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Despite established exposure limits and safety standards as well as the availability of carbon monoxide (CO) alarms, each year 50,000 people in the United States visit emergency departments for CO poisoning. Rapamycin mTOR inhibitor Carbon monoxide poisoning can occur from brief exposures to high levels of CO or from longer exposures to lower levels. Common symptoms can include headaches, nausea and vomiting, dizziness, general malaise, and altered mental status. Some patients may have chest pain, shortness of breath, and myocardial ischemia, and may require mechanical ventilation and treatment of shock. Individuals poisoned by CO often develop brain injury manifested by neurological problems, including cognitive sequelae, anxiety and depression, persistent headaches, dizziness, sleep problems, motor weakness, vestibular and balance problems, gaze abnormalities, peripheral neuropathies, hearing loss, tinnitus, Parkinsonian-like syndrome, and other problems. In addition, some will have cardiac issues or other ailments. While breathing oxygen hastens the removal of carboxyhemoglobin (COHb), hyperbaric oxygen (HBO2) hastens COHb elimination and favorably modulates inflammatory processes instigated by CO poisoning, an effect not observed with breathing normobaric oxygen. Hyperbaric oxygen improves mitochondrial function, inhibits lipid peroxidation transiently, impairs leukocyte adhesion to injured microvasculature, and reduces brain inflammation caused by the CO-induced adduct formation of myelin basic protein. Based upon three supportive randomized clinical trials in humans and considerable evidence from animal studies, HBO2 should be considered for all cases of acute symptomatic CO poisoning. Hyperbaric oxygen is indicated for CO poisoning complicated by cyanide poisoning, often concomitantly with smoke inhalation. Copyright© Undersea and Hyperbaric Medical Society.Carbon monoxide (CO) exposure is a prevalent cause of poisoning worldwide. The cardiac effects of CO poisoning are well described and can manifest as angina, myocardial ischemia or infarction, cardiogenic shock, and/or life-threatening arrhythmias. Atrial fibrillation has been associated with severe CO poisoning; however, few cases have described atrial fibrillation in acute CO poisoning with regard to hyperbaric oxygen (HBO2) therapy. Herein, we describe a case of severe CO poisoning that caused atrial fibrillation with successful conversion to sinus rhythm following HBO2 therapy and discuss implications for further research. Copyright© Undersea and Hyperbaric Medical Society.Carbon monoxide (CO) poisoning presents with many different cardiac effects, but one important presentation is its effect as a CO stress test to reveal underlying coronary artery disease (CAD). There are a limited number of publications detailing this phenomenon, but after CO intoxication it is important to suspect CAD in association with mild troponin leak or non-ST segment elevation myocardial infarction (NSTEMI) shown on electrocardiogram (EKG). We recently treated three patients with CO poisoning who had underlying CAD. In the first case a man presented to the emergency department with CO toxicity and an ST segment elevation myocardial infarction (STEMI), resulting in emergent angioplasty and the discovery of severe CAD. The second case involved an individual who presented with CO poisoning with rising troponin levels. An angioplasty discovered a stable 90% occlusion. The third case was a patient with CO poisoning and transient inferior T wave inversion EKG with borderline troponin elevation. Angioplasty showed only 30% occlusion, so the patient's presentation was likely due to direct CO cardiac toxicity. These cases demonstrate the varied presentations that CO poisoning can have on patients with underlying heart disease. Copyright© Undersea and Hyperbaric Medical Society.Introduction Altitude chamber exposures are used for training to allow aircrew to experience their hypoxia and pressure effect symptoms. Decompression illness (DCI) can occur subsequent to altitude chamber training or in operational aircraft when the cabin altitude is at least 18,000 feet. Definitive emergent treatment is hyperbaric oxygen (HBO2) to decrease bubble size, dissipate excess nitrogen, hyperoxygenate tissue and reduce inflammation. Case report A 27-year-old female underwent altitude chamber training to 25,000 feet. She developed tingling in both legs and left arm, headache, dizziness, malaise, then difficulty talking. She underwent two HBO2 treatments. Over the next 12 months, she had paresthesia, decreased memory and cognitive function similar to symptoms seen following traumatic brain injury. She was referred 14 months after the event for evaluation. Using pre-deployment Automated Neuropsychological Assessment Metrics (ANAM) and serial tests over 58 HBO2 treatments, the patient demonstrated near-return to her pre-deployment test scores.. Discussion The reason for HBO2 treatment was based on previous experience with chronic traumatic brain injury subjects where HBO2 improved outcome. The patient's chronic neurological symptoms mimicked chronic TBI. The patient was unique in that baseline cognitive tests existed that could be used to monitor her changes during the treatment series. Copyright© Undersea and Hyperbaric Medical Society.Hemorrhagic cystitis (HC) after allogeneic hematopoietic stem cell transplantation (AHSCT) in both children and adults has been associated with significant morbidity and mortality. Early HC can occur within 48 hours of completing the chemotherapy conditioning regimen, is usually associated with agents such as cyclophosphamide, and generally resolves promptly. Late HC is commonly associated with BK and other viruses and can prove refractory to antiviral and supportive therapy. There are limited reports of hyperbaric oxygen (HBO2) therapy showing benefit for refractory HC cases. We describe our experience with salvage HBO2 for a 15-year-old male with refractory HC beginning one month post AHSCT and associated with BK virus. Despite supportive therapies including hyperhydration, forced diuresis, transfusions, intravenous and intravesical cidofovir, macroscopic hematuria persisted and resulted in post-obstructive acute renal failure, need for a suprapubic catheter, then bilateral percutaneous nephrostomy tubes. HBO2 was started two months after the AHSCT and one month after detection of BK viremia.
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