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Query: UMLS:C0023380 (
lethargy
)
5,697
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
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.
...
PMID:Acute respiratory distress in the dog associated with paraquat poisoning. 86 Mar 82
Primary hypoadrenocorticism was diagnosed in ten young to middle-aged cats of mixed breeding. Five of the cats were male, and five were female. Historic signs included
lethargy
(n = 10), anorexia (n = 10), weight loss (n = 9), vomiting (n = 4), and polyuria (n = 3). Dehydration (n = 9), hypothermia (n = 8), prolonged capillary refill time (n = 5), weak pulse (n = 5),
collapse
(n = 3), and sinus bradycardia (n = 2) were found on physical examination. Results of initial laboratory tests revealed anemia (n = 3), absolute lymphocytosis (n = 2), absolute eosinophilia (n = 1), and azotemia and hyperphosphatemia (n = 10). Serum electrolyte changes included hyponatremia (n = 10), hyperkalemia (n = 9), hypochloremia (n = 9), and hypercalcemia (n = 1). The diagnosis of primary adrenocortical insufficiency was established on the basis of results of adrenocorticotropic hormone (ACTH) stimulation tests (n = 10) and endogenous plasma ACTH determinations (n = 7). Initial therapy for hypoadrenocorticism included intravenous administration of 0.9% saline and dexamethasone and intramuscular administration of desoxycorticosterone acetate in oil. Three cats were euthanatized shortly after diagnosis because of poor clinical response. Results of necropsy examination were unremarkable except for complete destruction of both adrenal cortices. Seven cats were treated chronically with oral prednisone or intramuscular methylprednisolone acetate for glucocorticoid supplementation and with oral fludrocortisone acetate or intramuscular injections of repository desoxycorticosterone pivalate for mineralocorticoid replacement. One cat died after 47 days of therapy from unknown causes; the other six cats are still alive and well after 3 to 70 months of treatment.
...
PMID:Primary hypoadrenocorticism in ten cats. 246 93
Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular
collapse
and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular
collapse
, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness,
lethargy
, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
...
PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13
Two weeks after daily topical application of hexachlorophene, a 4-week-old female kitten developed cardiovascular
collapse
, corneal ulcers, trembling,
lethargy
, and weakness. The kitten was euthanatized. At necropsy, the tissues appeared macroscopically normal; however, microscopic examination of tissue specimens indicated status spongiosis, astrocytosis, and microgliosis of the cerebral and cerebellar white matter and corticospinal tracts. Neuronal cell bodies forming the affected white matter were intact, indicating that demyelination may have been the cause of the lesions. The neurologic lesions were considered compatible with those of hexachlorophene-induced toxicosis.
...
PMID:Neurotoxicosis associated with the use of hexachlorophene in a cat. 358 87
Atherosclerosis was diagnosed on necropsy in 21 dogs in a 14-year period. Nine dogs died and 12 were euthanatized because of complications associated with the disease. The mean age was 8.5 +/- 0.5 years; 18 dogs were male. Three breeds (Miniature Schnauzer, Doberman Pinscher, and Labrador Retriever) had a higher prevalence of the disease than other breeds in the canine necropsy population of The Animal Medical Center. Most common clinical signs were
lethargy
, anorexia, weakness, dyspnea,
collapse
, and vomiting. Hypercholesterolemia, lipidemia, and hypothyroidism were common in affected dogs tested, and protein electrophoresis revealed high values for alpha 2 and beta fractions in all dogs tested. Electrocardiography indicated conduction abnormalities and myocardial infarction in 3 of 7 dogs. Necropsy revealed that affected arteries (including coronary, myocardial, renal, carotid, thyroidal, intestinal, pancreatic, splenic, gastric, prostatic, cerebral, and mesenteric) were yellow-white, thick and nodular, and had narrow lumens. Myocardial fibrosis and infarction also were observed in the myocardium. Histologically, affected arterial walls contained foamy cells or vacuoles, cystic spaces, mineralized material, debris with or without eroded intima, and degenerated muscle cells.
...
PMID:Clinical and pathologic findings in dogs with atherosclerosis: 21 cases (1970-1983). 374 84
Nineteen cases of primary autoimmune haemolytic anaemia are reported in the dog. The clinical features included pale mucous membranes, weakness,
lethargy
and
collapse
. The intravascular haemolytic type of the disease was seen in nine cases and was characterised by evidence of haemolysis (eg, marked bilirubinaemia). The other 10 cases were classed as the extravascular destructive type of autoimmune haemolytic anaemia. The presence of autoantibodies (of the IgG class) and complement (C3) on the red blood cells from affected patients was demonstrated by a commercial Coombs' (antiglobulin) test which, although it has disadvantages, is satisfactory providing it is interpreted in association with the clinical, haematological and biochemical features. Treatment of these 19 dogs was with prednisolone and was successful in most cases.
