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Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista de Educación e Investigación en Emergencias is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: The progression of 10-30% of prostate cancer (PC) to metastasis and its resistance to androgen deprivation therapy (ADT) constitutes metastatic castration-resistant prostate cancer (mCRPC), in which new therapies such as abiraterone improve survival, but with significant cardiovascular side effects such as QT prolongation and hypokalemia. The association between torsade de pointes (TdP) ventricular arrhythmias and abiraterone is rare, which is why we report this case. Clinical case: An 81-year-old man was seen in the emergency room after syncope, with an initial ECG showing a right bundle branch block, supraventricular extrasystoles with QTc prolongation, and subsequent TdP associated with severe hypokalemia and hypomagnesemia. Ventricular systolic function was slightly reduced, and he was found to have mild coronary artery disease. His management required defibrillation along with hypokalemia and hypomagnesemia correction, resulting in QTc normalization. Abiraterone was discontinued and corticosteroid supplementation was added. The adrenal axis results were compatible with hyperaldosteronism secondary to the recent use of abiraterone. The patient was discharged without any complications. Conclusions: Hormone therapy in PC has cardiovascular repercussions; therefore, a multidisciplinary approach and follow-up is essential in elderly patients with structural abnormalities that predispose them to major complications such as acquired long QTc and TdP. [ABSTRACT FROM AUTHOR]

Copyright of Acta Medica Colombiana is the property of Acta Medica Colombiana and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Médicas UIS is the property of Universidad Industrial de Santander and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Ginecología y Obstetricia de México is the property of Federacion Mexicana de Ginecologia y Obstetricia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Potassium is an essential cation for multiple physiological processes and potassium disorders, also known as dyskalemias, imply an increased risk of cardiovascular and neurological complications. The present review aims to outline the main strategies for the management of patients with potassium disorders in the hospital setting. For the management of hyperkalemia, we propose that the therapeutic approach should include etiologic evaluation, evidence-based pharmacologic management, monitoring of therapeutic response, and timely decision on initiation of dialysis. For hypokalemia, we suggest initial assessment of severity, pharmacologic management, and monitoring of response to therapy. Despite the limitations of the primary evidence for the management of potassium disorders, the present recommendations emphasize practices based on the best available evidence. [ABSTRACT FROM AUTHOR]

Copyright of Revista Mexicana de Endocrinología, Metabolismo y Nutrición is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Thyrotoxic Hypokalemic Periodic paralysis (PPHT) is a rare complication of hyperthyroidism. The case of a 50-year-old patient with no previous history of chronic diseases is presented, who presented recurrent episodes of weakness and quadriparesis, with normokalemia and without obvious symptoms of hyperthyroidism, which delayed the diagnosis of thyrotoxic periodic paralysis, until the frank presentation of hypokalemia. [ABSTRACT FROM AUTHOR]

Background: Thyrotoxic Periodic Paralysis (PPT) is an uncommon complication of hyperthyroidism, it is the most frequent cause of acute flaccid paralysis in adults. Material and methods: A retrospective observational study was carried out in 2 reference hospitals of the social security in Lima-Peru, which included 22 patients diagnosed with PPT during the period 2014-2021. Results: the average age at diagnosis was 35.77 ± 9.6 years, all of mixed race, in 82% of the patients the diagnosis of hyperthyroidism was established from this entity, the etiology in 95% was autoimmune (Graves-Basedow) except for one whose etiology was toxic multinodular goiter. The triggering event reported in 54% of patients was the intake of copious food high in carbohydrates, followed by exercise (27%), the most frequent presentation time was during the morning (41% of the cases), the main weakness pattern compromised lower limbs (45% paraplegia, 18% paraparesis), only 36% were diagnosed with PPT in their first episode of motor weakness. Conclusions: We consider that this condition should be suspected in any young male patient of any ethnicity with acute muscle weakness, associated with low serum potassium levels and symptoms of thyrotoxicosis, although its absence should not rule out the diagnosis. The precipitating factor should be identified as much as possible and initial therapy with propanolol with or without intravenous or oral potassium replacement should be established, with adequate subsequent monitoring to minimize the risk of rebound hyperkalemia. [ABSTRACT FROM AUTHOR]

