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 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Emergent conditions arising in patients with advanced terminal disease are inevitable and create stressful situations for patients, caregivers, and health care personnel. Discussions regarding appropriate levels of intervention based on parameters such as patient wishes, proper access to documentation of those wishes, location of care, cognitive status and extent of clinical decline are important to have before crisis situations. Common emergencies to be addressed include those that may or may not be associated with advanced malignancies, including compression syndromes, superior vena cava syndrome, hypercalcemia, acute dyspnea, seizures, acute urinary and bowel obstructions, massive hemorrhage, cardiac tamponade, acute embolic phenomenon, and psychiatric emergencies. Although not all clinical scenarios will be addressed in this article, the more common ones will be discussed.
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PMID:Management of emergent conditions in palliative care. 1140 37

We report two cases of localized benign pleural mesothelioma with different clinical features. Neuropsychiatric symptoms, including coma, hemiplegia, seizures and misbehavior predominated in the first case, associated with hypoglycemia. The symptoms in the second case were essentially respiratory (cough, dyspnea, and chest pain). Treatment consisted in thoracotomy and complete surgical resection. Histopathology revealed fusiform cells and collagen stroma. These two cases illustrate the diversity of clinical expression of benign localized pleural mesothelioma and confirm their complete resolution after surgical treatment.
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PMID:[Localized benign pleural mesothelioma observed at the Dakar University Hospital]. 1146 93

Moxidectin is a macrolide endectocide available as a 2% equine oral gel in the US. This report presents clinical signs of moxidectin toxicosis and its treatment in equines as reported to the ASPCA Animal Poison Control Center (APCC) from January 1998 to December 2000. Nine cases of moxidectin overdose in equines occurred: 5 had signs of toxicosis such as coma, dyspnea, depression, ataxia, tremors, seizures, or weakness. The approximate dose of moxidectin at which these signs were observed ranged from 1.0 to 5.1 mg/kg. The 4 equines that ingested moxidectin between 0.9 mg/kg to 1.7 mg/kg did not show signs of toxicosis. Clinical signs were seen within 6-22 h and lasted for 36-168 h. Only 1/5 clinical equines was an adult, the others were < 4 month of age. This study supports earlier report that young foals are more susceptible to moxidectin toxicosis. All 4 equines with known outcomes recovered with treatment that included decontamination, seizure control, thermoregulation, fluid therapy, and supportive care.
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PMID:A review of moxidectin overdose cases in equines from 1998 through 2000. 1213 74

The general health of a German shepherd dog had deteriorated slightly when it was found after being loose for one hour. After 10 hours of observation, the dog showed signs of pain for the first time and signs of poisoning, such as tenseness of muscles, slight opisthotonus, regurgitation, salivation, mydriasis, dyspnoea and cyanosis, were observed; it died 15 minutes after showing the first clinical signs but it had no seizures or tetanic spasms at any time. A postmortem examination did not reveal any pathological changes. A screening test for alkaloids was positive for strychnine (strychnidin-10-one). The presence of strychnine was confirmed and its concentration was determined by gas chromatography/mass spectrometry in urine (728.5 ng/ml) and in the stomach contents (44.6m microg/g). No strychnine was detected in the dog's serum, but traces of brucine (2,3-dimethoxystrychnidin-10-one), the dimethoxy derivative of strychnine, were detected. This case was compared with other strychnine poisonings recorded in the authors' laboratory over the previous six years, taking into account the species, type of samples, the clinical signs and their duration, the postmortem findings, and the concentrations of strychnine. This was the only case to show such an atypical time course of clinical signs.
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PMID:Atypical time course of clinical signs in a dog poisoned by strychnine. 1213 20

