Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032290 (aspiration pneumonia)
 2,291 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Based on the discussion of NMS, certain conclusions may be reached in regard to this patient. In the psychiatric setting, agitation and confusion alone are not suggestive of NMS. However in this patient, the symptoms of agitation, the rapid development of EPS symptoms unresponsive to anticholinergic therapy, autonomic changes (tachycardia, diaphoresis, and incontinence), and elevated CPK, met most of the diagnostic criteria described in Table VI. However, this case may have described an atypical presentation of NMS because of the absence of temperature increases during the onset of symptoms and the 7-week hospitalization for NMS. The patient's later onset of temperature elevations was a result of an aspiration pneumonia. Pneumonia and renal failure significantly increased the morbidity and extended the course of the illness. As a result, the diagnosis and specific treatment of NMS were delayed because of atypical symptoms and complications. In this patient, treatment of NMS with bromocriptine did not start until 10 days into hospitalization. A delay in pharmacologic therapy in this patient may have contributed to persistence of symptoms. The patient showed signs of improvement on day 21 during combination bromocriptine, benztropine, and dantrolene therapy. Moreover, this case exemplifies the rigorous need for supportive therapy and adjunctive pharmacologic therapy for primary and secondary complications resulting from NMS. In conclusion, because of the wide range of risk factors and variations of NMS, a systematic approach to diagnosing and treating NMS is critical to a successful outcome. Discontinuation of antipsychotics, maintenance of supportive therapy aimed at preventing dehydration, hemodynamic, and electrolyte imbalances, and pharmacotherapy are essential in the treatment of NMS.
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PMID:An atypical course of neuroleptic malignant syndrome. 800

From Dec. 1993 to May, 1994, coronary artery bypass grafting (CABG) was performed in 7 patients under bradycardia induced by an ultra-short acting beta blocker (esmolol). The ages ranged from 51 to 68 years. There was one patient with low ejection fraction (EF = 31%) and two patients with porcelain aorta. A tepid temperature was maintained during cardiopulmonary bypass (CPB). A high flow rate of 2.2-2.6 liter/min/m2 was applied to control perfusion pressure above 50 mmHg during CPB. After CPB was started, a high dose of esomolol was added (10-30 mg/kg intravenous bolus followed by a continuous infusion of 1-4 mg/kg/min). Severe bradycardia was achieved by the initial loading of esmolol. The mean heart rate was significantly (p < 0.01) decreased from 78 +/- 12 bpm to 49 +/- 7 bpm by the loading. Altogether, 25 anastomoses (11 ITA, 6 GEA, 8 SVG) were performed to LAD (10), Cx (7) and RCA (8), with an average of 3.6 +/- 0.9 anastomoses/patient. IABP was required for 2 patients postoperatively. There was no operative death, but one hospital death due to aspiration pneumonia 3 months later. Postoperative max CPK-MB was low (17.4 +/- 9.7 IU/L) in 6 patients. The postoperative angiography was performed in all patients with a patency rate of 88%. It was considered that esmolol facilitated CABG under beating heart and this technique is suitable for patients with severe atheromatous disease of the ascending aorta or patients with a low ejection fraction to avoid aortic cross-clamping.
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PMID:[Coronary artery bypass grafting under bradycardia induced by ultra-short acting beta blocker]. 875 90