number of cases with ready accessibility to the specialized HBO chambers. In previous studies, we developed an extracorporeal veno-venous membrane oxygenator that facilitates exposure of blood to an external visible light source to photo-dissociate carboxyhemoglobin (COHb) and significantly increase CO removal from CO-poisoned blood (photo-extracorporeal veno-venous membrane oxygenator [p-ECMO]). One objective of this study was to describe in vitro experiments with different laser wavelength sources to compare CO elimination rates in a small unit-cell ECMO device integrated with a light-diffusing optical fiber. A second objective was to develop a mathematical model that predicts CO elimination rates in the unit-cell p-ECMO  device design upon which larger devices can be based. STUDY DESIGN/MATERIAL AND METHODS: Two small unit-cell p-ECMO devices consisted of a plastic capillary with a length and inside diameter of 10 cm and 1.15 mm, respectively. Either five (4-1 device) or seven (6-1 device) gas exchange tubes were placed in the plastic capillary and a light-diffusing fiber was inserted into one of the gas exchange tubes. Light from lasers emitting either 635 nm or 465 nm wavelengths was coupled into the light-diffusing fiber as oxygen flowed through the gas exchange membranes. To assess the ability of the device to remove CO from blood in vitro, the percent COHb reduction in a single pass through the device was assessed with and without light. The Navier Stokes equations, Carreau-Yesuda model, Boltzman equation for light distribution, and hemoglobin kinetic rate equations, including photo-dissociation, were combined in a mathematical model to predict COHb elimination in the experiments. RESULTS: For the unit-cell devices, the COHb removal rate increases with increased 635 nm laser power, increased blood time in the device, and greater gas exchange membrane surface-to-blood volume ratio. The 6-1 device COHb half-life versus that of the 4-1 device with 4 W at 635 nm light was 1.5 min versus 4.25 min, respectively. At 1 W laser power, 635 nm and 465 nm exhibited similar CO removal rates. The COHb half-life times of the 6-1 device were 1.25, 2.67, and 8.5 min at 635 nm (4 W), 465 nm (1 W), and 100% oxygen only, respectively. The mathematical model predicted the experimental results. An analysis of the in vivo COHb half-life of oxygen respiration therapy versus an adjunct therapy with a p-ECMO device and oxygen respiration shows a reduction from 90 min to as low as 10 min, depending on the device design. CONCLUSION: In this study, we experimentally studied and developed a mathematical model of a small unit-cell ECMO device integrated with a light-diffusing fiber illuminated with laser light. The unit-cell device forms the basis for a larger device and, in an adjunct therapy with oxygen respiration, has the potential to remove COHb at much higher rates than oxygen therapy alone. The mathematical model can be used to optimize the design in practical implementations to quickly and efficiently remove CO from CO-poisoned blood.

Prevalence of Carbon Monoxide Poisoning and Hyperbaric Oxygen Therapy in Korea: Analysis of National Claims Data in 2010-2019.

This study aimed to investigate the prevalence of carbon monoxide (CO) poisoning and the provision of hyperbaric oxygen therapy (HBOT) in South Korea. We used data from the Korea Health Insurance Review and Assessment service. In total, 44,361 patients with CO poisoning were identified across 10 years (2010-2019). The prevalence of CO poisoning was found to be 8.64/10,000 people, with a gradual annual increment. The highest prevalence was 11.01/10,000 individuals, among those aged 30-39 years. In 2010, HBOT was claimed from 15 hospitals, and increased to 30 hospitals in 2019. A total of 4,473 patients received HBOT in 10 years and 2,684 (60%) were treated for more than 2 hours. This study suggested that the prevalence of both CO poisoning and HBOT in Korea gradually increased over the past 10 years, and disparities in prevalence were observed by region.

Hyperbaric oxygenation improve red blood cell deformability in patients with acute or chronic inflammation.

