Poisoned patients as potential organ donors: postal survey of transplant centres and intensive care units.
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BACKGROUND: The number of patients awaiting allograft transplantation in the UK exceeds the number of organs offered for transplantation each year. Most organ donors tend to be young, fit and healthy individuals who die because of trauma or sudden cardiac arrest. Patients who die from drug and poison intoxication tend to have similar characteristics but are less frequently offered as potential organ donors. METHODS: A postal questionnaire survey of all transplantation centres and an equal number of intensive care units in the UK was undertaken. The use of kidney, heart, lung, liver and pancreas transplants from poisoned patients following deliberate methanol ingestion, cardiac arrest presumed secondary to cocaine overdose, accidental domestic carbon monoxide inhalation and industrial cyanide exposure were used as case scenarios. RESULTS: Response rates were 70% for transplantation centres and 50% for intensive care unit directors. Over 80% of organs would be offered or discussed with transplant coordinators by intensive care unit directors. Transplantation physicians/surgeons would consider transplanting organs in up to 100% of case scenarios, depending on the organ and poisoning or intoxication involved. DISCUSSION: The postal survey presented here shows that most transplantation physicians and surgeons and intensive care unit directors would consider those who die following acute drug intoxication and poisoning as potential organ donors. The previously reported literature shows in general that transplanted organs from poisoned patients have good long-term survival, although the number of reports is small. Poisoned patients are another pool of organ donors who at present are probably underused by transplantation services. (+info)
A multicompartment model of carboxyhemoglobin and carboxymyoglobin responses to inhalation of carbon monoxide.
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We have developed a model that predicts the distribution of carbon monoxide (CO) in the body resulting from acute inhalation exposures to CO. The model includes a lung compartment, arterial and venous blood compartments, and muscle and nonmuscle soft tissues with both vascular and nonvascular subcompartments. In the model, CO is allowed to diffuse between the vascular and nonvascular subcompartments of the tissues and to combine with myoglobin in the nonvascular subcompartment of muscle tissue. The oxyhemoglobin dissociation curve is represented by a modified Hill equation whose parameters are functions of the carboxyhemoglobin (HbCO) level. Values for skeletal muscle mass and cardiac output are calculated from prediction formulas based on age, weight, and height of individual subjects. We demonstrate that the model fits data from CO rebreathing studies when diffusion of CO into the muscle compartment is considered. The model also fits responses of HbCO to single or multiple exposures to CO lasting for a few minutes each. In addition, the model reproduces reported differences between arterial and venous HbCO levels and replicates predictions from the Coburn-Forster-Kane equation for CO exposures of a 1- to 83-h duration. In contrast to approaches based on the Coburn-Forster-Kane equation, the present model predicts uptake and distribution of CO in both vascular and tissue compartments during inhalation of either constant or variable levels of CO. (+info)
During the acute stage of carbon monoxide poisoning, diffusion MR images obtained at b=1000 s/mm2 revealed high signal intensity lesions in the white matter, consistent with restricted diffusion. Low apparent diffusion coefficient values (0.18-0.34 x 10(-3) mm2/s) were noted in the affected white matter regions. Follow-up MR imaging performed 16 days later revealed disappearance of white matter lesions, suggesting that during the acute stage of carbon monoxide poisoning, white matter can be more sensitive than gray matter to ischemia. (+info)
Mitochondrial oxidative stress after carbon monoxide hypoxia in the rat brain.
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To better understand the mechanisms of tissue injury during and after carbon monoxide (CO) hypoxia, we studied the generation of partially reduced oxygen species (PROS) in the brains of rats subjected to 1% CO for 30 min, and then reoxygenated on air for 0-180 min. By determining H2O2-dependent inactivation of catalase in the presence of 3-amino-1,2,4-triazole (ATZ), we found increased H2O2 production in the forebrain after reoxygenation. The localization of catalase to brain microperoxisomes indicated an intracellular site of H2O2 production; subsequent studies of forebrain mitochondria isolated during and after CO hypoxia implicated nearby mitochondria as the source of H2O2. In the mitochondria, two periods of PROS production were indicated by decreases in the ratio of reduced to oxidized glutathione (GSH/GSSG). These periods of oxidative stress occurred immediately after CO exposure and 120 min after reoxygenation, as indicated by 50 and 43% decreases in GSH/GSSG, respectively. The glutathione depletion data were supported by studies of hydroxyl radical generation using a salicylate probe. The salicylate hydroxylation products, 2,3 and 2,5-dihydroxybenzoic acid (DHBA), were detected in mitochondria from CO exposed rats in significantly increased amounts during the same time intervals as decreases in GSH/GSSG. The DHBA products were increased 3.4-fold immediately after CO exposure, and threefold after 120 min reoxygenation. Because these indications of oxidative stress were not prominent in the postmitochondrial fraction, we propose that PROS generated in the brain after CO hypoxia originate primarily from mitochondria. These PROS may contribute to CO-mediated neuronal damage during reoxygenation after severe CO intoxication. (+info)
Delayed encephalopathy of acute carbon monoxide intoxication: diffusivity of cerebral white matter lesions.
