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

The roles of inflammation and coagulation in the pathophysiology of sepsis are described. Sepsis results when an infectious insult triggers a localized inflammatory reaction that then spills over to cause systemic symptoms of fever or hypothermia, tachycardia, tachypnea, and either leukocytosis or leukopenia. These clinical symptoms are called the systemic inflammatory response syndrome. Severe sepsis is defined by dysfunction of one of the major organ systems or unexplained metabolic acidosis. The inflammatory reaction is mediated by the release of cytokines, including tumor necrosis factor-alpha, interleukins, and prostaglandins, from neutrophils and macrophages. The cytokines activate the extrinsic coagulation cascade and inhibit fibrinolysis. These overlapping processes result in microvascular thrombosis; thrombosis is one potential factor producing organ dysfunction. Activation of the coagulation system leads to consumption of endogenous anticoagulants (e.g., protein C and antithrombin); this may be an important factor in the development of microvascular coagulation. Antiinflammatory mediators as well as inflammatory mediators have a role in sepsis, and an excess of either can result in poor patient outcomes. Sepsis is a complex syndrome involving activation of a variety of systems.
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PMID:Pathophysiology of sepsis. 1188 12

Records of 127 cats with arterial thromboembolism (ATE) were reviewed. Abyssinian, Birman, Ragdoll, and male cats were overrepresented. Tachypnea (91%), hypothermia (66%), and absent limb motor function (66%) were common. Of 90 cats with diagnostics performed, underlying diseases were hyperthyroidism (12), cardiomyopathy (dilated [8], unclassified [33], hypertrophic obstructive [5], hypertrophic [19]), neoplasia (6), other (4), and none (3). Common abnormalities were left atrial enlargement (93%), congestive heart failure (CHF, 44%), and arrhythmias (44%). Of cats without CHF, 89% were tachypneic. Common biochemical abnormalities were hyperglycemia, azotemia, and abnormally high serum concentrations of muscle enzymes. Of 87 cats treated for acute limb ATE, 39 (45%) survived to be discharged. Significant differences were found between survivors and nonsurvivors for temperature (P < .00001), heart rate (P = .038), serum phosphorus concentration (P = .024), motor function (P = .008), and number of limbs affected (P = .001). No significant difference was found between survivors and nonsurvivors when compared by age, respiratory rate, other biochemical analytes, or concurrent CHE A logistic regression model based on rectal temperature predicted a 50% probability of survival at 98.9 degrees F (37.2 degrees C). Median survival time (MST) for discharged cats was 117 days. Eleven cats had ATE recurrences, and 5 cats developed limb problems. Cats with CHF (MST: 77 days) had significantly shorter survival than cats without CHF (MST: 223 days; P = .016). No significant difference was found in survival or recurrence rate between cats receiving high-dose aspirin (> or = 40 mg/cat q72h) and cats receiving low-dose aspirin (5 mg/cat q72h). Adverse effects were less frequent and milder for the lower dosage.
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PMID:Arterial thromboembolism in cats: acute crisis in 127 cases (1992-2001) and long-term management with low-dose aspirin in 24 cases. 1256 30

Claude Bernard in the late 19th century, was one of the first who recognized that acute injury was associated with the development of hyperglycemia. In 1942 David Cutherbertson introduced the terms ebb and flow to describe the phases of hypo- and hypermetabolism, which follow traumatic injury. Hyperglycemia during the ebb phase is promoted by hepatic glycogenolysis secondary to catecholamine release, as well as by direct sympathetic stimulation of glycogen breakdown. Hyperglycemia is a prominent feature of the flow phase in patients who sustain more severely injured or in whom septic complications develop. It results from augmented glucose production in the presence of insulin resistance in peripheral tissues. The flow phase is clinically expressed as a syndrome consisting of: hypermetabolism (manifested by hyperglycemia, hyperlactatemia and protein catabolism), hyperdynamic cardiovascular state and clinical manifestations of fever or hypothermia, tachycardia, tachypnoea and leucocytosis. The hypermetabolic response to stress may be prolonged when there is stimulus for continuous formation of mediators--a persistent focus of injury or infection. Three systems are responsible for translating the initial insult into the stress response: nervous, endocrine and humoral (cytokine). These systems are interrelated. Maximal metabolic response to stress requires the participation of all three systems. Although glycogenolysis increases hepatic glucose output during the ebb phase, this effect is transient because glycogen stores are rapidly depleted. In contrast, the flow phase is characterized by a sustained increase in gluconeogenesis, which in turn promotes hyperglycemia. Hyperglycemia is common following stress, despite the fact that many tissues exhibit increased cellular uptake and utilization of glucose. Peripheral insulin resistance is central to this process by limiting insulin-mediated glucose uptake in skeletal muscles. In addition, hepatic insulin resistance also plays a role in the genesis of hyperglycemia during stress. In general, the degree of hyperglycemia and insulin resistance are directly proportional to the severity of the stress response. Hyperlactatemia and oxygen consumption also increase concurrently with the severity of stress. Modest hyperglycemia during stress may be of potential benefit by promoting cellular glucose uptake, however, severe hyperglycemia may be associated with complications, this in turn could result in organs dysfunction.
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PMID:[Alterations of blood glucose homeostasis during septic or injury stress--hyperglycemia]. 1271 56

