Hipodermóclise para correção de desidratação hiperosmolar e distúrbios eletrolíticos graves: relato de caso / Hypodermoclysis for correction of hyperosmolar dehydration and severe electrolyte disturbances: a case report

O tratamento de desidratação e distúrbios eletrolíticos graves é contraindicado por meio de hipodermóclise, mas o nível de evidência da recomendação se baseia na opinião de especialistas. Descreve-se caso clínico de paciente com idade avançada, com indicação de cuidados paliativos, que evoluiu com desidratação hiperosmolar com hipernatremia grave, injúria renal aguda e hipercalemia. Tratou-se a paciente com solução hipotônica por meio da técnica de hipodermóclise, com resolução completa do quadro. Conclui-se que há necessidade de mais estudos sobre o uso da hipodermóclise para o tratamento de distúrbios hidroeletrolíticos graves.

The treatment of dehydration and severe electrolyte disturbances using hypodermoclysis is usually contraindicated, but the level of evidence for its recommendation is based on expert opinion. This case report describes an older patient receiving palliative care who developed hyperosmolar dehydration with severe hypernatremia, acute kidney injury, and hyperkalemia. She was treated with hypodermoclysis using a hypotonic solution, which led to complete resolution of the condition. In conclusion, further studies on the use of hypodermoclysis for the treatment of severe hydroelectrolytic disorders are needed.

A physiology-based approach to a patient with hyperkalemic renal tubular acidosis / Abordagem diagnóstica de um paciente com acidose tubular renal hipercalêmica

ABSTRACT Hyperkalemic renal tubular acidosis is a non-anion gap metabolic acidosis that invariably indicates an abnormality in potassium, ammonium, and hydrogen ion secretion. In clinical practice, it is usually attributed to real or apparent hypoaldosteronism caused by diseases or drug toxicity. We describe a 54-year-old liver transplant patient that was admitted with flaccid muscle weakness associated with plasma potassium level of 9.25 mEq/L. Additional investigation revealed type 4 renal tubular acidosis and marked hypomagnesemia with high fractional excretion of magnesium. Relevant past medical history included a recent diagnosis of Paracoccidioidomycosis, a systemic fungal infection that is endemic in some parts of South America, and his outpatient medications contained trimethoprim-sulfamethoxazole, tacrolimus, and propranolol. In the present acid-base and electrolyte case study, we discuss a clinical approach for the diagnosis of hyperkalemic renal tubular acidosis and review the pathophysiology of this disorder.

RESUMO A acidose tubular renal hipercalêmica é uma acidose metabólica de ânion gap normal que invariavelmente indica anormalidade na secreção de íons potássio, amônio e hidrogênio. Na prática clínica, está geralmente atribuída a um estado de hipoaldosteronismo real ou aparente, causado por doenças ou toxicidade por drogas. Descrevemos um paciente de 54 anos, transplantado hepático, que foi admitido com fraqueza muscular associada à hipercalemia, potássio plasmático de 9,25 mEq/L. A investigação adicional revelou acidose tubular renal tipo 4 e importante hipomagnesemia com elevada fração de excreção de magnésio. A história patológica pregressa incluía um diagnóstico recente de Paracoccidioidomicose - uma infecção sistêmica fúngica endêmica que ocorre em algumas partes da América do Sul -, e as medicações de uso habitual continham sulfametoxazol-trimetoprim, tacrolimus e propranolol. No presente relato de caso, discutiremos uma abordagem clínico-laboratorial para o diagnóstico da acidose tubular renal hipercalêmica, assim como da hipomagnesemia, revisando a fisiopatologia desses transtornos.