A 42-yr-old woman presented with hyperthyroidism and a large, firm, irregular goiter. Within a few weeks she became hypothyroid. Five months later she developed increasingly severe neck pain and compressive symptoms. The goiter had become rock hard. A fine needle aspiration biopsy showed features of chronic thyroiditis and fibrosis. She partially responded to a course of glucocorticoids. Tamoxifen was added, with marked improvement in goiter size and pain. Both medications were tapered off. Two months later the patient experienced paresthesias of the fingertips, perioral numbness, and a seizure. She was found to have spontaneous primary hypoparathyroidism. Three months later the patient became hoarse and experienced difficulty in breathing. She was found to have a massively enlarged thyroid with compression of the right internal jugular vein and encasement of the right carotid artery as well as tracheal narrowing. She also had right vocal cord paralysis due to recurrent laryngeal nerve involvement. Because of airway compromise, an emergency isthmusectomy was performed, and the patient was given a postoperative course of glucocorticoids with gradual improvement. Postoperative diagnosis was Riedel's thyroiditis. Two months later she presented with near-syncope and was found to have bradycardia, hypotension, and right Horner's syndrome, presumably due to compression of the right carotid sheath. She was given i.v. glucocorticoids and tamoxifen. Six months later and 18 months after her initial presentation, the patient is doing remarkably well. Her goiter has regressed by more than 50%, and she no longer has any pain or difficulty breathing. She remains a little hoarse and has persistent hypothyroidism and hypoparathyroidism. She is taking prednisone (5 mg, this is being tapered very slowly) and tamoxifen (20 mg) daily. This case illustrates the protean manifestations of Riedel's thyroiditis, a rare but fascinating disease. The epidemiology of this disease, its pathophysiology and complications, and the roles of surgery and medical therapy are reviewed.
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PMID:Clinical case seminar: Riedel's thyroiditis: report of a case complicated by spontaneous hypoparathyroidism, recurrent laryngeal nerve injury, and Horner's syndrome. 1216 72

Although olanzapine therapy has been associated with fewer extrapyramidal side effects than the traditional antipsychotic medications, reported side effects include dystonia, tardive dyskinesia, hypotension, diabetes mellitus, seizures and neuroleptic malignant syndrome. There are no previous published reports of hyperventilation associated with olanzapine therapy, but we present the case of a male patient who developed dyspnea and hyperventilation while taking olanzapine.
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PMID:Olanzapine-induced hyperventilation: case report. 1227 91

The effects of sodium azide administration on the central cholinergic functions were investigated utilizing mice to evaluate the neurotoxicity in the acute poisoning. Seven oral doses of the toxicant, ranging in dosage from 12.3 to 59.3 mg/kg, based upon a multiple of 1.3 x 27 mg/kg (an empirical LD50 for mice) or 27 mg/kg divided by 1.3 to calculate the lower three doses, were administered to facilitate the acute signs and to observe behavior. The behavior included locomotor activity, rectal temperature and rotarod performance which are convenient for the evaluation of central cholinergic involvement even if it may be partial, since no behavioral methods to study totally the cholinergic system have been known. Measurements of the activities of acetylcholinesterase (AChE) and choline acetyltransferase (ChAT), enzymes that hydrolyze and synthesize acetylcholine (ACh) and high-affinity choline uptake (HACU), a rate-limiting step in the synthesis of ACh, were determined in the presence of various concentrations of sodium azide in vitro. Adult (12-15 weeks) female ICR strain mice were utilized in this study. Mice were orally given sodium azide in doses from 27 to 59.3 mg/kg and appeared sedated within 5 min. Next we observed hyperpnea and dyspnea, which were followed by seizure and death for mouse groups which received more than 35.1 mg/kg. Oral administration of the sodium azide solution produced an increase in locomotor activity for the 12.3 mg/kg group and a decrease for the higher doses (ranging from 16.0 to 27.0 mg/kg). The sodium azide administration suppressed rectal temperature dose-dependently as well as rotarod performance at high doses (20.8 and 27.0 mg/kg). Such behavioral changes elicited by sodium azide administration suggest an involvement of the central cholinergic system. Sodium azide also caused a measured decrease in the activity of AChE, but an increase in the activities of ChAT and HACU, dose-dependently, in vitro. From the results obtained from the behavioral and the in vitro experiments, we concluded that acute sodium azide poisoning significantly affects the central cholinergic system.
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PMID:[Neurotoxicity in sodium azide poisoning]. 1241 70