Copyright of Ginecología y Obstetricia de México is the property of Federacion Mexicana de Ginecologia y Obstetricia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: we present the case of a patient with hypokalemic periodic paralysis (HPP), which is a type of muscular channelopathy caused by a genetic alteration. Clinical case: a 13-year-old male adolescent with no significant family history. He started with episodes of flaccid paralysis of the four extremities upon awakening, the duration was variable, and without compromise of mental functions. In one of the episodes, severe hypokalemia (1.6 mmol/L) was documented, with recovery after electrolyte correction. HPP was suspected, requesting a genetic panel in which a heterozygous pathogenic variant was identified in the CACNA1S gene, classifying it as type 1 HPPH. Conclusions: HPP is a diagnostic and therapeutic challenge; its early identification can help to reduce comorbidities in these patients. [ABSTRACT FROM AUTHOR]

Copyright of Médicas UIS is the property of Universidad Industrial de Santander and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Enfermería en Cardiologia is the property of Asociacion Espanola de Enfermeria en Cardiologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: The aim of this study was to synthesize the evidence on the causes of sudden cardiac death (SCD) associated with hypokalemia in individuals ≥15 to <65 years of age without structural heart disease. Case report. We reported a case and collected SCD cases following the PECO strategy. We conducted a bibliographic search of the literature published up to November 30, 2021. We included 25 cases. The mean age was 33.8 ± 2.4 years. Of the total cases, 60% were male and 60% corresponded to acquired etiologies. Thyrotoxicosis was the etiology of 8% of cases. The QTc interval was prolonged in 90% of the cases in which it could be recorded. Sixty percent of cases occurred out of hospital. Only 24% of episodes resulted in death. Conclusions. Thyrotoxicosis is a rare cause of hypokalemic sudden cardiac arrest (SCA). Hypokalemic SCA seems to be associated with better clinical results compared to SCA associated with hyperkalemia or normokalemia. [ABSTRACT FROM AUTHOR]

Copyright of Revista Facultad de Medicina de la Universidad Nacional de Colombia is the property of Universidad Nacional de Colombia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Acta Médica Peruana is the property of Colegio Medico del Peru and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Mexicana de Endocrinología, Metabolismo y Nutrición is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Thyrotoxic periodic paralysis is an infrequent and potentially lethal complication of hyperthyroidism. It is characterized by muscle weakness episodes affecting legs more than arms with proximal muscle predominance. The incidence in Asians is 2% and of 0.1-0.2% in the rest of the hyperthyroid population, with no epidemiologic records in Mexico that can establish the real incidence of this condition. CLINICAL CASES: There are reported two cases: Case number 1. A 28-year-old male patient, with a history of thinner and adhesive inhalation, presented to the emergency department with new onset of weakness of lower limbs and fall from his own height. He presented thyrotoxic signs and symptoms (tachycardia, thyroid orbitopathy and diffuse goiter) and hypokalemia. Hyperthyroidism was subsequently diagnosed biochemically. Case number 2. A 38-year-old male patient, with history of vitiligo, presented to the emergency department with acute muscle weakness of the lower limbs that impeded him from walking. No thyrotoxic signs were found on examination. Hypokalemia was documented and the patient was later diagnosed with hyperthyroidism. CONCLUSIONS: Only a few cases of this condition have been described in Mexico. Because of its lethal potential, the performance of a thyroid profile made routinely in patients with paralysis and hypokalemia would be useful since the absence of thyrotoxic signs and symptoms does not exclude the diagnosis. [ABSTRACT FROM AUTHOR]

Ondansetron belongs to a class of medications called 5HT3 receptor antagonists with antiemetic use indicated for the control of nausea induced by chemotherapy, radiotherapy, and surgery. This medication has been associated with very few serious side effects. Currently, Ondansetron has been linked to cases of ventricular arrhythmias and sudden death. This case is of a 67-year-old male patient treated in the emergency department for a chronic hypokalemia, treated with fluid therapy, ranitidine, amlodipine, and ondansetron in a time of 20 minutes, after the administration of the latter, he presented with sudden death. [ABSTRACT FROM AUTHOR]