Diabetes mellitus and hyperkalemic renal tubular acidosis: case reports and literature review / Diabetes mellitus e acidose tubular renal hipercalêmica: relatos de caso e revisão da literatura

ABSTRACT Hyporeninemic hypoaldosteronism, despite being common, remains an underdiagnosed entity that is more prevalent in patients with diabetes mellitus. It presents with asymptomatic hyperkalemia along with hyperchloraemic metabolic acidosis without significant renal function impairment. The underlying pathophysiological mechanism is not fully understood, but it is postulated that either aldosterone deficiency (hyporeninemic hypoaldosteronism) and/or target organ aldosterone resistance (pseudohypoaldosteronism) may be responsible. Diagnosis is based on laboratory parameters. Treatment strategy varies according to the underlying pathophysiological mechanism and etiology and aims to normalize serum potassium. Two clínical cases are reported and the relevant literature is revisited.

RESUMO Apesar de comum, o hipoaldosteronismo hiporeninêmico continua a ser uma entidade sub-diagnosticada, com maior prevalência em pacientes com diabetes mellitus. A doença cursa com hipercalemia assintomática acompanhada de acidose metabólica hiperclorêmica sem disfunção renal significativa. O mecanismo fisiopatológico subjacente não é entendido em sua totalidade, mas postula-se que a deficiência de aldosterona (hipoaldosteronismo hiporeninêmico) e/ou a resistência à aldosterona no órgão-alvo (pseudo-hipoaldosteronismo) possam ser responsáveis. O diagnóstico é fundamentado em parâmetros laboratoriais. A estratégia terapêutica varia de acordo com o mecanismo fisiopatológico subjacente e a etiologia, mas seu objetivo é normalizar o potássio sérico. O presente artigo relata dois casos e analisa a literatura relevante sobre o assunto.

Pseudohiperkalemia por trombocitosis esencial: una entidad pobremente reconocida / Pseudohyperkalaemia in essential thrombocytosis: a poorly recognized

INTRODUCCIÓN: La hiperkalemia representa una emergencia médica frecuentemente manejada en servicios de urgencia. Identificar una pseudohiperkalemia en pacientes que presentan recuentos plaquetarios elevados permite evitar terapias innecesarias e iatrogenia que pueden tener consecuencias potencialmente fatales. PRESENTACIÓN DEL CASO: Mujer de 73 años, con enfermedad renal crónica (ERC) etapa-3a (etiología no precisada). En consulta neurológica por crisis isquémica transitoria (abril 2011), se demostró hiperkalemia de 6,0 mEq/L (suero), tasa de filtración glomerular(TFG) de 51 mL/min y trombocitosis de 1.113.000 plaquetas/mm3. Se trata la hiperkalemia con furosemida y dieta pobre en potasio. Inició hidroxiurea indicada por hematología. En control nefrológico (diciembre 2012) presenta hiperkalemia de 7,5 mEq/L (suero), TFG de 37 ml/min y trombocitosis de 1.052.000 plaquetas/mm3. Electrocardiograma (ECG), sin signos de cardiotoxicidad acordes al nivel de kalemia. Se sospechó pseudohiperkalemia secundaria a trombocitosis esencial (PSTE), se suspendió atenolol, furosemida y se continuó hidroxiurea. En febrero de 2013 presentó kalemia de 6,1 mEq/L (suero), trombocitosis de 713.000 plaquetas/mm3 y TFG de 31 mL/min. En mayo de 2014 la kalemia en suero fue de 5,5 mEq/L y en plasma de 5,2 mEq/L; trombocitosis de 503.000plaquetas/mm3 y TFG de 23 ml/min, confirmándose la PSTE. DISCUSIÓN: Hiperkalemia asociada a trombocitosis exige descartar PSTE. La regresión de la kalemia junto con la trombocitosis y ECG sin alteraciones en hiperkalemia, apoyan este diagnóstico. Su confirmación exige demostrar una hiperpotasemia mayor en suero que en plasma (0,36 +/-0,18 meq/L). Tratar una pseudohiperkalemia, puede generar iatrogenia (hipokalemia y/o hemoconcentración que aumenta riesgo de trombosis). Se descarta hiperkalemia secundaria a ERC con TFG>15ml/min

