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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hydrogen peroxide is an oxidising agent that is used in a number of household products, including general-purpose disinfectants, chlorine-free bleaches, fabric stain removers, contact lens disinfectants and hair dyes, and it is a component of some tooth whitening products. In industry, the principal use of hydrogen peroxide is as a bleaching agent in the manufacture of paper and pulp. Hydrogen peroxide has been employed medicinally for wound irrigation and for the sterilisation of ophthalmic and endoscopic instruments. Hydrogen peroxide causes toxicity via three main mechanisms: corrosive damage, oxygen gas formation and lipid peroxidation. Concentrated hydrogen peroxide is caustic and exposure may result in local tissue damage. Ingestion of concentrated (>35%) hydrogen peroxide can also result in the generation of substantial volumes of oxygen. Where the amount of oxygen evolved exceeds its maximum solubility in blood, venous or arterial gas embolism may occur. The mechanism of CNS damage is thought to be arterial gas embolisation with subsequent brain infarction. Rapid generation of oxygen in closed body cavities can also cause mechanical distension and there is potential for the rupture of the hollow viscus secondary to oxygen liberation. In addition, intravascular foaming following absorption can seriously impede right ventricular output and produce complete loss of cardiac output. Hydrogen peroxide can also exert a direct cytotoxic effect via lipid peroxidation. Ingestion of hydrogen peroxide may cause irritation of the gastrointestinal tract with nausea, vomiting, haematemesis and foaming at the mouth; the foam may obstruct the respiratory tract or result in pulmonary aspiration. Painful gastric distension and belching may be caused by the liberation of large volumes of oxygen in the stomach. Blistering of the mucosae and oropharyngeal burns are common following ingestion of concentrated solutions, and laryngospasm and haemorrhagic gastritis have been reported. Sinus tachycardia, lethargy, confusion, coma, convulsions, stridor, sub-epiglottic narrowing, apnoea, cyanosis and cardiorespiratory arrest may ensue within minutes of ingestion. Oxygen gas embolism may produce multiple cerebral infarctions. Although most inhalational exposures cause little more than coughing and transient dyspnoea, inhalation of highly concentrated solutions of hydrogen peroxide can cause severe irritation and inflammation of mucous membranes, with coughing and dyspnoea. Shock, coma and convulsions may ensue and pulmonary oedema may occur up to 24-72 hours post exposure. Severe toxicity has resulted from the use of hydrogen peroxide solutions to irrigate wounds within closed body cavities or under pressure as oxygen gas embolism has resulted. Inflammation, blistering and severe skin damage may follow dermal contact. Ocular exposure to 3% solutions may cause immediate stinging, irritation, lacrimation and blurred vision, but severe injury is unlikely. Exposure to more concentrated hydrogen peroxide solutions (>10%) may result in ulceration or perforation of the cornea. Gut decontamination is not indicated following ingestion, due to the rapid decomposition of hydrogen peroxide by catalase to oxygen and water. If gastric distension is painful, a gastric tube should be passed to release gas. Early aggressive airway management is critical in patients who have ingested concentrated hydrogen peroxide, as respiratory failure and arrest appear to be the proximate cause of death. Endoscopy should be considered if there is persistent vomiting, haematemesis, significant oral burns, severe abdominal pain, dysphagia or stridor. Corticosteroids in high dosage have been recommended if laryngeal and pulmonary oedema supervene, but their value is unproven. Endotracheal intubation, or rarely, tracheostomy may be required for life-threatening laryngeal oedema. Contaminated skin should be washed with copious amounts of water. Skin lesions should be treated as thermal burns; surgery may be required for deep burns. In the case of eye exposure, the affected eye(s) shod eye(s) should be irrigated immediately and thoroughly with water or 0.9% saline for at least 10-15 minutes. Instillation of a local anaesthetic may reduce discomfort and assist more thorough decontamination.
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PMID:Hydrogen peroxide poisoning. 1529 93

