Demographic characteristics and delayed neurological sequelae risk factors in carbon monoxide poisoning.

AIM: Carbon monoxide (CO) is a colorless, odorless gas and tasteless. CO poisoning (COP) is one of the most frequently encountered inhalation poisonings. The most common cause of morbidity in COP is delayed neurological sequelae (DNS). DNS is the occurrence of neuropsychiatric findings within 2-240 days after discharge of patients with COP and there are no definitive diagnostic criteria. The aim of our study is; to determine the risk factors and incidence of DNS. METHOD: Our study is a retrospective, observational study. Patients with the diagnosis of COP in the emergency department between 2015 and 2016 were included in the study. Patients age, gender, findings in the initial physical examination (PE) and neurological examination (NE), blood carboxyhemoglobin (COHb) level, relation between hyperbaric oxygen (HBO) treatment and DNS were assessed. RESULTS: Total of 72 patients were included in the study. Mean age was 33.43 ±â€¯20.89. It was determined that pathological findings in the initial NE are a significant predictive factor for DNS (Odds ratio 18.600, p:0.004). Significant relation between NE and HBO treatment was present (p:00.1). There was no statistically significant relationship between initial COHb level and receiving HBO treatment (p:0.9). Median COHb level of patients with DNS was 30 (min:10, max: 43), median COHb level of patients without DNS was 25 (min:10, max:44) and there was no statistically significant relationship between the two groups according to COHb levels (p:0.7). CONCLUSION: Pathological findings in the initial neurological examination had a predictive value for delayed neurological sequelae in patients with carbon monoxide poisoning.

Effect of free radical scavenger, edaravone, for patients with carbon monoxide poisoning.

OBJECTIVE: Chronic neurological symptoms after carbon monoxide (CO) poisoning are caused by various biological processes in the damaged brain, with free radicals playing roles as mediators in establishing pathological processes leading to chronic neurological symptoms under CO poisoning. This study aimed to clarify the effects of a free radical scavenger, edaravone, in patients with CO poisoning. METHODS: We retrospectively compared two groups comprising patients treated with hyperbaric oxygenation alone (Group A, n=25) or edaravone in addition to hyperbaric oxygenation (Group B, n=25). Edaravone was administrated intravenously at 30 mg every 12h for 7 days. Patient characteristics, general conditions on admission, and frequency of chronic neurological symptoms were compared between groups. Among patients showing chronic neurological symptoms, cognitive function and daily activity were also compared between groups. RESULTS: No significant differences in characteristics or general conditions on admission were identified between groups. In Group B, no patients presented with marked complications caused by edaravone. Although chronic persisting symptoms were less frequent in Group B (n=1, 0.04%) than in Group A (n=5, 20%), this difference was not significant. In the 11 patients showing chronic symptoms, scores for cognitive function and daily activity in the chronic phase were better in Group B than in Group A, but no significant differences were apparent. CONCLUSIONS: The present results suggest that edaravone represents a tolerable and feasible treatment for CO-poisoned patients. Further studies are needed to clarify whether edaravone can favorably influence chronic neurological symptoms caused by CO poisoning.

[Delayed neurological syndrome after CO intoxication of elderly female]. / Laattijdige neuropsychologisch syndroom na CO-intoxicatie bij een bejaarde vrouw.

This article discusses the case history of an 87-year old woman with loss of consciousness following accidental CO intoxication. A few weeks later, the patient's cognitive abilities progressively deteriorated. This is hence a case of Delayed Neurological Symptoms after CO intoxication. This condition occurs in 40% of patients with CO intoxication and manifests itself 3-240 days after apparent recovery. Symptoms can linger for a long time and are in some cases even permanent. Treatment of CO intoxication usually consists of administering normobaric oxygen and in certain cases hyperbaric oxygen. The role of treatment with hyberbaric oxygen in delayed neurological symptoms after CO intoxication remains controversial, however.

The relationship between blood lactate, carboxy-hemoglobin and clinical status in CO poisoning.

