Cases reported "Carbon Monoxide Poisoning"

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1/23. Delayed transient loss of consciousness in acute carbon monoxide intoxication.

    In acute carbon monoxide intoxication the presence of altered consciousness, ranging from transient loss of consciousness to coma, represents a poor prognostic factor and modifies the approach to therapy. Transient loss of consciousness is, as a rule, contemporaneous to the exposure, generally occurring at the scene of the intoxication. We report an unusual case of delayed transient loss of consciousness, occurring in the absence of any other evident aetiology, in one member of an orchestra composed of 110 members after a mass carbon monoxide poisoning.
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2/23. Apoptotic and necrotic brain lesions in a fatal case of carbon monoxide poisoning.

    A 41-year-old man was accidentally exposed to carbon monoxide (CO) gas and found in a state of cardiopulmonary arrest while he took bath. After admission, he was resuscitated and underwent artificial ventilation in a comatose state and died about 19h later. Computed tomography (CT) examination disclosed bilateral low density area in the basal ganglia and the thalamus, a well-known finding in the CO intoxication. Necropsy, histological examination, dna ladder assay gave the first line of evidence for the presence of apoptosis as well as necrosis in the human case of CO intoxication. TdT-mediated dUTP-biotin nick-end labeling (TUNEL) positive apoptotic cells were more predominant in the CA2 area than in CA1 area. There is general co-relation between the ratio of TUNEL-positive cells and the dna laddering on the agarose gel. basal ganglia and thalamus, which showed bilateral low density area in CT, were revealed to be severe edema. The two types of cell death occurred in the cortex, basal ganglia, hippocampus, thalamus, and cerebellum. Hypoxia caused by CO-hemoglobin formation alone cannot explain the phenomena.
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3/23. Management of the moribund carbon monoxide victim.

    Carbon monoxide (CO) poisoning is the commonest single cause of fatal poisoning in the U.K. (Broome & Pearson, 1988). The clinical features are numerous and include headache, fatigue, dizziness, confusion, memory loss, paraesthesia, chest pain, abdominal pain, nausea, and diarrhoea as well as coma, convulsions and death. Without adequate treatment many patients develop neuropsychiatric sequelae including headaches, irritability, memory loss, confusion and personality changes. The diagnosis of CO poisoning is often suggested only by circumstances surrounding the victim, and remains a challenge to the A&E department. Hyperbaric oxygen therapy (HBO) is internationally accepted as the most powerful form of treatment in severe cases (Drug & therapeutics Bulletin, 1988; Lowe-Ponsford & Henry, 1989). However, in the U.K. treatment with HBO is often not considered due to lack of hyperbaric facilities (Meredith & Vale, 1988; Anand et al., 1988), and due to inadequate awareness on the part of hospital staff. We report a case of a patient deeply unconscious as a result of CO poisoning, in which serial treatments with HBO over a period of 14 days, produced dramatic results.
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4/23. Post-interval syndrome after carbon monoxide poisoning.

    Carbon monoxide (CO) exposure and toxicity is a potentially lethal disorder with immediate and delayed side effects. A 24-y-old driver was admitted to the University-based emergency department with altered mental status. He was found unconscious in the driver's seat of his vehicle in an indoor garage the morning before. An estimated 7 h later, he was comatose and taken to a nearby village clinic. oxygen was administered immediately. Later, he was transferred to the university hospital. At the 12th h after exposure, the glasgow coma scale score was 12/15 (E3, M5, V4). Co-oximetry disclosed a carboxyhemoglobin concentration of 10.5%. Normobaric oxygen was administered. He recovered completely the 3rd d after exposure; however, on the 7th d disorientation and agitation was noted, and the interval form of CO poisoning and leukoencephelopaty were suspected, for which he was readmitted the 10th d after exposure. Analysis of cerebrospinal fluid and blood revealed no abnormalities. magnetic resonance imaging on the 11th d after exposure demonstrated an ischemic area in the posterior temporoparietal area. The patient continued improvement to discharge at 7th d of the second admission. Close follow-up should be scheduled for CO-poisoned patients to rule out the post-interval syndrome for at least 1 mo. This should also include those with apparent clinical and laboratory recovery.
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5/23. Carbon monoxide brain toxicity: clinical, magnetic resonance imaging, magnetic resonance spectroscopy, and neuropsychological effects in 9 people.