INTRODUCTION: Red blood cells (RBC) are one of the key elements of the microcirculation. Their ability to pass through capillaries and to deliver oxygen to cells is due to their large degree of deformability linked to the characteristics of the RBC membrane. Alterations in RBC deformability as a result of membrane damage, linked in part to increased synthesis of reactive oxygen species (ROS), can be observed in several diseases, such as sepsis, and may contribute to the altered microcirculation observed in these pathologies. Hyperbaric oxygen therapy (HBOT), with inhalation of 100 % oxygen, has been proposed in several acute or chronic pathologies, including carbon monoxide poisoning. OBJECTIVE: We investigated the effects of HBOT on oxidative stress from ROS produced by myeloperoxidase (MPO) and on RBC deformability in patients with acute or chronic inflammation (n = 10), in patients with acute carbon monoxide poisoning (n = 10), and in healthy volunteers (n = 10). METHODS: RBC deformability was evaluated before and after HBOT in the various populations using the ektacytometry technique (Laser-assisted Optical Rotational Red Cell Analyzer - LORRCA). Deformability was determined by the elongation index (EI) in relation to the shear stress (SS) over a range of 0.3 to 50 Pa. Oxidative stress was estimated through changes in proteins (chlorotyrosine and homocitrulline) induced by MPO activity measured by liquid chromatography-tandem mass spectrometry analysis. RESULTS: Before HBOT, EI was significantly lower in patients with acute or chronic inflammation than in healthy volunteers and patients with acute carbon monoxide poisoning for the majority of SS values studied. After one session of HBOT, the EI was significantly higher than before HBOT for SS values of 1.93 Pa or higher in patients with acute or chronic inflammation. This effect remains constant after 10 sessions. There were no differences before and after HBOT in protein or amino acid oxidation due to ROS generation mediated by MPO in the three populations. CONCLUSIONS: Our results confirm altered RBC deformability in patients with acute and chronic conditions associated with an underlying inflammatory process. HBOT improves deformability only after one session and therefore may improve microcirculation in this population. According to our results, this improvement does not seem mediated by the ROS pathway via MPO. These results need to be confirmed in a larger population.

Systemic Venous Air Emboli After Emergent Hyperbaric Therapy for Carbon Monoxide Poisoning.

BACKGROUND A venous air embolism is a rare condition but could have a disastrous effect on vital organs. It usually occurs due to iatrogenic sources, such as central venous catheter insertion, neurosurgery, and other invasive procedures. In most cases, hyperbaric oxygen therapy (HBOT) is the best treatment for those conditions. However, multiple venous air emboli after hyperbaric oxygen therapy has not been reported in the literature. CASE REPORT An 82-yr-old woman came to the Emergency Department after inhalation of fumes at the scene of a house fire. She had dizziness and nausea. Her vital signs were normal at the time of presentation. She received HBOT for carbon monoxide poisoning. Soon after the HBOT, the patient started to have dizziness, abdominal pain, and leg pains. Computed tomography scans showed multiple systemic venous air emboli throughout the portal venous system and femoral veins. The air emboli totally disappeared after HBOT with a longer ascent time. CONCLUSIONS To the best of our knowledge, this is the first case of multiple systemic venous air bubbles after emergent HBOT. Physicians should be aware of any kind of complications when treating patients who need HBOT in the emergent setting. Although decompression sickness following HBOT is extremely rare, it should not be ignored by emergency physicians.

Clinical and Laboratory Characteristics Predicting the Severity of Carbon Monoxide Poisoning in Children: A Single-Center Retrospective Study.

OBJECTIVES: Carbon monoxide poisoning (COP) is extremely common throughout the world. The purpose of this study was to assess the demographic, clinical, and laboratory characteristics predicting the severity COP in children. METHODS: The study included 380 children diagnosed with COP between January 2017 and January 2021 and 380 healthy controls. Carbon monoxide poisoning was diagnosed based on the medical history and a carboxyhemoglobin (COHb) level of more than 5%. The patients were classified as mild (COHb 10%), moderate (COHb 10%-25%), or severely (COHb > 25%) poisoned. RESULTS: The mean age of the severe group was 8.60 ± 6.30, for the moderate group was 9.50 ± 5.81, for the mild group was 8.79 ± 5.94, and for the control group was 8.95 ± 5.98. The most common place of exposure was at home and all cases were affected accidentally. The coal stove was the most common source of exposure, followed by natural gas. The most common symptoms were nausea/vomiting, vertigo, and headache. Neurologic symptoms such as syncope, confusion, dyspnea, and seizures were more common in the severe group. A total of 91.3% of the children had hyperbaric oxygen therapy, 3.8% were intubated, and 3.8% were transferred to intensive care in the severe group, whereas no death or sequela was observed. Mean platelet volume and red cell distribution width had the highest area under the curve in the receiver operating characteristic analysis (0.659; 0.379). A positive and low statistically significant relationship was found between COHb levels and troponin and lactate levels in the severe group ( P < 0.05). CONCLUSIONS: Carbon monoxide poisoning progressed more severely in children presented with neurological symptoms and have elevated red cell distribution width and mean platelet volume. Even in severe COP cases, satisfactory results have been obtained with early and appropriate treatment.

