Cases reported "Hyponatremia"

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1/40. Dual facets of hyponatraemia and arginine vasopressin in patients with ACTH deficiency.

    OBJECTIVE: Hyponatraemia is often observed in patients with ACTH deficiency who are thought not to suffer from volume depletion. Their high plasma AVP levels relative to plasma osmolality are presumed to be maintained by non-osmotic mechanisms. We attempted to assess volume status from changes in selected clinical measurements related to body fluid balance in the course of i.v. fluid supplementation and following glucocorticoid (GC) replacement in ACTH-deficient patients, and to interpret plasma AVP levels in the context of the estimated volume status. PATIENTS AND DESIGN: This report consists of three parts. First, an ACTH-deficient patient with hyponatraemia and volume depletion who was followed through volume replacement to recovery after GC replacement is described (case report). Secondly, medical records of five ACTH-deficient patients with hypovolaemia and hyponatraemia were surveyed retrospectively to observe changes in serum levels of sodium, uric acid (UA) and haematocrit (Hct) following i.v. fluid supplementation of low sodium content (retrospective study). Thirdly, five ACTH-deficient patients with or without overt dehydration were studied with regard to body weight, blood pressure, serum sodium, total proteins, Hct and blood urea nitrogen before and after GC replacement (prospective study). plasma AVP levels were measured after i.v. fluid supplementation without GC replacement in the patients of the retrospective study, and before and after GC replacement in the patients of the prospective study. RESULTS: The first patient became more hyponatraemic after i.v. fluid supplementation and recovered ultimately from hyponatraemia after GC replacement. In five patients studied retrospectively, the serum sodium levels fell progressively following i.v. fluid supplementation, concurrent with reduction in UA levels and Hct, which indicated the dilutional nature of the hyponatraemia. In the patients observed prospectively, the accumulation of fluid and sodium was indicated by a rise in body weight, blood pressure and serum sodium levels and a decline in Hct and total proteins after GC replacement. plasma AVP levels rose similarly in patients with dilutional hyponatraemia and in patients with borderline hyponatraemia before GC replacement. CONCLUSION: Patients with untreated ACTH deficiency may have either of two kinds of hyponatraemia--i.e. borderline hyponatraemia associated with subclinical hypovolaemia, or dilutional hyponatraemia. Similarity of plasma AVP levels in two hyponatraemic states suggests their AVP secretion is regulated by non-osmotic, non-volume mechanisms, possibly released from GC suppression at low plasma osmolality.
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2/40. Hyponatraemia: biochemical and clinical perspectives.

    Hyponatraemia is a common bio-chemical abnormality, occurring in about 15% of hospital inpatients. It is often associated with severe illness and relatively poor outcome. Pathophysiologically, hyponatraemia may be spurious, dilutional, depletional or redistributional. Particularly difficult causes and concepts of hyponatraemia are the syndrome of inappropriate antidiuresis and the sick cell syndrome, which are discussed here in detail. Therapy should always be targeted at the underlying disease process. 'Hyponatraemic symptoms' are of doubtful importance, and may be more related to water overload and/or the causative disease, than to hyponatraemia per se. Artificial elevation of plasma sodium by saline infusion carries the risk of induction of osmotic demyelination (central pontine myelinolysis).
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3/40. Hyponatraemia and seizures after ecstasy use.

    A patient presented to our unit with seizures and profound hyponatraemia after ingestion of a single tablet of ecstasy. The seizures proved resistant to therapy and ventilation on the intensive care unit was required. Resolution of the seizures occurred on correction of the metabolic abnormalities. The pathogenesis of seizures and hyponatraemia after ecstasy use is discussed. Ecstasy use should be considered in any young patient presenting with unexplained seizures and attention should be directed towards electrolyte levels, particularly sodium.
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4/40. A patient with pseudohypoaldosteronism type 1 and respiratory distress syndrome.

