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)

Few studies have been published about analgesic management practices during sickle cell pain crisis. Therefore, we reviewed the records of all hospitalized children with this complication during a recent five-year period. The 38 patients (98 painful episodes) who received intravenous narcotic therapy were the subjects of this review. In 76 patients, an initial intravenous bolus injection of morphine sulfate or meperidine hydrochloride was followed by a continuous intravenous infusion of one of these two drugs. To achieve adequate pain control, adjustments in infusion rates were made according to a written protocol. In 22 other patients, subsequent narcotic treatment consisted only of intermittent intravenous bolus injections of meperidine. Satisfactory pain relief was achieved in all 98 episodes. Patients given continuous infusions required more narcotic to control their pain and had more side effects than those treated with bolus injections alone, suggesting a dose-response relationship between narcotic dose and several known side effects. Common side effects included nausea and vomiting, lethargy, and abdominal distention. Although clinically evident respiratory depression was quite uncommon, chest syndrome was a frequent complication, and severe respiratory distress occurred in three patients. Narcotic withdrawal or addiction was not observed. With careful monitoring (including special attention directed to avoiding dosing error), continuous intravenous narcotic infusions are safe and provide effective pain relief for severe sickle cell pain crisis.
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PMID:Intravenous narcotic therapy for children with severe sickle cell pain crisis. 377 42

Five cases of coagulopathy caused by consumption of indanedione (diphacinone)-based rodenticides are reported. In each case, acute onset of lethargy and respiratory distress were the predominant initial clinical signs. Thoracic radiography revealed pulmonary edema, pleural effusion, and/or pericardial effusion as consistent findings. Laboratory evaluations confirmed coagulopathies that responded to vitamin K1 therapy.
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PMID:Diphacinone-induced coagulopathy in the dog. 394 17

We reviewed clinical data in 33 patients with transient hyperammonemia of the newborn (THAN): six previously unreported cases and 27 from the literature. Thirteen neonates with urea cycle enzyme deficiencies (UCED) served for comparison. No differences were found in the incidence of perinatal complications, route of delivery, Apgar scores, sex, or incidence or time of onset of seizures. On the other hand, neonates with THAN had significantly lower birth weights (mean +/- SEM 2282 +/- 78 gm vs 3336 +/- 222 gm, P less than 0.001) and gestational ages (35.1 +/- 0.5 weeks vs 39.6 +/- 0.5 weeks, P less than 0.001). Mean time of onset of respiratory distress (3.9 +/- 1.4 hours vs 71.5 +/- 26.1 hours, P less than 0.001), ventilatory support (P less than 0.001), lethargy (P less than 0.005), and coma (P less than 0.005) occurred earlier in THAN. Distinctive laboratory findings in patients with THAN included abnormal chest radiographic findings and plasma ammonium concentrations that were higher (1871 +/- 209 microM vs 973 +/- 169 microM, P less than 0.02) at an earlier age. Respiratory distress occurred in all but one patient with THAN before 24 hours; in contrast, only 62% of infants with UCED had respiratory symptoms, and none before 30 hours. In this retrospective study, the clinical presentation alone differentiated THAN from UCED.
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PMID:Differentiation of transient hyperammonemia of the newborn and urea cycle enzyme defects by clinical presentation. 405 69

Two female infants with nonketotic hyperglycinemia (NKH) were treated with diazepam for the control of seizures. The first infant had seizures, lethargy, and respiratory distress in the first 24 hours of life. The diagnosis of NKH was made at 3 weeks of age and she was then placed on a regimen of strychnine and a low-protein diet. Strychnine therapy was discontinued after three months of treatment because there was no improvement in the seizure control or in the patient's condition. At 5 months of age the patient was referred to our clinic for further work-up. The second infant had seizures, hypotonia, and respiratory distress shortly after birth. She was treated with phenobarbital and diphenylhydantoin, which had no effect on her seizures. The baby was referred to our clinic at 8 months of age and diagnostic studies revealed NKH. All previous medications were stopped and both infants were placed on diazepam, a competitor for glycine receptors in the CNS. Choline and folic acid were added for one-carbon unit transfer and sodium benzoate to bind excessive glycine. Both infants responded to this treatment with cessation of seizures; they became more responsive and alert, and their EEGs showed remarkable improvement despite the persistence of elevated glycine levels in plasma, CSF, and urine. Diazepam as a competitor for the receptors of glycine may prove helpful in controlling the intractable seizures associated with NKH.
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PMID:Nonketotic hyperglycinemia: treatment with diazepam--a competitor for glycine receptors. 630 Jul 46

A symptomatic elevation in plasma ammonium concentration, termed hyperammonemia, is associated with numerous congenital and acquired conditions (Table 11). In some cases, such as urea cycle disorders, ammonia is the principal toxin. In other instances, such as portal systemic encephalopathy, it is but one of a number of metabolic disturbances, However, in either case hyperammonemic episodes should be treated aggressively to prevent coma, subsequent brain damage, or death. This involves restricting protein intake, providing adequate calories, and giving agents that remove accumulated nitrogen. Long-term therapy relies on diagnosing the specific disease rate. This rarely requires invasive procedures such as liver biopsy. In most cases measurement of plasma amino acids and urinary organic acids will identify the defect. Treatment involving restriction of nitrogen intake, vitamin supplementation, or stimulation of alternative pathways of waste nitrogen excretion can then be instituted. Early therapy, especially in patients with neonatal-onset hyperammonemia, is imperative to avoid severe brain damage. On this basis, the plasma ammonium level should be determined in virtually every newborn with lethargy, hypotonia, poor feeding, seizures, and/or respiratory distress of unclear origin (Table 12).
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PMID:Hyperammonemia. 651 17

