Cases reported "Hypernatremia"

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1/39. hypercalcemia accompanied by hypothalamic hypopituitarism, central diabetes inspidus and hyperthyroidism.

    We present here a case of prominent hypercalcemia accompanied by hypothalamic tumor and Graves' disease. A 24-year-old man with hypothalamic tumor showed hypopituitarism, central diabetes inspidus (DI) and hyperthyroidism. nausea, loss of thirst and appetite, and general fatigue were found with the unveiling of hypercalcemia and hypernatremia. parathyroid hormone (PTH) and 1alpha-dihydroxyvitamin D levels were suppressed with a normal range of PTH-related protein values. One-desamino-(8-D-arginine)-vasopressin (DDAVP) and half-saline administration normalized hypernatremia, while hypercalcemia was still sustained. Administration of cortisone acetate and thiamazole reduced the elevated serum Ca level. In the present case, concurrent hyperthyroidism was assumed to accelerate skeletal mobilization of calcium into the circulation. Hypocortisolism and central DI was also considered to contribute, to some extent, to the hypercalcemia through renal handling of Ca.
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2/39. infant hypernatremia: a case report.

    A 7-month-old infant presented to the emergency department with diarrhea, vomiting, and decreased activity. The infant was febrile, tachycardic, tachypneic, lethargic, and had a prolonged capillary refill. Initial serum sodium was 197 mmol/L. Ultimately, the infant was diagnosed with central diabetes insipidus complicated by severe dehydration secondary to rotavirus infection. A brief review of infant hypernatremia and its evaluation and treatment in the emergency department follows.
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3/39. hypernatremia in a non insulin dependent (type 2) diabetic patient with central diabetes insipidus.

    We describe a patient with central diabetes insipidus who presented with hyperosmolar, non-ketotic hyperglycaemia. The role in this case of reduced thirst sensation with decreased water intake and abnormal AVP production illustrates the importance of these protective mechanisms in normal physiology regarding maintenance of normal plasma osmolality. Despite the complex pathophysiology in this patient, fluid resuscitation aimed at normalisation of the water deficit resulted in full recovery.
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4/39. peritoneal dialysis in an infant with type 1 diabetes and hyperosmolar coma.

    Hyperosmolar coma which is characterized by severe hyperglycemia in absence of chetosis is very rare in pediatric age with only 11 cases reported in the literature. The outcome of the condition is usually poor with mental retardation being the most common event. Here a case of hyperosmolar coma is described in a female of three months of age who was treated with peritoneal dialysis 11 hours after admittance to hospital. This female patient has been receiving insulin from three months of age and today at the age of 10 years she leads a normal life despite being on insulin therapy. A very low level of c-peptide (<0.3 ng/ml) clearly confirms she is affected by Type 1 diabetes. To our knowledge this is the first case report of hyperosmolar coma in a neonate with Type 1 diabetes who survived this condition without late neurological consequences.
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5/39. Idiopathic hypothalamic dysfunction with precocious puberty and adipsic hypernatremia first presenting in adolescence.

    BACKGROUND: Idiopathic hypothalamic dysfunction is a rare syndrome that has been described in young children. This syndrome is characterized by a disturbance of thirst regulation with hypernatremia, hyperosmolarity, and altered hypothalamic function. PATIENT REPORT: At age 6 years the reported patients presented with precocious puberty, by age 12 years she had hypernatremia presumed secondary to central diabetes insipidus and was treated with DDAVP, and at age 14 was identified to have hyperprolactinemia. At age 19 she presented with serum sodium of 185 mg/dl during an episode of illness associated with dehydration. After hydration, her sodium remained elevated. arginine vasopressin was measurable but inappropriate to serum sodium, while urinary cyclic amp response to vasopressin was appropriate. CONCLUSIONS: This is the first case of precocious puberty identified in association with the more classic features of idiopathic hypothalamic dysfunction, including later-onset hypernatremia, poor thermoregulatory function, obesity, and hyperprolactinemia.
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6/39. Hypodipsic hypernatremia and diabetes insipidus following anterior communicating artery aneurysm clipping: diagnostic and therapeutic challenges in the amnestic rehabilitation patient.