AIM: We aimed to determine the relationship between blood lactate, carboxy-hemoglobin (COHb) levels and the severity of clinical findings in patients with CO poisoning. PATIENTS AND METHODS: Patients over 18 years old and of both gender who were admitted to Emergency Department with the diagnosis of CO poisoning between 10.02.2008 and 17.03.2011 were enrolled in this study. Detailed physical examination of each patient was performed, patients and their relatives were informed about the study and written consents were noted. The levels of consciousness, physical examination findings, electrocardiographic findings, Glasgow Coma Scale (GCS) scores, laboratory results (lactate, COHb, CK-MB, Troponin-I levels) and applied treatments [normobaric oxygen therapy (NBOT), hyperbaric oxygen therapy (HBOT)] were recorded to standart data entry form for each patient. "SPSS for Windows version 18" package program was used for statistical analysis of the data. RESULTS: Total 201 patients were included in this study. Thirty five patients (17.4%) received HBOT and lactate; COHb, CKMB, Troponin-I levels of this group were higher than the other patients. Lactate and COHb levels were statistically significantly higher in patients with GCS < 15 than the ones with GCS = 15 (p < 0.01). The patients whose both Troponin-I and CK-MB levels increased have higher lactate levels (p = 0.038), but COHb levels of these patients did not change (p = 0.495). CONCLUSIONS: According to our study, blood lactate and COHb levels were both correlated with the changes of consciousness in CO poisoning. Blood lactate levels together with COHb in defining indications for HBO treatment might be suggested.

[Carboxyhemoglobin concentration in carbon monoxide poisoning. Critical appraisal of the predictive value]. / Carboxyhämoglobinkonzentration bei Kohlenmonoxidvergiftung. Kritische Betrachtung der prädiktiven Aussagekraft.

In cases of unclear depression of conciousness, arrhythmia and symptoms of cardiac insufficiency inadvertent carbon monoxide intoxication should always be taken into consideration. Rapid diagnosis of acute carbon monoxide intoxication with mostly unspecific symptoms requires an immediate supply of high dose oxygen which enables a distinct reduction of mortality and long-term morbidity. Levels of carboxyhemoglobin, however, should not be used as a parameter to decide whether to supply normobaric or the more efficient hyperbaric oxygen. There is no sufficient coherence between carboxyhemoglobin blood levels and clinical symptoms. Increased carboxyhemoglobin concentrations help to diagnose acute carbon monoxide intoxication but do not allow conclusions to be drawn about possible long-term neuropsychiatric or cardiac consequences.

Apolipoprotein E genotype and response of carbon monoxide poisoning to hyperbaric oxygen treatment.

RATIONALE: Hyperbaric oxygen (HBO2) reduced the incidence of cognitive sequelae 6 weeks after carbon monoxide (CO) poisoning compared with normobaric oxygen (NBO2). The apolipoprotein (APOE) epsilon4 allele predicts unfavorable neurologic outcome after brain injury and stroke. OBJECTIVES: To assess the effects of the epsilon4 allele on 6-week cognitive sequelae after CO poisoning. METHODS: We tested APOE genotypes in 86 of 152 CO-poisoned patients from our randomized trial. Logistic regression was used to control for risk factors while testing for effects with the epsilon4 allele or interactions with epsilon4 and treatment on 6-week and 6- and 12-month cognitive sequelae. MEASUREMENTS AND MAIN RESULTS: We enrolled 86 patients: 44 received HBO2 and 42 NBO2 therapy. A total of 31 (36%) patients had at least one epsilon4 allele. Six-week cognitive sequelae rates for patients treated with HBO2 and NBO2, respectively: epsilon4 allele absent, 11% (3/27) and 43% (12/28); epsilon4 allele present, 35% (6/17) and 29% (4/14). The epsilon4 allele was not associated with 6-week cognitive sequelae, 27% (15/55) without and 32% (10/31) with the epsilon4 allele (P = 0.323). The interaction between the epsilon4 allele and treatment was significantly associated with 6-week cognitive sequelae (P = 0.048). The interaction between the epsilon4 allele and treatment was not associated with 6- and 12-month cognitive sequelae. CONCLUSIONS: HBO2 therapy reduces cognitive sequelae after CO poisoning in the absence of the epsilon4 allele. Because apolipoprotein genotype is unknown at the time of poisoning, we recommend that patients with acute CO poisoning receive HBO2.

