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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Urethral obstruction induced in adult male cats caused clinical signs identical with those observed in naturally occurring disease. Central nervous system depression, anorexia, dehydration, vomiting, muscle weakness, and hypothermia occurred. Weight loss (due to water loss and catabolism), metabolic acidosis, mild hyponatremia, hyperkalemia, hypermagnesemia, hypocalcemia, hyperphosphatemia, hyperglycemia, azotemia, and hyperproteinemia were also observed. Serum amylase, alkaline phosphatase, and alanine aminotransferase activities were normal. Ten of 13 cats (group 1), with 72 hours' induced obstruction but not treated with parenteral fluids, died either before the obstruction was relieved or within 8 days afterward. Eight cats (group 2) with induced obstruction for 49 to 98 hours developed severe clinical and biochemical alterations. Treatment with a multiple-electrolyte solution, in addition to relief of urethral obstruction, resulted in favorable clinical and biochemical responses. These cats survived and were clinically healthy at 9 to 10 days after relief of obstruction. It was concluded that use of a multiple-electrolyte solution to correct acidosis, restore circulatory volume, and enhance renal excretion of potassium was effective supportive therapy after urethral obstruction was removed.
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PMID:Characterization and treatment of water, electrolyte, and acid-base imbalances of induced urethral obstruction in the cat. 87 80

Idiopathic hypoparathyroidism was diagnosed in five young to middle-aged cats of mixed breeding. Three of the cats were male and two were female. Historic signs included lethargy (n = 5), anorexia (n = 5), muscle tremors (n = 4), weakness (n = 4), generalized seizures (n = 3), ataxia (n = 3), mental dullness or disorientation (n = 3), panting (n = 2), pruritus (n = 1), ptyalism (n = 1) and dysphagia (n = 1). Weakness (n = 4), dehydration (n = 2), cataracts (n = 2), hypothermia (n = 1), and bradycardia (n = 1) were found on physical examination. Results of electrocardiography revealed a prolonged Q-T interval in two cats. Results of initial laboratory tests revealed profound hypocalcemia and severe hyperphosphatemia with normal renal function. The diagnosis of hypoparathyroidism was made on the basis of the history, clinical signs, and results serum biochemical testing (i.e., severe hypocalcemia and hyperphosphatemia); in two cats, the diagnosis was also confirmed by histologic examination of parathyroid glands. Initial treatment included intravenous administration of 10% calcium gluconate and oral administration of large loading doses of calcium and vitamin D (dihydrotachysterol). Successful long-term management with dihydrotachysterol and calcium was achieved in all cats. The final dosage of dihydrotachysterol required to maintain normocalcemia in the five cats ranged from 0.004 to 0.04 mg/kg/day (mean = 0.015 mg/kg/day). Long-term calcium supplementation was given to three of the cats in dosages ranging from 29 to 53 mg/kg/day (mean = 42 mg/kg/day) of elemental calcium. One cat died after 28 months of therapy from widely metastatic hemangiosarcoma; the other three cats are still alive and well after 5 to 37 months of treatment.
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PMID:Idiopathic hypoparathyroidism in five cats. 202 14

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.
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PMID:Primary hypoadrenocorticism in ten cats. 246 93

Severe electrolyte disturbances developed after the administration of hypertonic phosphate enemas in 2 chronically obstipated cats. Hyperphosphatemia, hypernatremia, and hypocalcemia were detected in both cats. Physical findings included weakness, anxiety, tachycardia, hypothermia, and dehydration. Intravenous fluid and electrolyte therapy led to prompt, dramatic improvement in both cats. Although well tolerated by most healthy animals, hypertonic phosphate enemas should be avoided in small animals, especially those that are dehydrated, severely obstipated, or suffering from renal or colonic disease.
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PMID:Electrolyte abnormalities induced by hypertonic phosphate enemas in two cats. 408 55

Clinicopathologic findings were retrospectively evaluated in 26 cats and 24 dogs with ethylene glycol intoxication. Common clinical signs were ataxia, depression, vomiting, and hypothermia. Characteristic alterations in the hemogram and serum chemical profile included neutrophilia, lymphopenia, azotemia, hyperphosphatemia, hypocalcemia, hyperglycemia, and decreased whole blood bicarbonate. Common urinalysis findings included isosthenuria, proteinuria, glucosuria, hematuria, calcium oxalate and hippurate crystalluria, and the presence of renal epithelial cells, white blood cells, and granular and cellular casts in the urine sediment. The high death rate (78%) was attributed to delays in presentation, diagnosis, and therapy.
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PMID:Clinicopathologic findings in dogs and cats with ethylene glycol intoxication. 669 34

