Cases reported "Carbon Monoxide Poisoning"

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1/10. Acute carbon monoxide poisoning as the cause of rhabdomyolysis and acute renal failure.

    Acute renal failure (ARF) is a severe complication of acute CO poisoning which, combined with other organ lesions, may result in lethal outcome. In all vague cases of ARF with nontraumatic rhabdomyolysis, CO poisoning should be considered as a possible etiologic factor. The diagnosis is made on the basis of several simple laboratory tests: determination of carboxyhemoglobin concentration, demonstration of myoglobin in urine or pigment granulated cylindres in urinary sediment, positive orthotoluidine test, and high CPK values originating from skeletal musculature. Many authors report on excellent prognosis in ARF due to nontraumatic rhabdomyolysis of various causes. Our case report shows that the prognosis of CO poisoned patient greatly depends on timely and appropriate treatment, severity of damage to other organs, and success of the treatment of complications such as hospital infections.
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2/10. 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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3/10. Successful cardiac transplantation with methanol or carbon monoxide-poisoned donors.

    BACKGROUND: patients succumbing to methanol or carbon monoxide poisoning are usually rejected for heart donation. Increasing demand for donors has lead to the expansion of acceptance criteria and increased use of the marginal donor. methods: We transplanted hearts from donors who had had methanol intoxication in three cases and carbon monoxide exposure in two cases. Standard donor evaluation criteria and transplantation techniques were used. RESULTS: All of the transplants were successful. Three of the recipients required significant inotropic support for a few days postoperatively; however, all of the hearts functioned well over the intermediate and long term. Two recipients (1 from each group) died of complications other than heart failure (1.5 and 2 years postoperatively). CONCLUSIONS: Successful heart transplantation can be achieved using the hearts from patients succumbing to methanol or carbon monoxide poisoning. Routine evaluation of cardiac function and myocardial damage is adequate for screening these donors. Hearts from methanol-poisoning victims may require longer inotropic support postoperatively before complete recovery, but can provide excellent long-term function and results.
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4/10. Suicidal inhalation of motorbike exhaust: adding new data to the literature about the contribution of gasoline in the cause of death.

    We would like to alert toxicologists to the importance of testing for gasoline, and for volatile hydrocarbons in general, in deaths involving inhalation of exhaust fumes occurring in closed spaces with running motors or machinery. We present here a case of suicidal inhalation of motorbike exhaust, a mixture of carbon monoxide (CO) and gasoline vapor, by a 38-year-old female. She was found in her closed home garage with a hose extending from the exhaust pipe of a motorbike through a cellophane plastic device into a closed tent in which the victim lay. She left two suicide notes nearby. The carboxyhemoglobin (COHb) was measured using visible spectrophotometry. The toxicological screening and quantitation of gasoline was performed by means of gas chromatography with flame-ionization detector and confirmation was performed using gas chromatography-mass spectrometry. The %COHb determined in blood was 73%. gasoline concentrations in heart blood and vitreous humor were 22.3 and 1.0 mg/L, respectively. Although fatalities with CO at this rate are common, we would like to highlight the role of gasoline and add new quantitative data of this toxic substance to the scarce literature. Based upon the toxicological data, along with the information provided by the medical examiner, the cause of death was determined to be CO and gasoline poisoning and the manner of death suicide.
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5/10. Carbon monoxide effect on alveolar epithelial permeability.

    A carbon monoxide (CO)-intoxicated patient developed increased permeability-type pulmonary edema demonstrated by a normal capillary wedge pressure and production of protein-rich edema fluid. To investigate the effect of CO on alveolar-epithelial permeability, a radio-active labelled isotope, 51Cr-EDTA (MW 377), was instilled into the airways of rabbits. Subsequent egress of the marker from the lungs into arterial blood was determined in serial arterial blood samples. The 51Cr-EDTA counts increased significantly within 15 minutes in the CO-exposed animals, compared with the control animals, while dynamic lung compliance fell, airways resistance rose, and arterial blood pressure decreased. Ultrastructural study of the lungs of CO-exposed animals revealed epithelial and endothelial cell swelling, in terstitial edema, and alveolar type II cells depleted of lamellar bodies. These findings support the possibility that carbon monoxide intoxication is associated with increased alveolar-epithelial permeability.
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6/10. carbon monoxide poisoning and nonoliguric acute renal failure.

    carbon monoxide poisoning in a 37-year-old man was complicated by neurologic damage, skin changes, muscle necrosis and nonoliguric renal failure. The relation between nontraumatic rhabdomyolysis and acute renal failure in carbon monoxide poisoning is reviewed. Recognition of the acute renal failure in such cases is important, for this complication can be fatal; the prognosis is excellent, however, if proper medical management is provided.
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7/10. Increased blood viscosity in a patient with sickle cell anemia.

