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。     

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。     

低钾性周期性麻痹28例临床分析

目的：观察分析低钾性周期性麻痹的临床特点。方法：对1992年1月～2003年1月确诊的28例低钾性周期性麻痹的患者进行临床分析。结果：28例患者中原发性18例，无明显的家族史。继发性10例，其中继发于甲亢者6例，激素引起者4例。有心电图资料者26例，正常7例，有低血钾改变者19例。有血清肌酸磷酸激酶资料者12例，升高者6例。28例中有四肢麻木者4例，肌肉酸痛3例。结论：部分患者可有感觉异常及肌酶增高，血清钾及心电图的检查有利于早期诊断及治疗。继发性者要加强病因治疗，避免各种诱因以防止复发。     

低钾型周期性麻痹的肌酶学变化及诊断意义

低钾型周期性麻痹 (HOPP)是一种以反复发作的突发骨骼肌弛缓性瘫痪为特征的常见疾病 ,发病时伴有血钾降低 ,而且常有一些患者因为合并肌酶学升高给确断造成疑问。而长期以来人们一直认为 ,肌酶学升高是多发性肌炎和肌营养不良的重要临床特征 ,在其他肌肉疾病较为少见 ,HOPP不会出现肌酶学改变〔1〕。本研究分析 34例 HOPP患者肌酶学改变及其特点 ,探讨其对诊断的意义。1　临床资料1.1　病例 :诊断按侯熙德主编的第 3版《神经病学》HOPP标准。 34例患者中男2 9例 ,女 5例 ;年龄 16～ 6 0岁 ,平均 38岁 ;合并甲状腺功能亢进 5例 ,合并…     

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。     

低钾型周期性麻痹28例临床分析及文献复习

目的:探讨低钾型周期性麻痹(HOKPP)的临床特点,诱发因素及治疗方法.方法:分析28例病人的临床表现及辅助检查结果.结果:本组病人发病有早晨和下午两个发病高峰,腱反射呈多样性,全部病例肌张力降低,无病理征.6例(21.4%)为甲亢继发低钾型周期性麻痹,75%有心电图异常改变,所有病人经静脉及口服补钾后症状完全缓解.结论:进一步认识了低钾型周期性麻痹的临床及辅助检查特点,有利于诊断、鉴别诊断及治疗.     

低钾血症伴血清肌酸激酶增高临床意义的研究与护理对策

目的探讨低钾血症患者血清肌酸激酶(CK)改变的临床意义及护理。方法收集杭州市第一人民医院1992—2006年收治的116例低钾血症患者资料,根据患者是否有周期性麻痹分为周期性麻痹组32例和非周期性麻痹组84例,观察其血清CK改变与血钾降低程度的关系。结果周期性麻痹组32例中有23例CK升高(占71.9%),且升高的程度与血钾降低的程度呈负线性关系,在非低钾型周期性麻痹组,84例中有8例CK升高(占9.5%),但升高程度与血钾降低不具有相关性。结论CK是反映低钾患者病情的重要指标,低钾血症合并CK升高时要考虑到低钾型周期性麻痹可能。     

49例甲亢合并低钾性周期性麻痹原因分析及护理干预

目的 探讨甲亢合并低钾性周期性麻痹发生原因,以提高对此类疾病护理的重视,为临床护理奠定基础.方法 采集5年49例住院甲亢合并低钾性周期麻痹患者回顾性资料,总结分析发病原因并提出护理干预措施.结果 49例甲亢合并低钾周期性麻痹患者,经积极治疗、护理低钾症状好转带药出院.结论 甲亢合并低钾性周期性麻痹护理上要重视评估,注重原发病的积极治疗,帮助患者寻找原因,积极预防,可以减少其发病率,提高患者工作、生活质量.     

低钾性周期性麻痹病人的发病诱因分析及观察护理

笔者对52例低钾性周期性麻痹病人发病诱因进行回顾性的分析,发现其发病诱因与上呼吸道感染、腹泻、劳累、合并甲亢等多方面的因素相关。护理上加强补钾的观察,注意血清钾的监测,为治疗及护理提供重要的依据,同时加强卫生宣教,指导患者保持良好的生活习惯,积极治疗合并症,是预防低钾性周期性麻痹发病的关键。     

低钾型周期性麻痹71例临床分析

目的:探讨低钾型周期性麻痹的临床特点。方法:统计分析71例低钾型周期性麻痹的临床资料。结果:低钾型周期性麻痹好发于20～50岁青壮年,男性明显高于女性,四季均可发作,夏秋较多,部分病例临床表现不典型,可继发于甲亢等全身疾病。结论:临床上应重视对不典型病例和继发性周期性麻痹的认识,周期性麻痹应常规进行甲亢指标检查。     

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 in an African male: a case report

Thyrotoxic hypokalemic periodic paralysis is a rare manifestation of thyrotoxicosis and is rarely reported in non‐Asian populations. A 26‐year‐old Ethiopian male who presented with recurrent flaccid tetraparesis, hypokalemia, and hyperthyroidism is reported here. Thyroid function should be routinely checked in patients with acute or recurrent hypokalemic paralysis.     