INTRODUCTION: Hyperkalemia is a medical emergency often managed in emergency services. Identifying a pseudohiperkalemia in patients with high platelet counts will avoid unnecessary iatrogenic therapies, which can have potentially fatal consequences. CASE REPORT: 73 year old woman, with chronic kidney disease (CKD) stage-3a (unknown etiology). In neurological consultation by transient ischemic attack (april 2011) it was evidenced a hyperkalemia of 6.0 mEq/L (serum), glomerular filtration rate (GFR) of 51 mL/min and thrombocytosis of 1,113,000 platelets/mm3. Hyperkalemia is treated with furosemide and potassium poor diet. Started on hydroxyurea indicated by hematology. Nephrology consultant (december 2012) realized hyperkalemia of 7.5 mEq/L (serum), GFR of 37mL/min and thrombocytosis of 1,052,000 platelets/mm3. EKG with no sign of cardiotoxicity was found in relation to potassium serum level. A pseudohyperkalemia secondary to essential thrombocytosis (PSET) was suspected. Atenolol and furosemide were discontinued and hidroxiurea was continued. In February 2013 potassium serum level was 6.1 mEq/L, platelet count: 713,000/ mm3 and GFR: 31 mL/min. In may 2014 serum potassium was 5.5 mEq/L and plasma potassium was 5.2 mEq/L; platelet count: 503,000//mm3 and GFR: 23 mL/min, confirming PSET. DISCUSSION: Hiperkalemia associated with thrombocytosis requires to rule out PSET. Regression of serum potassium with platelet count and the abscense of EKG changes with simultaneous hyperkalemia, support this diagnosis. Confirmation of PSTE diagnosis needs to demonstrate a potassium serum level greater than in plasma (0.36 +/- 0.18 mEq/L). Treating a pseudohiperkalemia can generate iatrogenia (hypokalemia and/or hemoconcentration, increasing the risk of thrombosis). A hyperkalemia secondary to CKD is ruled out with GFR >15mL/min

A Case of Myotonic Dystrophy with Electrolyte Imbalance

Type 1 myotonic dystrophy (DM1) is an autosomal-dominant inherited disorder with a multisystem involvement, caused by an abnormal expansion of the CTG sequence of the dystrophic myotonia protein kinase (DMPK) gene. DM1 is a variable multisystem disorder with muscular and nonmuscular abnormalities. Increasingly, endocrine abnormalities, such as gonadal, pancreatic, and adrenal dysfunction are being reported. But, Electrolytes imbalance is a very rare condition in patients with DM1 yet. Herein we present a 42-yr-old Korean male of DM1 with abnormally elevated serum sodium and potassium. The patient had minimum volume of maximally concentrated urine without water loss. It was only cured by normal saline hydration. The cause of hypernatremia was considered by primary hypodipsia. Hyperkalemic conditions such as renal failure, pseudohyperkalemia, cortisol deficiency and hyperkalemic periodic paralysis were excluded. Further endocrine evaluation suggested selective hyperreninemic hypoaldosteronism as a cause of hyperkalemia.

Hiperpotassemia: conduta sinoventricular em paciente idoso, em insuficiência renal e cetoacidose diabética / Hyperpotassemia and sinoventricular conduction in elderly patient with renal insufficiency and diabetic ketoacidosis

Paciente idoso, portador de cardiomiopatia isquêmica, hipertenso, com leve disfunção renal e diabético insulinodependente, por suspensão do uso da insulina desenvolveu cetoacidose com grave desidratação e severa hiperpotassemia, que reverteu com o uso de medicações. Analisam-se interessantes aspectos eletrocardiográficos inerentes ao caso.

An elderly patient with ischemic cardiomyopathy, hypertension, slight renal dysfunction and insulindependentdiabetes developed ketoacidosis aftersuspending insulin use, with severe dehydration and severe hyperpotassemia, both reverted throughmedications. This paper analyzes interesting eletrocardiographic aspects of this case.

