deamino-arginine-vasopressin and Brain-Edema

Hyponatremia causes significant morbidity, mortality, and disability. This review considers the literature of the past 18 months to improve understanding of these complications and to identify therapeutic strategies to prevent them.. Acute hyponatremia causes serious brain swelling that can lead to permanent disability or death. A 4-6 mEq/l increase in serum sodium is sufficient to reverse impending herniation. Brain swelling is minimal in chronic hyponatremia, and to avoid osmotic demyelination, correction should not exceed 8 mEq/l/day. In high-risk patients, correction should not exceed 4-6 mEq/l/day. Inadvertent overcorrection of hyponatremia is common and preventable by controlling unwanted urinary water losses with desmopressin. Even mild chronic hyponatremia is associated with increased mortality, attention deficit, gait instability, osteoporosis, and fractures, but it is not known if the correction of mild hyponatremia improves outcomes.. Controlled trials are needed to identify affordable treatments for hyponatremia that reduce the need for hospitalization, decrease hospital length of stay, and decrease morbidity. Such trials could also help answer the question of whether hyponatremia causes excess mortality or whether it is simply a marker for severe, lethal, underlying disease.

Topics: Animals; Brain Edema; Cognition Disorders; Deamino Arginine Vasopressin; Fractures, Bone; Gait Disorders, Neurologic; Humans; Hypernatremia; Hyponatremia; Osteoporosis; Saline Solution, Hypertonic; Sodium; Sodium Chloride

Central pontine myelinolysis (CPM) and extrapontine myelinolysis (EPM) are dire neurological disorders, characterized by severe damage to the myelin sheath of neurons, which typically result from rapid correction or overcorrection of systemic hyponatremia. For many years, both conditions have been considered universally fatal, though survivors have been reported more recently. Pediatric cases are rare. We present a 13-year-old boy with panhypopituitarism secondary to repair of a nasofrontal encephalocele in infancy, managed on long-term corticosteroid, deamino arginine vasopressin and thyroid hormone. He presented with severe hyponatremia (116 mEq/l), which during correction rapidly and unexpectedly increased to 176 mEq/l, resulting in profoundly impaired consciousness. Brain imaging revealed multiple bilateral changes in the basal ganglia, thalamus, pons and cerebral white matter, consistent with both CPM and EPM. Malignant cerebellar edema necessitated emergent suboccipital craniectomy, with subsequent improvement in level of consciousness and imaging postoperatively. However, he succumbed to acute cardiorespiratory arrest 8 weeks later. Nine similar cases from the literature are reviewed.

Topics: Adolescent; Antidiuretic Agents; Brain Edema; Cerebellum; Deamino Arginine Vasopressin; Humans; Hyponatremia; Magnetic Resonance Imaging; Male; Myelinolysis, Central Pontine; Osmotic Pressure

DDAVP is a drug that should be used with caution for each patient individually. Particular care is needed to avoid fluid overload and rapid fluctuations in sodium concentration. Not only families but physicians as well should be educated and aware of the adverse effects of DDAVP, especially in high risk patients. Extreme caution is needed in children with severe neurological and developmental problems who cannot control their fluid intake themselves. Similarly, caution is needed in patients with hypodipsia and DI who have difficulty in balancing water intake and DDAVP dose. The treatment of DI is water; however, DDAVP is given to avoid a large fluid intake which can result in medullary washout. Frequent home monitoring of body weight and regular determinations of serum sodium may help to disclose the early phase of over-hydration or dehydration. DDAVP therapy should be temporarily interrupted during acute illness, febrile episodes, hot days and other conditions with increased water intake. It should be used with considerable caution in patients with cystic fibrosis, or renal or cardiovascular diseases. In patients with enuresis, it is recommended that DDAVP medication should not be continued for longer than 3 months without stopping for 1 week for full reassessment. Fluid intake should be limited 1 hour before and 8 hours after the dose. Generally, undertreatment with vasopressin analogue is safer than overtreatment. A simple measure to avoid overtreatment is to miss one dose once a week; a rapid onset diuresis ('washout' effect) provides considerable reassurance.