This study compared the efficacy of yohimbine with atipamezole, a new alpha2 adrenergic antagonist, to treat canine amitraz intoxication. Thirty dogs were divided equally into 3 groups (A, AY, and AA). Group A received 2.5% amitraz iv at 1 mg/kg; Group AY received the same dose of amitraz followed 30 min later by 0.1 mg/kg (2 mg/mL) yohimbine iv; and Group AA received the same dose of amitraz followed 30 min later by 0.2 mg/kg (5 mg/ mL) atipamezole iv. Temperature, heart rate, respiratory frequency, mean arterial pressure, degree of sedation, mean time of tranquilization and diameter of pupils were monitored for 360 min. Sedation, loss of reflexes, hypothermia, bradycardia, hypotension, bradypnea and mydriasis were observed in Group A, with 3rd eyelid prolapse, increased diuresis and vomiting in some animals. Yohimbine reversed all alterations induced by amitraz, but induced significant cardiorespiratory effects such as tachycardia and tachypnea. Atipamezole was a useful antagonist for amitraz, with less cardiorespiratory effects, suggesting its potential role as an alternative treatment of amitraz intoxication in dogs.
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PMID:The comparative efficacy of yohimbine and atipamezole to treat amitraz intoxication in dogs. 1277 86

Vipera palaestinae (Vp), formerly a subspecies of the near east viper Vipera xanthina, is the most common poisonous snake in Israel and neighbouring countries (Jordan, Lebanon and Syria), and is responsible for most envenomations in humans and domestic animals. Hospital records were retrospectively reviewed for confirmed cases of Vp envenomations in dogs over a 13-year period and 327 cases were included in the study. Most envenomations occurred between May and October, and between 02:00 and 10:00 PM. The most frequent clinical signs included: local swelling and oedema (99.6%), viper teeth penetration marks (51%), tachypnoea (50%), panting (44%), increased body temperature (19.2%), tachycardia (>160/min, 19%), salivation (18%) and lameness (15.6%). Common haematological findings included: increased haematocrit (47%), increased haemoglobin concentration (45%), leucocytosis (39%), and thrombocytopenia (30%). The prothrombin time and activated partial thromboplastin time were prolonged in 68 and 21% of the dogs, respectively. Blood biochemistry abnormalities included increased activities of muscle enzymes, hyperglycaemia, hyperbilirubinaemia, hyperglobulinaemia and hypocholesterolaemia. The mortality rate was 4% (13 dogs). The following variables were significantly (p < 0.05) associated with mortality: body weight below 15 kg (p = 0.01), limb envenomation (0.008), envenomation at night (p = 0.025), severe lethargy (P < 0.001), hypothermia (p = 0.04), systemic bleeding (p = 0.001), shock (p = 0.007), dyspnoea (p = 0.002), tachycardia (p = 0.002), thrombocytopenia (p = 0.02), and glucocorticosteroid therapy (p = 0.002). Dogs younger than 4 years had a lower death risk (p = 0.01). The association of steroid therapy with increased mortality suggests that the use of steroids in Vp envenomations may be harmful. Specific antivenom therapy (10 ml/dog) was not associated with a higher survival rate, thus its use, dose and timing of administration should be further investigated.
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PMID:Vipera palaestinae envenomation in 327 dogs: a retrospective cohort study and analysis of risk factors for mortality. 1510 90

Anesthetized rams envenomed s.c. with 40 microg/kg Tityus discrepans scorpion venom developed fasciculation, hypothermia, polyuria, pulmonary wet rales, tachypnea, respiratory distress and arrhythmia. Rams developed a cascade of inflammation reactions, characterized by activation of macrophages, fibroblasts and neutrophils, neutrophil infiltration and aggregation, vasculitis, arteritis and abundant fibrin deposition. At the inoculation site, venom was detected by immunohistochemistry in the extra cellular matrix, lymphatic vessels' and venules' lumen, inside macrophages and surrounding nerves. Extra cellular matrix was degraded at the inoculation site perhaps by activated neutrophils. Envenoming produced hepatocytes with Mallory body-like vacuoles which may be due to the increased plasmatic levels of TNF-alpha and IL6. Venom produced degranulation and vacuolization of acinary cells as well as interstitial swelling and necrosis. Necrosis of the Langerhan's islets occurred occasionally. Lungs showed the most deleterious effects developing wall collapse and necrosis, diffuse injury of the alveolar capillary barrier, interstitial and alveolar fibrin deposits with strong neutrophil infiltration. Massive infiltration of lymphocytes and macrophage occurred in the intestinal submucose, to the point that it modified villi and intestinal folding morphology. Envenomation developed a marked leukocyte aggregation surrounding nerves at the inoculation site. This study reveals that beyond its neurotoxicity, Tityus venom produces a severe and widespread inflammatory syndrome, expressed as histopathological changes at the site of inoculation, as well as in remote organs such as pancreas, lungs, intestine and liver. Our results suggest that not all remote targets are directly affected by the venom but that, as proposed earlier, are modified by inflammation by products produced elsewhere.
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PMID:Histopathological changes and inflammatory response induced by Tityus discrepans scorpion venom in rams. 1553 Sep 67