^131I治疗甲亢604例近期疗效分析

目的分析^131I治疗甲亢近期临床疗效。方法根据甲状腺质量和最高吸碘率等给予604例甲亢患者个性化^131I治疗,^131I于治疗后1、3、6、12个月随访,对甲亢、Graves眼病、甲亢性心脏病、低钾周期性麻痹、谷丙转氨酶升高、粒细胞减少及甲状腺大小等的转归进行回顾性分析。结果痊愈374例（61．9％）,部分缓解101例（16．8％）,甲减112例（18．5％）,无效17（2．8％）,总有效率为97．2％,治愈率为80．4％。^131I治疗Graves眼病总有效率83．7％,治疗甲亢性心脏病总有效率95．6％,同时可以缓解低钾周期性麻痹症状,改善肝功能,升高粒细胞,缩小甲状腺。结论^131I治疗甲亢及其伴发症安全有效,但要注意甲减等并发症的发生。     

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.     

Graves病与低钾性周期性麻痹和胸腺增生的关系

目的 观察Graves病与低钾性周期性麻痹和胸腺增生的关系.方法 收集2010年1月至2011年1月临床确诊的Graves病患者62例分为两组：Graves病不伴胸腺增生组33例;Graves病伴胸腺增生组29例,同期门诊体检健康人为正常对照组30名.结果 Graves病伴胸腺增生组与不伴胸腺增生组相比,在性别、年龄、病程、是否伴有甲状腺肿大、突眼、周期性麻痹及血清游离三碘甲状腺原氨酸、血清游离甲状腺素、促甲状腺素方面,差异均无统计学意义（P均＞0.05）,正常对照组均无胸腺增生;男性Graves病伴胸腺增生患者周期性麻痹发生率62％ （8/13）,明显高于女性6％ （1/16）,差异有统计学意义（x2=10.24,P＜0.05）;男性Graves病患者周期性麻痹发生率62％（16/26）,明显高于女性6％（2/36）,差异有统计学意义（x2=22.96,P＜0.05）;Graves病患者是否伴胸腺增生与性别、年龄、病程、是否伴有甲状腺肿大、突眼、周期性麻痹及游离三碘甲状腺原氨酸、血清游离甲状腺素、促甲状腺激素无相关性（P均＞0.05）.结论 男性Graves病伴胸腺增生患者周期性麻痹发生率高于女性,在临床工作中应予鉴别,以免漏诊误诊.     

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.     

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.     

An unrecognized cause of paralysis in ED: thyrotoxic normokalemic periodic paralysis

Hypokalemic paralysis associated with hyperthyroidism (TPP) is a well-known acute electrolyte and muscle function disorder. Lesser known is normokalemic periodic paralysis associated with hyperthyroidism. We describe two cases of young men with acute muscular paralysis and bilateral impairment of sensation over the lower legs who had normal plasma potassium concentrations. They were initially misdiagnosed as having Guillain-Barré syndrome or hysterical paralysis. However, thyroid function tests showed elevated serum T(3) and T(4) and markedly depressed thyroid-stimulating hormone findings consistent with hyperthyroidism. Control of the hyperthyroidism completely abolished their periodic paralysis. Thyrotoxic normokalemic periodic paralysis (TNPP) should be kept in mind as a cause of acute muscle weakness to avoid missing a treatable and curable condition.     

Hypokalemic paralysis in a professional bodybuilder

Severe hypokalemia is a potentially life-threatening disorder and is associated with variable degrees of skeletal muscle weakness, even to the point of paralysis. On rare occasions, diaphragmatic paralysis from hypokalemia can lead to respiratory arrest. There may also be decreased motility of smooth muscle, manifesting with ileus or urinary retention. Rarely, severe hypokalemia may result in rhabdomyolysis. Other manifestations of severe hypokalemia include alteration of cardiac tissue excitability and conduction. Hypokalemia can produce electrocardiographic changes such as U waves, T-wave flattening, and arrhythmias, especially if the patient is taking digoxin. Common causes of hypokalemia include extrarenal potassium losses (vomiting and diarrhea) and renal potassium losses (eg, hyperaldosteronism, renal tubular acidosis, severe hyperglycemia, potassium-depleting diuretics) as well as hypokalemia due to potassium shifts (eg, insulin administration, catecholamine excess, familial periodic hypokalemic paralysis, thyrotoxic hypokalemic paralysis). Although the extent of diuretic misuse in professional bodybuilding is unknown, it may be regarded as substantial. Hence, diuretics must always be considered as a cause of hypokalemic paralysis in bodybuilders.