Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clonidine hydrochloride (CH) is an antihypertensive drug with complex pharmacologic activity including central and peripheral alpha-adrenergic stimulation and CNS depression. We reviewed the records of 5 children admitted to our Pediatric Intensive Care Unit following accidental ingestion of CH. All patients presented with lethargy or stupor, beginning 20-60 minutes after ingestion. Respiratory depression or apnea occurred in 4, requiring endotracheal intubation in 2 and mechanical ventilation in 1. All 5 developed mild to moderate hypertension, and 3 developed asymptomatic bradycardia. The dose of CH ingested was estimated to be 0.2-0.4 mg in 4 out of 5 patients. Treatment consisted of efforts to prevent absorption of CH from the GI tract and supportive care. All signs of CH toxicity resolved within 6-14 hours. Four patients were transferred from ICU within 24 hours and discharged home the following day. One patient developed post-extubation stridor and atelectasis. Significant toxicity occurred even though the amount of CH ingested was relatively small in at least 4 or 5 patients. Transient hypertension occurred early in the hospital course of all patients and resolved without treatment. Hypotension and symptomatic bradycardia were not observed. Apnea was the most serious abnormality observed. All patients recovered without significant morbidity.
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PMID:Hypertension associated with clonidine ingestion. 652 27

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

Mycobacterium microti, a member of the Mycobacterium tuberculosis complex, causes tuberculosis in small rodents and occasionally in other mammals including man. Three adult male squirrel monkeys, two with a history of lethargy, weakness and stridor and one with paralysis of the hind legs, were presented for necropsy. One of the two lethargic animals showed multiple granulomas in the mesentery, mesenteric lymph nodes, lung, liver, kidneys and spleen, while the other showed granulomas only in the lung. The animal with paralysis of the legs had an abscess-like lesion in the skeletal muscle of the neck, granulomas in the mesenteric and mediastinal lymph nodes, and a fracture of the thirteenth thoracic vertebra with severe lesions of the spinal cord. Histologically the granulomas showed typical features of tuberculous granulomas, i.e., central necrosis surrounded by epithelioid cells, multinucleated giant cells, inflammatory cells and a border of connective tissue. Ziehl-Neelsen stain demonstrated sporadic acid-fast bacilli within the granulomas, these organisms being identified as M. microti by microbiological and molecular methods.
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PMID:Multiple granulomas in three squirrel monkeys (Saimiri sciureus) caused by Mycobacterium microti. 1788 48

On April 17, 2012, two adult females presented to the hospital with symptoms of botulism. Patient A displayed shortness of breath, increasing lethargy, ptosis, and fixed and dilated pupils, and was intubated after admission. Patient B presented with shortness of breath, vomiting, and stridor. Both patients consumed a meal consisting of a traditionally prepared salted fish, fesikh, on the evening of April 16 during a gathering to celebrate Sham el-Nessim, an Egyptian holiday marking the beginning of spring. Foodborne botulism was suspected based on symptoms and consumption of potentially hazardous food. Antitoxin was administered to both patients on April 18. Another attendee of the Sham el-Nessim gathering (patient C), who also consumed the implicated food, developed symptoms consistent with botulism on April 18. Clinical specimens from all three symptomatic attendees tested positive for either Clostridium botulinum or type E botulinum neurotoxin. Fesikh remaining from the shared meal contained both type E botulinum neurotoxin and C. botulinum type E organisms. Unsold fesikh shad and fesikh sardines tested positive for C. botulinum type E, while unsold fesikh mullet pieces in oil tested positive for both C. botulinum type E and type E botulinum neurotoxin. After consultation with public health investigators, all fesikh products were voluntarily withheld from sale by the manufacturer prior to laboratory confirmation of contamination. Additional illnesses were likely prevented by these precautionary holds, which underscores the importance of timely public health action based on epidemiological evidence available in advance of laboratory results. This is the first documented outbreak of foodborne botulism associated with fesikh to occur in Canada.
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PMID:Outbreak of type E foodborne botulism linked to traditionally prepared salted fish in Ontario, Canada. 2518 79