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排序方式: 共有379条查询结果,搜索用时 31 毫秒
81.
目的 探讨低钾性周期性麻痹的临床特点及诊治原则。方法 综合分析58例低钾性周期性麻痹病例的一般临床资料、主要症状及体征,重要辅助检查及治疗转归。结果 病人均有低钾、瘫痪、补钾后迅速恢复等特点,16例心电图有P-R间期、Q-T间期延长、QRS增宽或ST段低、T波变平、U波出现等改变,6例有浅感觉减退,18例肌张力正常,11例腱反射增高,38例腱反射降低,有5例出现尿潴留,有1例出现呼吸肌麻痹。结论 低钾性周期性麻痹临床上有低钾、下运动神经元瘫痪、肌张力减低、腱反射减弱、心电图改变等典型症状,也可有浅感觉减腿、腱反射增高等特殊变化,诊断上须注意与格林-巴林综合征、急性脊髓炎等疾病鉴别。治疗上主要是迅速补钾。 相似文献
82.
目的探讨ICU-应用微量泵中心静脉高浓度补钾的有效性及安全性。方法回顾性分析ICU发生低钾血症78例患者的临床资料。随机分为常规组和高浓度组,每组各39例,补钾均在心电监护下进行。常规组钾浓度为40mmol/L,补钾速度为10~20mmol/h;高浓度组钾浓度为100~300mmol/L,补钾速度为加~200mmol/h,同时计算达到目标血钾浓度所需补钾量,监测两组血钾浓度、每小时尿量、达到目标血钾浓度所需时间及患者局部不良反应。结果两组患者治疗前均存在低钾血症,设定目标血钾浓度为4.0mmol/L,两组治疗前血钾浓度、所需补钾量比较差异无统计学意义,分别为(2.9±0.2)、(3.0±0.2)mmol/L和(85.2±8.7)、(92.3±7.6)mmol。常规组与高浓度组相比达到目标血钾浓度所需时间较长[(17.25±4.49)h比(5.67±0.75)h,P〈0.01]。结论在ICU严密监护下应用微量泵中心静脉高浓度补钾安全、有效.有一定的临床廊用价值。 相似文献
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Renal tubular acidosis, associated with hypothyroidism, is rare. We present the case of a woman with known renal tubular acidosis and treated hypothyroidism who underwent emergency cesarean delivery under uneventful combined spinal-epidural anesthesia. The rationale for choosing the anesthetic technique and the potential risks associated with anesthesia and renal tubular acidosis are discussed. 相似文献
87.
《Current medical research and opinion》2013,29(10):584-590
SummaryTwo-hundred and ten patients from general practice with a mean age of 75 years were assessed for the signs and symptoms of potassium deficiency, before and after receiving a potassium supplement (‘Slow-K’) 8.06 mEq. three times a day. The assessment included potassium and haemoglobin levels, diet, and symptomatic ratings. Following treatment, 86% of patients showed symptomatic improvement, and there was a highly significant increase in mean potassium levels from 3.8 to 4.4 mEq./l. Interestingly there was a slight but significant increase in mean haemoglobin levels from 12.1 to 12.8?g./100ml. It was not possible, because of the trial design, to correlate conclusively the symptomatic improvement with the therapy. 相似文献
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89.
《Journal of emergency nursing》2022,48(3):310-316
PurposeHypokalemic cardiac arrest is an uncommon occurrence in the emergency department. Electrocardiogram findings related to hypokalemic cardiac arrest include prolonged QT, U waves, and preventricular contractions leading to Torsades de Pointes and then arrest. Literature evaluating the prevalence of hypokalemic cardiac arrest is scarce, and its management is lacking. This review provides a summary of current literature, recommendations from current guidelines, and proposed management strategies of hypokalemic cardiac arrest.SummaryIntravenous potassium administration is the treatment for hypokalemic cardiac arrest. Although the treatment for hypokalemic cardiac arrest is known, there is limited evidence on the proper procedure for administering intravenous potassium appropriately and safely. Owing to the time-sensitive nature of treating hypokalemic cardiac arrest, rapid administration of intravenous potassium (10 mEq/100 mL of potassium chloride over 5 minutes) is warranted. Concerns regarding rapid potassium administration are not without merit; however, a risk-benefit analysis and potential mitigation strategies for unwanted side effects need to be considered if hypokalemic cardiac arrest is to remain a reversible cause. It is imperative to identify hypokalemia as the cause for arrest as soon as possible and administer potassium before systemic acidosis, ischemia, and irreversible cell death.ConclusionsMore evidence is necessary to support treatment recommendations for hypokalemic cardiac arrest; however, it is the authors' opinion that, if identified early during cardiac arrest, intravenous potassium should be administered to treat a reversible cause for cardiac arrest. 相似文献
90.
《Journal of clinical neuroscience》2014,21(11):1989-1990
Levetiracetam (LEV), used for both partial and generalized seizures, is a frequently preferred antiepileptic because of its few side effects. We present a 23-year-old man who developed hypokalemia after switching from valproate to LEV. The patient was sent to our clinic due to hypokalemia 1 month after initiation of LEV, and his neurological examination was normal. Further examinations revealed hypokalemia (3.1 mmol/L) and hypomagnesaemia (0.56 mmol/L). His hemogram, blood urea nitrogen, creatinine, total cortisol, thyroid function tests, creatinine clearance, and renal Doppler ultrasound were normal. LEV was tapered off and treatment with 200 mg/day lamotrigine begun. Potassium and magnesium levels returned to normal ranges in subsequent tests. While hypokalemia and hypomagnesaemia have not been reported before to our knowledge, interstitial nephritis and renal failure after the use of LEV have been. Hypokalemia, found in the early period in this case, may be an indicator of a recently developed renal tubular disorder. This experience indicates that unpredictable side effects of increasingly used new antiepileptic drugs should be taken into consideration. 相似文献