Cases reported "Hyponatremia"

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1/40. Hyponatraemic convulsion secondary to desmopressin treatment for primary enuresis.

    The case of a 6 year old child who presented with convulsions and coma after unsupervised self administration of intranasal desmopressin (DDAVP) for nocturnal enuresis is presented. Children with enuresis can be embarassed by their condition and may believe that multiple doses of their nasal spray may bring about a rapid resolution. water intoxication is an uncommon but serious adverse effect of treatment with intranasal DDAVP. These patients may present with seizure, mental state changes, or both. Basic management consists of stopping the drug, fluid restriction, and suppressive treatment for seizures. Recovery is usually rapid and complete. Administration of the nasal spray in children should be supervised by parents to prevent highly motivated children from accidental overdose. The risks of high fluid intake need to be carefully explained to both parents and children.
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2/40. Fatal child abuse by forced water intoxication.

    BACKGROUND: Although water intoxication leading to brain damage is common in children, fatal child abuse by forced water intoxication is virtually unknown. methods: During the prosecution of the homicide of an abused child by forced water intoxication, we reviewed all similar cases in the united states where the perpetrators were found guilty of homicide. In 3 children punished by forced water intoxication who died, we evaluated: the types of child abuse, clinical presentation, electrolytes, blood gases, autopsy findings, and the fate of the perpetrators. FINDINGS: Three children were forced to drink copious amounts of water (over 6 L). All had seizures, emesis, and coma, presenting to hospitals with hypoxemia (PO2 = 44 /- 8 mm Hg) and hyponatremia (plasma Na = 112 /- 2 mmol/L). Although all showed evidence of extensive physical abuse, the history of forced water intoxication was not revealed to medical personnel, thus none of the 3 children were treated for their hyponatremia. All 3 patients died and at autopsy had cerebral edema and aspiration pneumonia. The perpetrators of all three deaths by forced water intoxication were eventually tried and convicted. INTERPRETATION: Forced water intoxication is a new generally fatal syndrome of child abuse that occurs in children previously subjected to other types of physical abuse. Patients present with coma, hyponatraemia, and hypoxemia of unknown etiology. If health providers were made aware of the association, the hyponatremia is potentially treatable.
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3/40. Postoperative coma induced by hyponatremia after laparoscopy--a case report.

    hyponatremia is a common clinical entity which may occur during the course of many medical illnesses. However disastrous sequelae or even death may develop in young, generally healthy patients who receive simple elective surgery. Here we present a case of a 34-year-old female, without past history of cardiopulmonary or renal disease, after undergoing laparoscopic surgery developed mental status changes and lapsed into coma on the second postoperative day. She was found to have a serum sodium level of 110 mEq/L. After careful treatment and a protracted hospital stay, the patient recovered uneventfully. The pathophysiology of postoperative hyponatremia is discussed and attention is called to the special vulnerability of menstruant women who carry a much increased risk of mortality and morbidity associated with hyponatremia.
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4/40. Can delirium relieve psychosis?

    A delirium presages a poor prognosis in hospitalized patients, but an incidental delirium is a feature of some psychiatric treatments. We report five cases in which delirium preceded the relief of affective and psychotic symptoms of a major mental illness. The experience stimulated a review of the literature on delirium in psychiatric treatments. Five inpatients (aged 53 to 69 years) with an exacerbation of chronic mental illness developed deliria from medications (n = 4) and electrolyte disturbance (n = 1). The deliria were managed with medication washout or correction of electrolyte imbalance. The progress of the patients was noted clinically and summarized. The clinical signs of delirium such as confusion, disorganized speech, sleep-wake cycle changes, and hallucinations persisted for 24 to 72 hours. As the delirium cleared, psychotic and affective symptoms improved or resolved. The improvements persisted for 1 to 5 months, with low doses of medications in two of the cases. A delirium may precede clinical improvement in affective and psychotic symptoms. Historically, some treatments for mental illness induce an incidental delirium (e.g., electroconvulsive therapy [ECT] and insulin coma). Why a delirium should presage a beneficial effect on psychosis is unclear, but the emergence of delirium may herald a beneficial pathophysiology.
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5/40. citalopram-induced severe hyponatraemia with coma and seizure. Case report with literature and spontaneous reports review.

    Numerous case reports of hyponatraemia followed increasing use of selective serotonin re-uptake inhibitors (SSRIs) but this adverse effect was only rarely observed in relation to citalopram. We report a case of severe hyponatraemia associated with deep coma, seizure, atrial fibrillation and muscle damage in a 92-year-old woman after only two doses of citalopram, and review 14 cases previously published in the literature and 28 cases spontaneously reported to Australian Drug Reaction Advisory Committee (ADRAC). The data presented suggest that citalopram, as well as SSRIs may cause hyponatraemia secondary to syndrome of inappropriate secretion of antidiuretic hormone (SIADH). The majority of symptomatic cases occurred in elderly patients (79% were older than 70 years) and in women (74%). Polymedication and concomitant use of another psychotropic drug or thiazide diuretic may precipitate and/or augment the development of hyponatraemia/SIADH. In 84% of cases, the hyponatraemia associated with citalopram was detected during the first month of treatment. High level of suspicion, close and careful monitoring of serum sodium concentration particularly in elderly patients and especially in the first month of therapy with citalopram may reduce the incidence of this serious and likely not rare adverse effect.
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6/40. Hyponatraemic coma induced by desmopressin and ibuprofen in a woman with von Willebrand's disease.