Potassium is the main intracellular cation, its asymmetric distribution between intra and extracellular space relies mainly on the activity of the Na+/K+ ATPase pump. Any variation in potassium levels may alter the functionality of excitable tissues, underlining the importance of these precise regulatory processes. In this article we review the mechanisms responsible for the regulation of potassium balance with particular emphasis on the renal regulation of potassium excretion. This is followed by a brief discussion of the classification, pathophysiology and diagnostic approach of the most common tubulopathies. The internal balance of potassium refers to the regulation of the intra/extracellular distribution of this cation, avoiding short term fluctuations in potassium concentration induced by variations in dietary potassium content. Internal balance is regulated by insulin and catecholamines acting through specific intracellular signaling mechanisms. The external balance of potassium are the predominantly renal mechanisms that adjust potassium excretion to match the potassium dietary intake. The excretion of potassium by the kidney results from the balance between potassium reabsorption in the proximal nephron and the complex potassium secretory mechanisms of the distal nephron. Among the principal regulating factors of potassium secretion in the distal nephron are the delivery of sodium and water and aldosterone. Mineralocorticoid activity is regulated intracellularly by WNK proteins. The electrolyte and acid-base profile as well as the presence of hypo or hyperkalemia are the cornerstones for the diagnostic approach of hereditary or acquired tubulopathies. Knowledge of the homeostatic mechanisms that regulate potassium balance are a guide for the clinician to the correct diagnosis and therapy of the most common disorders of potassium excretion. [ABSTRACT FROM AUTHOR]

Copyright of Nefrologia is the property of Revista Nefrologia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Habanera de Ciencias Médicas is the property of Universidad de Ciencias Medicas de La Habana and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Hypokalemic periodic paralysis is generally caused by autosomal dominant mutations in the voltage-dependent calcium channel gene; seizures of weakness usually persist for hours or days before gradually resolving; the serum potassium level may be low or normal during the crisis. This disorder can present in an acquired way in conditions such as digestive losses of potassium, potassium-depleting diuretics, among others. The case of a 53-year-old white-skinned patient who came to the clinic due to loss of muscle strength in all four limbs, and preserved osteotendinous reflexes it is describe. In the tests, only the low serum potassium values (1.99 mmol / L) stand out. The rare frequency with which this disorder occurs, the form of presentation in this patient, and the probability of confusing it with other diseases, motivated the publication of the article. [ABSTRACT FROM AUTHOR]

Objective: To describe electrolyte and acid-base imbalances in patients with hyperglycemic crisis attended at emergency in a general hospital in Chiclayo. Methods: A case series of diabetic patients with hyperglycemic crisis that were followed for 3 hours. Clinical, demographic, blood gases, serum glucose and electrolytes were gathered from patient's charts. Results: 52 patients were evaluated; mean age was 55.1 ± 16.9 years and 29 (55.8%) were females. Mean time to diagnosis was 4.3 ± 5.4 months; 13 (25.0%) occurred at onset of diabetes and 4 (7.7%) died. The most common symptom was mental confusion in 14 (26,9%) of patients, 30 (57,7%) had acute renal failure. Hyponatremia in 26 (50.0%) patients and hypokalemia in 18 (34.6%) were the most common electrolyte abnormalities found. Metabolic acidosis was more frequently found in patients with ketoacidosis than in hyperosmolar coma (85.0 vs 15.0%; p<0.0001). Acute renal failure occurred in 76.7% among patients with ketoacidosis and in 23.3% of patients with hyperosmolar coma (p=0.74). Conclusions: the frequency and complications of diabetic ketoacidosis and of hyperosmolar coma as well as the electrolyte abnormalities differed from those reported in the literature. [ABSTRACT FROM AUTHOR]

Copyright of Biomédica: Revista del Instituto Nacional de Salud is the property of Instituto Nacional de Salud of Colombia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

BACKGROUND: Arterial hypertension secondary to primary hyperaldosteronism is becoming more frequent. Unilateral adrenal adenoma is a common cause of primary hyperaldosteronism, its clinical and biochemical presentation is similar to that of the aldosterone-producing adenoma. CLINICAL CASE: A 59-year-old male patient who attended to the emergency room due to sudden diminishment of muscle strength of right hemibody, limitation of gait, difficulty for articulating words and deviation of the commissure to the left. In imaging studies, computed tomography of the adrenal glands showed a hypodense image between 8-12 UH compatible with right adrenal adenoma of 12 x 16 x 16 mm. CONCLUSION: Although its diagnosis remains a challenge, the importance in the recognition of this disease is that most of the times it allows a specific therapy of surgical and curable type, thus avoiding the deleterious effects of aldosterone in the cardiovascular system and in the beta cells. [ABSTRACT FROM AUTHOR]

Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Universidad Médica Pinareña is the property of Editorial Ciencias Medicas and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Medicina (Buenos Aires) is the property of Medicina (Buenos Aires) and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Revista Medicina is the property of Revista Medicina and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Background: The most dispensed phytotherapeutic products in Spain are laxatives. Anthracenic laxatives such as aloe vera (Aloe spp.) or cascara sagrada (Rhamnus purshianus) could be involved in drug interactions due to the risk of hypokalemia caused by their continued use. Objectives: To carry out an analysis of the dispensing situation of these laxatives and detect potential interactions in pharmacies of the Province of Seville. Material / Methods: A descriptive, observational study made from 14 Pharmacy Offices, through the application of a questionnaire about the use of medicinal herbs. The potential interactions described in the EMA and ESCOP monographs were identified, and the risk factors for them (advanced age, polymedication and frequency of use) were analyzed. Results: The sample was constituted by 252 patients. 24.6% (n=62) consumed anthracene laxatives, more than 50% daily. The percentage of association with other drugs was 70%. Potential interactions have been identified in 40% (n=26) of the patients, based on the association of the laxative with diuretic drugs, with drugs that could prolong the QT interval, or with both at the same time. In all of them, the existence of one or several Risk Factors for Interaction (FRI) was detected. *Conclusions: The results obtained show the need for updated training by community pharmacists on the benefits and risks of these phytoterapics products. Its protocolized dispensation would favor the identification of possible pharmacological interactions and their safe and rational use. [ABSTRACT FROM AUTHOR]

Copyright of Revista Mexicana de Endocrinología, Metabolismo y Nutrición is the property of Publicidad Permanyer SLU and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Rhabdomyolysis is a condition with a broad spectrum of presentation that can range from mild asymptomatic disease to fatal complications due to electrolyte imbalance, arrhythmias and/or acute renal injury. We report the case of a 35-year-old woman, hypertensive, who was admitted for muscle weakness following a gastrointestinal condition. Biochemically with severe hypokalemia, elevated creatinekinase, conserved renal function, hypocalcemia and metabolic alkalosis. Their comprehensive evaluation culminated in the diagnosis of primary hyperaldosteronism secondary to an aldosterone-producing adenoma which was surgically removed without complications. The presentation of Conn's syndrome with hypokalemia rhabdomyolysis is exceptional since most cases are diagnosed with normokalemia or mild hypokalemia from the secondary hypertension protocol. A high level of suspicion and integral evaluation are necessary to arrive at the correct diagnosis. [ABSTRACT FROM AUTHOR]

Aldosteronoma is a suprarrenal cortex tumor producer of aldosterona and it is the main cause of primary hyperaldosteronism, is diagnosed mainly among 30 and 60 years old, predominantly in women 1.5:1, usually unilateral but occasionally bilateral (8%). Most patients with hyperaldosteronism have normal serum potassium levels at diagnosis, which should not be an exclusion criterion for the diagnosis. We must suspect aldosteronoma in patients with hypertension, hypokalemia and metabolic alkalosis. Also we can search in patients with family history of primary hyperaldosteronism, incidentaloma, hypertension and previous study of secondary hypertension. This paper reports the case of a 39-year-old female patient, with hypertension and hipokalemia. The diagnosis has made with high aldosteron serum levels and abdominal computed axial tomography, which showed a right adrenal tumor without renal involvement. The laparoscopic adrenalectomy and pathology study confirmed aldosteronoma. Aldosteronoma has a diverse clinical presentation, this is why we need to establish it as a differential diagnosis in patients with secondary hypertension. Laparoscopic adrenalectomy is the gold standard treatment for the aldosteronoma. [ABSTRACT FROM AUTHOR]

Thyrotoxic periodic paralysis is an unusual complication of hyperthyroidism that frequently presents in a dramatic fashion, needing treatment in an emergency department or admission to an intensive care unit. It is characterized by recurrent episodes of flaccid muscle paralysis, hypokalemia and elevated levels of triiodothyronine (T3) and thyroxine (T4). Potassium supplementation and B-adrenergic blockers are essential in the prevention of cardiopulmonary complications, and the effective control of hyperthyroidism is indicated to prevent the recurrence of paralysis. [ABSTRACT FROM AUTHOR]