    Although intracellular viscosity is greatly increased in deoxygenated sickle cells, the viscosity of blood is not, because patients' packed cell volumes (PCV) are usually extremely low (15-25%). A young women with sickle cell anemia was admitted with a typical painful crisis, and was found to have a PCV of 39% with a reticulocyte count of 3.6%. During a hospitalization of 48 h, the PCV rose to 46%; her pain subsided but her behavior became bizarre, cardiopulmonary arrest occurred, and she could not be resuscitated. At autopsy, no abnormalities were found except for congested blood vessels containing sickle cells. It was subsequently discovered that she and her family had been exposed to carbon monoxide for a week prior to admission. Blood samples from another patient studied with a PCV of 40% showed progressively decreased viscosity if they contained 13-20% carboxyhemoglobin. It is suggested that preexisting accelerated erythropoesis was further stimulated by CO, and caused "compensatory polycythemia", but that the CO prevented most of the newly formed cells from sickling and being destroyed. Admission to hospital caused a gradual disappearance of CO but the patient's PXV continued to rise. Her death may have been due to a rare form of hyperviscosity syndrome, when the level of carboxyhemoglobin in her blood fell to more normal levels and her cells regained the ability to sickle. Treatment of sickle cell anemia with an effective non-covalently bound agent could have a similar effect, if the agent were withdrawn abruptly.
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8/10. Cardiac allograft harvesting after carbon monoxide poisoning. Report of a successful orthotopic heart transplantation.

    Hearts from brain dead victims of carbon monoxide poisoning have been reported to be unsuitable for heart transplantation. We present the case of a 30-year-old male donor who was the victim of carbon monoxide poisoning. He was on ventilation for 16 days before the organs were offered for harvesting. A liver biopsy indicated focal liver cell necrosis. The liver graft was not used. heart transplantation was performed successfully. No evidence of ischemic areas or myocardial cell necrosis could be found in all heart biopsy specimens. Four months after transplantation, graft function remains excellent.
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9/10. myocardial infarction with normal coronary artery after carbon monoxide exposure: a case report.

    Carbon monoxide intoxication usually disturbs the normal human biochemical respiratory chain cascade from which high affinity of carboxyhemoglobin to oxygen causes ischemic insult to the human tissues and cells. Ubiquitous injuries to human cells have already been well documented for a long period of time. Here we reported a 42-year-old female who was sent to the medical emergent unit under the suspicion of carbon monoxide exposure mainly with neurologic deficits. serum carboxyhemoglobin level was found to be 18%. Serial revolutional changes of serum CK level and ECG were noted. The echocardiogram showed hypokinesia of left ventricular apical lateral wall. Normal coronary arteriogram was found in later admission date. The patient received hyperbaric oxygen therapy and was discharged with residual psychotic symptoms. This report presented normal coronary arteriogram with serial EKG and biochemical changes in a victim of CO intoxication with evidence of myocardial infarction. Impaired oxygen delivery and disturbed intracellular mitochondrial metabolism were considered to be responsible for the ischemic insult associated with carbon monoxide exposure. The role of hyperbaric oxygen therapy was also discussed in this report; however, more experiences in application are needed to determine it's benefits for patients.
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10/10. Functional and ultrastructural evidence of myocardial stunning after acute carbon monoxide poisoning.

    OBJECTIVE: To study human myocardial ultrastructural changes after carbon monoxide (CO) poisoning inducing reversible cardiac failure. DESIGN: Case report: clinical, functional and morphologic findings. SETTINGS: Public university-affiliated hospital and electron microscopy laboratory. PATIENT: A 25-yr-old woman with functional evidence of cardiac failure after acute CO poisoning. INTERVENTIONS: Hyperbaric and intensive care treatment over 10 days. Scintigraphic and cardiac angiography with endomyocardial biopsy. MEASUREMENTS AND MAIN RESULTS: Scintigraphy with 99mTc hexakis 2-methoxy-2-isobutyl isonitrile (sestaMIBI) showed an uptake defect in the left anterior descending artery territory. The cardiac angiography demonstrated a slight hypokinesis of the superior two thirds of the anterior wall and of the septal region with completely normal coronary angiograms. Electron microscopy of left ventricular biopsies showed slight ultrastructural changes in the myocytes. In addition, large glycogen deposits were mostly associated with swollen mitochondria. The patient was discharged in good clinical condition on day 10. CONCLUSIONS: Presence of glycogen deposits associated with abnormal mitochondria may be signs of the incapability of myocardial cells in utilizing energy substrata. In the presence of normal myocardial perfusion, our findings are consistent with the presence of a stunned myocardium-like syndrome. Early recognition and treatment of this clinical syndrome allow the prevention of myocardial infarction.
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