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)

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

An acute respiratory distress syndrome in 10 adult dogs was usually preceded by vomiting, anorexia and lethargy followed, after a short interval, by dyspnoea. The dyspnoea became increasingly severe, despite oxygen therapy, and cyanotic respiratory failure ensued. All 10 dogs died or were killed after illnesses lasting between one and eight days. Necropsies revealed pulmonary congestion, oedema, collapse and haemorrhage with loss of alveolar epithelial cells. Early alveolar fibrosis was also found. Paraquat was identified in post mortem samples from four of the 10 dogs.
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PMID:Acute respiratory distress in the dog associated with paraquat poisoning. 86 Mar 82

We reported a clinical course and autopsy results of an 8-year-old severely handicapped girl with marked periventricular leukomalacia. She was well until 3 days prior to first admission in local hospital. Two days prior to admission, she began to vomit. Twelve hours later, she was noted to be lethargic and developed malaise with frequent vomiting. At physical examination on admission, she had frequent fits and her posture was decerebrate rigidity. Consciousness disturbance continued for two weeks. Thereafter, she became severely handicapped with spastic quadriplegia, mental retardation and intractable epilepsy. She was transferred to our hospital one month later. We cared her totally and carefully with our rehabilitation staff, but during her course several rare happening occurred; she suffered from subdural hemorrhage due to hypocupremia and received an operation for the release of contracture of her hips. She died of acute cardio-respiratory failure at 8 years and 5 months of age. Her autopsy findings were characteristic of the damage to an immature brain during development; cactus formation of cerebellar cortex and periventricular leukomalacia.
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PMID:[A clinical course and autopsy results of an 8-year-old severely handicapped girl with marked periventricular leukomalacia]. 138 94

Symptomatic viral hepatitis A usually only requires supportive therapy and the majority of cases are managed in the community. The prodromal symptoms of nausea, anorexia and lethargy tend to improve with the onset of clinical jaundice. Fulminant hepatic failure is said to be an uncommon complication, occurring in only 0.14-0.35% of hospitalized cases. However, an increasing incidence has been documented in some northern European countries where up to 20% of cases of fulminant viral hepatitis is due to hepatitis A. This trend parallels the increasingly delayed exposure to hepatitis A and the increased severity of the illness when contracted in later life. The risk of developing fulminant hepatic failure is best monitored using coagulation factor assays, with the prothrombin time and factor V levels being the most favoured. The diagnosis is established with the onset of encephalopathy. Patients progressing to grade 4 encephalopathy have a reasonably good prognosis compared to other aetiologies and survival rates of up to 67% have been obtained with medical management, despite the co-existence of such complications as cerebral oedema, renal and respiratory failure and the metabolic sequelae of acute liver failure. Nevertheless, some patients require emergency liver transplantation and 10 such patients have been reported to date. Transplantation is especially required in older patients (> 40 years) and those who are jaundiced for > 7 days before the onset of encephalopathy. The serum bilirubin and the prothrombin time complement these parameters in the decision making process.
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PMID:Management of acute and fulminant hepatitis A. 147

We describe two siblings who presented with lethargy, decreased sucking, respiratory failure and seizures in their first days of life. Pin-point pupils were noted in both siblings. Amino acid analysis revealed elevated concentrations of glycine in plasma and cerebrospinal fluid (CSF), with abnormal CSF/plasma ratios, compatible with hyperglycinemia. Urine organic acid analysis was unremarkable. Hyperammonemia was found in both siblings, but this subsided within 24-72 h. We suggest that pin-point pupils may be an additional presenting sign of nonketotic hyperglycinemia and, if looked for early enough, hyperammonemia may be found in this disorder.
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PMID:Nonketotic hyperglycinemia presenting with pin-point pupils and hyperammonemia. 155 2

