低钾性瘫痪24例临床分析

目的探讨低钾性瘫痪的急诊诊断及治疗方法。方法分析24例低钾性瘫痪患者的临床特点及诊治过程。结果 24例低钾性瘫痪患者多为男性青壮年,多于夜间或晨起急性起病,四肢对称性软瘫,发作时血清钾低,补钾后短期内恢复。结论提高对低钾性瘫痪的认识,及时诊断治疗对低钾性瘫痪具有重要临床意义。     

低钾性周期性麻痹41例临床分析

目的提高对低钾性周期性麻痹临床表现的认识,提出治疗及预防措施以及护理建议。方法分析41例周期性麻痹病例的临床表现及辅助检查结果。结果男29例,女12例,年龄17～55岁,平均32.1岁,其中40岁以下30例,占73.2%。发病季节为5～9月份者32例,占78.0%。均表现为不同程度的骨骼肌驰缓性瘫痪,合并感觉障碍8例,伴有甲状腺功能亢进者9例（22.0%）。16例肌酶学指标均有不同程度的升高,有低钾性心电图改变者35例,占85.4%。结论低钾性周期性麻痹的发病以青壮年男性为主。多发于夏秋季节,可有多种诱因存在。急性肌无力为其临床特点,低钾血症、特征性心电图改变有利于确立诊断。部分不典型病例合并有甲亢,血清肌酶升高,以及感觉异常,临床注意与急性脊髓病变,以及格林巴利综合征、肌炎等相鉴别。治疗上主要是快速补钾,以口服为主。注意适当的心理疏导。     

甲亢性周期性瘫痪80例临床观察

目的:探讨以低钾性瘫痪为主要临床表现的甲状腺功能亢进症(甲亢)的发病相关因素及治疗方法。方法:对80例甲亢性周期性瘫痪(TPP)的临床资料进行回顾性分析。结果:发作时均有不同程度双下肢或四肢瘫痪;T3、T4均高于正常。结论:甲亢性周期性瘫痪以年轻男性多见,补钾短期内可改善TPP症状,抗甲亢治疗是预防TPP复发的关键。     

老年低钾性周期性麻痹补钾探讨

<正> 周期性麻痹是以周期性发作的迟缓性瘫痪为特征的一组疾病。临床上的低钾性周期性麻痹为多见。该型患者发病较急,病情较重,处理不及时或处理不当可危及生命,而补钾是主要治疗措施。本文对我科自1994年10月～1997年2月收治的20例低钾性周期性麻痹患者补钾有关问题探讨如下:     

微泵持续静脉补钾治疗低钾型周期性瘫痪的护理

[目的]总结微泵持续静脉补钾治疗低钾型周期性瘫痪中需注意的护理问题.[方法]对40 例低钾型周期性瘫痪的患者给予微泵持续静脉补钾中给予全程护理.[结果]血清钾在1～2 d恢复正常,且无高血钾症状,无心律失常.[结论]使用微泵持续补钾,可使患者血清钾浓度缓慢而持续上升,并稳定在正常水平加上全程有效的护理,避免了高钾相关并发症的发生,治疗安全有效.     

低钾性瘫痪104例临床分析

目的：总结低钾性瘫痪的常见病因和临床表现。方法：回顾分析104例低钾性瘫痪患者的主要临床表现及辅助检查。结果：低钾性瘫痪的常见病因有低钾性周期性瘫痪，甲亢性周期性瘫痪，肾小管性酸中毒等。血钾水平与肌无力不完全平行，血钾越低患者临床症状及其他辅助检查的变化也就越重，治疗效果也越差。患者肌力下降可不对称，71例(68％)有肌痛或主观感觉障碍，58例(56％)有肌酸磷酸激酶(cPK)增高。呼吸肌麻痹和致命性心律失常是死亡的主要原因。结论：血钾水平与肌无力症状不完全平行，可出现肌痛、主观感觉异常、cPK增高。呼吸肌麻痹和致命性心律失常是死亡的主要原因，不典型低钾性瘫痪应与格林一巴利综合征、多发性肌炎等进行鉴别。     

低钾型周期性麻痹36例临床分析

目的:探讨低钾型周期性麻痹的临床特点,进一步认识低钾型周期性麻痹的诊断及治疗。方法:对36例低钾型周期性麻痹患者的临床表现及辅助检查结果进行回顾性分析。结果:男女比例8∶1,青年男性为高发,散发多见。36例患者中继发于甲亢者15例。四肢腱反射变化显著,36例患者中反射消失6例、减退18例、正常8例、活跃4例。有心电图资料者36例,有典型心电图低血钾改变者30例。有血清CPK资料者18例,升高者6例。结论:低钾型周期性麻痹的正确诊断是关键,治疗及时与否与预后密切相关。     

