Severe hypernatremia from a urea-induced diuresis due to body protein wasting in an insulin-resistant type 2 diabetic patient.

CONTEXT: Hypernatremia is encountered after pituitary or hypothalamic surgery and typically is secondary to vasopressin deficiency resulting in increased free water clearance with inadequate water replacement. OBJECTIVE: We report a type 2 diabetic patient with severe hypernatremia (Na⁺ = 161 mEq/L) after hypothalamic surgery. Unexpectedly, this was accompanied by persistent urinary hypertonicity and negative total but positive electrolyte free water clearance. MAIN OUTCOME MEASURE: Measurement of urinary electrolytes and urea revealed that an osmotic diuresis induced by urea derived principally by breakdown of endogenous protein was causative. Body protein losses over 48 hours were estimated to exceed 2 kg of lean mass. High-dose glucocorticoid, insulin resistance, and a postsurgical catabolic stress likely contributed. CONCLUSION: In surgically severely stressed individuals, proteolysis of endogenous protein can strongly impact body water metabolism and contribute to severe hypernatremia.

Extreme hypernatremia combined with rhabdomyolysis and acute renal failure.

Rhabdomyolysis is a life-threatening condition that involves muscle cell destruction. Among its etiologies, severe hypernatremia is a less common cause. We report a teenage girl with congenital central hypoventilation syndrome and hypothalamus dysfunction syndrome who presented with extreme hypernatremia (sodium, 211 mmol/L) with rhabdomyolysis (creatine kinase, 32,850 U/L) and acute renal failure (creatinine, 6.1 mg/dL) following gastroenteritis with 7-kg weight loss. Rhabdomyolysis subsequently led to acute renal failure and hyperkalemia. Acute hemodialysis was initiated on hospital day 3 for hyperkalemia. This resulted in a 13 mmol/L fall in serum sodium in 3 hours despite using a 156 mmol/L sodium bath, but without the development of cerebral edema or neurological defect. This report highlights an unusual cause of rhabdomyolysis in children and the experience of managing such a difficult clinical situation.

Severe hypernatremia and hyperosmolality exacerbated by an herbal preparation in a patient with diabetic ketoacidosis.

This article reports a case of severe reversible hypernatremia exacerbated by an herbal agent "goldenseal" (Hydrastis canadensis) in an 11-year-old girl with new onset type I diabetes mellitus presented with diabetic ketoacidosis. A literature review is presented and possible mechanism of hypernatremia caused by this herbal preparation is discussed.

¿Es frecuente la deshidratación hipernatrémica como causa de readmisión hospitalaria en recién nacidos? / Is hypernatremic dehydration a common readmission cause in newborns?

Objetivo: conocer la incidencia de deshidratación hipernatrémica (DH) asociada a ictericia así como sus características clínicas en neonatos ingresados a un hospital general. Material y Métodos: estudio exploratorio, prospectivo, descriptivo. Se incluyeron neonatos de término, ingresados por hiperbilirrubinemia, divididos en dos grupos, con y sin hipernatremia. Se compararon características perinatales, edad en la readmisión, pérdida de peso, fiebre, bilirrubina, manejo con antimicrobianos, presencia de alteraciones neurológicas y mortalidad. Resultados: se ingresaron 24 pacientes en un año, de los cuales 12 tuvieron sodio sérico elevado, con un promedio de 163,92 mmol/L. La incidencia fue de 5/1000 nacidos vivos. No se encontraron diferencias en cuanto a las características perinatales o cifras de bilirrubinas. La pérdida ponderal fue mayor en el grupo con DH. Dos pacientes presentaron alteraciones neurológicas y uno falleció. Conclusiones: la incidencia de la triada de deshidratación hipernatrémica, fiebre e ictericia puede ser mayor a la reportada.

[A case of extrapontine myelinolysis precipitated by correction of a hyper-osmolar state].

We report a case of extrapontine myelinolysis (EPM) precipitated by correction of a hyper-osmolar state. A 7-year-old boy presented with disturbed consciousness. Serum BUN and Na level were 48 mg/dl and 196 mmol/L, respectively. T2-weighted images and FLAIR images of MRI visualized symmetrical bilateral high signal intensity areas in the external capsule and in the thalamus. In addition, the splenium of the corpus callosum showed high signal intensity. All these lesions showed high signal intensity on diffusion-weighted images. Extrapontine myelinolysis is precipitated not only by the rapid correction of a hypo-osmolar state but also by that of a hyper-osmolar state.