Topics: Adolescent; Antidiuretic Agents; Brain Edema; Child; Deamino Arginine Vasopressin; Diabetes Insipidus; Drinking; Enuresis; Hemostatics; Humans; Hyponatremia; Myelinolysis, Central Pontine; Sodium; Water Intoxication

Induction of cellular cerebral edema (CE) was achieved by a standard method of water intoxication which consisted of fractionated intraperitoneal administration of distilled water (DW) together with the injection of desmopressin (DP). Using metabolic cage, fluid and food balance was studied in two groups of eight animals: group C - control; group CE - cellular edema induced by water intoxication. For each rat the intake (food pellets and water) and excretion (solid excrements and urine) were recorded for 48 h together with the initial and final body weight. CE animals consumed significantly less food, drank less water and eliminated the smallest amount of excrements. The induction of cellular cerebral edema was accompanied with a significant loss of body weight (representing on average 13 % of the initial values) mainly due to a reduction of food intake. This phenomenon has not yet been reported.

Topics: Animals; Antidiuretic Agents; Body Weight; Brain Edema; Deamino Arginine Vasopressin; Male; Rats; Rats, Wistar; Water Intoxication; Weight Loss

Topics: Adult; Antidiuretic Agents; Brain Edema; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Humans; Hyponatremia; Magnetic Resonance Imaging; Male; Myelinolysis, Central Pontine; Syndrome

To determine the occurrence rate of central diabetes insipidus in pediatric patients with severe traumatic brain injury and to describe the clinical, injury, biochemical, imaging, and intervention variables associated with mortality.. Retrospective chart and imaging review.. Children's Hospital, level 1 trauma center.. Severely injured (Injury Severity Score ≥ 12) pediatric trauma patients (>1 month and <18 yr) with severe traumatic brain injury (presedation Glasgow Coma Scale ≤ 8 and head Maximum Abbreviated Injury Scale ≥ 4) that developed acute central diabetes insipidus between January 2000 and December 2011.. Of 818 severely injured trauma patients, 180 had severe traumatic brain injury with an overall mortality rate of 27.2%. Thirty-two of the severe traumatic brain injury patients developed acute central diabetes insipidus that responded to desamino-8-D-arginine vasopressin and/or vasopressin infusion, providing an occurrence rate of 18%. At the time of central diabetes insipidus diagnosis, median urine output and serum sodium were 6.8 ml/kg/hr (interquartile range = 5-11) and 154 mmol/L (interquartile range = 149-159), respectively. The mortality rate of central diabetes insipidus patients was 87.5%, with 71.4% declared brain dead after central diabetes insipidus diagnosis. Early central diabetes insipidus onset, within the first 2 days of severe traumatic brain injury, was strongly associated with mortality (p < 0.001), as were a lower presedation Glasgow Coma Scale (p = 0.03), a lower motor Glasgow Coma Scale (p = 0.01), an occurrence of fixed pupils (p = 0.04), and a prolonged partial thromboplastin time (p = 0.04). Cerebral edema on the initial computed tomography, obtained in the first 24 hrs after injury, was the only imaging finding associated with death (p = 0.002). Survivors of central diabetes insipidus were more likely to have intracranial pressure monitoring (p = 0.03), have thiopental administered to induce coma (p = 0.04) and have received a decompressive craniectomy for elevated intracranial pressure (p = 0.04).. The incidence of central diabetes insipidus in pediatric patients with severe traumatic brain injury is 18%. Mortality was associated with early central diabetes insipidus onset and cerebral edema on head computed tomography. Central diabetes insipidus nonsurvivors were less likely to have received intracranial pressure monitoring, thiopental coma and decompressive craniectomy.

Topics: Adolescent; Antidiuretic Agents; Brain Edema; Brain Injuries; Child; Child, Preschool; Coma; Deamino Arginine Vasopressin; Decompressive Craniectomy; Diabetes Insipidus, Neurogenic; Female; Glasgow Coma Scale; Humans; Hypnotics and Sedatives; Incidence; Intracranial Hypertension; Intracranial Pressure; Male; Monitoring, Physiologic; Partial Thromboplastin Time; Pupil Disorders; Radiography; Retrospective Studies; Thiopental; Time Factors

