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.

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.

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.

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.

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.

[Carbon monoxide intoxication-New aspects and current guideline-based recommendations]. / Kohlenmonoxidintoxikation ­ neue Aspekte und aktuelle leitlinienbasierte Empfehlungen.

Carbon monoxide poisoning is a common and potentially life-threatening intoxication, showing an interindividual variety of unspecific symptoms as well as late neurological and other sequelae. Two new German guidelines (S2k guidelines diagnosis and treatment of carbon monoxide poisoning as well as S3 guidelines oxygen therapy in the acute care of adult patients) focus on current evidence-based information on diagnostics as well as therapeutic options with considerable uncertainty remaining. This review summarizes current information and presents a flow scheme for daily practical use.

Carbon Monoxide Toxicity.

Carbon monoxide accounts for thousands of deaths worldwide each year. Clinical effects can be diverse and include headache, dizziness, nausea, vomiting, syncope, seizures, coma, dysrhythmias, and cardiac ischemia, and severe toxicity generally affects the nervous and cardiovascular systems. Because of its complex pathophysiology, effects of toxicity can be acute or delayed. The diagnosis can be elusive, as carboxyhemoglobin levels do not always correlate with the degree of poisoning. Even when the diagnosis is certain, appropriate therapy is widely debated. Normobaric oxygen is the standard therapy, and the efficacy of hyperbaric oxygen is unclear.

S2k guideline diagnosis and treatment of carbon monoxide poisoning.

Carbon monoxide (CO) can occur in numerous situations and ambient conditions, such as fire smoke, indoor fireplaces, silos containing large quantities of wood pellets, engine exhaust fumes, and when using hookahs. Symptoms of CO poisoning are nonspecific and can range from dizziness, headache, and angina pectoris to unconsciousness and death. This guideline presents the current state of knowledge and national recommendations on the diagnosis and treatment of patients with CO poisoning. The diagnosis of CO poisoning is based on clinical symptoms and proven or probable exposure to CO. Negative carboxyhemoglobin (COHb) levels should not rule out CO poisoning if the history and symptoms are consistent with this phenomenon. Reduced oxygen-carrying capacity, impairment of the cellular respiratory chain, and immunomodulatory processes may result in myocardial and central nervous tissue damage even after a reduction in COHb. If CO poisoning is suspected, 100% oxygen breathing should be immediately initiated in the prehospital setting. Clinical symptoms do not correlate with COHb elimination from the blood; therefore, COHb monitoring alone is unsuitable for treatment management. Especially in the absence of improvement despite treatment, a reevaluation for other possible differential diagnoses ought to be performed. Evidence regarding the benefit of hyperbaric oxygen therapy (HBOT) is scant and the subject of controversy due to the heterogeneity of studies. If required, HBOT should be initiated within 6 h. All patients with CO poisoning should be informed about the risk of delayed neurological sequelae (DNS).

The History of Carbon Monoxide Intoxication.

Intoxication with carbon monoxide in organisms needing oxygen has probably existed on Earth as long as fire and its smoke. What was observed in antiquity and the Middle Ages, and usually ended fatally, was first successfully treated in the last century. Since then, diagnostics and treatments have undergone exciting developments, in particular specific treatments such as hyperbaric oxygen therapy. In this review, different historic aspects of the etiology, diagnosis and treatment of carbon monoxide intoxication are described and discussed.

Sensitive quantification of carbon monoxide in vivo reveals a protective role of circulating hemoglobin in CO intoxication.

Carbon monoxide (CO) is a gaseous molecule known as the silent killer. It is widely believed that an increase in blood carboxyhemoglobin (CO-Hb) is the best biomarker to define CO intoxication, while the fact that CO accumulation in tissues is the most likely direct cause of mortality is less investigated. There is no reliable method other than gas chromatography to accurately determine CO content in tissues. Here we report the properties and usage of hemoCD1, a synthetic supramolecular compound composed of an iron(II)porphyrin and a cyclodextrin dimer, as an accessible reagent for a simple colorimetric assay to quantify CO in biological samples. The assay was validated in various organ tissues collected from rats under normal conditions and after exposure to CO. The kinetic profile of CO in blood and tissues after CO treatment suggested that CO accumulation in tissues is prevented by circulating Hb, revealing a protective role of Hb in CO intoxication. Furthermore, hemoCD1 was used in vivo as a CO removal agent, showing that it acts as an effective adjuvant to O2 ventilation to eliminate residual CO accumulated in organs, including the brain. These findings open new therapeutic perspectives to counteract the toxicity associated with CO poisoning.

Predictors of Severe Clinical Course in Children With Carbon Monoxide Poisoning.