...
PMID:Primary autoimmune haemolytic anaemia in the dog. 732 59
Congenital Adrenal Hyperplasia (C.A.H.) is an autosomal recessive disorder which is often life threatening during the neonatal period prior to establishment of the diagnosis and instigation of appropriate treatment. In females the condition is usually detected at birth due to genital ambiguity. Unfortunately males or extremely virilized females often remain undetected until they suffer a potentially fatal adrenal crisis. Typically, a crisis occurs within the first couple of weeks of life and is preceded by a history of failure to thrive,
lethargy
and vomiting which may be misdiagnosed as resulting from pyloric stenosis. Vascular
collapse
and diminished consciousness ensue if adrenal insufficiency remains undetected. Initial biochemical investigation of the shocked neonate with C.A.H. reveals severe hyperkalaemia and hyponatraemia, which initially may be thought to be due to renal failure. Hypoglycaemia may also be a feature. Initial resuscitation requires intravenous saline and hydrocortisone. Once physiologically stable, oral steroids are used to replace absent glucocorticoids and mineralocorticoids. The psychosocial impact of having a critically ill baby, with a relatively uncommon genetic disorder, who requires lifelong treatment can be overwhelming for parents. There is an ongoing risk of adrenal crisis throughout the child's life during periods of physiological stress. Parents require education on the management of medication during normal childhood illnesses; the early indicators of crisis and instruction in injection technique. In addition to skilled technical nursing interventions for their baby, parents can benefit from accurate information and contact with the C.A.H. support group.
...
PMID:Congenital adrenal hyperplasia: a potential diagnosis for the neonate in shock. 762 Feb 64
We describe a patient with a long history of psoriasis who developed severe erythrodermic psoriasis associated with
lethargy
, muscular weakness and
collapse
. Serum biochemical screening at the time revealed severe hypophosphataemia, and when this was corrected by intravenous phosphate replacement her symptoms resolved and her psoriasis improved. Hypophosphataemia may therefore be another metabolic complication of erythrodermic psoriasis.
...
PMID:Erythrodermic psoriasis. Report of a case associated with symptomatic hypophosphataemia. 848 98
Passive immunization with monoclonal antibodies (MAbs) specific for the major capsular polysaccharide of Cryptococcus neoformans alters the course of murine cryptococcosis. During studies of passive immunization for treatment of murine cryptococcosis, we noted the occurrence of an acute, lethal toxicity. Toxicity was characterized by scratching,
lethargy
, respiratory distress,
collapse
, and death within 20 to 60 min after injection of antibody. The toxic effect was observed only in mice with a cryptococcal infection and was reduced or absent in the early and late stages of disease. The clinical course and histopathology were consistent with those for shock. There was considerable variation between mouse strains in susceptibility to toxicity. Swiss Webster mice from the Charles River colony were most susceptible, followed by C3H/He, BALB/c, and C57BL/6 mice. DBA/2 mice and Swiss Webster mice from the Simonsen colony were resistant. Acute toxicity was mimicked by injection of preformed complexes of MAb and purified polysaccharide. The toxic effect was also produced by injection of MAbs into mice that were preloaded with polysaccharide. The toxic effect was not blocked by treatment of mice with chloropheniramine or anti-tumor necrosis factor alpha antibodies or by depletion of complement components via pretreatment with cobra venom factor. Toxicity was reduced by treatment of mice with high doses of epinephrine, dexamethasone, or chlorpromazine. Finally, the toxic effect was completely blocked by treatment of mice with the platelet-activating factor antagonist WEB 2170 BS or by pretreatment of mice with the liposome-encapsulated drug dichloromethylene diphosphonate, a procedure which depletes macrophages from the spleen and liver.
...
PMID:Acute lethal toxicity following passive immunization for treatment of murine cryptococcosis. 912 64
Two, young adult, male pugs presented for spontaneous left-cranial lung lobe torsions. Clinical signs associated with these two cases included increased weakness, increased respiratory effort, tachypnea, acute
collapse
,
lethargy
, anorexia, and cyanosis. The torsed lung lobes were excised using a thoracoabdominal stapling device without detorsing the lobes. Both dogs recovered uneventfully, and at least one year postoperatively, no clinical abnormalities were noted by their owners. Results of this report suggest that spontaneous lung lobe torsion in pugs occurs and should be a differential diagnosis for pugs with increased respiratory effort, tachypnea, nonproductive cough, acute
collapse
, cyanosis, and
lethargy
. Surgical excision may be curative.
...
PMID:Spontaneous lung lobe torsion in two pugs. 1130 May 18
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