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BACKGROUND AND PURPOSE: Carbon monoxide intoxication has delayed effects on the cerebral white matter characterized by bilateral, confluent lesions that reflect diffuse demyelination. To increase our understanding of this process, we assessed the diffusion characteristics of these lesions. METHODS: Five consecutive patients with delayed encephalopathy of CO intoxication were examined with diffusion MR imaging. Diffusion-weighted images (DWIs) were obtained 25-95 days after their exposure to CO and during a relapse of neuropsychiatric symptoms, which occurred after an initial recovery. Imaging was performed at 1.5 T by using a spin-echo echo-planar sequence with diffusion gradients of 0, 500, and 1000 s/mm(2). DWIs and apparent diffusion coefficient (ADC) maps were visually evaluated, and mean ADCs were calculated from the periventricular white matter and the centrum semiovale, where confluent hyperintensity was seen on T2-weighted images. Findings were compared with those of normal-looking white matter. RESULTS: In all five patients, both T2-weighted images and DWIs showed the white matter lesions as bilateral, diffuse, confluent areas of hyperintensity in the periventricular white matter and centrum semiovale. On ADC maps, these lesions were isointense, with focal areas of hypointensity (n = 4) or diffuse hypointensity (n = 1). Mean ADC values of the white matter lesions were significantly lower than those of normal-looking white matter, regardless of their isointensity or hypointensity on ADC maps (P <.05). CONCLUSION: Bilateral, confluent, white matter lesions in patients with delayed encephalopathy of CO intoxication show decreased diffusivity. (+info)
Management of the moribund carbon monoxide victim.
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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. (+info)
TRAFFIC ACCIDENTS--EPIDEMIOLOGY AND MEDICAL ASPECTS OF PREVENTION.
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Injuries and deaths from traffic accidents are a public health problem of epidemic proportions and justify intensive epidemiological research. The human factor is responsible for the majority of traffic accidents. The literature concerning the human factor is reviewed, and it is concluded that psychosocial influences are most important, though medical conditions may be responsible for 3 to 4% of accidents. Problems concerning the medical examination of drivers are discussed and the need is emphasized to find some means of removing from the road those drivers who continue to drive in spite of repeated medical advice not to do so. Some of the medical conditions influencing driver safety are discussed. It is recommended that each Division of The Canadian Medical Association should publish a guide for physicians who examine drivers. The advantages of a uniform guide in Canada are stressed. (+info)
Technetium-99m HM-PAO SPECT in patients with delayed neurologic sequelae after carbon monoxide poisoning.
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We used single photon emission computed tomography (SPECT) with technetium-99m hexamethylpropylene amine oxime (99mTc-HM-PAO) in 14 studies on 6 patients with delayed neurologic sequelae from carbon monoxide (CO) poisoning to determine whether any changes in cerebral blood flow could be correlated with clinical or computed tomographic evidence of delayed deficits. Among the six initial CT brain scans, two showed low density of both basal ganglia and two showed decreased density of the cerebral white matter. There was no correlation between the clinical outcome and the findings of the follow-up CT brain scans. Of the two SPECTS with 99mTc-HM-PAO performed during acute anoxic insult, one showed focal hypoperfusion which appeared 20 days prior to the onset of delayed neurologic sequelae after CO poisoning. Seven SPECTs in the six patients performing the delayed phase showed diffuse patched patterns of hypoperfusion which improved on follow-up images. There was good correlation between the clinical outcome and the findings of the 99mTc-HM-PAO SPECT. In preliminary conclusion, 9Tc-HM-PAO brain SPECT can be used for predicting or evaluating the outcome of delayed neurologic sequelae after CO poisoning. Cerebral vascular changes may be the possible cause of hypoperfusion in patients with CO poisoning. (+info)