To induce luteal regression-related abortion/delivery and treat pyometra in dogs, various PGF2alpha-analogues (PGAs) are administered, but a PGA most appropriate for clinical application in dogs, with a low incidence of side effects, is being investigated. In this study, we compared the effects of etiproston tromethamine (PGA-E), which has not been investigated in dogs, with those of cloprostenol (PGA-C), which is routinely used in dogs. A single dose of PGA-E at 100, 200, 400 or 800 microg or PGA-C at 12.5, 25, 50 or 100 microg was administered to beagles (n=5 per group) 25 days after ovulation, when the corpus luteum was in the functional phase. We compared the state of luteal regression by measuring plasma progesterone levels. As side effects, the incidences of salivation, vomiting, tachypnea, diarrhea and the drop in body temperature were investigated. In the 400-microg and 800-microg groups treated with PGA-E, the mean intervals from administration until luteal regression were 18.6 days and 31.2 days, respectively. In the dogs treated with 50 microg or more of PGA-C, luteal regression was noted 2 days after administration. The above side effects were observed for 3 hr after administration of PGA-E/PGA-C. In the dogs treated with 800 microg of PGA-E, the mean body temperature was 36.7 degrees C 4 hr after administration; hypothermia persisted. PGA-E may be less useful than PGA-C for promoting luteal regression in dogs in clinical application.
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PMID:Influence of a PGF2alpha-analogue, etiproston tromethamine, on the functional corpus luteum of dogs. 1569 86

Sodium fluoroacetate (SFAC) or Compound 1080 is a potent rodenticide, largely used after 1946 for rodent and home pest control. The toxic effects of SFAC are caused by fluorocitrate action, a toxic metabolite, which has a competitive action with aconitase enzyme, leading to citrate accumulation and resulting in interference in energy production by Krebs cycle blockade. In the present study, domestic cats were intoxicated with oral doses of fluoroacetate (0.45 mg/kg). The intoxicated animals presented emesis, diarrhea with abdominal pain posture and an abdominal palpation, tachypnea, bilateral midriasis, hypothermia, hyperexcitability and convulsions. Blood gas analysis indicated decreased pH and bicarbonate levels. Serum ionized calcium was also decreased. ECG showed non-specific changes in ventricular repolarization and ventricular arrhythmias. The survival rate was 75% in the treated group with calcium gluconate and sodium succinate and 37.5% in the nontreated group.
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PMID:Calcium gluconate and sodium succinate for therapy of sodium fluoroacetate experimental intoxication in cats: clinical and electrocardiographic evaluation. 1669 92

The concepts of systemic inflammatory response syndrome (SIRS) and scoring system were defined by the journal of Bone in 1992. SIRS was described as occurrence of two or more clinical criteria in four ones (fever or hypothermia, tachypnea, tachycardia, and leukocytosis). An early diagnosis and estimation of systemic inflammation in patients is helpful for treatment selection. This paper reviews the application of SIRS scoring system, which has been extensively validated for large groups of critical care patients with severe injury and critical surgical diseases. Recent studies have documented SIRS score as a significant predictive parameter of adverse outcome in critical care patients. Furthermore, some studies also give us a suggestion on how to reduce the overload systemic response.
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PMID:Clinical significance of scoring system for systemic inflammatory response syndrome. 1702 66

A seven month old domestic shorthaired male cat was presented with a known history of acetaminophen ingestion. Clinical findings included icterus, depression, hypothermia, tachypnea and pronounced edema of the head and neck. Treatment was aimed at providing substrate to assist in conjugation of the drug and reversing methemoglobinemia. Administration of oral acetylcysteine, ascorbic acid and IV fluids was insufficient in this case due to a delay in initiation of treatment. The salient postmortem findings were icterus, subcutaneous and pulmonary edema and evidence of hemolysis in the liver, spleen and urinary tract.The pathophysiology of the toxicosis and the current recommendations for treatment are reviewed.
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PMID:Acetaminophen toxicosis in a cat. 1742 85


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