Diffusion-tensor MR imaging for evaluation of the efficacy of hyperbaric oxygen therapy in patients with delayed neuropsychiatric syndrome caused by carbon monoxide inhalation.

The purpose of this study is to assess the efficacy of hyperbaric oxygen therapy (HBOT) in patients with delayed neuropsychiatric syndrome (DNS) caused by carbon monoxide (CO) inhalation using diffusion tensor magnetic resonance (MR) imaging and neuropsychological test. Conventional and diffusion tensor brain MR imaging exams were performed in six patients with DNS immediately before and 3 months after the HBOT to obtain fractional anisotropy (FA) values. Six age- and sex-matched normal control subjects also received MR exams for comparison. Mini-Mental State Examination (MMSE) was also performed in patients immediately before and 3 months after the HBOT. A significantly higher mean FA value was found in control subjects as compared with the patients both before and 3 months after the HBOT (P < 0.001). The mean FA value 3 months after the HBOT was also significantly higher than that before the HBOT in the patient group (P < 0.001). All of the patients regained full scores in the MMSE 3 months after the HBOT. Diffusion tensor MR imaging can be a quantitative method for the assessment of the white matter change and monitor the treatment response in patients of CO-induced DNS with a good clinical correlation. HBO may be an effective therapy for DNS.

Delayed neuropsychiatric syndrome in a child following carbon monoxide poisoning.

Here, we report the case of a five-year-old boy with carbonic monoxide (CO) poisoning. The patient initially recovered after the initiation of hyperbaric oxygen (HBO) therapy, but lethargy as well as visual and gait disturbances appeared two days later. Left hemiparesis and mood lability also subsequently appeared. Slow frontal activity was noted on electroencephalography, while fluid-attenuation inversion recovery and diffusion-weighted magnetic resonance imaging (MRI) revealed high signal-intensity lesions in the hippocampus and deeper layers of the occipital and frontal cerebral cortex. The neurological symptoms subsided gradually during the 10-day course of HBO therapy, but the left-hand paresis and quadrantic hemianopsia persisted, in association with impaired attention, slow mental processing, and incontinence. Lesions in the globus pallidum were noted on follow-up MRI at 14 days, and cortical lesions became evident as linear, low signal-intensity areas on T1-weighted imaging 4 months after presentation. Delayed neuropsychiatric syndrome in CO poisoning is rare in childhood, although children should be carefully monitored after CO exposure. The finding of cortical laminar necrosis in this patient is quite atypical in CO poisoning, and suggests a broader and previously nonpredicted pathomechanism in this condition.

Affective outcome following carbon monoxide poisoning: a prospective longitudinal study.

OBJECTIVE: To longitudinally assess the prevalence of depression and anxiety following carbon monoxide (CO) poisoning and to assess the contributions of mode of poisoning (accidental versus suicide attempt), cognitive sequelae, and oxygen dose (hyperbaric oxygen versus normobaric oxygen) to depression and anxiety. BACKGROUND: CO is the most common cause of poisoning in the United States and may result in neuropathologic changes and cognitive and neurologic sequelae, yet little is known regarding affective outcomes. METHOD: We prospectively assessed affect in 127 CO-poisoned patients. Self-report inventories of depression and anxiety were administered at 6 weeks and at 6 and 12 months post CO poisoning. The primary outcome was prevalence of depression and anxiety at 6 weeks. To determine the effect of mode of poisoning, cognitive sequelae, and oxygen dose, odds ratio estimates were calculated at all three times using logistic regression. RESULTS: Depression and anxiety were present in 45% of patients at 6 weeks, 44% at 6 months, and 43% at 12 months. Patients with suicide attempt and cognitive sequelae had higher prevalence of depression and anxiety at 6 weeks. At 12 months, there were no differences in depression or anxiety regardless of mode of poisoning, presence of cognitive sequelae, or oxygen dose. CONCLUSIONS: CO poisoning results in significant depression and anxiety that persist to at least 12 months. Patients with cognitive sequelae and suicide attempt had a higher rate of depression and anxiety at 6 weeks but not at 12 months. Clinicians need to be aware of affective morbidity following CO poisoning and remain vigilant about CO prevention.

