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

Extensive water, sodium, chloride, bicarbonate, and potassium losses occur in the diarrheal calf. The water loss is entirely from the extracellular space. In severe cases, hypovolemic shock occurs with the blood volume decreased by as much as one-half. Acidosis, which results from fecal bicarbonate loss, lactic acidosis, and renal dysfunction, results in tissue buffering, which in turn causes the efflux of cellular potassium ions. Although there is a total body potassium deficit, plasma potassium concentration is increased. This, in conjunction with an intracellular deficit, causes weakness, lethargy, and potassium cardiotoxicosis resulting in death. Hypoglycemia also contributes to the weakness and lethargy seem as calves become moribund. These losses from the body and shifts in fluids and electrolytes must be understood to develop the most effective rationale for supportive therapy.
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PMID:Pathophysiologic changes due to coronavirus-induced diarrhea in the calf. 21 8

The continuous infusion of a concentrated, high-caloric glucose solution intravenously into underfed or 3-day-starved rats at a rate of 390 kcal/kg/day results in hypophosphatemia, muscular weakness, neuropathy, lethargy, occasional convulsions, and eventual coma and death. This sequence of events is not observed in similarly infused normal rats. It is a model of a fatal parenteral nutrition syndrome which occurs in undernourished patients. Rats in coma had an eightfold increase in the blood glucose level, a 1.6-fold increase in serum osmolarity, a 16% to 20( decrease in brain water content, and normal blood ketones. A lag phase of at least 8 hr and often 12 to 24 hr occurred following the start of the hyperosmotic glucose infusion before the blood glucose began to accumulate progressively and the syndrome developed. The onset of the syndrome could be prevented by the administration of large amounts of insulin required to keep the blood sugar from exceeding 250 mg/dl. Thus the rat model of the fatal hyperalimentation syndrome is a form of hyperglycemic, hyperosmolar, nonketotic coma caused by brain dehydration.
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PMID:Weakness, neuropathy, and coma following total parenteral nutrition in underfed or starved rats: relationship to blood hyperosmolarity and brain water loss. 21 10

Hyperviscosity syndrome was associated with increased plasma content of monoclonal immunoglobulin (IgA or IgM) in 3 dogs with lymphocytic leukemia. The diagnosis of lymphocytic leukemia was based on the finding of a large number of mature lymphocytes in the blood and bone marrow. The clinical signs included weakness, lethargy, depression, and coughing due to congestive heart failure. Consistent physical findings were splenomegaly, with or without peripheral lymphadenopathy, and funduscopic abnormalities. Of the 2 dogs treated successfully with chlorambucil, 1 remains in remission after withdrawal of the drug for over 1 year.
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PMID:Hyperviscosity syndrome associated with lymphocytic leukemia in three dogs. 40 53

The pathogenesis of the rare hypernatremia, usually described in the literature as "neurogenic" or "essential" hypernatremia, consists of defective thirst mechanism either alone or in combination with impaired osmoregulation of ADH release. As etiology, disturbances of the neoplastic, vascular and degenerative type and malformations in the hypothalamic area are known. In patients with the hypodipsia-hypernatremia syndrome, dysfunction of the anterior pituitary lobe, obesity, abnormal regulation of body temperature, psychomotor retardation and episodic muscular weakness are frequently encountered as additional abnormalities. A 6-year-old patient is described with hypodipsia-hypernatremia syndrome manifest for 3 years. Besides hypernatremia, hypodipsia and the relative insensitivity of the osmoreceptors regulating ADH release, elevated body temperature, polyphagia and obesity, partial hypothalamic-hypophyseal dysfunction, lethargy and psychomotor retardation are the principal findings. An inflammatory lesion or one occupying an intracranial space was not demonstrable until now. Under forced water intake and hypocaloric diet the patient has progressed well with nearly complete normalization of the hypernatremia, body temperature and obesity.
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PMID:Hypodipsia-hypernatremia syndrome. 42 94

A case report of lead poisoning in Canada geese at Cheyenne Bottom Wildlife Management Area in Kansas is presented. Seventy-nine dead geese and 10 geese too weak too fly were found by management personnel. Clinical signs in the live geese were weakness, lethargy, anorexia, emaciation and bile stained diarrhea. Seventeen geese were necropsied. Lesions were impacted roots and fibrous stalks in the esophagus and proventriculus and numerous lead shot in the gizzard. One to 44 lead shot (mean 13) were found in the 17 gizzards examined. The concentration of lead in liver and kidney was 9.21 to 102.56 ug/g (wet weight). The presence of lead shot in the gizzard, characteristic clinical signs, and the concentration of lead in the liver and kidney confirmed the diagnosis of lead poisoning.
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PMID:Lead poisoning in Canada geese: a case report. 49 80

