Cases reported • Carbon Monoxide Poisoning; Illuminating Gas Poisoning

1/27. Neuropsychiatric aspects of carbon monoxide poisoning: a review and single case report suggesting a role for amphetamines.

Sublethal exposure to carbon monoxide (CO) can result in severe neurologic and psychiatric complications. Once in the body, CO can wreak havoc on virtually every organ system, with the brain being the most vulnerable to the damaging effects. Neuropathological injury is frequently widespread, and while white matter injury is most common, both gray and white matter injury occurs. Consequently, no neurologic or psychiatric syndrome is pathognomonic for CO poisoning. There are currently no effective treatments for the delayed neuropsychiatric sequelae of CO poisoning, and medical management focuses on correcting immediate symptoms through the use of oxygen, hyperbaric oxygen therapy, and supportive measures. Preliminary data suggest, however, that dopaminergic agents may be useful for the treatment of some of the delayed sequelae of CO neurotoxicity. To our knowledge, ours is the first case report in which dextroamphetamine (DAMP), a potent dopaminergic agent, has been used for treating the neuropsychiatric symptoms of CO poisoning. Our data demonstrate that it is effective in shortening cognitive and motor recovery time, that psychostimulant actions occur slightly sooner than locomotor effects, and that theraputic benefit is most dramatic within the first ten days of use. Therefore, DAMP appears to be a pharmacological agent that can be combined with supportive interventions to reverse, attenuate, or symptomatically improve the delayed sequelae that occur in these patients.

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2/27. Recognition of chronic carbon monoxide poisoning.

Chronic exposure to low levels of carbon monoxide can cause vague symptoms that are easily mistaken for other common illnesses. During the past 5 years, three families have contacted the wisconsin Division of public health to report illnesses that may have been caused by chronic exposure to carbon monoxide. Members of these families were diagnosed with a variety of conditions including chronic fatigue syndrome, depression and influenza. Carbon monoxide exposure was not suspected as a cause of these illnesses until heating contractors discovered that gas appliances in these families' homes were not properly vented. These cases serve as reminders that carbon monoxide exposure should be considered in the differential diagnosis of patients who present with chronic symptoms of headache, fatigue, dizziness, nausea and mental confusion--especially when these symptoms onset during the winter heating season.

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3/27. Extracorporeal support in an adult with severe carbon monoxide poisoning and shock following smoke inhalation: a case report.

The objective of this study was to discuss the case of a patient with severe smoke inhalation-related respiratory failure treated with extracorporeal support. The study was set in a 12-bed multi-trauma intensive care unit at a level one trauma center and hyperbaric medicine center. The patient under investigation had carbon monoxide poisoning, and developed acute respiratory distress syndrome and cardiovascular collapse following smoke inhalation. Rapid initiation of extracorporeal support, extreme inverse-ratio ventilation and intermittent prone positioning therapy were carried out. Admission and serial carboxyhemoglobin levels, blood gases, and computerized tomography of the chest were obtained. The patient developed severe hypoxia and progressed to cardiovascular collapse resistant to resuscitation and vasoactive infusions. Veno-venous extracorporeal support was initiated. Cardiovascular parameters of blood pressure, cardiac output, and oxygen delivery were maximized; oxygenation and ventilation were supported via the extracorporeal circuit. Airway pressure release ventilation and intermittent prone positioning therapy were instituted. Following 7 days of extracorporeal support, the patient was decannulated and subsequently discharged to a transitional care facility,neurologically intact. smoke inhalation and carbon monoxide poisoning may lead to life-threatening hypoxemia associated with resultant cardiovascular instability. When oxygenation and ventilation cannot be achieved via maximal ventilatory management, extracorporeal support may prevent death if initiated rapidly.

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4/27. Cardiac damage in pediatric carbon monoxide poisoning.

BACKGROUND: Cardiovascular disorders including myocardial ischemia and heart failure have been described in both laboratory animals and humans following carbon monoxide poisoning. Carbon monoxide cardiotoxicity may be clinically occult and often remains undiagnosed because of the lack of overt symptoms and specific ischemic changes in the electrocardiogram. Routine myocardial necrosis markers have low diagnostic efficiency, particularly in patients with concomitant skeletal muscle necrosis or multiple organ failure complicating carbon monoxide poisoning. Carbon monoxide-induced cardiotoxicity has been investigated rarely in children. CASE REPORT: This paper describes carbon monoxide poisoning in a 12-year-old child who suffered from occult cardiac damage despite mild symptoms and low carboxy hemoglobin concentrations. Myocardial and mitral valve dysfunctions were observed, suggesting an ischemia-like syndrome. Cardiac damage was completely reversible within 1 month. CONCLUSION: This case report supports that a prolonged carbon monoxide exposure can cause cardiac damage in children even in the absence of specific symptoms, cerebral failure and high carboxyhemoglobin concentrations.

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5/27. Selective sparing of face learning in a global amnesic patient.