[A case of interval form of carbon monoxide poisoning with a remarkable recovery].

A 69-year-old woman was admitted to our hospital due to an interval form of carbon monoxide (CO) poisoning one month after acute CO poisoning. On admission, she had disorientation, memory disturbance, apathy, masked face, muscle rigidity, bradykinesia and parkisonian gait. An MRI (FLAIR image) revealed high signal intensity lesions in the bilateral globus pallidus and the white matter of the frontal lobe. Hyperbaric oxygen (HBO) therapy at 2 atmospheres for 60 min was given every day, in addition to citicoline, levodopa/DCI and selegiline hydrochloride. Cognitive disturbance and parkinsonism gradually decreased, and abnormal signals in the bilateral globus pallidus and the cerebral white matter were attenuated after the treatment. Neuropsychiatric abnormalities except for a slight gait disturbance disappeared one and a half month after starting the treatment. In addition to HBO therapy, administration of citicoline, lovodopa and selegiline may be useful in the case of the interval form of CO poisoning.

Neuropsychologic and functional recovery from severe carbon monoxide poisoning without hyperbaric oxygen therapy.

STUDY OBJECTIVE: To test the hypothesis that neuropsychologic test results and functional outcome will be abnormal if hyperbaric oxygen (HBO) is not used in patients with severe carbon monoxide (CO) poisoning. METHODS: For a 1-year interval, we retrospectively identified all CO-poisoned patients who were comatose on presentation at a large, urban tertiary hospital and did not receive HBO therapy. Prospectively, 6 and 12 months after CO poisoning, we administered standardized questionnaires to assess functional outcome. At 6 months, we performed extensive neuropsychologic testing. RESULTS: All four patients exhibited normal performance on a neuropsychologic test battery at 6 months. The Folstein Mini-Mental Status Examination was normal in all patients. All patients had normal functional outcomes. CONCLUSION: Normal neuropsychologic and functional outcomes are possible after severe CO poisoning without the use of HBO therapy.

Preserved visual imagery in visual form agnosia.

We investigated the ability of a patient (D.F.) with profound visual form agnosia to perform a variety of tasks requiring visual imagery. Despite her inability to discriminate between objects and patterns of different shapes, sizes, and orientations, D.F. showed quite normal visual imagery involving these same 'visual' properties when the images were drawn from long-term memory. Thus, she was able both to scan mental images in search of particular features and to form new images by combining several known images. While there is growing evidence that perception and imagery share common neural substrates, the fact that D.F. shows intact visual imagery in the face of a massive perceptual deficit in form vision challenges recent suggestions that these two psychological processes share common input pathways in early vision. It is suggested that regions in the occipitotemporal pathway may be important for the generation of visual images while regions in the posterior parietal system might be involved in the manipulation of these images.

Delayed neuropsychologic sequelae after carbon monoxide poisoning: prevention by treatment with hyperbaric oxygen.