Botulism is a serious intoxication caused by ingestion of food containing preformed botulinus toxin and characterized by rapidly progressive bulbar paralysis, generalized weakness, and respiratory insufficiency. In 1976 a distinct clinical entity of infant botulism was recognized. The disease apparently results from intraintestinal toxin production which produces a defect in neuromuscular transmission by interfering with release of acetylcholine at cholinergic synapses. Five cases of infant botulism were identified at the Children's Hospital of Philadelphia between 1975 and 1977. Initial symptoms included constipation, slow feeding, lethargy and weak cry. Four of the patients progressed to respiratory insufficiency requiring nasotracheal intubation. Three of the infants with respiratory failure required tracheotomy. Because infants with respiratory failure may require support for months, we recommend that a tracheotomy be performed early in the management to avoid the complications associated with prolonged intubation. The effectiveness of antitoxin or antibiotics to treat infant botulism remains questionable and therefore prolonged respiratory supportive care is the mainstay of therapy. In addition, we offer guidelines for decannulation in cases of infant botulism. None of the patients in our series could be decannulated prior to initial discharge from the hospital.
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PMID:Tracheotomy for infant botulism. 51 32

Underfed rats infused intravenously with a glucose-amino acid solution at the rate of 390 kcal/kg/day developed a syndrome of muscular weakness, neuropathy, lethargy and precoma or coma associated with severe hypophosphatemia. The movement of phosphate into the cells was studied to determine where it went and into which organic compounds it was incorporated. All but 8% of the labeled phosphate was found in liver, muscle, bone, and carcass residue. Liver cells took up as much phosphate as bone and twice as much as muscle, on weight basis. About 90% of the labeled phosphate entering liver was found in the acid-soluble fraction. The specific activity of liver phosphate increased in the infused underfed rats compared to uninfused underfed rats. Infusion of the underfed rat until signs of the syndrome appeared was associated with a 2.7- to 5-fold increase over the correspondingly infused normal rat in the labeling of glucose-6-phosphate, glucose-1-phosphate, and 6-phosphogluconate. No increase over the infused normal rat was observed in most of the other sugar phosphate compounds nor in the non-sugar phosphate compounds such as phospholipids, nucleic acids or proteins. he changes in sugar phosphates observed in the underfed rats probably reflect the enzymatic atrophy associated with underfeeding and the consequent inability to respond to the huge glucose load.
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PMID:Intracellular distribution of phosphate in the underfed rat developing weakness and coma following total parenteral nutrition. 82 10

Neuroblastoma is one of the most common malignant neoplasms in infants and children under 5 years of age. The commonest manifestations are abdominal masses or metastases. The case reported showed unusual manifestations as the presenting features simulated myasthenia gravis in all aspects. He was a child, aged 3 years, who was admitted because of generalized weakness, inability to open his eyes and lethargy. Radiography showed an oval opacity at the right upper zone of the chest. A thorocotomy was performed and a tumour was removed from the posterior mediastinum. Histopathology confirmed diagnosis of ganglioneuroblastoma. There is only one similar report in the medical literature.
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PMID:Ganglioneuroblastoma presenting as myasthenia gravis. 86 63

During the summer and fall of 1973, a few horses, goats, and cattle in the Napa Valley of California became intoxicated by bromide via the ingestion of volunteer oat hay that had been cut from a field treated with methyl bromide, a soil fumigant. The bromide content of the hay ranged from 6,00 to 8,400 ppm. Signs of intoxication were lethargy, weakness, and ataxia. Animals experimentally fed the contaminated hay developed signs of intoxication between the 7th and 9th days.
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PMID:Bromide intoxication of horses, goats, and cattle. 90 90

A case of a 76-year-old man with the syndrome of inappropriate secretion of antidiuretic hormone (ADH) is discussed. The patient was initially treated with fluid restriction followed by the administration of hypertonic saline. After failure to achieve rapid correction of the condition and continued lethargy and muscle weakness in the patient, a trial with lithium carbonate 300 mg three times daily via nasogastric tube was initiated. This resulted in a prompt reversal of the hyperosmolar state and improvement in electrolyte balance. However, despite the apparent success in treating his inappropriate ADH, the patient expired as a result of a massive cerebral vascular accident. The potential benefit of using lithium in the treatment of the syndrome of inappropriate secretion of ADH, and possible mechanisms of action, are reviewed.
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PMID:Lithium carbonate treatment in the syndrome of inappropriate secretion of antidiuretic hormone. 92 Jul 46


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