    Hypodipsic hypernatremia (HH) represents a pathological increase in serum sodium due to a lack of thirst and defect in hypothalamic osmoreceptors. While 15% of patients with HH have a vascular aetiology, few cases have been described. Moreover, the presence of such abnormalities in the amnestic patient can have particularly threatening implications, as HH tends to recur unless the patient complies with a regimen of water intake. This study reports the case of a 46-year-old male admitted for rehabilitation of functional deficits following subarachnoid haemorrhage (SAH), with clipping of an anterior communicating artery (ACoA) aneurysm. Clinical examination was remarkable for profound short-term memory loss and inability to retain new information. blood chemistry on admission showed a serum sodium level of 160 mEq/L, increasing to 167 mEq/L the following day. The patient denied thirst, and showed no clinical signs of dehydration. Neuroendocrine evaluation revealed diabetes insipidus (DI) and HH. Treatment initially included DDAVP and intravenous hydration, later supplemented with chlorpropramide. Stabilization of serum sodium and osmolality did not ensue until the treatment regimen included hydrochlorothiazide and supervision of enforced fluid intake. Endocrine abnormalities may be encountered among patients with vascular lesions adjacent to the hypothalamus. rehabilitation interventions include establishing a structured medication regimen with fluid administration in the amnestic patient with hypothalamic dysfunction.
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7/39. Hypodipsia-hypernatremia syndrome associated with holoprosencephaly in a child: a case report.

    We report a child with diabetes insipidus and hypodipsia associated with holoprosencephaly. A two-year-old girl with the history of several admittances to hospital during and after the newborn period with hypernatremic dehydration, acute renal failure and convulsions is presented. The patient had hypodipsia, hypernatremia, microcephaly, failure to thrive, and unilateral cleft lip and palate. magnetic resonance imaging revealed lobar type holoprosencephaly. Increased plasma osmolality and decreased urinary osmolality were detected. Her urine ADH level was 10 ng/day. plasma osmolality levels returned to normal after hydration and administration of a vasopressin analogue. These findings suggest that in children with hypernatremia-hypodipsia syndrome, the possibility of cerebral malformations should always be kept in mind.
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8/39. survival with serum sodium level of 180 mEq/L: permanent disorientation to place and time.

    A 41-year-old woman who had undergone transfrontal craniotomy for a pituitary tumor 4 months before presentation was admitted with confusion and orientation only to self. She had a fever of 40 degrees C. serum sodium and chloride levels on admission were 180 and 139 mEq/L, respectively. Measured serum osmolality was 380 mOsmol/L with a urine osmolality of 360 mOsmol/L. magnetic resonance imaging revealed a 1.5-cm mass in the sella turcica, which was nonfunctioning on endocrine evaluation. The "bright spot" of a normal posterior pituitary was absent. Central diabetes insipidus was confirmed by a 300% increase in urine osmolality with desmopressin. The patient survived her severe hypernatremia, which has 70% mortality with a serum sodium level of 160 mEq/L or above. However, she developed permanent (6 months) disorientation to time and place even when hypernatremia was corrected, which has not been described previously.
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9/39. Dural sinus thrombosis with severe hypernatremia developing in a patient on long-term lithium therapy.

    Dural sinus thrombosis has not been described in a patient with hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus. A 63-year-old man on chronic lithium therapy for schizoaffective disorder was transferred to the Emergency Department with dehydration and signs of central nervous system dysfunction after a 3-week isolation in a room in a psychiatric hospital due to exacerbation of psychiatric disorder, during which he refused to eat. Laboratory examination revealed hypertonic hypernatremia (osmolality, 359 mOsm/kg and Na, 171 mEq/L) and hyposthenuria (specific gravity, 1.010 and osmolality, 249 mOsm/kg), with normal serum endogenous vasopressin concentration (2.3 pg/mL). The serum lithium concentration was within the therapeutic range (0.94 mEq/L). Cranial computed tomography demonstrated subarachnoid hemorrhage and suggested dural sinus thrombosis. Although treatment with indomethacin (25 mg parenterally at 8-hour intervals) was somewhat effective in restoring renal concentrating capacity, he died of massive hemorrhagic infarction on the sixth hospital day, probably secondary to dural sinus thrombosis. The clinical diagnosis was confirmed by postmortem examination. physicians should be alert for the possibility of dural sinus thrombosis as a complication of hypernatremia resulting from lithium-induced nephrogenic diabetes insipidus.
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10/39. Severe hypernatremia after cesarean delivery secondary to transient diabetes insipidus of pregnancy.

    BACKGROUND: Transient diabetes insipidus is an uncommon complication of pregnancy, usually manifesting with polydipsia and polyuria. This condition is considered to result from excess placental vasopressinase activity and is managed with deamino D arginine vasopressin. CASE: While on restricted oral intake after cesarean delivery, the patient gradually became disoriented and agitated in conjunction with markedly increased urine output disproportional to her intravenous crystalloid fluid intake. Marked hypernatremia of 178 mEq/dL was noted. urine osmolality was low at 248 mOsm/L. The clinical presentation and electrolyte abnormalities were considered consistent with transient diabetes insipidus of pregnancy. The patient responded well to nasal-spray-administered deamino D arginine vasopressin and increased intravenous fluid intake, with resolution of symptoms and gradual normalization of serum sodium levels. CONCLUSION: Transient diabetes insipidus of pregnancy should be considered in the differential diagnosis of severe hypernatremia in obstetric patients with restricted oral intake after operative delivery.
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