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。     

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.     

心理护理对低钾性周期性麻痹患者抑郁的影响

目的探讨低钾性周期性麻痹患者抑郁心理状态及心理护理干预措施。方法对46例低钾性周期性麻痹患者及30名健康成年人采用Zung抑郁量表（SDS）进行抑郁心理评分比较,进而制订针对低钾性周期性麻痹患者的心理干预措施。将46例低钾性周期性麻痹患者随机分为干预组和对照组各23例。分别接受心理护理干预和常规护理。比较干预前后2组SDS评分及抑郁发生率。结果低钾性周期性麻痹患者SDS评分分值及抑郁心理发生率高于健康成年人。给予心理干预后,干预组SDS评分分值及抑郁发生率显著低于对照组。结论低钾性周期性麻痹患者SDS评分分值偏高,抑郁发生率较高,心理护理干预能够有效改善患者的心理状态,促进患者身心健康。     

心理护理对低钾性周期性麻痹患者抑郁的影响

目的 探讨低钾性周期性麻痹患者抑郁心理状态及心理护理干预措施.方法 对46例低钾性周期性麻痹患者及30名健康成年人采用Zung抑郁量表(SDS)进行抑郁心理评分比较,进而制订针对低钾性周期性麻痹患者的心理干预措施.将46例低钾性周期性麻痹患者随机分为干预组和对照组各23例.分别接受心理护理干预和常规护理.比较干预前后2组SDS评分及抑郁发生率.结果 低钾性周期性麻痹患者SDS评分分值及抑郁心理发生率高于健康成年人.给予心理干预后.干预组SDS评分分值及抑郁发生率显著低于对照组.结论 低钾性周期性麻痹患者SDS评分分值偏高,抑郁发生率较高,心理护理干预能够有效改善患者的心理状态,促进患者身心健康.     

新莞人低钾型周期性麻痹的调查分析及护理

目的：探讨新莞人低钾型周期性麻痹发生原因及特征,提出护理干预及预防措施。方法：选择低钾型周期性麻痹患者78例,总结分析发病原因及特征。并提出护理干预措施。结果：低钾型周期性麻痹以新莞人为主,男性多于女性,多发于青壮年为,与来莞时间、劳动强度、生活习惯、居住环境、饮食习惯、基础疾病有密切联系。经积极治疗及护理,78例患者低钾症状缓解,肌力恢复正常。仅3例患者在补钾过程中出现反跳性高血钾,经使用胰岛素、利尿、补液处理后血钾浓度恢复正常。结论：对低钾型周期性麻痹患者要注重原发病的积极治疗,加强对新莞人的健康教育,提高患者工作生活质量,减少低钾型周期性麻痹的发生或复发。     

低钾性瘫痪40例临床分析

目的:探讨低钾性瘫痪的诊断及治疗。方法:分析40例低钾性瘫痪患者的一般情况、临床表现、辅助检查及诊断分型,并给予相应治疗。结果:40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,少数累及呼吸肌,发作时血清钾低,补钾后短期内恢复。20例原发性低钾性瘫痪者中1例为家族性,19例为散发性;20例继发性低钾性瘫痪者中2例为肾上腺皮质腺瘤,2例为肾小管性酸中毒,16例为甲亢。治疗应首选口服补钾,同时行病因治疗。结论:全面认识低钾性瘫痪的临床表现、诊断及治疗将会给低钾性瘫痪患者带来良好疗效。     

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.     

个体化护理在治疗低钾型周期性麻痹的意义

目的 探讨个体化护理时治疗低血钾型周期性麻痹的意义。方法对43例低血钾型周期性麻痹住院患者实施个体化护理进行总结。结果依据患者的不同心理状态、症状、体征、病情经过及治疗中的反应，实施有针对性的个体化护理后，不但能及时发现患者起病的原因，而且能够尽早地予以治疗，使本组的治愈率达97．7％。结论个体化护理对低血钾型周期性麻痹的诊断及治疗有着极其重要的作用。     

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     

周期性麻痹发作期患者一氧化氮表达的临床意义

目的了解一氧化氮(NO)对周期性麻痹患者发病的影响.方法低钾型周期性麻痹患者,在弛缓性瘫痪发作期及肌力恢复后,同时检测血钾、NO、一氧化氮合酶(NOS).观察不同病期患者血NO、NOS的变化与疾病的关系.结果42例患者在瘫痪发作期血NO、NOS均明显降低;经治疗后,NO、NOS随血钾和肌力的恢复而趋于正常.瘫痪期NO的变化与血钾降低的程度呈正相关(r=0.3511,P＜0.05);与肌无力程度无明显相关.结论NO参与了周期性麻痹患者弛缓性瘫痪的发病.其作用机理可能与操纵钾离子通道而使血钾降低有关.     

Apparently persistent weakness after recurrent hypokalemic paralysis: a tale of two disorders

A 19-year-old woman presented with recurrent hypokalemic paralysis, followed by apparently persistent symptoms due to coexisting osteomalacia. Distal renal tubular acidosis type 1 (dRTA1) linked the metabolic abnormalities and occurred as an extraglandular feature of Sj?gren syndrome (SS). This case highlights the fact that in the setting of recurrent hypokalemia, apparently progressive weakness should be distinguished from primary hypokalemic paralysis and evaluated for dRTA1, as the metabolic alterations are potentially treatable. Further dRTA1 may precede the occurrence of sicca syndrome in SS.     

Lower-Extremity Weakness in a Teenager Due to Thyrotoxic Periodic Paralysis

Background

Thyrotoxic hypokalemic paralysis is the hallmark of thyrotoxic periodic paralysis (TPP). TPP is a potentially deadly complication of hyperthyroidism that occurs because of rapid and dramatic intracellular shift of potassium. This transference results in severe hypokalemia and clinically manifests itself as muscle weakness or paralysis. This condition predominantly affects males of Asian descent, and its presentation can range from mild to severe, as seen in our case.

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。     

Severe hypokalemia in thyrotoxic periodic paralysis

Thyrotoxic hypokalemic periodic paralysis is an uncommon but sometimes fatal disease in which early recognition and therapy may prevent untoward complications. The case of a 26-year-old Chinese man who presented to the emergency department with rapidly progressive profound weakness and severe hypokalemia (serum potassium, 1.2 mEq/L) is presented. The patient required endotracheal intubation, ventilatory assistance, and intravenous potassium administration. Emergency medical evaluation and management of this entity are discussed.     

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。     

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。     

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.     

重症低钾型周期性瘫痪原因分析及护理干预

目的探讨低钾型周期性瘫痪发生原因，以提高对该病护理的重视，为临床护理奠定基础。方法选择低钾型周期性瘫痪患者64例，总结分析发病原因并提出护理干预措施。结果低钾型周期性瘫痪患者，经积极治疗及护理，低钾症状缓解出院。结论护理上要重视评估，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。     

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.