急诊低钾性周期性麻痹48例临床分析

目的 总结低钾性周期性麻痹（HOKPP）的临床表现和治疗，探讨其发病机制及预防措施。方法回顾分析48例急诊低钾性周期性麻痹患者的临床资料。结果 48例患者中，原发性40例，其中有家族史者3例，散发37例；继发于甲亢者8例。有心电图资料者48例，其中，正常10例，有典型低血钾改变者38例。经过口服和静脉注射钾后，全部病例均痊愈出院。结论 血清钾及心电图的检查有利于早期诊断及治疗HOKPP。继发性HOKPP者要加强原发病治疗，避免各种诱因是防止复发的关键。     

低钾性瘫痪63例临床分析

低钾性瘫痪是急诊内科的常见症状,一组与钾离子代谢有关的代谢性疾病,以突发性骨骼肌弛缓性瘫痪为特征,病因复杂多样。现对我科收治的63例低钾性瘫痪患者临床表现、病因以及治疗效果进行分析,以期提高对本病的诊疗水平。     

低钾型周期性麻痹46例临床分析

周期性麻痹是临床上常见的疾病,以周期性反复发作的骨骼肌短暂性弛缓性瘫痪为特点的一组疾病,多伴有钾离子代谢的异常,以低钾型周期性麻痹最常见。低钾型周期性麻痹如何治疗及补钾的量及速度是否恰当直接影响患者的预后。1999年1月~2003年12月我科共收治低钾型周期性麻痹患者46例,现报告如下。1临床资料1.1一般资料本组46例,男39例,女7例,年龄15~52岁,平均33.5岁。反复发作两次以上者19例。临床表现:46例均有肢体对称麻木、乏力,尤以下肢为显著。双上肢肌力1级6例,2级5例,3极16例,4级12例,5级7例。双下肢肌力0级4例,1级8例,2级16例,3级12例,…     

低血钾麻痹临床分析

目的 :观察低钾型麻痹的临床特点 ,探讨其治疗方法。方法 :分析 30例低血钾麻痹病人的临床表现、辅助检查及治疗方法。结果 :本组病人以男性居多 ,肢体软瘫以双下肢近端为重 ,肌张力低 ,90 %心电图异常 ,一般病人按常规补钾方法完全缓解 ,重度及危重病人应当增加静脉补钾浓度和速度。结论 :该病根据临床特点 ,不难作出正确诊断 ,补钾浓度和速度视病情而定     

低钾性周期性麻痹患者的病因分析及护理经验总结

目的分析低钾性周期性麻痹患者的病因,并总结其护理经验。方法选取2013—2019年于广西医科大学第九附属医院急诊科就诊的97例低钾性周期性麻痹患者作为研究对象,根据患者临床资料,分析其发病诱因、总结护理经验。结果97例低钾性周期性麻痹患者中,性别以男性为主;发作季节以夏季为主;麻痹部位以四肢为主。51例低钾性周期性麻痹患者有明显诱因,占52.58%,其中上呼吸道感染导致21例,运动导致9例,饮料导致21例。42例低钾性周期性麻痹患者为甲亢性低钾性周期性麻痹,占43.30%。经补钾治疗、健康教育等措施后,所有患者均救治成功。结论临床应重视低钾性周期性麻痹患者的护理评估、治疗中护理及康复后护理,使患者得到全面、有效的护理干预,进而提升治疗效果。     

Cisplatin-induced hypokalemic paralysis

INTRODUCTION: Profound hypokalemic conditions resulting from cisplatin therapy have been known to produce hypokalemic paralysis in rare cases. We describe such a case of cisplatin-induced hypokalemic paralysis. CASE SUMMARY: A 15-year-old Persian girl with ovarian dysgerminoma presented with severe generalized weakness and paraplegia 1 week after the fourth course of cisplatin-based chemotherapy. On physical examination, there was symmetric flaccid paralysis and areflexia in all of the extremities and particularly in the lower limbs. Her serum potassium concentration was 1.7 mmol/L. Metastatic disease was excluded by a comprehensive systemic evaluation. Complete clinical and paraclinical recovery was achieved after short-term administration of potassium supplement. DISCUSSION: Adverse drug reactions are common with cisplatin, but the drug is only rarely associated with hypokalemic paralysis. Based on the Naranjo causality algorithm, an objective assessment revealed cisplatin to be a probable cause of hypokalemic paralysis in this case. This adverse drug event--whether isolated or secondary to hypomagnesemia--may be deceptive, leading to a fatal mistake in the oncology setting, and should therefore be precisely differentiated from cancer-related complications. CONCLUSIONS: This case suggests that cisplatin should be added to the list of agents causing hypokalemic paralysis. Regular serum electrolyte measurement, the early detection of cation deficiency, and appropriate replacement of cations are all recommended.     