Optical, flow, and thermal analysis of a phototherapy extracorporeal membrane oxygenator for treating carbon monoxide poisoning.

BACKGROUND: Extracorporeal membrane oxygenators (ECMO) are currently utilized to mechanically ventilate blood when lung or lung and heart function are impaired, like in cases of acute respiratory distress syndrome (ARDS). ARDS can be caused by severe cases of carbon monoxide (CO) inhalation, which is the leading cause of poison-related deaths in the United States. ECMOs can be further optimized for severe CO inhalation using visible light to photo-dissociate CO from hemoglobin (Hb). In previous studies, we combined phototherapy with an ECMO to design a photo-ECMO device, which significantly increased CO elimination and improved survival in CO-poisoned animal models using light at 460, 523, and 620 nm wavelengths. Light at 620 nm was the most effective in removing CO. OBJECTIVE: The aim of this study is to analyze the light propagation at 460, 523, and 620 nm wavelengths and the 3D blood flow and heating distribution within the photo-ECMO device that increased CO elimination in CO-poisoned animal models. METHODS: Light propagation, blood flow dynamics, and heat diffusion were modeled using the Monte Carlo method and the laminar Navier-Stokes and heat diffusion equations, respectively. RESULTS: Light at 620 nm propagated through the device blood compartment (4 mm), while light at 460 and 523 nm only penetrated 48% to 50% (~2 mm). The blood flow velocity in the blood compartment varied with regions of high (5 mm/s) and low (1 mm/s) velocity, including stagnant flow. The blood temperatures at the device outlet for 460, 523, and 620 nm wavelengths were approximately 26.7°C, 27.4°C, and 20°C, respectively. However, the maximum temperatures within the blood treatment compartment rose to approximately 71°C, 77°C, and 21°C, respectively. CONCLUSIONS: As the extent of light propagation correlates with efficiency in photodissociation, the light at 620 nm is the optimal wavelength for removing CO from Hb while maintaining blood temperatures below thermal damage. Measuring the inlet and outlet blood temperatures is not enough to avoid unintentional thermal damage by light irradiation. Computational models can help eliminate risks of excessive heating and improve device development by analyzing design modifications that improve blood flow, like suppressing stagnant flow, further increasing the rate of CO elimination.

Speech therapy and hyperbaric oxygen for aphasia after carbon monoxide intoxication.

Acute carbon monoxide (CO) intoxication may result in delayed neurological sequelae, which can include amnesia, ataxia, aphasia, emotional lability, disorientation, dysphagia, and other manifestations. A 27-year-old man reported symptoms of aphasia with agraphia and alexia in a review after CO intoxication. The patient received outpatient speech therapy, as well as repeated sessions of hyperbaric oxygen for 15 days, interspersing speech therapy with hyperbaric oxygen therapy for two months. After this period of combined treatment the aphasic symptomatology remitted, and oral and written language was normal. The complete disappearance of aphasia with agraphia and alexia confirms the efficacy of the combined intervention. More data from large clinical studies are needed to assess the outcomes of hyperbaric oxygen treatment in patients with delayed neurological sequelae after CO intoxication, but this case suggests it may be a good therapeutic option in combination with specific speech therapy.

Hyperbaric oxygen therapy in carbon monoxide poisoning in Moroccan patients.

Describe the epidemiological, clinical characteristics of acute carbon monoxide poisoning (COP), and the therapeutic effect of hyperbaric oxygen therapy on patient's clinical outcome. This is the first study in this field in Morocco. It studies retrospectively 309 victims of acute COP with major neurological signs. All patients have been treated with hyperbaric oxygen therapy, and have been admitted by the emergency department of the Mohammed V military training hospital in Rabat, between January 2015 and December 2018. All poisonings were accidental and occurred especially in winter (50%), with a predominance in urban areas (93%). The poisoning was often caused by a non-compliant water heater (91%), multi-causality was in half of the cases, and affected adults and women (mean age: 21 ± 17 years, gender (male:female) 1:1.5. The average admission time to the hyperbaric chamber lasted 9 h 04 min (± 12 h 32 min). Clinical signs were mainly unconsciousness (151 cases), headache (85 cases), vomiting (63 cases), nausea (53 cases), and dizziness (51 cases). All the patients benefitted from hyperbaric oxygen therapy sessions. The clinical outcome was positive in the majority of cases, but 23% of the cases presented minor or major sequelae. Patients with sequelae had a longer length of admission than those who had not. COP is a major public health problem in Morocco. Through this study, we suggest the interest of hyperbaric oxygen therapy, especially when it is administered timely without delay.