Bloqueo AV completo, reversible, en relación a hiperkalemia grave por enalapril y espironolactona: caso clínico / Complete atrioventricular block, reversible, related to serious hyperkalemia due to enalapril and spironolactone: case report

La hiperkalemia es una de las principales complicaciones potenciales del uso de drogas del tipo IECA, bloqueadores ARAII y antagonistas del receptor de aldosterona, en relación a su dosis, su eventual uso combinado y la función renal del paciente. A continuación se reporta el caso de un paciente de 71 años de edad, hipertenso y diabético que se encontraba en tratamiento con Enalapril 10 mg c/12 h y Furosemida 40 mg a/ 12 h, que sufre una bloqueo aurículo ventricular de 3º grado, secundario a una hiperkalemia de 8.53 mEq/l.

Successful resuscitation of prolonged hyperkalemic cardiac arrest following succinylcholine administration in possibly undiagnosed myopathy

We report a 3 years old male with undiagnosed myopathy, who developed cardiac arrest secondary to hyperkalemia following succinylcholine administration.The patient underwent prolonged cardiopulmonary resuscitation [CPR], which ended successfully after applying external pace maker. He was discharged home eleven days after the cardiac arrest for follow up of his myopathy

Continuous arteriovenous haemofiltration to regulate hyperkalaemia during renal transplantation: a case report.

Progressive hyperkalaemia is common in end stage renal disease patients waiting for renal transplantation. Ventricular tachycardia and ventricular fibrillation due to hyperkalaemia are life-threatening complications in these patients. In live and related renal transplant, after induction and anaesthesia, ventricular fibrillation and pulmonary oedema occurred. After immediate resuscitation by defibrillation and intravenous injection of adrenaline, the patient was put on continuous femoral arteriovenous haemofiltration (CAVH). This improved his pulmonary oedema, controlled hyperkalaemia and surgery could be completed uninterruptedly. After anaesthetising live and related kidney donor for nephrectomy, since it is not prudent to stop recipient surgery because of unforeseen complication, the authors wish to recommend CAVH as an alternative method to prevent life threatening cardiac complication of hyperkalaemia.

Pseudo-hypo aldosteronism Type II.

A 50-day-old infant diagnosed as meningitis had persistently elevated serum potassium, low serum bicarbonate and normal serum sodium. She had metabolic acidosis with low TTKG, low serum renin and low normal serum aldosterone with no renal failure or extra renal causes of hyperkalemia. Hence a diagnosis of Type II pseudo-hypoaldosteronism was made. She was started on oral thiazide following which her serum electrolytes normalized.

Severe muscle weakness due to hyperkalemia.

Hyperkalemia is a commonly encountered electrolyte disturbance in patients with renal insufficiency. It develops very rapidly when potassium is supplemented while a patient is on a potassium-sparing diuretic. Most often it remains asymptomatic and manifests in the form of electrocardiographic changes. Muscle weakness and paralysis although described is seldom observed in clinical practice. We report one such case.

Comparison of aminophylline and insulin-dextrose infusions in acute therapy of hyperkalemia in end-stage renal disease patients.