Force assessment in periodic paralysis after electrical muscle stimulation

OBJECTIVE: To obtain an objective measure of muscle force in periodic paralysis, we studied ankle dorsiflexion torque during induced paralytic attacks in hyperkalemic and hypokalemic patients. SUBJECTS, PATIENTS, AND METHODS: Dorsiflexor torque after peroneal nerve stimulation was recorded during provocative tests on 5 patients with hypokalemic or hyperkalemic disorders and on 2 control subjects (1995-2001). Manual strength assessment was simultaneously performed in a blinded fashion. Standardized provocation procedures were used. RESULTS: The loss of torque in hyperkalemic patients roughly paralleled the loss of clinically detectable strength, whereas in the hypokalemic patients, pronounced torque loss occurred well before observed clinical effects. No dramatic changes occurred in the control subjects. Torque amplitude decreased more than 70% in all patients during the provocation tests; such decreases were associated with alterations induced in serum potassium concentrations. CONCLUSIONS: Stimulated torque measurement offers several advantages in characterizing muscle dysfunction in periodic paralysis: (1) it is independent of patient effort; (2) it can show a definitely abnormal response early during provocative maneuvers; and (3) characteristics of muscle contraction can be measured that are unobservable during voluntary contraction. Stimulated torque measurements can characterize phenotypic muscle function in neuromuscular diseases.     

Licorice consumption causing severe hypokalemic paralysis

Hypokalemic paralysis due to licorice consumption is extremely rare, with only 40 cases in the English literature describing paralysis secondary to exposure to licorice in candies, medications, chewing tobacco, and herbal preparations. We describe a patient who suffered life-threatening hypokalemic paralysis caused by consumption of licorice in the form of a tea sweetener superimposed on long-term consumption of licorice candy. Aggressive fluid and potassium replenishment produced complete and lasting recovery. To our knowledge, this is the first report of hypokalemic paralysis due to exposure to licorice as a tea sweetener, a common custom among the Arab population. The case emphasizes the importance of considering patients' cultural backgrounds and local customs, which often may lead the treating physician to the correct clinical diagnosis.     

Hypokalemic paralyses: a review of the etiologies, pathophysiology, presentation, and therapy.

Acute hypokalemic paralysis is an uncommon cause of acute weakness. Morbidity and mortality associated with unrecognized disease include respiratory failure and death. Hence, it is imperative for physicians to be knowledgeable about the causes of hypokalemic paralysis, and consider them diagnostically. The hypokalemic paralyses represent a heterogeneous group of disorders with a final common pathway presenting as acute weakness and hypokalemia. Most cases are due to familial hypokalemic paralysis; however, sporadic cases are associated with diverse underlying etiologies including thyrotoxic periodic paralysis, barium poisoning, renal tubular acidosis, primary hyperaldosteronism, licorice ingestion, and gastrointestinal potassium losses. The approach to the patient with hypokalemic paralysis includes a vigorous search for the underlying etiology and potassium replacement therapy. Further therapy depends on the etiology of the hypokalemia. Disposition depends on severity of symptoms, degree of hypokalemia, and chronicity of disease.     

甲状腺功能亢进症合并低钾性周期性麻痹的观察及护理

通过对48例甲状腺功能亢进症合并低钾性周期性麻痹病人的观察及护理,分析其发病特点,采取针对性的治疗和相应的整体护理措施进行防治.包括预防诱发因素,有效补钾,控制原发病,加强肌力、生命体征的观察,进行心理护理和健康宣教等.结果48例病人均在原发病控制的基础上痊愈出院.     

低钾型周期性瘫痪临床特点分析

目的总结分析低钾型周期性瘫痪(HOPP)的临床特点。方法回顾分析38例HOPP患者的临床表现及主要辅助检查。结果 38例HOPP患者中有18例由多种诱因诱发,8例为甲状腺功能亢进症,其症状与甲状腺功能无平行关系。HOPP表现为肢体瘫痪,呈对称性,近端重于远端,从下肢发展到上肢。血清钾均降低,22例出现白细胞、中性粒细胞增高,22例有肌酶学变化,以肌酸磷酸激酶(CK)增高为主。口服补钾治疗为主要措施,甲亢性低钾型周期瘫痪须合用抗甲状腺药物及β受体阻滞剂。结论 HOPP发作由多种诱因诱发,部分与甲状腺功能亢进症有关。多数有肌酶学变化,以CK增高明显。     

Thyrotoxic hypokalemic periodic paralysis triggered by high carbohydrate diet

Thyrotoxic hypokalemic periodic paralysis is an uncommon disorder characterized by elevated thyroid hormone, muscle weakness or paralysis, and intracellular shifts of potassium leading to hypokalemia. This article presents a case of thyrotoxic hypokalemic periodic paralysis in a 22-year old Hispanic man with nonfamilial thyrotoxic hypokalemic periodic paralysis triggered by a high carbohydrate diet. Laboratory studies showed elevated thyroid hormone, decreased thyroid-stimulating hormone, and hypokalemia. Rapid reduction in thyroid hormone levels by giving antithyroid drugs such as propylthiouracil and prompt potassium therapy with frequent measurements of serum potassium levels during therapy to avoid catastrophic hyperkalemia when potassium starts to shift back from intracellular to extracellular compartments can lead to successful outcome.