Acute kidney injury (AKI) is encountered in a variety of settings (e.g., hospitalized and outpatient, non-intensive and intensive care unit patients, pediatric, adult, and elderly), with varied clinical manifestations ranging from a minimal elevation of serum creatinine (SCr) to anuric renal failure and/or multi organ failure (MOF), and a wide variation in causes, risk factors and comorbiditis. There is no hard and fast rule as to when renal replacement therapy (RRT) should be initiated, but is clearly not sensible to wait until an obvious uremic complication arises. Modern practice is to initiate RRT sooner rather than later, for example, when the SCr concentration reaches 500-700 micromol/L, perhaps even earlier, unless there is clear evidence that renal function is about to recover. The choice of the treatment will depend on the clinical practice, technical resources, and well-trained nurses of a given department, than on precise clinical indication. The ideal RRT should mimic the functions and physiological mechanisms of the native organ, ensuring qualitative and quantitative blood purification, be free of complications, have good clinical tolerance and restore and maintain homeostasis, thus favouring organ recovery. Now available RRT options /peritoneal dialysis (PD), 2. intermittent hemodialysis (IHD), 3. continuous therapies (CRRT), and 4. hybrid therapies/, differ in the method of delivery, efficiency, and their clinical tolerability. AKI without MOF is less complex, can be managed outside intensive care unit and the same RRT techniques used for the treatment of chronic renal failure may be applied. AKI associated with MOF is a more complex condition and requires more flexible RRT. Acute PD remains a viable option for the treatment of selected patients with AKI, particularly pediatric population, and those who are hemodynamically compromised, have severe coagulation abnormalities, difficulty in obtaining blood access, removal of high molecular weight toxins (> 10 kD), and clinically significant hypothermia and hyperthermia. Patients that are hemodynamically stable can be managed with IHD techniques. Maintaining hemodynamic stability is probably one of the most important aspects of dialysis technique as well as one of the most difficult challenges. With CRRT, the continuous regulation of volume homeostasis could lessen the hourly rate of required UF, thereby improving hemodynamic stability compared with IHD. Clinical data suggest that CRRT should be strongly considered for patients with severe hyperphosphatemia, elevated intracranial pressure, cerebral edema complicating acute liver failure, sepsis or septic shock, might be a useful component of therapy for lithium intoxication, and because of continuous nature of process prevents the post-dialytic "rebound" elevation of plasma concentration of uremic toxins typically seen with IHD. Hybrid therapies using a variety of machines are safe and convenient, providing excellent control of electrolytes and fluid balance, and offers several advantages over CRRT, including less cumbersome technique, patient mobility, and decreased requirements for anticoagulation, while providing similar hemodynamic stability and volume control. Currently, it has been found no difference in mortality or renal recovery between hybrid RRT, CRRT or IHD for critically ill patients with AKI. However, future investigations should collect detailed information on long-term costs and the relative likelihood of renal recovery associated with dialysis modality.
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PMID:New experiences with the therapy of acute kidney injury. 1925 43

Hypothermia or cold-stunning is a condition in which the body temperature of an animal decreases below normal physiologic range and which has been linked to severe morbidity in sea turtles. Reports have focused on the physiologic changes caused by cold-stunning in Kemp's Ridley sea turtles (Lepidochelys kempii) and loggerhead sea turtles (Caretta caretta), but few have evaluated the green sea turtle (Chelonia mydas). This study evaluated hematologic and serum biochemical profiles of cold-stunned green sea turtles in North Carolina, USA. When compared with healthy, free-ranging juvenile green turtles from the same region, cold-stunned turtles exhibited hypoglycemia, hypocalcemia (both total and ionized calcium), hyponatremia, hypokalemia, hypoproteinemia, hypoalbuminemia, hyperphosphatemia, and elevations in uric acid and blood urea nitrogen. These findings contrast with some previously reported changes in cold-stunned Kemp's Ridley and loggerhead sea turtles. These results emphasize the importance of basing therapeutic regimens on biochemical analyses in cold-stunned sea turtles.
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PMID:Evaluation of hematology and serum biochemistry of cold-stunned green sea turtles (Chelonia mydas) in North Carolina, U.S.A. 2294 2

Two pet rabbits were presented with an acute decrease in appetite and activity. Rabbit 1 showed severe hypothermia, bradycardia, arrhythmias, a heart murmur, dyspnea, occlusion of the nares with secretions, icterus, dehydration, and gaseous gastrointestinal dilation. The urine was dark yellow. Rabbit 2 was overweight, apathetic, and dehydrated; this animal presented with a heart murmur, gastric dilation, and intermittent nystagmus with dorsal strabismus in the right eye. Blood gas, electrolyte, hematology, plasma clinical biochemistry analysis, coagulation profile, plasma protein electrophoresis, urinalysis, and radiographic examinations were performed. The main shared findings were moderate thrombocytopenia, markedly decreased aspartate aminotransferase and alanine aminotransferase activities and fibrinogen concentrations, prolonged prothrombin and activated partial thromboplastin times, profoundly increased alkaline phosphatase and gamma-glutamyl transferase (GGT) activities, and high bile acid and bilirubin concentrations. Rabbit 1 also had respiratory acidosis, marked hypoglycemia, hyperphosphatemia, and a profoundly increased creatine kinase activity. Gastric dilation was observed on both radiographic exams. A low urinary pH of 5-6, marked bilirubinuria and proteinuria, and high urinary GGT levels were present in both patients. Marked icterus developed before death, which occurred within 22 and 30 hours post admission in rabbits 1 and 2, respectively. The necropsy of rabbit 1 showed a markedly accentuated hepatic lobular pattern, pulmonary hemorrhages, pericardial effusion with adhesions, peritoneal petechiae, and icteric and hemorrhagic abdominal fat. Histopathologic findings included hemorrhagic diathesis, severe centroacinar and midzonal hepatocellular necrosis, severe necrosuppurative bronchopneumonia, and moderate cardiomyocyte necrosis. A liver PCR assay was positive for Rabbit Hemorrhagic Disease Virus (RHDV) 2 (RHDV2) and negative for classic RHDV. This is the first description of the gross clinicopathologic abnormalities associated with naturally occurring RHDV2 infection in pet rabbits.
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PMID:Clinicopathologic findings of naturally occurring Rabbit Hemorrhagic Disease Virus 2 infection in pet rabbits. 3086 86