OBJECTIVE: This study was performed to compare the efficacy of aminophylline and insulin-dextrose infusion as acute treatment modality of hyperkalemia in patients with end-stage renal disease (ESRD). METHODS: This study was conducted on 30 ESRD patients with serum potassium > 6.0 mEq/L. These patients were divided in two groups of 15 each. Group A patients were treated with aminophylline infusion, whereas group B patients were treated with insulin-dextrose infusion. Serum potassium and other biochemical parameters such as blood sugar were measured at beginning of treatment followed by at 60 minutes, 180 minutes, and 360 minutes after treatment. RESULTS: Intervenous infusion of aminophylline lowered plasma potassium from 6.48 +/- 0.39 mEq/L to 5.92 +/- 0.40 mEq/L at 180 minutes (p < 0.001 Vs basal) and 6.05 +/- 0.53 mEq/L at 360 minutes (p < 0.01 Vs basal). Whereas, intravenous infusion of insulin-dextrose decreased plasma potassium from 6.59 +/- 0.31 mEq/L to 5.76 +/- 0.32 mEq/L (p < 0.001 Vs basal) and 5.84 +/- 0.21 mEq/L (p < 0.001 Vs basal). Thus in both groups, plasma potassium levels were significantly less than basal levels throughout the study. The decrease in plasma potassium was significantly more in group B patients (p value is < 0.001 after 60 minutes, < 0.05 after 180 minutes and < 0.05 after 360 minutes) when compared to group A patients. There was one episode of hypoglycemia (blood sugar < 60 mg%) in insulin-dextrose infusion group. No other side effects were observed throughout the study. CONCLUSION: Aminophylline is an effective modality for acute treatment of hyperkalemia, though it is less effective than insulin-dextrose infusion. However, more studies are required to confirm these results.

Un caso atípico de abdomen agudo / Atipical case of acute abdomen

Introducción: El potasio es el ión más importante en el funcionamiento de las células excitables, la hiperkalemia se relaciona con efectos peligrosos sobre miocardio, músculo liso y nervios periféricos. A pesar de la clara asociación fisiopatológica entre el aumento del potasio y el íleo paralítico, no se han hallado casos que mencionen al abdomen agudo como forma de presentación en la búsqueda bibliográfica por Medline de los últimos diez años. Se presenta por tanto un caso en el cual el motivo de consulta fue dolor abdominal. Presentación: Paciente de sexo femenino, 83 años, consulta por dolor abdominal muy intenso asociado a náuseas y oliguria de 24 hs de evolución. Antecedentes: tromboembolismo de pulmón a repetición a pesar de estar anticoagulada de forma suficiente, hipertensión pulmonar, fibrilación auricular, medicada con furosemida, espironolactoma, digoxina, acenocumarol. Examen físico: desasosegada, taquipneica, soplo de regurgitación tricúspidea, abdomen doloroso, sin ruidos hidroaéreos. Urea: 108 mg por ciento, creatinina: 1,91 mg/dl, K: 6,8 meq, Ph: 7,52, Po2: 142, PCo2 35, COH3 29,9. ECG: ritmo nodal. Colon por enema: dolicocolon. Ecografía abdominal y endoscopía esófago-gástrica normales. Se trata con soluciones polarizantes, cediendo el dolor abdominal y retornando el ritmo cardíaco a fibrilación auricular, recupera el ritmo diurético y normaliza urea y creatinina. Conclusiones: 1) Esta hiperkalemia sin fallo renal crónico previo fue multifactorial. a- Uso prolongado de espironolactona en paciente deshidratada con escaso aporte de Na. b- Seudohipoaldosteronismo. c- Alcalosis mixta. 2) Debido a la acción del potasio sobre las células excitables, la hiperkalemia puede provocar íleo paralítico y presentarse como abdomen agudo sobre todo en pacientes polimedicados

Paralisia periódica: análise clínica de 20 pacientes / Periodic paralysis: clinical analysis in 20 patients