    Carbon monoxide (CO) exposure is a common cause of toxic brain damage, whereby effects range from transient neurological dysfunction to coma and death. A spectrum of severity of magnetic resonance imaging (MRI) findings after CO brain toxicity, including globus pallidus and white matter lesions, is well documented. Reports of MR spectroscopy (MRS) findings re main sparse. This article reports 9 people exposed to CO because of an apartment house's faulty gas heater. Four, with transient loss of consciousness after chronic moderate level CO exposure, suffered intellectual impairment without MRI abnormalities. The MRS of 1 individual demonstrated decreased n-acetyl aspartase in the basal ganglia, bilaterally. Of 5 exposed to high levels for about 12 hours, 1 died prior to clinical and/or MRI evaluation. One who suffered coma recovered but was lost to evaluation. Three, who were unconscious for hours to days, exhibited T2 MRI white matter signal abnormalities. MRS showed decreased basal ganglia n-acetyl aspartase in 2. One of these suffers a Parkinsonian syndrome. All 3 are intellectually impaired. This study demonstrates that although MRI and MRS are useful markers of CO-induced brain damage, they are not always sensitive to resultant intellectual dysfunction.
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keywords = coma
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6/23. Partial recovery from cortical blindness following carbon monoxide intoxication.

    patients with carbon monoxide (CO) intoxication may show neurological signs such as headache, seizures, extrapyramidal findings, and coma. However, cortical blindness is rare in these cases. This study describes a woman exhibiting confusion and axial rigidity after CO intoxication. Ten days after intoxication, her pupils were isonormocoric and reactive to light. A fundoscopic examination was normal, but visual acuity was light-perception in both eyes. There were diffuse EEG slow waves. magnetic resonance imaging (MRI) demonstrated bilateral hyperintensity in the basal ganglia. The P100 latencies of visual evoked potentials (VEP) were increased and dispersed. One year later, the patient's visual acuity was almost normal and VEPs showed mild dispersion in P100 latencies. The authors found this case of interest because cortical blindness due to CO intoxication is only rarely seen with a relatively good outcome.
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7/23. skin lesions in carbon monoxide intoxication.

    A 25-year-old man who survived carbon monoxide intoxication presented erythematous cutaneous lesions with blister formation in pressure areas. Histologic examination revealed subepidermal vesicles with extensive sweat gland necrosis. We discuss the clinicopathological findings of carbon monoxide poisoning. Similar cutaneous features have been observed in patients with various kinds of drug-induced coma.
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keywords = coma
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8/23. The diagnostic utility of flumazenil (a benzodiazepine antagonist) in coma of unknown etiology.

    The use of flumazenil, a benzodiazepine antagonist, was studied in two patients with coma of unknown etiology. One patient ingested 20.5 mg alprazolam before crashing his truck into parked automobiles. The patient was awakened by flumazenil administration, and the severity of his injuries was evaluated reliably. A second patient ingested 7.5 mg triazolam and attempted suicide with carbon monoxide from car exhaust. His coma resolved completely after the administration of the double-blind study drug, obviating treatment with hyperbaric oxygen. flumazenil had a clear diagnostic and therapeutic role in the treatment of these patients and should be a useful tool for emergency physicians and toxicologists.
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keywords = coma
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9/23. Acute carbon monoxide poisoning. risk of late sequelae and treatment by hyperbaric oxygen.

    The indications for hyperbaric oxygen therapy (HBO) in the treatment of acute carbon monoxide (CO) poisoning are discussed far too little in the literature. Depending on the author reasons for referral to a hyperbaric center include the carboxyhemoglobin level, change in state of consciousness or neurological abnormalities. In our opinion, HBO should be used on much wider indications than is usual, not only because of the rapid relief from symptoms it provides but mainly because it may prevent severe delayed sequelae. During a period of 9 months 230 patients with CO poisoning were admitted to our intensive care unit; 203 were treated with HBO and 27 with normobaric oxygen. Our indications for HBO treatment were: coma, pathological neurological findings or loss of consciousness during CO exposure irrespective of normal clinical findings on admission. Four patients died and the others were discharged 12 hours to 25 days after the incident. Seven patients had minor neurological problems within two weeks of discharge and which disappeared within one month. Two patients were re-hospitalized for neuropsychiatric sequelae and recovered in 3 and 6 months respectively. Neither the clinical status upon admission nor COHb predicted the outcome of the poisoning. Referral to a HBO center should be considered when: --the patient is comatose --there are abnormal clinical findings --patients have been unconsciousness during exposure, irrespective of whether they are conscious on admission and have normal clinical status.
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ranking = 2
keywords = coma
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10/23. carbon monoxide poisoning with features of Gilles de la Tourette's syndrome.

    A previously healthy 58-year-old man had severe carbon monoxide poisoning. Following a comatose state, tics of the head, coprolalia, fits of shouting, and abnormal vocal utterances developed. In addition to the signs of diffuse encephalopathy, he had some of the features associated with idiopathic Gilles de la Tourette's syndrome. The computed tomographic scan showed ventricular enlargement and low-density areas in the basal ganglia.
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keywords = coma
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