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Thread: CO poisoning case pictures - NEURORADIOLOGY ATLAS

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    Default CO poisoning case pictures - NEURORADIOLOGY ATLAS

    Case Vignette
    Ms. A, a 57-year-old woman with a history notable for alcoholism and depression, attempted suicide by ingesting a large amount of alcohol and medications, then lying down in a bathtub next to a pan of lit charcoal briquettes in a closed room. Police found her some hours later after her therapist called 911 when Ms. A failed to show for a regularly scheduled appointment. She was rushed to a nearby city hospital. On arrival, her vital signs were stable, but she was obtunded; her CO level was elevated (31.7%; normal, < 5%). Quetiapine, zolpidem, oxycodone, and citalopram were present in her serum. She was intubated for airway protection and was transferred to a large general hospital, where she received 1 hyperbaric oxygen (HBO2) treatment at a pressure of 3.0 atm for 90 minutes. Her CO level after HBO2 therapy was 7.3%. She was admitted to the medical intensive care unit, where she was treated for an aspiration pneumonia (with intravenous antibiotics), and she was extubated.

    Her mental status examination was notable for profound psychomotor retardation, hypophonia, and prolonged speech latency. While lying on the bed (hugging a pillow and curled into a fetal position), she exhibited athetoid movements of her trunk, feet, and hands. Her eye contact was poor, her affect was flat, and she manifested word-finding difficulty. She endorsed poor sleep, a lack of interests, feelings of guilt, low energy, poor concentration, lethargy, and a continued desire to end her life. The next week in the general hospital she received antibiotics (for aspiration pneumonia) and hydration for mild rhabdomyolysis. A brain magnetic resonance imaging (MRI) scan revealed a focus in the right globus pallidus consistent with a subacute stroke and no other abnormalities. She was tranferred to the inpatient psychiatric unit for further treatment of her depression and thoughts of suicide.

    Screening neuropsychological tests to assess cognitive deficits included a 100-point Mental Status Examination; her score (97 of 100) was not indicative of gross cognitive impairment. Her score on a test of working memory, the Wechsler Memory Scale Digit Span subtest, was in the normal range, and she reported no subjective cognitive dysfunction. Her psychological evaluation revealed that she was socially detached and had difficulty asserting herself and reaching out to others in times of distress, with no evidence of thought disorder or personality pathology. After 1 week, she was discharged from the unit to a residential program.
    poisoning case pictures NEURORADIOLOGY ATLAS attachment.php?s=1008f426671f0f7f5bcf58b809c2023f&attachmentid=1529&d=1440347185

    Three days after discharge, Ms. A grew more withdrawn, became less communicative, and developed odd, stereotyped movements (such as holding a sock in the air for minutes at a time and slowly crossing and uncrossing her legs). She was admitted to a second inpatient psychiatric unit for depression with catatonic features. Results of screening laboratory tests, a chest x-ray, and an electrocardiogram, as well as her vital signs, were all unremarkable. However, she displayed bizarre posturing and waxy flexibility, frequently grimaced, was mute, had urinary and fecal incontinence, and was resistant to passive movement. She also manifested periodic nonpurposeful athetotic movements in her limbs (e.g., repetitive fanning of the fingers). She was abulic and spoke in short phrases (e.g., “This is torture”). Her muscles were not rigid, and there was no evidence of autonomic instability. Her mental status failed to improve with oral or intramuscular lorazepam; a CO-related encephalopathy was considered. Brain MRI demonstrated new diffuse, bifrontal white matter T2 hyperintensities as well as partial necrosis of the right globus pallidus, consistent with anoxic injury due to CO poisoning. An EEG revealed moderate to severe generalized slowing with diffuse sharp elements intermixed, suggestive of moderate to severe cortical dysfunction; no epileptiform activity was observed. A trial of dextroamphetamine (10 mg daily) led to minimal improvement in her affect and ability to engage with others. After a 16-day hospital stay with negligible change in her clinical status, Ms. A was transferred to a rehabilitation hospital for further care.

    hat Signs and Symptoms Suggest CO Poisoning?
    Carbon monoxide poisoning is a common phenomenon. According to a 1991 study by the Centers for Disease Control and Prevention, 56,133 deaths occurred in the United States because of CO poisoning over a 10-year period from 1979 to 1988. Of that number, 25,889 deaths, or approximately 46% of all CO poisonings, were suicides by CO poisoning.1

