Hyponatremia-induced Seizures in Schizophrenic Patient Treated with Olanzapine

Severe hyponatremia (serum sodium concentration <120 mEq/L) is a well-known etiology of acute symptomatic seizure. Severe hyponatremia may occur as a rare but clinically important adverse reaction of psychotrophic drugs. Among them, patients with psychogenic polydipsia have especially higher risk of severe hyponatremia. We present a schizophrenic patient with polydipsia who developed severe hyponatremia and symptomatic seizures while receiving olanzapine treatment.

Primary Polydipsia in Children: Two Case Reports

Primary polydipsia (PP) is marked by an increase in thirst, and most often presents in patients with psychiatric illnesses. Although uncommon in children, we experienced cases of PP in a 15-month-old boy and a 5-year-old girl. Both were admitted to the hospital with symptoms of polydipsia and polyuria that appeared 1–3 months before admission. Brain magnetic resonance imaging in both patients was normal. A water restriction test was performed after hospitalization and showed normal results. The symptoms improved after the parents were instructed to implement water-intake restriction for 2 weeks. Our report provides useful information for the treatment of PP in children.

Rabdomiólise recorrente secundária à hiponatremia em doente com polidipsia psicogênica primária / Recurrent rhabdomyolysis secondary to hyponatremia in a patient with primary psychogenic polydipsia

A rabdomiólise é caracterizada por destruição de tecido muscular esquelético, sendo as suas principais causas o trauma, os tóxicos e os distúrbios hidroeletrolíticos. Entre esses últimos, inclui-se a rabdomiólise induzida por hiponatremia, uma situação rara, que ocorre principalmente em doentes com polidipsia psicogênica. Esta acomete maioritariamente doentes com esquizofrenia, cursando com hiponatremia em quase 25% dos casos. É também nesse contexto que a rabdomiólise secundária a hiponatremia ocorre mais frequentemente. Neste artigo, descreveu-se o caso de um homem de 49 anos, com antecedentes de esquizofrenia, medicado com clozapina, trazido ao serviço de urgência por quadro de coma e convulsões. Foi objetivada hiponatremia hiposmolar grave, com edema cerebral em tomografia computorizada, sendo feito posteriormente o diagnóstico de hiponatremia secundária à polidipsia psicogênica. Foi iniciada terapêutica de correção de hiponatremia e internado em unidade de terapia intensiva. Feita correção de hiponatremia, contudo apresentou analiticamente marcada rabdomiólise, de agravamento crescente, com creatinofosfoquinase de 44.058UI/L no 3º dia de internação. Houve posterior redução progressiva com a terapêutica, sem ocorrência de lesão renal. Este caso alerta para a necessidade de monitorização dos marcadores de rabdomiólise na hiponatremia grave, ilustrando um quadro de rabdomiólise secundária à hiponatremia induzida por polidipsia psicogênica, situação a considerar em doentes sob terapêutica com neurolépticos.

Rhabdomyolysis is characterized by the destruction of skeletal muscle tissue, and its main causes are trauma, toxic substances and electrolyte disturbances. Among the latter is hyponatremia-induced rhabdomyolysis, a rare condition that occurs mainly in patients with psychogenic polydipsia. Psycogenic polydipsia mostly affects patients with schizophrenia, coursing with hyponatremia in almost 25% of the cases. It is also in this context that rhabdomyolysis secondary to hyponatremia occurs most often. In this article, the case of a 49-year-old male with a history of schizophrenia, medicated with clozapine, and brought to the emergency room in a state of coma and seizures is described. Severe hypoosmolar hyponatremia with cerebral edema was found on a computed tomography examination, and a subsequent diagnosis of hyponatremia secondary to psychogenic polydipsia was made. Hyponatremia correction therapy was started, and the patient was admitted to the intensive care unit. After the hyponatremia correction, the patient presented with analytical worsening, showing marked rhabdomyolysis with a creatine phosphokinase level of 44.058UI/L on day 3 of hospitalization. The condition showed a subsequent progressive improvement with therapy, with no occurrence of kidney damage. This case stresses the need for monitoring rhabdomyolysis markers in severe hyponatremia, illustrating the condition of rhabdomyolysis secondary to hyponatremia induced by psychogenic polydipsia, which should be considered in patients undergoing treatment with neuroleptics.

Hypotonic hyponatremia by primary polydipsia caused brain death in a 10-year-old boy

Hypotonic hyponatremia by primary polydipsia can cause severe neurologic complications due to cerebral edema. A 10-year-and-4-month-old boy with a psychiatric history of intellectual disability and behavioral disorders who presented with chief complaints of seizure and mental change showed severe hypotonic hyponatremia with low urine osmolality (serum sodium, 101 mmol/L; serum osmolality, 215 mOsm/kg; urine osmolality, 108 mOsm/kg). The patient had been polydipsic for a few months prior, and this had been worse in the previous few days. A diagnosis of hypotonic hyponatremia caused by primary polydipsia was made. The patient was in a coma, and developed respiratory arrest and became brain death shortly after admission, despite the treatment. The initial brain magnetic resonance imaging showed severe brain swelling with tonsillar and uncal herniation, and the patient was declared as brain death. It has been reported that antidiuretic hormone suppression is inadequate in patients with chronic polydipsia, and that this inadequate suppression of antidiuretic hormone is aggravated in patients with acute psychosis. Therefore, hyponatremia by primary polydipsia, although it is rare, can cause serious and life-threatening neurologic complications.