Este estudo consiste da avaliaçäo de 20 pacientes com diagnóstico de paralisia periódica (PP) sendo descritos aspectos epidemiológicos, manifestaçöes clínicas, exames subsidiário, tratamento e evoluçäo. Dezesseis pacientes tinham a forma hipocalêmica (5 familiares, 5 esporádicos, 5 tireotóxicas e 1 secundária). Näo houve casos de PP normocalêmica. Houve predomínio do sexo masculino (14 pacientes). Todos os 5 pacientes com forma tireotóxica eram do sexo masculino e nenhum deles tinha origem oriental. Somente 4 pacientes tinham a forma hipercalêmica (3 familiares, 1 esporádico). Nas duas formas os ataques ocorreram preferencialmente no período da manhä sendo o repouso após exercício o fator desencadeante mais importante. No entanto observamos que 75 por cento dos pacientes com a forma hipercalêmica referiram crises de curta duraçäo (< 12 horas). Crises mais prolongadas foram referidas por 43 por cento dos pacientes com a forma hipocalêmica. A maioria das crises caracterizava-se por fraqueza generalizada, predominando nos membros inferiores e sendo sua frequência variável. A creatinoquinase foi avaliada em 10 pacientes e 8 tinham níveis elevados que variaram de 1,1 a 5 vezes o valor normal. A eletroneuromiografia foi realizada em 6, mas o fenômeno miotônico foi a única alteraçäo encontrada em 2 pacientes. Inibidores da anidrase carbônica, principalmente a acetazolamida, usados no tratamento profilático em 9 pacientes mostraram uma boa resposta em todos. Embora a PP seja algumas vezes considerada doença benigna, encontramos sintomas respiratórios em 5 pacientes, miopatia permanente em 1, alteraçöes eletrocardiográficas durante crise em 4; óbito durante paralisia ocorreu em 2 pacientes. Assim, o correto diagnóstico e o tratamento imediato säo cruciais. Este estudo mostra que o hipertireoidismo é importante causa de PP em nosso meio, mesmo em pacientes näo orientais. Assim, a investigaçäo endócrina é mandatória já que as crises de paralisia só desaparecem após a normalizaçäo dos níveis hormonais

Mechanisms of hyperkalemia associated with hyporeninemic hypoaldosteronism in streptozotocin-induced diabetic rats

This study was aimed at investigating the mechanisms of clinically important overt hyperkalemia in diabetes mellitus with underlying hyporeninemic hypoaldosteronism known as a classic model of the syndrome of hyporeninemic hypoaldosteronism (SHH). Rats (Sprague-Dawley, male) were streptozotocin-treated (60 mg/kg, ip) and used after 60 days. Rats with plasma glucose levels higher than 300 mg/dL (mean +/- SEM, 423 +/- 20 mg/dL, n = 8) were selected as the diabetic group. Age-matched normal rats served as control (mean plasma glucose, 88 +/- 2, mg/dL, n = 8). Serum potassium concentrations and osmolalities as well as serum creatinine levels were significantly higher in the diabetic than in the control group (5.07 +/- 0.09 vs. 4.68 +/- 0.11 mEq/L; 330 +/- 14 vs 290 +/- 3 mOsm/L; 0.40 +/- 0.03 vs 0.31 +/- 0.02 mg/dL, p < 0.05). Plasma renin activity (PRA) in the diabetic group was significantly lower than that in the control group (6.0 +/- 1.0 vs 12.1 +/- 1.1 ng Al/ml/h, p < 0.001). Plasma aldosterone concentration (PAC) was also significantly lower in the former than in the latter (368 +/- 30 vs 761 +/- 57 pg/ml, p < 0.001). Renomegaly, abnormal distal tubular cells with few organelles, and increased lipid droplets with pyknotic nucleus in zona glomerulosa of the adrenal glands were noted in the diabetic group. In conclusion, multifactorial causes including insulinopenia, hyperosmolality, elevated serum creatinine level and hypoaldosteronism with possible contribution of altered distal tubular response to aldosterone may have interacted to develop hyperkalemia in these diabetic rats.

Hyperkalemic periodic paralysis associated with thyrotoxicosis.

A 32 year old male presented with episodic pure motor weakness for 1 1/2 months. On evaluation he was found to be thyrotoxic. Hyperkalemic challenge test provoked similar weakness with raised serum potassium (6 meq/L). He responded to treatment with neomercazole. Till he became euthyroid, he responded to the addition of acetazolamide to his medication. He is symptom free on antithyroid drug alone over 8 months of follow up.