    We present a patient born at 36 weeks' gestation with respiratory distress, who required 6 days of mechanical ventilation, without a demonstrable infectious cause. He also developed hyponatremia, hypernatriuria, elevated serum aldosterone levels, and probable pseudohypoaldosteronism type 1 (PHA-1). This appears to be the first reported human case of both respiratory distress and a renal salt wasting process with elevated serum aldosterone. In animal models, abnormalities of subunits of the epithelial sodium channel produce respiratory distress and PHA-1. This patient's clinical presentation could be due to the same processes.
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5/40. hyponatremia in the postoperative craniofacial pediatric patient population: a connection to cerebral salt wasting syndrome and management of the disorder.

    hyponatremia after cranial vault remodeling has been noted in a pediatric patient population. If left untreated, the patients may develop a clinical hypoosmotic condition that can lead to cerebral edema, increased intracranial pressure, and eventually, to central nervous system and circulatory compromise. The hyponatremia has traditionally been attributed to the syndrome of inappropriate secretion of antidiuretic hormone (SIADH); however, in our patients the treatment has been resuscitation with normal saline as opposed to fluid restriction (the accepted treatment of SIADH), thus placing the diagnosis of SIADH in question. Patients who developed hyponatremia after intracranial injury or surgery were, until recently, grouped together as having SIADH. However, there are diagnosis and treatment differences between SIADH and another distinct but poorly understood disorder that is designated cerebral salt wasting syndrome (CSW). CSW is associated with increased urine output and increased urine sodium concentration and volume contraction, and it is frequently seen after a central nervous system trauma. We therefore developed a prospective study to evaluate the cause of the sodium imbalance.Ten consecutive pediatric patients who underwent intracranial surgery for various craniosynostotic disorders were postoperatively monitored in the pediatric intensive care unit for hemodynamic, respiratory, and fluid management. The first four patients were evaluated for electrolyte changes and overall fluid balance to determine the consistency with which these changes occurred. The remaining six patients had daily (including preoperative) measurement of serum electrolytes, urine electrolytes, urine osmolarity, serum antidiuretic hormone (ADH), aldosterone, and atrial natriuretic hormone (ANH). All patients received normal saline intravenous replacement fluid in the postoperative period.All of the patients developed a transient hyponatremia postoperatively, despite normal saline resuscitation. serum sodium levels as low as 128 to 133 mEq per liter (normal, 137 to 145 mEq per liter) were documented in the patients. All patients had increased urine outputs through the fourth postoperative day (>1 cc/kg/h). The six patients who were measured had an increased ANH level, with a peak value as high as 277 pg/ml (normal, 25 to 77 pg/ml). ADH levels were low or normal in all but one patient, who had a marked increase in ADH and ANH. aldosterone levels were variable. On the basis of these results, all but one patient showed evidence of CSW characterized by increased urine output, normal or increased urine sodium, low serum sodium, and increased ANH levels. The other patient had similar clinical findings consistent with CSW but also had an increase in ADH, thus giving a mixed laboratory picture of SIADH and CSW.The association of CSW to cranial vault remodeling has previously been ignored. This study should prompt reevaluation of the broad grouping of SIADH as the cause of all hyponatremic episodes in our postoperative patient population. An etiologic role has been given to ANH and to other, as yet undiscovered, central nervous system natriuretic factors. All of the patients studied required normal saline resuscitation, a treatment approach that is contrary to the usual management of SIADH. These findings should dictate a change in the postoperative care for these patients. After cranial vault remodeling, patients should prophylactically receive normal saline, rather than a more hypotonic solution, to avoid sodium balance problems.
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6/40. Very delayed hyponatremia after surgery and radiotherapy for a pituitary macroadenoma.

    Severe hyponatremia (118 mmol/l) with natriuresis, consistent with cerebral salt wasting syndrome (CSWS), occurred 38 days after transsphenoidal surgery in a 59-year-old woman affected by a pituitary non-functioning macroadenoma. From the 35th day after surgery, she showed progressive polyuria, hypotension and hyponatremia associated with natriuresis, decreased plasma and increased urinary osmolality. The clinical examination revealed signs of dehydration and gradual decline in the level of consciousness. The anterior pituitary function was normal due to appropriate replacement of thyroid and adrenal axis. The patient was treated with saline administration until normal natremia and water balance were restored and neurological symptoms had completely disappeared. This case focuses on the unusually prolonged time of development of post-surgery hyponatremia, despite delayed symptomatic hyponatremia being reported to commonly occur 7 days after transsphenoidal surgery. Therefore, we would advise not to limit the periodic follow-up of the hydroelectrolytic balance to the first two weeks after surgery, but to prolong it until after discharge from hospital. In fact, an early diagnosis is of great importance to prevent permanent neurological damage or death. Since CSWS and syndrome of inappropriate secretion of ADH, the two disorders alternatively imputed to generate post-surgical hyponatremia, are characterized by different pathogenic mechanisms and require opposing therapeutic approaches, the occurrence of extracellular volume dilution or of increased sodium renal loss should be carefully investigated. The evidences in favor of CSWS, the possible mechanisms behind the syndrome and diagnosis and management of patients with post-transsphenoidal surgery CSWS are discussed.
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7/40. hyponatremia in a pediatric stroke patient: syndrome of inappropriate antidiuretic hormone secretion or cerebral salt wasting?