The remarkable time-resolution enhancement by deep lethargic hypothermia (15 degrees C rectal temperature, "cold narcosis," "anesthesia by internal cold") of metabolic events in the rat brain after oxygen deprivation has been exploited to monitor metabolic changes by in vivo (31)P-NMR. A correlation was established between the bioenergetic status of the brain and physiological descriptors of tolerance (survival and revival times) determined in parallel experiments with large series of animals. Spectral peak integrals were transformed into absolute concentrations by comparison to biochemically determined time series of data obtained in freeze-trapping experiments conducted under identical conditions. Serial spectra were used to reconstruct the time-course kinetics of intracellular brain pH and of concentration changes of inorganic phosphate, phosphocreatine, ATP, and ADP. Both the biochemical and NMR time series of data were simultaneously fitted by a set of exponential kinetic equations accounting for relationships imposed by the Lohmann and adenylate kinase reactions. Depletion profiles were then computed for a number of descriptors of brain energy status (energy charge, phosphorylation potential, total adenylate, and primary energy stores expressed as the sum of high-energy phosphate-bond equivalents). The results contribute to the understanding of the role of brain energetics in tolerance to oxygen deprivation.
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PMID:Brain energetics and tolerance to anoxia in deep hypothermia. 1615 18

The toxic effects of four commercial detergents (two washing powders and two cakes) are reported in this paper on behavior, mortality and RBC counts of a freshwater fish Gambusia affinis. During acute toxicity studies (96h), surface movements of fish increased markedly for 24h, only at higher concentrations (>10 ppm) of all the four detergents. Thereafter, they were lethargic and bottom dwellers similar to those exposed for a period of 30 days in the longterm ecotoxicological studies made on detergent powders at a sublethal concentration (10 ppm). The detergents exposed to fish were found slippery due to mucous secretion. Hemorrhage regions were also found on their gills. The dissolved oxygen content also decreased (10-18%) in the detergent treatments of higher concentration (> 10 ppm). During acute toxicity studies, cakes (LC50 = 6.69 - 19.98ppm) were found more toxic than powders (LC50 = 18.34-20.72ppm). In comparison to the control fish, RBC counts decreased (12-64%) in the detergent exposed fish, being more pronounced among those exposed to cakes. The chronic exposure (30 days) of the fish also resulted in reduction in the RBC counts (41-58%). It is thus evident that all the four detergents are toxic to the fish Gambusia affinis.
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PMID:Effect of an acute and chronic toxicity of four commercial detergents on the freshwater fish Gambusia affinis Baird & Gerard. 1664 15

Rosiglitazone is a peroxisome proliferator active receptor. gamma agonist, which increases insulin sensitivity in adipose tissue, muscle, and liver. Rosiglitazone is a member of the thiazolidinedione group, and because of its significantly positive effect on glycemic control, it is especially preferred in type 2 diabetic patients with a high cardiovascular disease risk. This drug, because of its decreasing effect on insulin resistance, is used alone or combined with type 2 diabetic drugs. A 73-year-old female patient was admitted to the emergency department with dyspnea, pink frothing phlegm, cyanosis, and tiredness. She was lethargic, uncooperative, and had no orientation. In arterial blood gases, hypoxemia and hypercapnia were found. She was taken to the general intensive care unit, and oxygen was applied via mask. The patient had a history of 10 years of diabetes mellitus, hypertension, and atherosclerotic cardiac disease, and she was using rosiglitazone for the past 6 weeks. Her chest x-ray was taken, and acute pulmonary edema was diagnosed. In her last echocardiography, which was performed 1 year before, no signs indicating cardiac failure and pleural effusion could be found. Therefore, it was concluded that pulmonary edema occurred as a complication of rosiglitazone use. After stabilizing the patient's vital signs, blood glucose levels, and lactate levels, medical treatment of diabetes mellitus was rearranged, and she was discharged on the seventh day after her admittance. In a patient with diabetes mellitus who has been admitted to the intensive care unit because of acute pulmonary edema, for differential diagnosis, use of rosiglitazone should be kept in mind during the determination of treatment. Therefore, the authors aim to discuss the effect of rosiglitazone on creating acute pulmonary edema with a case report presentation.
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PMID:Acute pulmonary edema due to rosiglitazone use in a patient with diabetes mellitus. 1669 44