    Unfortunately, the symptoms of CO poisoning are subtle and nonspecific. When CO poisoning is mild, it can go unrecognized, as its symptoms can mimic those of other illnesses.2 As a general rule, as the level of CO in the blood (carboxyhemoglobin [COHgb]) increases, so does the severity of symptoms. However, the ability of CO levels to predict sequelae of CO poisoning is poor. At low levels (COHgb < 25%), headache is the most common symptom, and it may be accompanied by malaise, nausea, and dizziness.3 At higher levels (COHgb 25%–50%), mental status changes (including confusion), dyspnea, and syncope may occur. Carboxyhemoglobin levels greater than 50% to 60% often lead to myocardial ischemia, ventricular arrhythmias, pulmonary edema, lactic acidosis, hypotension, coma, seizures, and death.3 Survivors of severe, acute CO poisoning can develop long-term neurologic sequelae (e.g., impairments in memory, concentration, and speech, as well as depression and parkinsonism).4 These sequelae may arise immediately after CO poisoning or may be delayed (occurring 2–21 days after CO poisoning)

    How Does CO Poisoning Cause Damage?
    Carbon monoxide absorption in plasma is diffusion-limited and binds 200 to 250 times more avidly to hemoglobin than oxygen, effectively displacing oxygen from heme-binding sites. CO decreases oxygen saturation in dose-dependent fashion and shifts the oxygen dissociation curve to the left, despite a normal partial pressure of oxygen (PO2). A leftward shift of the oxygen dissociation curve causes decreased binding of oxygen to hemoglobin.

    In addition to binding to hemoglobin, 10% to 15% of CO binds to other proteins, particularly myoglobin within cardiac muscle.5 This binding interferes with oxidative phosphorylation, which is necessary for myocardial contraction, and impairs intracellular mitochondrial cytochrome oxidase function. Chest pain, arrhythmias, hypoperfusion, and myocardial injury/ischemia can occur with moderate exposure.The cardiovascular compensatory mechanisms to maintain O2 concentration in the brain can be overwhelmed by the hypoxemic hypoxia of CO.Nonetheless, the formation of COHgb alone does not account for all the pathophysiologic sequelae. In dog studies, Goldbaum and colleagues9 found that neither the transfusion of erythrocytes containing 80% COHgb nor the intraperitoneal injection of CO gas produced CO toxicity, even though the serum COHgb level was above 50%. Dogs inhaling CO died within 2 hours, with an average COHgb level of 65%. This difference in effect is thought to be related to the compensatory cerebrovascular vasodilation and increased cardiac output to maintain O2 delivery to the central nervous system (CNS). In addition to cardiovascular hypoperfusion, CNS toxicity also occurs from synergistic effects of COHgb-mediated hypoxic stress and intracellular oxidative disruption.

    Multiple hypotheses explain the mechanism by which CO toxicity leads to cerebral injury. There are acute and delayed neuropathologic changes related to direct CO toxicity (i.e., they are independent of hypoxia-induced injury). Animal models and postmortem human studies suggest the following: (1) Neurotoxicity is secondary to a massive release of excitatory amino acids, particularly glutamate. Glutamate release triggers an ischemic cascade that causes excessive calcium influx, free radical–mediated injury, and inhibition of antioxidant defenses.12,13 Carbon monoxide activates neutrophils that produce reactive O2 species and cause brain lipid peroxidation. Peroxidation leads to the degradation of unsaturated fatty acids and the reversible demyelination of CNS lipids.14,15 (3) Carbon monoxide increases the production and deposition of peroxynitrite a potent oxidant) within blood vessel endothelium and brain parenchyma, leading to vascular compromise and cell death in neurons and neuronal cell lines.16) Reoxygenation injury occurs secondary to the production of partially reduced oxygen species, created during HBO2 treatment. Oxygen species can oxidize essential proteins and nucleic acids, creating injury similar to reperfusion damage

    References:
    Complications of Carbon Monoxide Poisoning: A Case Discussion and Review of the Literature











    Last edited by Medical Photos; 08-23-2015 at 04:26 PM.

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