1. We have studied the time course of the numbers of arterial monocytes and their superoxide anion (O2-) production in a chronically instrumented sheep model of subacute endotoxaemia induced by a continuous intravenous infusion of Escherichia coli lipopolysaccharide (20 ng min-1 kg-1). 2. Four out of 11 animals died from irreversible respiratory and cardiovascular failure within 21 h of the start of lipopolysaccharide administration ('non-survivors'), whereas in the seven surviving sheep ('survivors') there was a persistence of decreased systemic vascular resistance, systemic hypotension, pulmonary hypertension, anorexia and lethargy. 3. O2- generation by isolated monocytes was measured by the O2- dismutase-inhibitable reduction of ferricytochrome c after stimulation with phorbol myristate acetate (100 ng/ml) or opsonized zymosan (3 mg/ml). Basal mean value of phorbol myristate acetate-stimulated O2- production was significantly (P = 0.008) higher for non-survivors (31.3 +/- 8.8 nmol 30 min-1 10(-6) cells; n = 4) than for survivors (6.2 +/- 2.3 nmol 30 min-1 10(-6) cells; n = 7). 4. For both survivors and non-survivors, monocyte counts and phorbol myristate acetate-stimulated O2- production increased over time to reach in survivors a plateau after 2 days of continuous lipopolysaccharide infusion. Similar results were obtained when monocytes were stimulated for O2- production with opsonized zymosan. 5. These results suggest that (1) increased O2- production by monocytes and monocytosis appear with a precise, delayed time course during the development of subacute endotoxaemia in sheep; and (2) a high stimulated O2- production by monocytes before lipopolysaccharide administration may represent a predictive factor for the subsequent respiratory failure and outcome of endotoxaemia.
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PMID:Superoxide production by peripheral blood monocytes during sustained endotoxaemia in sheep. 166 89

A 3-day-old girl had a syndrome of lethargy and lactic acidosis. Pregnancy and delivery had been normal; there was no consanguinity or family history of neuromuscular disease. At age 4 1/2 months, she had generalized weakness, hypotonia, areflexia, and macroglossia. She developed cyanosis and respiratory failure, and marked cardiomegaly was noted. She died at age 8 1/2 months of cardiac arrest. Results from a muscle biopsy specimen obtained at age 4 1/2 months showed ragged-red fibers and increased glycogen and lipid droplets. With the cytochrome c oxidase reaction, only 5% of the fibers stained positively in the biopsy specimen. Cytochrome c oxidase activity was 7.3% of normal in muscle mitochondria and 12.2% of normal in heart mitochondria. Reduced-minus-oxidized cytochrome spectra showed lack of the cytochrome aa3 peak. Immunotitration using antibodies against purified human heart cytochrome c oxidase showed normal amount of cross-reacting material in both heart and muscle. The genetic error could have involved a cytochrome c oxidase isozyme common to heart and muscle.
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PMID:Myopathy and fatal cardiopathy due to cytochrome c oxidase deficiency. 302 95

Nine children, hospitalized for severe respiratory failure following scorpion envenomation, were a part of a group of 61 youngsters and infants admitted to the Pediatric Intensive Care Unit of the Soroka Medical Center, Beer-Sheva during the years 1983-87 because of scorpion venom intoxication. Four out of the nine had cardiogenic shock, three had severe systemic hypertension and one had severe airway obstruction. All nine patients had central nervous system manifestations, including lethargy, confusion and agitation (three cases), and markedly reduced level of consciousness (six cases). Hemodynamic studies performed in two patients showed 'high pressure' (cardiogenic) pulmonary edema. Seven patients recovered completely, one died and another one was left severely handicapped. Hydralazine i.v. showed a remarkable effect on the systemic blood pressure and central nervous system disturbances in addition to mechanical ventilation. Based on our own experience and previous clinical and experimental studies, the possible pathogenetic mechanisms underlying the respiratory and central nervous system dysfunction following scorpion sting are discussed.
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PMID:Respiratory failure in children following envenomation by the scorpion Leiurus quinquestriatus: hemodynamic and neurological aspects. 320 82

Two adolescent boys with Kearns-Sayre syndrome (progressive external ophthalmoplegia, heart block, elevated CSF protein, and ragged-red muscle fibers) developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria after a brief course of steroid therapy. Both had hyperglycemia and acidosis. Nonketotic, lactic acidosis was present in one and ketosis in the other. Severe respiratory failure developed, and both patients died. Postmortem revealed fatty infiltration of the pancreas in addition to a diffuse spongiform encephalopathy.
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PMID:Fatal metabolic acidosis, hyperglycemia, and coma after steroid therapy for Kearns-Sayre syndrome. 370 1

This paper presents the clinical and metabolic findings in two young boys with long-standing Kearns-Sayre syndrome. Following short exposure to oral prednisone, both boys developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria. Both presented in the emergency room with profound coma, hypotension, severe hyperglycemia, and acidosis. Nonketotic lactic acidosis was present in one and ketosis without a known serum lactate level was present in the other. Respiratory failure rapidly ensued and both patients expired in spite of efforts at resuscitation. We believe these two cases represent a newly described and catastrophic metabolic-endocrine failure in the Kearns-Sayre syndrome.
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PMID:Hyperglycemic acidotic coma and death in Kearns-Sayre syndrome. 370 9


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