OBJECTIVE: To test the hypothesis that visual memory for faces can be dissociated from visual memory for topographical material. METHOD: A patient who developed a global amnesic syndrome after acute carbon monoxide poisoning is described. A neuroradiological examination documented severe bilateral atrophy of the hippocampi. RESULTS: Despite a severe anterograde memory disorder involving verbal information, abstract figures, concrete objects, topographical scenes, and spatial information, the patient was still able to learn previously unknown human faces at a normal (and, in some cases, at a higher) rate. CONCLUSIONS: Together with previous neuropsychological evidence documenting selective sparing of topographical learning in otherwise amnesic patients, this case is indicative of the fact that the neural circuits involved in face recognition are distinct from those involved in the recognition of other visuoperceptual material (for example, topographical scenes).

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6/27. Pearls and pitfalls in the approach to patients with neurotoxic syndromes.

neurotoxins are an important cause of neurologic disorders. A vast number of potentially neurotoxic compounds exist, including prescription drugs, illicit substances, and exposures through the workplace, residence, hobbies, and the environment. Effects of neurotoxins can mimic neurologic illnesses; therefore, it is important to consider neurotoxins in the differential diagnosis of any patient with neurological dysfunction. Paramount to the diagnosis of a possible neurotoxic syndrome is establishing causation. This can be done by a systematic approach utilizing principles in epidemiology and applying them to the individual patient. This approach is discussed in the following article in an attempt to bring structure to solving problems in a complex area of medicine.

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7/27. Dissociations in routine behaviour across patients and everyday tasks.

We present a single case study of a patient, FK, who was severely impaired on routine, everyday tasks, such as preparing a cup of tea. We used the action coding system developed by Schwartz et al. to provide quantitative and qualitative measures of his performance in a number of experimental manipulations. In section A, we established FK's baseline performance on a range of tasks with (a) task-congruent objects only and (b) task-congruent objects and semantic distracters. In section B, we aimed to facilitate FK's performance by (a) giving him a pictorial representation of the goal, (b) giving him a set of written commands to follow, (c) giving him one command at a time, (d) demonstrating how the task should be performed and (e) dividing the task into smaller subgoals. We compared FK's performance with another patient, HG, to establish if there are qualitative differences between patients with 'action disorganization syndrome'. In section C, we aimed to hinder FK's performance by interrupting his execution of routine tasks. By comparing the factors that facilitated and impaired FK's performance in sections B and C, we hoped to isolate the key cognitive processes required to generate and control routine behaviour. In section D, we investigated how task demands impact on our ability to complete different everyday activities. The results of these experiments have important clinical implications for rehabilitation programmes for patients with action disorganization syndrome and can also help to distinguish between contemporary theoretical accounts of routine behaviour. In particular, we propose that patients who can be classified under the umbrella term of 'action disorganization syndrome' do not all have a reduction to 'non-specific cognitive resources' but can have qualitatively different impairments to a specialized action production system.

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8/27. rhabdomyolysis and acute renal failure following carbon monoxide poisoning: two case reports with muscle histopathology and enzyme activities.

Two patients with carbon monoxide poisoning are presented, both of whom suffered rhabdomyolysis complicated by acute renal failure. One patient, an attempted suicide, developed a compartment syndrome of the right thigh that required fasciotomy and recovered after a period of hemofiltration and hemodialysis. Muscle biopsy appearances were consistent with partial muscle infarction. The other patient, rescued from a smoke filled room, exhibited raised creatine kinase but no evidence of muscle swelling. He developed anuric renal failure and adult respiratory distress syndrome and died despite maximum intensive care. Muscle biopsy showed early evidence of muscle necrosis. In both cases there was a marked reduction of enzyme activities in the muscle biopsy consistent with metabolic derangement. Although there was a clinical compartment syndrome in the first case, there was no muscle swelling at the time of biopsy or subsequently in the second case. A direct toxic effect of carbon monoxide may thus have been an important mechanism contributing to the muscle necrosis in the second case, although local ischemia may have been an exacerbating factor in the first case.

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9/27. frontal lobe and cingulate cortical metabolic dysfunction in acquired akinetic mutism: a PET study of the interval form of carbon monoxide poisoning.

A middle-aged man suffering from acute carbon monoxide intoxication was clinically assessed to be in an akinetic and mute state. In order to elucidate regional cerebral disturbances, brain metabolism was investigated with fluoro-deoxyglucose positron emission tomography ((18)FDG-PET) 5.5 months after intoxication. Significantly reduced metabolic rates of glucose were revealed in selected brain regions, especially in both the frontal and anterior cingulate cortices, as well as in the subcortical white matter. Frontal and cingulate cortices showed a preserved metabolism of 35-53%, whereas the regional glucose consumption in cerebral white matter was reduced by more than 70%. In contrast, other areas of the brain such as the sensory-motor cortex, parts of the temporal lobes, basal ganglia and brainstem disclosed normal metabolic values. This lesion topography is discussed in relation to the development of akinetic mutism in the present case and in comparison with recent reports on the topic. Considering a plausible pathophysiology, akinetic mutism appears to be based on a different structural neuropathology when compared with the locked-in syndrome and the vegetative state. It is suggested that akinetic mutism is regarded as a specific condition characterized by injury of the frontal neuronal systems which promote executive functions.

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10/27. 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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