Metformin is a biguanide. Due to its effects in suppressing the hepatic production of endogenous glucose and in increasing insulin sensitivity in adipose tissue and skeletal muscle, the agent is used particularly in type 2 diabetes mellitus and metabolic syndrome, in which insulin resistance is especially pronounced. Lactic acidosis is one of the most important side effects of metformin. A male patient, born in 1923, was admitted to the emergency unit of our hospital for sudden vertigo, weakness, dyspnea, cyanosis, and lethargy. His history data showed that the patient had been suffering from type 2 diabetes mellitus for 10 years and taking Glargin (insulin), 12 U/kg, once daily and Glucophage (metformin), 850 mg thrice daily. The patient's general condition was fair; stupor, time and spatial orientation were absent. Analysis of arterial blood gases showed the presence of metabolic acidosis, hypokalemia, hypoxemia, and hypercapnia. Thereafter the patient was transferred to the intensive care unit of the hospital; intubated and connected to a T-bird ventilation apparatus. On the following day, an analysis of arterial blood gases indicated the proximity of the results to their physiological parameters. Ventilation was stopped; and monitoring of the patient continued by following the T-shape type of ventilation discontinuation. There were no X-ray signs of pneumonia or pulmonary edema. On the same day, the patient was extubated and oxygen inhalation in a dose of L/min was continued through a mask. On day 4 since therapy was initiated, the patient's vital signs, serum sugar and lactate levels became normal. By determining a new treatment regimen, the patient was discharged from the intensive care unit. Dyspnea, acidosis, and hypoxia developed in the patient resulted from lactic acidosis caused by the use of metformin. It should be remembered that dyspnea, acidosis, and hypoxia, which suddenly developed in metformin-treated patients with type 2 diabetes mellitus, may be caused by lactic acidosis.
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PMID:[A clinical case of development of lactic acid acidosis in a diabetic patient taking metformin]. 1675 49

Here, we report the case of a five-year-old boy with carbonic monoxide (CO) poisoning. The patient initially recovered after the initiation of hyperbaric oxygen (HBO) therapy, but lethargy as well as visual and gait disturbances appeared two days later. Left hemiparesis and mood lability also subsequently appeared. Slow frontal activity was noted on electroencephalography, while fluid-attenuation inversion recovery and diffusion-weighted magnetic resonance imaging (MRI) revealed high signal-intensity lesions in the hippocampus and deeper layers of the occipital and frontal cerebral cortex. The neurological symptoms subsided gradually during the 10-day course of HBO therapy, but the left-hand paresis and quadrantic hemianopsia persisted, in association with impaired attention, slow mental processing, and incontinence. Lesions in the globus pallidum were noted on follow-up MRI at 14 days, and cortical lesions became evident as linear, low signal-intensity areas on T1-weighted imaging 4 months after presentation. Delayed neuropsychiatric syndrome in CO poisoning is rare in childhood, although children should be carefully monitored after CO exposure. The finding of cortical laminar necrosis in this patient is quite atypical in CO poisoning, and suggests a broader and previously nonpredicted pathomechanism in this condition.
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PMID:Delayed neuropsychiatric syndrome in a child following carbon monoxide poisoning. 1700 41

Angina pectoris is usually the first clinical sign of underlying myocardial ischemia, which results from an imbalance between oxygen supply and oxygen demand in the heart. This report describes the pharmacology of beta-adrenoceptor antagonists as it relates to the treatment of angina. The beta-adrenoceptor antagonists are widely used in long-term maintenance therapy to prevent acute ischemic episodes in patients with chronic stable angina. Beta-adrenoceptor antagonists competitively inhibit the binding of endogenous catecholamines to beta1-adrenoceptors in the heart. Their anti-ischemic effects are due primarily to a reduction in myocardial oxygen demand. By decreasing heart rate, myocardial contractility and afterload, beta-adrenoceptor antagonists reduce myocardial workload and oxygen consumption at rest as well as during periods of exertion or stress. Predictable adverse effects include bradycardia and cardiac depression, both of which are a direct result of the blockade of cardiac beta1-adrenoceptors, but adverse effects related to the central nervous system (eg, lethargy, sleep disturbances, and depression) may also be bothersome to some patients. Beta-adrenoceptor antagonists must be used cautiously in patients with diabetes mellitus, peripheral vascular disease, heart failure, and asthma or other obstructive airway diseases. Beta-adrenoceptor antagonists may be used in combination with nitrates or calcium channel blockers, which takes advantage of the diverse mechanisms of action of drugs from each pharmacologic category. Moreover, concurrent use of beta-adrenoceptor antagonists may alleviate the reflex tachycardia that sometimes occurs with other antianginal agents.
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PMID:Antianginal actions of beta-adrenoceptor antagonists. 1799 92

