Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

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)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

A 64-year-old male with an incomplete spinal cord injury had been taking baclofen 20 mg tid for 2 1/2 months without side effects. His blood urea nitrogen and serum creatinine rose from 13 and 0.9 mg%, respectively, to 59 and 2.8 mg% after ibuprofen 600 mg tid was begun. The patient displayed baclofen toxicity, developing confusion, disorientation, bradycardia, and hypothermia. His blood pressure dropped and he complained of blurred vision. Ibuprofen discontinuation and fluid repletion corrected the renal indices. Rapid tapering of baclofen was accompanied by reversal of baclofen toxicity. Patients taking baclofen must be monitored closely for toxicity when declining renal function is present. Clinicians should be alert to the possibility of renal insufficiency developing when ibuprofen is initiated. This case demonstrates the potential for ibuprofen-induced renal insufficiency to reduce baclofen clearance, thereby leading to baclofen toxicity. Published reports of ibuprofen-induced renal insufficiency are reviewed and pertinent pharmacokinetics of baclofen discussed.
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PMID:Baclofen toxicity associated with declining renal clearance after ibuprofen. 648 61

An 18-year-old white woman had nausea, vomiting, weight loss, and a diagnosis of anorexia nervosa. Copper-colored skin was noted on physical examination, and serum chemistry values were normal. Subsequent fever, disorientation, and confusion led to the discovery of Addison's disease, which responded well to corticosteroid replacement therapy. Addisonian and anorexic patients exhibit clinical similarities, including nausea, vomiting, weight loss, abdominal pain, cold intolerance, hypothermia, and orthostasis. Other commonalities include prolongation of electrocardiographic PR and QT intervals and generalized slowing on electroencephalogram. Important differences include a brown color to the skin in Addison's disease instead of a yellowish color in anorexia. Addisonian patients also display hypocortisolism, hypoglycemia, and hyperkalemia, in contrast to the hypercortisolism, hyperglycemia, and hypokalemia seen in anorexia.
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PMID:Prompt differentiation of Addison's disease from anorexia nervosa during weight loss and vomiting. 949 78

In human diffuse axonal injury (DAI), axons are exposed to transient tensile strain. Over the ensuing several hours, injured axons enter a "pathological cascade" of events that lead to secondary axotomy. Use of animal models of traumatic axonal injury (TAI) has allowed description of a number of pathological changes before axotomy occurs, including structural and functional changes in the axolemma, disorientation, and/or loss of microtubules, either compaction and/or dispersion of neurofilaments together with focal compaction at sites where continuity of the axolemma is lost. Recent literature suggests that use of hypothermia may improve behavioral outcomes or reduce the number/density of injured axons in which axonal transport is altered after TAI. But there is presently no ultrastructural, pathological explanation as to how hypothermia may act at the level of the axon to reduce posttraumatic loss of axoplasmic transport. In this study, we tested the hypothesis that posttraumatic hypothermia may ameliorate (a) alteration of axonal transport and (b) early pathological changes in the axonal cytoskeleton prior to secondary axotomy. We have undertaken a pilot study within 4 h of stretch injury to adult guinea pig optic nerve axons as a model of TAI and applied stereological techniques to assess differences in pathology in animals either maintained at 37.5 degrees C or cooled to 32-32.5 degrees C for 2 or 4 h after injury. We provide quantitative evidence that posttraumatic hypothermia significantly reduces the number of axons labelled for beta-APP, a marker for disruption of fast axonal transport, and reduces the loss of microtubules and compaction of neurofilaments, which occurs in normothermic animals over the first 4 h after injury.
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PMID:Axonal cytoskeletal responses to nondisruptive axonal injury and the short-term effects of posttraumatic hypothermia. 1061