Clinical Application of V2 Receptor Antagonists / 대한내과학회지

Hyponatremia results from a relative excess of total body water compared with the sodium content. Except for primary polydipsia, vasopressin activation plays a major role in pathogenesis of water retention. Consequently, the increase of solute-free water clearance by inactivating vasopressin action would be a more reasonable therapeutic approach than the addition of sodium. The V2 vasopressin receptor is mainly localized to the collecting ducts in the kidney and causes water reabsorption via water channels. Selective V2 receptor antagonists or vaptans were recently introduced to clinical practices and may be useful for correcting dilutional hyponatremia. Clinical trials have shown that vaptans are effective in increasing the serum sodium concentration in patients with syndrome of inappropriate anti-diuresis and congestive heart failure and that they might be safe as long as patients are allowed free accesses to water. However, the indications for using vaptans need to be more refined, and the question of their long-term cost-effectiveness should be answered. In addition, the potential roles of vaptans in ameliorating the growth of cysts in polycystic kidney disease, saving diuretics in edematous disorders, and retarding the progression of chronic kidney disease are being explored.

Hyponatremia with Neurological Symptom in Patients with Chronic Schizophrenia : Five Cases / 대한정신약물학회지

Hyponatremia frequently occurs in patients with chronic schizophrenia and has various causes such as compulsive drinking, neuroleptics, and physical illness. If not corrected immediately, it leads to severe problems such as seizures, change in mental status, and even death. We detected five cases of hyponatremia with neurological symptoms in patients with chronic schizophrenia. One case had a long history of primary polydipsia, whereas the other four cases had no history of polydipsia. We speculated that the cause in these latter four cases was neuroleptics or physical illness. All five cases improved with conservative treatment. Possible implications and the need for future study are discussed.

The Significance of Plasma ADH in Differential Diagnosis of Central Diabetes Insipidus / 대한내분비학회지

BACKGROUND: Although the water restriction test(WRT) has been used as a standard test for the differential diagnosis of diabetes insipidus(DI), the measurement of plasma ADH concentration is also known to be useful method for differential diagnosis. Recent studies have shown that some patients with idiopathic central DI(CDI) were found to have a lesion on follow-up imaging studies. There have been no report in Korea on plasma ADH measurement for the differential diagnosis of DI, nor on follow-up imaging study of the idiopathic CDI. METHODS: We retrospectively reviewed the clinical and laboratory findings of 26 patients(12 men, 14 women, age 9-65 years) with CDI, including pituitary MRI or CT scan, who had been diagnosed with WRT and had undergone plasma ADH concentration measurement. RESULTS: 1) Clinical features of the patients with complete CDI did not differ from those of patients with partial CDI. 2) Maximal urine osmolality of complete CDI and partial CDI were 168+/-69mOsm/kg and 431+/-141mOsm/kg, respectively, and the percentage increase in the urinary osmolality after ADH injection was 209+/-149% and 29+/-17%, respectively. 3) Among the 26 patients, 10 patients had their plasma ADH measured. Nine patients in this group were diagnosed as CDI by WRT and plasma ADH concentration of the 9 was compatible for CDI. The plasma ADH level was also inappropriately low in one patient who had been diagnosed with primary polydipsia by WRT, the patient was diagnosed as partial CDI. 4) The findings of follow-up MRI revealed isolated thickening of the pituitary stalk in two cases of idiopathic CDI diagnosed initially with MRI. CONCLUSION: This study suggests that the measurement of plasma ADH can ensure a better differential diagnosis between partial CDI and primary polydipsia, and that the patients with idiopathic CDI should be examined regularly with MRI brain scan, including the pituitary gland.

A Case of Diabetes Insipidus Following Tuberculous Meningitis / 대한내과학회지

Tuberculous menigitis is relatively common disease and delay in treatment is associated with many neurologic sequelae. Of the neurologic disorder, diabets insipidus is extreamly rare. Diabetes insipidus is a syndrome characterized by the excretion of abnormally large volumes of dilute urine. It is divided into central diabets insipidus, nephrogenic diabetes insipidus, primary polydipsia and gestational daibetes insipidus. In this four type of diabetes insipidus, central diabetes insipidus is a polyuric disorder results from a lack of sufficient antidiuretic hormone to effect appropriate concentration of the urine for water conservration. We report a 25-year old male who had prolonged head ache and subsequently followed by polyuria. He was dia gonsed as the tuberculous meningitis by laboratory find ing and smear of CSF, and diagnosed central diabetes insipidus by serum osmolality & Na+ & AVP (arginine va sopressin), urine osmolality & specific gravity, adminis tration of vasopressin. He maintained the water balance of body by administration of vasopressin, but without im provement of mental status, sudden cardiac arrest occurs on 20th hospital day