Topics: Adult; Anticonvulsants; Antidiuretic Agents; Brain; Brain Edema; Craniocerebral Trauma; Craniotomy; Deamino Arginine Vasopressin; Diazepam; Fatal Outcome; Hematoma, Subdural; Humans; Hyponatremia; Intubation, Intratracheal; Male; Nocturnal Enuresis; Phenytoin; Saline Solution, Hypertonic; Seizures; Sodium; Tomography, X-Ray Computed

A patient was referred to the intensive care unit with sudden delirium and a serum sodium level of 111 mEq/L (mmol/L). A computerized tomographic scan revealed marked cerebral edema. Laboratory values were highly consistent with the action of the antidiuretic hormone. She had received desmopressin acetate (DDAVP) for 4 days preoperatively and postoperatively for putative van Willebrand's disease. Hyponatremia as a sequel to DDAVP treatment is an unusual complication and the medication is generally safe. However, our patient nevertheless teaches that vigilance equals avoidance.

Topics: Brain Edema; Deamino Arginine Vasopressin; Delirium; Drug Administration Schedule; Female; Humans; Hyponatremia; Middle Aged; Ovarian Cysts; Premedication; Sodium; Tomography, X-Ray Computed; von Willebrand Diseases

Seven cases of cerebral oedema have been observed in enuretic children during low-dose desmopressin (DDAVP) treatment given in a dose of 7-21 microg daily in the Czech Republic between 1995 and 1999, after the drug started to be marketed for this indication and delivered in simple bottles with a dropper. All seven children (age 5-11 years, four boys) experienced a period of unconsciousness but all recovered without sequelae. In most cases, safety measures were underestimated and natraemia was not regularly controlled. Two children developed cerebral oedema after excessive water intake in preparation for uroflowmetry, another one drank much during a hot summer day, in one diabetes insipidus was not recognised and two children were clearly non-compliant with reduced fluid intake on a long-term basis. Only in one child, no risk factor was found. Conclusion. Proper selection and instruction of patients is needed to avert cerebral oedema during treatment with desmopressin for nocturnal enuresis.

Topics: Brain Edema; Child; Child, Preschool; Consumer Product Safety; Deamino Arginine Vasopressin; Enuresis; Female; Humans; Hyponatremia; Male; Renal Agents; Water Intoxication

Topics: Adult; Blood Glucose; Brain Edema; Brain Neoplasms; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Mellitus, Type 1; Diabetic Coma; Diabetic Ketoacidosis; Diagnosis, Differential; Fatal Outcome; Female; Fluid Therapy; Headache; Humans; Hypernatremia; Insulin; Polyuria; Postoperative Complications; Radiography

Previous studies have demonstrated that hyponatremia induced by continuous sc infusion of desmopressin (dDAVP) in combination with a liquid diet allows brain volume adaptation with negligible morbidity and mortality in rats. In contrast, some studies of hyponatremia induced by injections of long-acting preparations of arginine vasopressin (AVP) have reported mortality rates as high as 20 to 80%. To evaluate the possibility that the use of AVP to produce antidiuresis may cause greater mortality as a result of increased brain edema, this study examined brain water and electrolyte contents of male and female rats after varying periods of hyponatremia induced by continuous sc infusions of either dDAVP (5 ng/h) or AVP (100 ng/h). Rats infused with AVP had AVP levels in plasma elevated into ranges reported in patients with the syndrome of inappropriate antidiuretic hormone secretion (17.5 +/- 2.0 pg/mL); however, despite the production of comparably severe degrees of hyponatremia with both AVP and dDAVP infusions (105 to 115 mmol/L), no mortality occurred in any of the rats (N = 40 AVP infused and N = 40 dDAVP infused). AVP- and dDAVP-induced hyponatremia both caused transient brain edema in female and male rats, but brain water content returned to the levels of normonatremic controls after 5 days in the females and 10 days in the males. However, at no time during the 10-day study period did brain water content differ significantly between rats infused with AVP or dDAVP, either in females or males. Decreases in brain electrolytes were also equivalent in the AVP- and dDAVP-infused male and female rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Arginine Vasopressin; Body Weight; Brain; Brain Edema; Deamino Arginine Vasopressin; Electrolytes; Female; Hyponatremia; Male; Rats; Rats, Sprague-Dawley; Reference Values; Sodium