Hypokalemic thyrotoxic periodic paralysis is a rare disorder characterized by severe muscle weakness with low serum potassium levels in hyperthyroid patients. We describe a 28- years-old man who was admitted to a first level health center with a history of muscle weakness and a fall from his height without loss of consciousness. He was transferred to a regional Hospital (in Colombia) where, in a physical examination, was noticed an enlarged size of thyroid gland. Thyroid function tests and levels of thyroid stimulating hormone (TSH) were requested, which were abnormal. This case report attempts to spread the knowledge of a disease considered rare in the region, in order to highlight some clinical and pathophysiological aspects, the importance of always be considered in patients with this clinical presentation and making an appropriate treatment and diagnosis. [ABSTRACT FROM AUTHOR]

Copyright of Acta Medica Colombiana is the property of Acta Medica Colombiana and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Introduction: The juxtaglomerular cell tumor is a rare cause of hypertension in young patients, which was first described by Robertson in 1967 and coined by Kihara en1968.1 Up to date, fewer than 100 cases have been reported. Clinically these patients have hypertension, hyperaldosteronism and hypokalemia secondary to excessive renin secretion of by juxtaglomerular cells. Case report: We present a case of juxtaglomerular cells tumor, functional producing renin, which was treated with laparoscopic lumpectomy, who evolved properly, referring symptoms characterized by hypertension and hypokalemia. Conclusion: The renal juxtaglomerular cell tumors are a rare pathology, although rarely malignant, this pathology in most cases it is a functional tumor which produces hiperreninemia and secondary hyperaldosteronism causing hypertension difficult to control and hypokalemia, so it should be considered for surgical treatment which becomes curative in almost 90% of cases. [ABSTRACT FROM AUTHOR]

Copyright of Iatreia is the property of Universidad de Antioquia and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

We describe a case of a 20 years old man, who consulted to the emergency room for two hours of paresthesias and loss of muscle strength In the lower limbs, until he presented complete Inability to rise from a chair. During the last two months, the patient presented five episodes similar to this, In the morning, mild, of short duration, and with spontaneous remissions. Four months earlier he had been having palpitations, loss of 12 kilograms of weight with polyphagia, heat sensitivity, abundant defecation, and tremor. Thyrotoxichypokalaemic periodic paralysis (PPHT) is an emergency that can occur predominantly from proximal muscle weakness until complete paralysis, with the risk of death secondary to severe hypokalemia. The diagnosis is confirmed by the presence of clinical or biochemical thyrotoxicosis associated with hypokalemia. In PPHT, there is activity increase of the Na K-ATPase pump given by an increase in beta-adrenergic stimulation associated with an excess of thyroid hormone. Common precipitating factors are a high carbohydrate intake and strenuous exercise, although there are many others. It is important to ask for hyperthyroidism in individuals with paralysis or muscle weakness and hypokalemia. This condition has been described mainly in Asian men, but should be considered also in our country. [ABSTRACT FROM AUTHOR]

With the widespread use of proton pump inhibitors (PPIs) have appeared unexpected effects adverse. Recently there have been case reports of severe hypomagnesaemia associated with PPIs with producing of hypokalemia, hypocalcaemia and hypoparathyroidism leading to clinical manifestations endanger life of the patients. The cause of hypomagnesaemia seems to be an alteration in the intestinal absorption induced by prolonged use of PPIs. This is an unknown adverse effect by clinicians and therefore goes unnoticed as the cause of hypomagnesaemia. The diagnosis requires a high degree of clinical suspicion. It should monitor serum magnesium levels in patients treated which PPIs. [ABSTRACT FROM AUTHOR]

A 57-year-old man with chronic alcoholism was admitted to our hospital due to disturbance of consciousness and polyradiculitis. Laboratory examination revealed metabolic acidosis, hypokalemia and hypophosphataemia. Alcoholic ketoacidosis is a common disorder in alcoholic patients. All patients present with a history of heavy alcohol misuse, preceding a bout of particularly excesive intake, which had been terminated by nausea, vomiting and abdominal pain. The most important laboratory results are: normal or low glucose level, metabolic acidosis with a raised anion GAP, low or absent blood alcohol level and urinary ketones. The greatest threats to patients are: hypovolemia, hypokaliemia, hypoglucemia and acidosis. Alcohol abuse may result in a wide range of electrolyte and acid-base disorders including hypophosphataemia, hypomagnesemia, hypocalcemia, hypokalemia, metabolic acidosis and respiratory alkalosis. Disturbance of consciousness in alcoholic patients is observed in several disorders, such drunkenness, Wernicke encephalopathy, alcohol withdrawal syndrome, central pontine myelinolysis, hepatic encephalopathy, hypoglucemia and electrolyte disorders. [ABSTRACT FROM AUTHOR]

