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.     

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.     

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。     

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.     

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.     

Severe hypokalemia, paralysis, and AIDS-associated isospora belli diarrhea

Background: Hypokalemia of clinical significance, severe enough to cause paralysis and cardiac dysrhythmias, is an uncommon life-threatening medical disorder. Hypokalemic periodic paralysis (HPP), where an abrupt intracellular shift of potassium has occurred, must be distinguished from hypokalemic non-periodic paralysis (non-HPP), where a total body potassium deficit exists. The challenge for emergency physicians is to swiftly and accurately differentiate disease etiology and institute prompt treatment. Aggressive potassium repletion, required in non-HPP etiologies, may predispose HPP patients to dangerous and potentially fatal rebound hyperkalemia as the intracellular potassium shift resolves. Objectives: Describe the process by which HPP and non-HPP can be differentiated on clinical and laboratory grounds leading to appropriate resuscitation from severe and clinically relevant hypokalemia. Chronic diarrhea syndromes and possibly normal alkaline phosphatase levels alert the clinician to the potential for non-HPP. Case Report: A case of HIV/AIDS-associated isospora belli diarrheal illness with severe hypokalemia of the non-HPP type is presented. Historical, laboratory, and clinical findings, which assisted in the differentiation from HPP, are emphasized. Clinical progression and treatment strategies, as well as electrocardiogram findings with T-U-P fusion waves, are described in detail. Conclusion: The history, especially the time course of disease, is essential in differentiating HPP and non-HPP, allowing treatment to proceed without overcorrection and rebound hyperkalemia. Although other infectious diseases have been linked to non-HPP, to our knowledge this is the first report linking non-HPP to isospora belli diarrheal illness.     

Thyrotoxic periodic paralysis: a case report and review of the literature

Hypokalemic periodic paralysis occurring in thyrotoxicosis is rare in Caucasians and is not often highlighted as an endocrine emergency. Periodic paralysis, without familial background, manifests only in the thyrotoxic patient. Thyrotoxic periodic paralysis is a self-limiting disorder that is cured by the treatment of the underlying hyperthyroidism. We report an unusual case of acute onset weakness from thyrotoxic periodic paralysis in a young Chinese migrant who had a normal serum potassium level at the time of initial presentation, though on subsequent presentation one week later, he had the typically associated hypokalemia. We also review the literature on thyrotoxic periodic paralysis.     

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 periodic paralysis

Generalized motor weakness is a common complaint in the emergency department and has a wide differential diagnosis that includes both organic and infectious etiologies. We report the case of a previously healthy young man with symptoms of muscular paralysis and associated hypokalemia. The clinical presentation of hypokalemic periodic paralysis, its differential diagnosis, and pertinent physical findings are discussed.     

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。     

Thyrotoxic Periodic Paralysis: A Case Report and Literature Review

Thyrotoxic periodic paralysis (TPP) is a rare presentation of thyrotoxicosis most commonly associated with Graves’ disease. It is rare in Caucasians, but it affects approximately 2% of Asians (occurring in those of Chinese, Japanese, Vietnamese, Filipino, and Korean descent) with thyrotoxicosis of any cause. Typical thyrotoxic features may be absent despite biochemical thyrotoxicosis. Hypokalemia and muscle paralysis are the result of an acute intracellular shift of potassium and not due to total body potassium deficiency. TPP is a self-limiting condition that is easily corrected by treatment of the thyrotoxicosis. We present a case of a Filipino man, aged 47 years, who presented to the emergency department with acute bilateral lower extremity weakness and hypokalemia who was subsequently diagnosed with TPP due to Graves’ disease.     

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.

Thyrotoxic Periodic Paralysis: A Case Report and Literature Review

We describe a 37-year-old man with a 4-month history of episodic muscular weakness, involving mainly lower-limbs. Hypokalemia was documented in one episode and managed with intravenous potassium chloride. Hyperthyroidism was diagnosed 4 months after onset of attacks because of mild symptoms. The patient was subsequently diagnosed as having thyrotoxic periodic paralysis associated with Graves’ disease. Treatment with propranolol and methimazol was initiated and one year later he remains euthyroid and symptom free. Thyrotoxic periodic paralysis is a rare disorder, especially among Caucasians, but it should always be considered in patients with acute paralysis and hypokalemia, and thyroid function should be evaluated.     