Diarrea aguda: tratamiento nutricional / Acute diarrhea: nutrtional treatment

El tratamiento de la diarrea aguda consistirá básicamente en rehidratación oral si existiera deshidratación, realimentación precoz y excepcionalmente farmacológico. La rehidratación debe durar 4-6 horas, que se prolonga a 8-12 horas si la deshidratación es hipernatrémica, pasando posteriormente a la fase de mantenimiento. Las soluciones de rehidratación oral son las recomendadas, usándose en países en vías de desarrollo la solución de la OMS por las pérdidas importantes de sodio en las heces y soluciones con menor contenido de sodio en los países industrializados al ser las pérdidas de sodio menores. La realimentación debe ser lo mas precoz y equilibrada posible, recoméndandose la lactancia materna si es la forma de alimentación o la fórmula sin diluir si realiza lactancia artificial. No es aconsejable sistemáticamente las fórmulas sin lactosa. El uso de probióticos mejora el cuadro. No se precisa tratamiento farmacológico y los antibióticos sólo están indicados en pacientes inmunodeprimidos, cólera, lactantes menores de 3 meses con coprocultivos bacterianos positivos, enfermedad sistémica, infección por amebas, giardias, clostridium difficile y shigella que permanece sintomática (AU)

Transient thalamic changes on MRI in a child with hypernatremia.

Severe hypernatremia has been associated with a wide variety of central nervous system lesions. Neurologic sequelae are the usual outcome in those cases in which a lesion has been documented neuroradiologically. The authors report a 7-month-old male with severe hypernatremia who developed obtundation after correction of the electrolyte imbalance. Magnetic resonance imaging revealed bilateral thalamic signal changes that resolved on follow-up study, in accordance with complete clinical recovery. To the authors' knowledge, bilateral thalamic signal changes are previously unreported findings associated with hypernatremia. Pertinent literature and the clinical course of the authors' patient are the basis for questioning currently recommended guidelines for the rate of correction of hypernatremia.

Adipsic hypernatremia in two sisters.

We describe two sisters with chronic hypernatremia, lack of thirst, and inappropriate osmoregulated vasopressin secretion. Only one sister, who presented with microcephaly and developmental delay, showed signs of dysplasia of the midline structures (ie, septum pellucidum and corpus callosum) and a large intracranial cyst. Neither sister showed any signs of thirst, even when osmolality exceeded 337 mmol/kg. In both patients, the vasopressin secretion did not respond to either osmotic or nonosmotic stimuli or was suppressed by a water load. Plasma osmolality values returned to normal after treatment with forced hydration and a vasopressin analogue, desamino-D-arginine vasopressin. These findings indicate a severe defect in the hypothalamic osmoreceptors that control thirst and vasopressin secretion. To our knowledge, this is the first report of such a disorder in two sisters.

Lateral pontine and extrapontine myelinolysis associated with hypernatremia and hyperglycemia.

Efforts to understand and prevent pontine and extrapontine myelinolysis have focused on the correction of hyponatremia, but controversy persists. We report a woman who presented in hyperosmolar diabetic coma with hypernatremia (169 mEq/l) and hyperglycemia (954 mg/dl). Plasma sodium rapidly increased to 188 mEq/l before gradually returning to normal. She remained obtunded and died 21 days later. Autopsy showed widespread, symmetrical demyelination involving the subcortical white matter, corpus callosum, anterior commissure, extreme, external, and internal capsules, fornix, thalamus, cerebellum, and lateral pons. The central pons and lateral geniculate nuclei were uninvolved. This case illustrates that lateral pontine and extrapontine myelinolysis can be associated with hypernatremia and hyperosmolality. In both hypo- and hypernatremic states, the significant event may be an increase in serum sodium or serum osmolality of sufficient rapidity and magnitude.

[Electrolyte metabolism and emergency].