Solvent abuse and intoxication are common and are associated with various disorders, such as muscle weakness, hypokalemia, severe metabolic acidosis, neurological, renal, gastrointestinal, and electrolytes alterations among others. We report eight cases in the service of Nephrology, Hospital Universitario, Monterrey Mexico, and review the pathophysiological mechanisms. [ABSTRACT FROM AUTHOR]

Oral rehydration is the method of choice for mild to moderate dehydration secondary to diarrhea. Intravenous hydration is indicated in hypovolemic shock, severe dehydration, severe hyponatremia or hypernatremia, persistent vomiting, paralytic ileus, in dehydrated patients with impaired consciousness or seizures, and when there is clinical deterioration or no improvement after 8 hours of oral rehydration. Intravenous hydration varies depending on the severity, type of dehydration (isonatrémic, hyponatremic or hypernatremic) and associated ion and acid-base deficits. It is performed in 2 phases: the first is the emergency phase to restore blood volume in cases of hypovolemic shock and the second phase to replenish deficits and to supply maintenance requirements and concurrent loss of fluid and electrolytes. Basal needs are calculated by the method of Holliday and Segar, and for patients weighing more than 30 kg. the patient's body surface is employed as the base for calculations. Fluid and electrolyte deficits are estimated according to specific schemes and formulas. Common complications of dehydration (metabolic acidosis and hypokalemia) should also be addressed with specific indications. Intravenous rehydration in the newborn with dehydration secondary to diarrhea is the same as in infants, but the particular electrolyte balance at this age should be considered in order to avoid complications. Examples of calculations for intravenous hydration for each type of dehydration (isonatrémic, hyponatremic and hypernatremic) are given. [ABSTRACT FROM AUTHOR]

We report of a 12 year-old girl who presented with severe hypokalemia, as low as 1.6 mEq/L, secondary to repeated vomiting and prolonged fasting. Management was complex due to the degree of the fluid and electrolyte imbalance. In the few published reports of severe hypokalemia in previously healthy patients we have not found cases as severe as the one which is presented. [ABSTRACT FROM AUTHOR]

Thyrotoxic hypokalemic periodic paralysis is an acute and reversible episode of muscular weakness associated with a thyrotoxic state. It most commonly occurs in Asiatic patients with Graves' disease, but it can be seen in any ethnic group. The crises are precipitated by b-adrenergic overstimulation or by hyperinsulinemia, factors associated with hyperactivity of the Na-K ATPase pump, a state that produces an intracellular K+ sequestration. Generally, it manifests itself at night or very early in the morning, commonly after a high-carbohydrate diet or intense physical activity. Proximal muscles of the lower extremities are first affected to later extend to the rest; in serious cases cranial nerves and respiratory muscles can be involved. The clinical episode can be spontaneously resolved in 3 to 36 hours but nevertheless, medical treatment is necessary to prevent lethal complications related to hypokalemia, such as cardiac arrhythmias or respiratory arrest. The definitive control of THPP is obtained by avoiding the precipitating events and by seeking a complete suppressive treatment of the hyperthyroid state. Periodic hypokalemic thyrotoxic paralysis is infrequent in clinical practice and as such is not recognized early during the diagnostic approach. It is important to spread its knowledge to all emergency medical services. [ABSTRACT FROM AUTHOR]

Hombre de 50 años de edad sin antecedentes patológicos que se presenta con imposibilidad para movilizar piernas y brazos de inicio súbito. A la exploración neurológica se encontró parálisis flácida de las cuatro extremidades, ausencia de reflejos osteotendinosos, sensibilidad conservada y precordio arrítmico; por lo que inicialmente se sospechó síndrome de Guillain-Barré (SGB). Los laboratorios iniciales reportaron potasio sérico de 1.3 mEq/L modificando la impresión diagnóstica hacia parálisis hipocalémica aguda. Las pruebas de función tiroidea mostraron patrón de hipertiroidismo. La recuperación de la función motora fue total tras la reposición de potasio. [ABSTRACT FROM AUTHOR]

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