Unusual cause of hypokalemic paralysis in aged men: Sjögren syndrome

Hypokalemic paralysis is a less recognized but reversible disorder in elderly patients. This report describes two elderly Chinese males (age 74 and 78 years) who had progressive muscle weakness and eventually paralysis. Physical examination showed symmetrical flaccid paralysis of extremities. Both had the major biochemical abnormality of profound hypokalemia (1.4 and 1.8 mmol/L) accompanied by high urine K+ excretion and hyperchloremic metabolic acidosis. A positive urine anion gap and alkaline urine pointed to the diagnosis of distal renal tubular acidosis. Large doses of potassium chloride supplementation were required to restore muscle strength. Pertinent investigations, including elevated titers of antinuclear antibody and rheumatoid factor, positive anti-Ro antibody, low serum C3 and C4 levels, and delayed saliva excretion on salivary scintigraphy suggested Sj?gren syndrome. Despite the lack of sicca syndrome at the initial presentation, both had development of typical sicca syndrome and positive Schirmer test at the 5-month and 1-year follow-up, respectively. Potassium citrate supplement and prednisolone therapy completely corrected the hypokalemia and metabolic acidosis. Extraglandular involvement with distal renal tubular acidosis preceding the typical sicca syndrome may induce hypokalemic paralysis and unveil Sj?gren syndrome in elderly males.     

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.     

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.     

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。     

Clinical perspectives on the rationale for potassium supplementation

Hypokalemia is a common electrolyte disturbance, observed in > 20% of hospitalized patients. Hypokalemia, although not formally defined, is generally considered to be when serum potassium levels fall below the normal value of 3.6 mmol/L. In contrast to other electrolytes, potassium is primarily an intracellular ion: only 2% of all potassium in the body is present in the extracellular fluid, so a small decrease in serum potassium may represent a significant decrease in intracellular potassium. Individuals with mildly decreased potassium levels (3.0–3.5 mmol/L) may be asymptomatic, but patients with more pronounced decreases may report symptoms including muscle weakness, fatigue, and constipation. Very low serum potassium levels (≤ 2.5 mmol/L) can lead to muscle necrosis, paralysis, cardiac arrhythmias, and impaired respiration, which can be life-threatening. Absent comprehensive and robust treatment guidelines, strategies for the prevention or treatment of hypokalemia, such as how to diagnose hypokalemia, when to treat patients, what dosage regimen of potassium supplementation to use and for how long, are often based on the experience of the physician and empirical evidence. However, proper evaluation and treatment of hypokalemia in patients is essential because of associated morbidities. Because small potassium deficits in serum represent large body losses, potassium repletion requires substantial and prolonged supplementation. For patients with known risk factors for hypokalemia (e.g. hypertension, heart failure, or diabetes), careful monitoring is crucial to avoid the adverse sequelae associated with potassium deficits and to ensure that adequate and timely preventive measures can be taken. In this review, we provide practical insights into the etiology, differential diagnosis, and treatment of hypokalemia, including treatment strategies for patients with known risk factors.     

Transient Hypokalemic Quadriplegia After a Lumbar Transforaminal Epidural Dexamethasone Injection: A Case Report

A 30-year-old man with no significant medical history presented with hypokalemic quadriplegia 4 hours after he received a lumbar transforaminal epidural steroid injection (ESI) containing dexamethasone and lidocaine. A comprehensive workup ruled out acquired and hereditary causes of hypokalemic paralysis. Symptoms gradually resolved within hours after potassium restoration with no residual neurologic deficits. Paralysis after transforaminal ESI is uncommon but has been associated with particulate steroids that can coalesce into aggregates and occlude vessels. To our knowledge, there have been no case reports of paralysis after ESI with dexamethasone, a nonparticulate steroid. This transient paralysis is possibly caused by the effects of glucocorticoids on Na-K channels and insulin resistance resulting in hyperglycemia and subsequent hypokalemia. We reviewed the differential diagnosis of transient paralysis after epidural steroid injection in this report.