To study effects of mitochondrial complex I (CI, NADH:ubiquinone oxidoreductase) deficiency, we inactivated the Ndufs4 gene, which encodes an 18 kDa subunit of the 45-protein CI complex. Although small, Ndufs4 knockout (KO) mice appeared healthy until approximately 5 weeks of age, when ataxic signs began, progressing to death at approximately 7 weeks. KO mice manifested encephalomyopathy including a retarded growth rate, lethargy, loss of motor skill, blindness, and elevated serum lactate. CI activity in submitochondrial particles from KO mice was undetectable by spectrophotometric assays. However, CI-driven oxygen consumption by intact tissue was about half that of controls. Native gel electrophoresis revealed reduced levels of intact CI. These data suggest that CI fails to assemble properly or is unstable without NDUFS4. KO muscle has normal morphology but low NADH dehydrogenase activity and subsarcolemmal aggregates of mitochondria. Nonetheless, total oxygen consumption and muscle ATP and phosphocreatine concentrations measured in vivo were within normal parameters.
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PMID:Mice with mitochondrial complex I deficiency develop a fatal encephalomyopathy. 1839 29

ABSTRACT Body packers are people who illegally carry drugs, mostly cocaine as well as opium and/or heroin, concealed within their bodies. The packets are inserted in the mouth, rectum, or vagina in order to get across borders without being detected. In this presentation we report a case of an opium body packer and review the available scientific literature by focusing on mechanisms of toxicity and treatment approach. The patient was a 35-year-old man who had lethargy, respiratory depression, tachycardia, normal blood pressure, hyperthermia, and pinpoint pupils on presentation. No past medical history was obtained and the only positive history was his travel from Afghanistan 2 days earlier, which he had given to emergency personnel before arriving at our hospital. Complete blood cells and kidney and liver tests were all in normal range. In the emergency department, the patient was treated with oxygen, naloxone, and hypertonic glucose. One dose of activated charcoal (1 g/kg) was administered orally. After intravenous injection of naloxone (4 mg), the lethargy, respiratory depression, and miosis were resolved. The patient was admitted to the intensive care unit and 90 min after admission, the patient redeveloped respiratory distress and lost consciousness. He was intubated and mechanically ventilated due to the suspicious of body packing. Plain abdominal x-ray showed multiple packets throughout the gastrointestinal tract; 81 packets were removed by surgery and three of them were left due to leaking. After removing the packets, the patient was treated conservatively. He suffered a pulmonary infection (aspiration pneumonia) and he regained consciousness after 4 days. Upon recovery the patient was seen by a psychiatrist prior to going to prison. Surgery is recommended for body packers who have significant signs or symptoms.
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PMID:A case report of opium body packer; review of the treatment protocols and mechanisms of poisoning. 2002 Sep 70

A series of artificial microcosms was used to test the effect of clam density on benthic iron biogeochemistry and, subsequently, if the response of clam Ruditapes decussatus to infection with Perkinsus olseni, a common opportunistic parasite known to be iron dependent, was correlated with the dynamics of iron sediment pore waters within the chambers. Three series of benthic microcosms were used in the experiment, comparing similar densities of clams (none, one, two, three, or four individuals/chamber) between a control set (no deliberate infection) and two parallel sets of clams that were deliberately infected with the parasite after 10 days of incubation. Fifteen chambers were used simultaneously and the experiment was conducted for 35 days. In order to avoid spurious effects of differential organic loading and clam feeding efficiency on the oxidative state of the sediment, the iron balance was tentatively shifted during incubation toward decreased dissolved iron in pore water. This was done by applying a constant flow of air to all chambers and refraining from supplying extra organic matter during the experimental run, which led to the reduction of benthic oxygen demand as the experiment progressed. Results showed that microcosms bearing both higher clam densities and lower infection levels were able to exert a quantitative influence in iron biogeochemistry through bioturbation activity. This effect was significantly depressed in chambers hosting clams with high infection levels. In addition, analysis of molecular markers responsive to iron and parasite stress revealed an upper regulation of HSP70 and ferritin in infected clams, thus suggesting a role of those molecules on both host protection and response to parasite presence by limiting iron availability. Together, these findings suggest a correlation between the expression of clam molecular iron/stress markers and iron bioavailability, which can be modified by the presence or absence of Perkinsus infection. In turn, we propose that clam lethargy in response to parasite invasion might help to combat infection by reducing iron mobilization in the surrounding sediment through a decrease in bioturbation activity, thus reducing its availability to the parasite.
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PMID:Changes in bioturbation of iron biogeochemistry and in molecular response of the clam Ruditapes decussates upon Perkinsus olseni infection. 2023 99


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