In outlining the pathology of various electrolyte metabolism abnormalities in cancer patients we considered the main clinical points between pathologies and emergency treatment. In regard to sodium (Na+) metabolism, one pathologic state that requires our attention is hypernatremia. Hypernatremia is accompanied with dehydration and is due to water loss, vomiting, diarrhea and renal insufficiency. One of the major causes of this condition is lack of the antidiuretic hormone due to intracranial metastasis of the tumor. When hypernatremia becomes severe, it is accompanied with circulatory failure, muscular asthenia, disorientation, convulsions, coma and other cerebral symptoms. Treatment consists of replenishing the water content by infusion of electrolyte solutions which should be carefully conducted after complete diagnose of the severity of the patient's pathological condition. Hyponatremia, like sick cell syndrome, is observed relatively frequently in cancer patients. When the serum Na level falls markedly, it induces cerebral edema and causes disorders of consciousness. The major treatment consists of providing both water and sodium supplements. Hyperkalemia is observed at the time of renal insufficiency, tissue lesions, vomiting, and diarrhea. When serum potassium level rises, it causes bradycardia, ventricular fibrillation, or cardiac arrest. It is important to diagnostically apprehend the severity of this condition using EKG and determining the serum K1+ level. For emergency treatment injection of calcium gluconate is very effective. Hypokalemia is often manifested by the loss of intestinal fluids due to diarrhea or during administration of diuretic agents. Clinical symptoms include neural paralysis but emergencies occur relatively infrequently. K C1 injections are used in treating this condition. Hypercalcemia is manifested in cancer patients during hyperparathyroidism. Its clinical symptoms include lassitude, tachycardia, nausea, vomiting, and renal dys-function, leading to neural symptoms in severe cases. The main treatment consists of injection of physiological saline solution and administration of calcitonin, mithramycin. Hypocalemia is manifested during renal insufficiency, lack of vitamin D, and hypothyroidism. In classic cases it causes tetanic spasms. Injection of calcium is an effective treatment but since during tetanic spasms alcalosis may easily occur, treatment should only be provided after obtaining a complete understanding of the patient's condition. The pathological conditions described above can not be said to specific to cancer but it should be kept in mind that one of their main causative factors is the involvement of mechanism which produces ectopic hormones from cancerous tissues.

Electrolyte and acid-base disturbances in the management of leukemia.

Electrolyte disturbances in leukemia can be the result of the disease process or drug therapy. One group of electrolyte abnormalities is related to the stage of the leukemic process. Included in this group are newly diagnosed patients who may show elevated serum potassium, phosphorus, and magnesium--a result of their release from malignant cells after cytotoxic therapy or their accumulation due to urate nephropathy. Patients in remission usually have normal serum electrolyte concentrations, but acute leukemia patients during relapse may have hypokalemia, hypophosphatemia, and hypomagnesemia. This imbalance may be related to cellular uptake of these electrolytes in the presence of inadequate dietary intake. Other factors contributing to electrolyte derangements, and related to the leukemic process, include hyponatremia and hypochloremia secondary to the SIADH, hypokalemia in acute monocytic or acute myelomonocytic leukemia due to lysozyme-induced tubular damage, hypercalcemia possibly secondary to leukemic infiltration of bone or parathyroid glands (with PTH release), or production of a PTH-like substance by leukemic cells. Nonspecific factors related to the disease process which may aggravate the electrolyte imbalance include gastrointestinal loss through nausea, vomiting, and malnutrition. The drug-related electrolyte abnormalities include cyclophosphamide- and vincristine-induced SIADH; decreased serum sodium, chloride, potassium, and calcium concentrations as a result of polymyxin B nephrotoxicity; hypokalemia and hypomagnesemia secondary to amphotericin B; hypocalcemia, hypophosphatemia, and hyperphosphaturia due to L-asparaginase-induced hypoparathyroidism; hypokalemia due to a nonreabsorbable anion effect of antibiotics in the distal tubule or changes in membrane ionic transport of all cells by large doses of antibiotics. Electrolyte disturbance in leukemia thus have a multifactorial pathogenesis which can best be delineated according to the stage of the leukemic process and the drugs being used. Recognition of the cause or causes in a particular patient is essential for an effective approach to management. This review emphasizes the need for routine measurement of serum electrolytes during all phases of the leukemic process.