Mycoplasma pneumonia usually follows a benign course and the patient does not require hospitalization. The present report summarizes the feature of eight children admitted for a moderately severe pneumonia during an epidemic of Mycoplasma pneumoniae in Victoria. All children were previously healthy. The usual presenting symptoms included cough, fever, lethargy, and weight loss. All children had moderately severe respiratory distress and physical signs in the chest consistent with extensive parenchymal involvement. Half of this group had radiological evidence of a small pleural effusion. Complement fixation titres for Mycoplasma pneumoniae in paired samples confirmed the diagnosis. Clinical and radiological resolution was complete after one to three months. It is suggested that severe mycoplasma pneumonia may be more common than previously appreciated.
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PMID:Severe mycoplasma pneumonia in previously healthy children. 721 82

Excessive unexplained mortality was observed in flocks of double-crested cormorants located at Snake Island in Green Bay, Michigan, in June 1992. Clinical signs included weakness, lethargy, diarrhea, respiratory distress, paralysis of the wings and legs, torticollis, and incoordination. The most significant and consistent gross lesions included edema of the eyelids and periocular tissues, pulmonary edema and congestion, marked splenomegaly, hepatic necrosis, and scattered hemorrhages in visceral organs. Histologically, the principal alterations were severe lymphocytic meningoencephalitis and myelitis, as well as splenic lymphoid necrosis with hemorrhage. A type 1 paramyxovirus was isolated from the affected birds and characterized as a velogenic neurotropic strain of Newcastle disease virus. Since the infection occurred in free-living migratory birds, there exists the potential for spread of the virus over a large area, thus posing a hazard to domestic poultry.
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PMID:Neurotropic velogenic Newcastle disease in cormorants in Michigan: pathology and virus characterization. 770 23

Whole-carcass residues of the rodenticide zinc phosphide (Zn3P2) and hydrolyzed phosphine (PH3) were determined for voles (Microtus spp.) that died following ingestion of a 2% Zn3P2 steam rolled oat (SRO) groats bait. Procedures involved: a three-day acceptance test to assess vole consumption (n = 27) of control SRO groats and several one-day Zn3P2- (n = 13) or control-bait (n = 4) tests to characterize onset of pharmacotoxic signs and to obtain fatally-dosed carcasses for residue analyses. Carcasses were stored in liquid nitrogen (LN2) to maximize retention of Zn3P2/PH3 residues prior to chemical determinations. Linear regressions were computed between pairs of consumption and residue variables. Main results were the following: (1) mean (+/- SD) consumption of control bait was 2.5 (+/- 0.9), 3.0 (+/- 0.9), and 2.8 (+/- 0.8) g on days 1, 2, and 3, respectively (> or = 10.6 +/- 4.6% of body weight); (2) all test-bait voles (n = 13) died approximately 4-12 h after bait presentation, with lethargy and respiratory distress key signs of toxicosis; (3) whole-carcass Zn3P2 residues averaged 1.73 mg (min-max: 0.31-4.95), and PH3 residues averaged 10.6 micrograms (min-max: 0.5-21.0); and (4) significant linear regressions were found between bait consumption/Zn3P2 intake and body weight (r2 = 0.64, p < or = 0.001), carcass Zn3P2 and bait consumption/Zn3P2 intake (r2 = 0.32, p < or = 0.043), and carcass Zn3P2 and body weight (r2 = 0.60, p < or = 0.002). Certain analytical and hazards issues are discussed.
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PMID:Regressors of whole-carcass zinc phosphide/phosphine residues in voles: indirect evidence of low hazards to predators/scavengers. 775 4

Multiple submissions of bobwhite quail (Colinus virginianus) were received for diagnosis from a commercial-size quail operation. The history and clinical signs included respiratory distress, lethargy, and substantial mortality. Reovirus was recovered from quail in the first submission, and both reovirus and adenovirus were isolated from later submissions. To determine the pathogenicity of the isolated reovirus, the initial isolate was inoculated into young quail from a different source. Those inoculated by the subcutaneous route became lethargic, and more than half died during the 2 weeks of the trial. Reovirus was recovered from a high percentage of those inoculated by this route. To the authors' knowledge, the isolation of reovirus from quail has rarely been reported, and reovirus has never before been suggested as a pathogen in this species.
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PMID:Reovirus associated with excessive mortality in young bobwhite quail. 814 44

An outbreak of narasin poisoning in swine is described. Forty nine out of 108 lactating sows died over a period of one month after being fed a ration accidentally contaminated with narasin. Clinical signs included anorexia, respiratory distress, lethargy and posterior paresis, progressing to lateral recumbency and death. Necropsy examination in 3 pigs revealed extensive myocardial and skeletal muscle damage. Analysis of the feed confirmed the presence of high concentrations of narasin.
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PMID:An outbreak of narasin poisoning in swine. 849 96


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