OBJECTIVE: Carbon monoxide (CO) is a gas, which is produced by incomplete combustion of hydrocarbon-containing substances, and causes significant tissue and organ damage in the common event of CO poisoning. This study aims to evaluate the demographic, clinical, and laboratory characteristics of patients diagnosed with CO poisoning in the emergency department and to determine the factors associated with severe course in the acute phase of poisoning. METHODS: A total of 331 patients diagnosed with CO poisoning in Hacettepe University Children's Hospital, Pediatric Emergency Unit, between January 2004 and March 2014 were included in the study. Their demographic characteristics, presenting complaints, physical examination findings, Glasgow Coma Scale scores, carboxyhemoglobin, leukocyte, hemoglobin, troponin T, pH and lactate levels, type of treatment (normobaric or hyperbaric oxygen), intensive care unit admissions, and outcome of poisoning were investigated. RESULTS: Ninety-three patients were given hyperbaric oxygen. Fifty-one patients were admitted to the pediatric intensive care unit, 18 patients have had a severe clinical course, and 6 patients have died. The risk factors associated with severe disease course were determined to be low Glasgow Coma Scale score, high leukocyte count, and high troponin T levels at presentation. CONCLUSIONS: Glasgow Coma Scale score, leukocyte count, and troponin T level may be beneficial in predicting clinical outcomes and tailoring therapy in children with CO poisoning.

A 7-Day-Old Male Infant With Carbon Monoxide Poisoning Treated With Hyperbaric Oxygen.

OBJECTIVE: Children are presented with an unknown intoxication at emergency department (ED) after carbon monoxide (CO) poisoning. Although CO poisoning is well defined in the adult literature, little information exists regarding CO poisoning in childhood, especially in infants. The only diagnostic test for CO poisoning is elevation of the carboxyhemoglobin level in the blood. CASE: We report the second youngest neonate in literature who was severely poisoned by CO and treated with hyperbaric oxygen at the ED. He present to the ED with fussiness and feeding difficulty. Upon arrival, he was lethargic, hypotonic, and crying weak. He had a high carboxyhemoglobin measurement, and the levels of cardiac markers elevated. He was treated with hyperbaric oxygen and discharged a good clinical condition. CONCLUSIONS: If there is a baby with unexplained neurologic symptoms and signs, CO poisoning should be considered in the differential diagnosis. Early diagnosis and treatment prevent complications and sequelaes.

Effects of Hyperbaric Oxygen Therapy on Acute Myocardial Infarction Following Carbon Monoxide Poisoning.

Carbon monoxide poisoning (COP) may increase the risk of myocardial infarction. We conducted a study to investigate the effects of hyperbaric oxygen therapy (HBOT) on the risk. We used the Nationwide Poisoning Database in Taiwan to identify COP patients diagnosed between 1999 and 2012. We compared the risk for myocardial infarction between patients with and without HBOT by following up through 2013 and identified the independent predictors of myocardial infarction. The risk of myocardial infarction in the 7278 patients with HBOT was lower than in the 18,459 patients without HBOT, but this difference did not reach statistical significance [adjusted hazard ratio (AHR): 0.69; 95% confidence interval (CI) 0.45-1.07]. Stratified analyses showed that the reductions in the risk associated with HBOT for myocardial infarction reached statistical significance in male patients (AHR: 0.45; 95% CI 0.24-0.83) and during the first 2 weeks of follow-up (AHR: 0.22; 95% CI 0.05-0.96). In patients without HBOT, independent predictors of myocardial infarction were old age, male sex, and the underlying comorbidities of hypertension, diabetes, coronary artery disease, and congestive heart failure. In patients with HBOT, however, old age, male sex, and the underlying comorbidities of diabetes, coronary artery disease, and congestive heart failure were not independent predictors. HBOT was associated with a reduced risk of myocardial infarction in male patients and within 2 weeks following COP. These results may provide important reference for using HBOT in treating COP.

Trends and characteristics of cases when serial carboxyhemoglobins are obtained.

BACKGROUND: Carboxyhemoglobin (COHb) levels are obtained when there is suspicion for carbon monoxide (CO) exposure. Serial COHb levels are sometimes obtained despite the well-established half-life of COHb with oxygen supplementation. We sought to evaluate the trends and characteristics associated with obtaining serial carboxyhemoglobin levels. METHODS: A retrospective review was performed at an academic medical center for all inpatient and emergency department cases with either single COHb or serial COHb levels from 1 April 2010 through 31 March 2015. Data collected included age, gender, pregnancy status, smoking history, encounter month, admission status, oxygen administration, fire or burn history, vital signs, presenting symptoms, hyperbaric oxygen (HBO2) therapy use, initial pH, troponin, lactate, and COHb levels. The time and change in values between serial levels were also obtained. RESULTS: 624 cases were identified, with 106 (17%) having multiple carboxyhemoglobin levels. A mean of 2.6 (range 2 - 9) serial COHb levels were obtained. The average initial COHb was 8.9%. Subsequent serial levels were obtained on average at 353, 663 and 1,095 minutes and averaged 2.8%, 1.8% and 1.1% respectively. Serial COHb levels were obtained more commonly in burn patients, those admitted to the ICU and those who had HBO2 therapy. Four patients had an increase in COHb level on serial testing. The largest increase of these was from 2.0% to 3.9%. CONCLUSION: Serial COHb levels were not infrequent in this study. No clinically significant increase in COHb was identified by serial testing. Further studies should examine the clinical utility of such practices.