Sodium azide, used mainly as a preservative in aqueous laboratory reagents and biologic fluids and as a fuel in automobile airbag gas generants, has caused deaths for decades. Its exposure potential for the general population increases as the use of airbags increase. In order to characterize the known health effects of sodium azide in humans and the circumstances of their exposure, the authors conducted a systematic review of the literature from 1927 to 2002 on human exposure to sodium azide and its health effects. The most commonly reported health effect from azide exposure is hypotension, almost independent of route of exposure. Most industrial exposures are by inhalation. Most laboratory exposures or suicide attempts are by ingestion. Most of the reported cases involved persons working in laboratories. The time between exposure and detection of hypotension can predict outcome. Fatal doses occur with exposures of >or=700 mg (10 mg/kg). Nonlethal doses ranged from 0.3 to 150 mg (0.004 to 2 mg/kg). Onset of hypotension within minutes or in less than an hour is indicative of a pharmacological response and a benign course. Hypotension with late onset (>1 hour) constitutes an ominous sign for death. All individuals with hypotension for more than an hour died. Additional health effects included mild complaints of nausea, vomiting, diarrhea, headache, dizziness, temporary loss of vision, palpitation, dyspnea, or temporary loss of consciousness or mental status decrease. More severe symptoms and signs included marked decreased mental status, seizure, coma, arrhythmia, tachypnea, pulmonary edema, metabolic acidosis, and cardiorespiratory arrest. The signs and symptoms from lower exposures (<700 mg) are physiological responses at the vascular level and those at or above are toxicological responses at the metabolic level. There is no specific antidote for sodium azide intoxication. Recommended preventive measures for sodium azide exposure consist of education of people at high risk, such as laboratory workers, regarding its chemical properties and toxicity, better labeling of products containing sodium azide, and strict enforcement of laboratory regulations and access control.
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PMID:Human health effects of sodium azide exposure: a literature review and analysis. 1285 Nov 50

Lymphomatoid granulomatosis (LYG)/angiocentric immunoproliferative lesions (AIL) consist of angiocentric and angiodestructive lymphoreticular proliferation predominantly involving the lungs and other extranodal sites, such as the central nervous system (CNS). This clinical entity is considered as a B cell process related to Epstein-Barr virus (EBV) infection and EBV positive diffuse large B-cell lymphoma. The CNS is involved in 20% of cases of LYG, but initial involvement is rare. In cases without pulmonary symptoms, diagnosis may be difficult. We report a rare case involving initial progression of CNS symptoms followed by a pulmonary abnormality.A 14-year-old girl suffered from high fever, ataxic gait and paraparesis. MRI revealed diffuse T2 high signals with multiple gadolinium enhancements in the cerebellum, brain stem and cerebral white matter. Her symptoms briefly improved after steroid therapy, but ataxia gradually progressed. Dyspnea due to pulmonary interstitial involvement appeared when she was 18 years old. Steroid therapy proved effective for respiratory symptoms. At 20 years old she suffered from disseminated intravascular coagulopathy (DIC) and hemophagocytic syndrome (HPS) with respiratory symptoms and repeated seizures. Her symptoms improved after the administration of cyclophosphamide. Mild hemiparesis and gait disturbance appeared when she was 22 years old. MRI revealed new lesions at the basal ganglia and subcortical white matter, brain atrophy and diffuse T2 high intensity of cerebral white matter. Cyclophosphamide was effective and there has been no recurrence of symptoms in the last 5 years. We reviewed the non-tumorous LYG/AIL involving the CNS, and discussed the clinical features, MRI imaging and diagnosis of the LYG/AIL.
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PMID:A case of lymphomatoid granulomatosis/angiocentric immunoproliferative lesion with long clinical course and diffuse brain involvement. 1287 57

Anxiety is a medical mimicker that can imitate both cardiac and neurological symptoms. Anxiety disorder research protocols regularly use hyperventilation or i.v. lactate infusion to trigger panic attacks in susceptible subjects. Susceptible patients experience panic attacks with slight decreases in CO2 or increases in lactate production seen in mild exercise such as stair climbing. To the unsuspecting physician this appears to be dyspnea on exertion. Hyperventilation during rapid eye movement (dream) sleep may trigger panic attacks in patients with panic disorder, mimicking paroxysmal nocturnal dyspnea. Syncope from panic-induced hyperventilation can mimic seizures. When panic-like anxiety is discovered in aircrew it necessitates grounding. The prognosis is frequently good after treatment with psychotherapy, with return to full flying status a strong possibility.
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PMID:You're the flight surgeon. Anxiety. 1292 69


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