Correct administration in the early postoperative phase is decisive in the final outcome of surgery and the presence of the Recovery Room (RR) contributes significantly to a reduction in the post-operative risk rate. The objectives of the RR are: removal of the pharmacological effect of general anaesthesia; stabilization of vital parameters (circulation and ventilation); stabilization of body temperature; control of the hydro-electrolytic balance; intensive intervention in the case of an acute complication; prescribing a suitable postoperative analgesia; recovering movement in the case of loco-regional anesthesia. Organization of RR must take into consideration: 1) aspect of environment and location; 2) transport of the patient from the operating room to the RR; 3) definition of the equipment necessary for the RR; 4) definition of the role and qualification of the medical and nursing staff; 5) definition of regulations of assistance and the clinical file; 6) definition of criteria for discharge and transfer; 7) definition of means of adjournment, improvement and comparison with other similar structures. RR is administered by an Anesthetist with clinical, therapeutic and decision-making responsibility for the discharge of patients, while the supervision and assistance patients is entrusted to specialised professional nurses. From a clinical point of view the following data are monitored and recorded: the vital signs (passage of air-ways, cardiac and respiratory frequency, arterial pressure, saturation of O2, EtCO2 (in patient with air-way support), body temperature and the state of consciousness, instrumental monitoring of the patient (at pre-established time intervals), control of the skin, the peripheral circulation, surgical wounds, drainage and catheters. The percentage of incidence of complications in RR varies from 6-7 to 30% depending on various studies, probably in relation to the diversity of criteria in defining the complication. The principal complications which can be found in RR, reported in several studies are: respiratory (obstruction of the air-way, hypoxemia, hypoventilation, inhalation), cardio-circulatory (hypotension, hypertension, arrhythmia, myocardial ischemia), postoperative nausea and vomiting, hypothermia and hyperthermia, delayed re-awakening, disorientation and hyper-excitability, postoperative shivering. As long as the patient can be discharged from the RR the following requisites must be satisfied: return of a state of consciousness, stable cardio-circulatory parameters, absence of respiratory depression, absence of bleeding, absence of nausea and vomiting, good analgesia and recovery of movement in the case of loco-regional anesthesia (on this last point not all authors agree). What has been said until now shows the function, usefulness and importance of RRs which must not replace the Intensive Therapy Units. In fact, they are places where the cure must be concluded, in which the Anesthetist is responsible for the whole process. This cure must begin in the preoperative period, continue in the intraoperative period and it is compulsory to proceed in the immediate postoperative period until such a time that, because of the anesthesia administered, the clinical situation of the patient ceases to be considered a potential medical-surgical urgency-emergency .
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PMID:[Recovery Room. Organization and clinical aspects]. 1160 73

Alprazolam is a benzodiazepine anti-anxiety agent that acts at the limbic, thalamic, and hypothalamic level of the CNS and has anxioytic. sedative, hypnotic, skeletal muscle relaxant, and anticonvulsant properties. A retrospective study was conducted of 415 alprazolam ingestions in dogs reported to the ASPCA Animal Poison Control Center between January 1998 and August 2000: 238 suspected alprazolam toxicoses in dogs were evaluated. Clinical signs were ataxia/disorientation, depression, hyperactivity, vomiting, weakness, tremors, vocalization, tachycardia, tachypnea, hypothermia, diarrhea, and increased salivation that developed within 10-30 min post-ingestion. Treatment included standard decontamination procedures, such as emesis and activated charcoal: the specific benzodiazepine antagonist, flumazenil, may be used for severe CNS depression.
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PMID:Accidental ingestion of alprazolam in 415 dogs. 1182 68

A 6-day-old, female roan antelope (Hippotragus equinus cottoni) was diagnosed with a single intrahepatic portosystemic venous shunt at necropsy. Clinical signs had included weakness, lethargy, hypothermia, diarrhea, and a weak suckle response. Multiple seizure episodes were associated with hypoglycemia and characterized by vocalization, muscle fasciculations, and disorientation. Hematologic abnormalities included anemia with hypochromasia, anisocytosis, poikilocytosis, and leukopenia with neutropenia and lymphopenia. Serum biochemical abnormalities included elevations in blood urea nitrogen and total serum bile acid concentration. A portosystemic vascular anomaly should be a differential diagnosis for nonthriving, exotic ruminant calves with overt or subtle neurologic signs, persistent hypoglycemia, and/or elevated bile acids. In very young calves, total bile acid concentration may be more useful in establishing a diagnosis than blood ammonia concentration.
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PMID:Intrahepatic portosystemic venous shunt in a neonatal roan antelope (Hippotragus equinus cottoni). 1731 83

Voltage-gated potassium channel antibody (VGKC-Ab)-associated limbic encephalitis (LE) is a recently described syndrome that broadens the spectrum of immunotherapy-responsive central nervous system disorders. Limbic encephalitis is typically characterised by a sub-acute onset of disorientation, amnesia and seizures, but the clinical spectrum is not yet fully defined and the syndrome could be under-diagnosed. We here describe the clinical profile of four patients with VGKC-Ab-associated LE who had intermittent, episodic hypothermia. One of the patients also described a prodrome of severe neuropathic pain preceding the development of limbic symptoms. Both of these novel symptoms responded well to immunosuppressive therapy, with concurrent amelioration of amnesia/seizures.
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PMID:Hypothermia in VGKC antibody-associated limbic encephalitis. 1820 10


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