    OBJECTIVE: To determine the potential role of atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in the pathogenesis of cerebral salt wasting. DESIGN: Clinical case report. SETTING: Regional pediatric intensive care unit. PATIENT: A 3-yr-old boy with a cerebral infarct secondary to traumatic carotid artery dissection who developed hyponatremia associated with weight loss and excessive renal sodium excretion on the sixth day after hospitalization. MEASUREMENTS AND MAIN RESULTS: plasma concentrations of ANP, BNP, antidiuretic hormone, and renin were determined serially and compared with concentrations measured in a group of eight healthy children undergoing elective surgical procedures. Compared with controls, ANP and BNP plasma concentrations on the eighth day after hospitalization were increased 1.9-fold and 7.7-fold, respectively. Thereafter, the course of ANP and BNP paralleled that of sodium and H2O excretion and remained elevated until the 14th (BNP) and 16th (ANP) days after hospitalization. serum antidiuretic hormone and renin concentrations were within normal ranges during the entire observation period. CONCLUSION: Cerebral salt wasting is associated with elevated plasma concentrations of ANP and BNP. natriuretic peptides may play a role in the pathogenesis of this syndrome.
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8/40. Perinatal water intoxication due to excessive oral intake during labour.

    The increased body water in pregnant women and the birth-related activation of water-sparing systems contribute to a high risk of perinatal water intoxication if the mother drinks too much water during labour. This study reports on four newborn term infants and one mother presenting with life-threatening symptoms due to hyponatraemia from excessive oral intake during labour. awareness of this diagnosis in the delivery unit is very important, because the clinical picture may mimic that of pre-eclampsia or dehydration. CONCLUSION: Guidelines are proposed to prevent and treat perinatal water intoxication due to excessive oral intake during labour.
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9/40. Neonatal ascites and hyponatraemia following umbilical venous catheterization.

    The complications associated with umbilical venous catheterization in neonates range from pericardial effusion, portal hypertension, and peritoneal perforation with ascites, to Wharton's jelly embolism. The case of a term neonate who developed ascites and severe hyponatraemia (serum sodium 119 mmol/L) most probably following peritoneal perforation by an umbilical venous catheter is reported. The presenting feature was convulsions associated with dilutional hyponatraemia, probably following absorption of a large quantity of ascitic fluid across the peritoneum. Conservative management was associated with gradual recovery over 24 h. The case highlights that, irrespective of the route, excessive administration of salt-free fluids can lead to dilutional hyponatraemia with adverse consequences. The present case illustrates the importance of confirming intravascular positioning of umbilical catheters by ensuring free flow of blood on aspiration, to prevent/detect inadvertent peritoneal perforation. Ideally, echocardiographic confirmation of optimal intravascular placement of such catheters is preferred as radiographic confirmation is reported to be unreliable.
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10/40. hyponatremia and hypoglycemia in acute Sheehan's syndrome.

    We report the case of a 23-year-old Saudi Arabian woman who presented to the medical intensive care unit with severe hyponatremia and hypoglycemia following a cesarean section delivery complicated by hemorrhage due to disseminated intravascular coagulopathy. She was treated successfully for adrenal insufficiency acutely, and was later discharged on hormone replacement therapy. To our knowledge, this is the first case report of acute Sheehan's syndrome presenting with both hyponatremia and suggestive hypoglycemia. Pituitary necrosis is an uncommon complication of peripartum hemorrhagic shock. Since the initial description by Sheehan in 1937, the incidence of the syndrome has gradually declined through improved management of hemodynamic complications leading to the infarction of the gland. There are many studies describing complications of late Sheehan's syndrome; however, relatively few contain descriptions of the acute phase. In addition, the diagnosis of this syndrome is often determined after resolution of the acute process with resultant lack of data regarding immediate endocrine and imaging abnormalities. In this report, we describe the complete endocrine and imaging assessment of a patient presenting in critical condition due to necrosis of the pituitary gland in the immediate postpartum period.
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