STUDY OBJECTIVE: Carbon monoxide (CO) poisoning is a major clinical problem. The risk of morbidity and the most effective treatment have not been clearly established. We measured the incidence of delayed neurologic sequelae (DNS) in a group of patients acutely poisoned with CO and tested the null hypothesis that the incidence would not be affected by treatment with hyperbaric oxygen (HBO). DESIGN: We conducted a prospective, randomized study in patients with mild to moderate CO poisoning who presented within 6 hours. Patients had no history of loss of consciousness or cardiac instability. INTERVENTIONS: The incidence of DNS was compared between groups treated with ambient pressure 100% oxygen or HBO (2.8 ATA for 30 minutes followed by 2.0 ATA oxygen for 90 minutes). DNS were defined as development of new symptoms after oxygen treatment plus deterioration on one or more subtests of a standardized neuropsychologic screening battery. RESULTS: In 7 of 30 patients (23%), DNS developed after treatment with ambient-pressure oxygen, whereas no sequelae developed in 30 patients after HBO treatment (P < .05). DNS occurred 6 +/- 1 (mean +/- SE) days after poisoning and persisted 41 +/- 8 days. At follow-up 4 weeks after poisoning, patients who had been treated with ambient pressure oxygen and had not sustained DNS exhibited a worse mean score on one subtest, Trail Making, compared with the group treated with HBO and with a control group matched according to age and education level. There were no differences in scores between the control group and the hyperbaric oxygen group. CONCLUSION: DNS after CO poisoning cannot be predicted on the basis of a patient's clinical history or CO level. HBO treatment decreased the incidence of DNS after CO poisoning.

Carbon monoxide, amnesia and hyperbaric oxygen therapy.

A case of carbon monoxide poisoning, initially misdiagnosed as conversion disorder, is presented. Cognitive deficits demonstrated at the time of psychiatric assessment were successfully reversed by hyperbaric oxygen therapy despite the 1 week delay. The clinical manifestations of carbon monoxide poisoning and the rationale for and timing of hyperbaric oxygen therapy are discussed. Emphasis is placed on the need for a high index of suspicion for carbon monoxide poisoning in the clinical situation of profound memory disturbance.

Gamma-aminobutyric acid-B (GABAB) binding sites in postmortem suicide brains.

Gamma-aminobutyric acid-B (GABAB) binding sites labelled with [3H]GABA were determined in postmortem frontal cortex samples of 20 control subjects and 16 suicides. The suicide group was further subdivided according to the method of suicide and the existence of depressive symptoms prior to death. No significant differences in GABAB binding were found either between overall suicide and control groups or between the control group and the other subgroups (violent suicide, nonviolent suicide, nondepressed and depressed suicide victims). A significant increase in GABAB binding was observed in those individuals dying from carbon monoxide poisoning. It is concluded that although GABAB binding sites are not altered in our suicide group, a presynaptic dysfunction might account for the increased GABAB binding found in the carbon monoxide subgroup.

A neuropsychological screening battery for emergency assessment of carbon-monoxide-poisoned patients.

The Carbon Monoxide Neuropsychological Screening Battery (CONSB) was developed to improve the neurological assessment of CO-poisoned patients in an emergency setting. Traditional assessment methods (clinical examination and carboxyhemoglobin [CoHb] levels) readily can identify unconscious, severely involved patients; however, many CO-intoxicated patients with cerebral impairment who also require aggressive hyperbaric oxygen therapy are assessed inadequately by such methods. Administration of the CONSB to 66 CO-poisoned patients and 66 volunteer controls revealed significant differences in performance between the two groups. It was concluded that the CONSB enhanced the accuracy of the evaluation of cerebrally impaired CO-poisoned patients. Failure to assess the cerebral functioning of patients exposed to CO and to identify those who require aggressive oxygen therapy could have neurological sequelae.

A historic case of visual agnosia revisited after 40 years.

In one of the seminal works on visual agnosia, Adler (1944, 1950) presented the case of a 22-yr-old woman who sustained carbon monoxide cerebral toxicity in the Cocoanut Grove nightclub diaster of 1942. We located this patient 40 yrs after injury and performed a detailed reevaluation. The patient demonstrated persistent deficits in visual recognition, characterized most prominently by defective recognition of elemental shape and form, associated with alexia, prosopagnosia, visuospatial disorientation and impaired visual imagery. Visual acuity, colour recognition, writing ability and verbal intelligence were relatively preserved. Isolated bilateral occipital injury was demonstrated by CT and MRI scanning. On comparison with previously reported cases, our results support the hypothesis that carbon monoxide toxicity can induce a visual agnosia of the apperceptive type with well defined characteristics, seldom seen with other types of cerebral injury. Prognosis for long-term recovery is poor.