    A middle-aged woman was admitted to the hospital after being found unconscious at home. A brain CT scan excluded an intracranial bleed or other focal abnormality. Laboratory analysis showed hyponatraemia (sodium: 121 mmol L(-1)) and a low plasma osmolality, with normal sodium excretion and urine osmolality. A diagnosis of hyponatraemic coma was made. The patient was treated with water restriction; 24 h later the sodium was 135 mmol L(-1) and the patient was neurologically fully recovered. The patient, who suffered from von Willebrand's disease, had received desmopressin and ibuprofen for analgesia 2 days before after a dental intervention. She had received desmopressin several times in the past without any complications. A few patients treated with desmopressin for coagulation abnormalities have been reported to develop water intoxication and severe hyponatraemia resulting in seizures and coma. By inhibiting prostaglandin synthesis, non-steroid anti-inflammatory agents (NSAIDs) potentiate the effect of water reabsorption in the renal tubules of vasopressin, therefore enhancing water retention. Desmopressin and NSAIDs should not be used in combination in patients with bleeding disorders, but it is often followed in clinical practice. In addition, this is probably not an unusual situation in patients treated with desmopressin for other 'non-haemorrhagic' indications. This report emphasizes the need for practitioners to be aware of this rare but severe complication.
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7/40. The syndrome of inappropriate antidiuretic hormone secretion associated with chemotherapy for hypopharyngeal cancer.

    The syndrome of inappropriate antidiuretic hormone secretion (SIADH) is characterized by hyponatremia and the plasma hypoosmolality induced by water retention attributable to persistent antidiuretic hormone (ADH) release. It has been reported that SIADH may occur due to various factors in patients with malignant tumor. We report a case of hypopharyngeal cancer complicated by SIADH following chemotherapy. A 72-year-old woman with hypopharyngeal cancer was treated by oral administration of S-1 and intravenous administration of low-dose cisplatin following radiation therapy. General fatigue and coma occurred during the third course of this chemotherapy, using S-1 and low-dose cisplatin. We believed that she had SIADH because of the results of examinations including hyponatremia, serum hypoosmolality and increasing serum ADH level. We treated her by fluid restriction and intravenous administration of hypertonic saline and furosemide, and she recovered. Unfortunately, her hypopharyngeal cancer gradually progressed and she died of acute pneumonia three months later.
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8/40. Hyponatremic coma under oxcarbazepine therapy.

    Oxcarbazepine (OXC) is considered to be a promising new antiepileptic drug with similar efficacy and better tolerability compared to carbamazepine (CBZ). However, hyponatremia is supposed to occur even more often than with CBZ. We report on a patient who developed hyponatremic coma under OXC with a serum sodium level of 115 mmol/l, the second published case of OXC-induced hyponatremia with serious clinical adverse effects.
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9/40. Peculiar venous lesions in fatal hyponatremic brain edema.

    A 19-year-old woman with a 3-year history of schizophrenia suddenly began to vomit, and rapidly developed a coma an hour after the onset of vomiting. A brain CT scan showed diffuse brain edema with compression of the ventricles. Laboratory tests showed a low serum sodium concentration of 117 mmol/L. She died 67 h after the onset of the first symptom. A postmortem examination showed diffuse swelling of the brain with bilateral uncal and tonsillar herniations. Histologically, no necrotic, hemorrhagic or encephalitic changes were seen. However, microvacuolar changes with lymphocytic infiltration were found in the venous walls (media and adventitia) mainly in the basal ganglia, thalamus and brainstem. To our knowledge, this is the first demonstration of venous alterations in fatal hyponatremic brain edema. These changes may have participated in the exacerbation of the brain edema due to functional disturbance of venous drainage.
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10/40. rhabdomyolysis after correction of hyponatremia in psychogenic polydipsia possibly complicated by ziprasidone.

    OBJECTIVE: To report a case of rhabdomyolysis related to correction of hyponatremia secondary to psychogenic polydipsia, possibly complicated by the use of ziprasidone. CASE SUMMARY: A 50-year-old white man treated for 3 weeks with ziprasidone 40 mg twice daily for chronic paranoid schizophrenia was admitted to the intensive care unit after a witnessed generalized seizure. Marked hypotonic hyponatremia was present secondary to psychogenic polydipsia. After correction of hyponatremia with intravenous NaCl 0.9%, he developed a substantial elevation in the creatine kinase level without any evidence of muscle trauma, stiffness, or swelling or any signs of neuroleptic malignant syndrome. Renal failure or compartment syndrome did not complicate the clinical picture. DISCUSSION: It is well known that severe hyponatremia can cause neurologic complications such as stupor, seizures, and even coma. hyponatremia from water intoxication (n = 28) and its correction with intravenous fluids (n = 2) may cause non-neurologic complications such as rhabdomyolysis. An explanation may lie within the calcium-sodium exchange mechanism across the skeletal myocyte or the failure of cell volume regulation secondary to extracellular hypo-osmolality. Neuroleptic medications have been linked to the development of rhabdomyolysis, with antipsychotics being the primary offenders. As of August 2005, there has been only one reported case of rhabdomyolysis related to correction of hyponatremia complicated by an atypical antipsychotic (clozapine). It is possible that ziprasidone, like clozapine, may enhance muscle cell permeability leading to rhabdomyolysis under similar conditions. CONCLUSIONS: Psychiatric patients treated with atypical antipsychotic medications should be closely monitored for rhabdomyolysis during correction of hyponatremia, thus permitting prompt therapy to limit its complications.
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