deamino-arginine-vasopressin and Brain-Injuries

Central diabetes insipidus (CDI) is a complex and heterogeneous clinical syndrome affecting the hypothalamic-neurohypophyseal network and water balance. A recent national surveillance in Denmark showed a prevalence rate of twenty-three CDI patients per 100,000 inhabitants in five years. The differential diagnosis between several presenting conditions with polyuria and polydipsia is puzzling, and the etiological diagnosis of CDI remains a challenge before the identification of an underlying cause. For clinical practice, a timely diagnosis for initiating specific treatment in order to avoid central nervous system damage, additional pituitary defects and the risk of dissemination of germ cell tumor is advisable. Proper etiological diagnosis can be achieved via a series of steps that start with careful clinical observation of several signs and endocrine symptoms and then progress to more sophisticated imaging tools. This review summarizes the best practice and approach for the diagnosis and treatment of patients with CDI.

Topics: Antidiuretic Agents; Brain Injuries; Brain Neoplasms; Child; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Disease Management; Histiocytosis, Langerhans-Cell; Humans; Magnetic Resonance Imaging; Neoplasms, Germ Cell and Embryonal

Central or neurogenic diabetes insipidus results from a deficiency in antidiuretic hormone (ADH) or arginine-vasopressin (AVP). Treatment is based on replacement therapy with the hormone analog desmopressin (d-DAVP). d-DAVP can be administered subcutaneously to infants or patients with postoperative or posttraumatic brain injury being monitored for transient diabetes insipidus. Intranasal and oral forms are also available. The recently introduced lyophilisate, which melts under the tongue, has replaced the tablet form (recently withdrawn from the market in France) and provides better bioavailability. Irrespective of the mode of administration, it is usually the patient who finds the effective minimal dose necessary for a normal life, i.e. without excessive polyuria, particularly at night. Patient education is necessary to avoid the risk of water intoxication and hyponatremia.

Topics: Antidiuretic Agents; Brain Injuries; Chemistry, Pharmaceutical; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Diagnosis, Differential; Dose-Response Relationship, Drug; Drug Administration Routes; Humans; Infant

Trauma and emergency department clinicians encounter a growing number of patients admitted with traumatic head injury on prehospital antithrombotic therapies. These patients appear to be at increased risk of developing life-threatening intracranial hemorrhage. It is imperative that trauma clinicians understand the mechanism and duration of commonly prescribed outpatient antithrombotics in order to appropriately assess and treat patients who develop intracranial hemorrhage. This review summarizes current literature on the morbidity and mortality associated with premorbid non-steroidal anti-inflammatory drugs, aspirin, clopidogrel, warfarin, and heparinoids in the setting of traumatic head injury, and also examines the current strategies for reversal of these therapies.

Topics: Aged; Anticoagulants; Brain Injuries; Cerebral Hemorrhage, Traumatic; Combined Modality Therapy; Critical Care; Deamino Arginine Vasopressin; Emergency Medical Services; Factor VIIa; Hematoma, Epidural, Cranial; Hematoma, Subdural; Hemostatics; Hospital Mortality; Humans; Middle Aged; Plasma; Platelet Aggregation Inhibitors; Platelet Transfusion; Protamines; Recombinant Proteins; Risk Factors; Vitamin K 1

The authors present a brief review of the problem of diabetes insipidus in neurosurgical patients, with particular emphasis on the differential diagnosis of postoperative and posttraumatic polyuria and the management of diabetes insipidus in these periods. A listing of drugs currently used in its treatment is given.

Topics: Administration, Intranasal; Benzothiadiazines; Brain Injuries; Carbamazepine; Chlorpropamide; Deamino Arginine Vasopressin; Diabetes Insipidus; Diabetes Mellitus; Diagnosis, Differential; Diuretics; Humans; Hypothalamo-Hypophyseal System; Lypressin; Methods; Polyuria; Postoperative Complications; Sodium Chloride Symporter Inhibitors; Vasopressins; Water-Electrolyte Balance

COVID-19 has changed the nature of medical consultations, emphasizing virtual patient counseling, with relevance for patients with diabetes insipidus (DI) or hyponatraemia. The main complication of desmopressin treatment in DI is dilutional hyponatraemia. Since plasma sodium monitoring is not always possible in times of COVID-19, we recommend to delay the desmopressin dose once a week until aquaresis occurs allowing excess retained water to be excreted. Patients should measure their body weight daily. Patients with DI admitted to the hospital with COVID-19 have a high risk for mortality due to volume depletion. Specialists must supervise fluid replacement and dosing of desmopressin. Patients after pituitary surgery should drink to thirst and measure their body weight daily to early recognize the development of the postoperative syndrome of inappropriate antidiuresis (SIAD). They should know hyponatraemia symptoms. The prevalence of hyponatraemia in patients with pneumonia due to COVID-19 is not yet known, but seems to be low. In contrast, hypernatraemia may develop in COVID-19 patients in ICU, from different multifactorial reasons, for example, due to insensible water losses from pyrexia, increased respiration rate and use of diuretics. Hypernatraemic dehydration may contribute to the high risk of acute kidney injury in COVID-19. IV fluid replacement should be administered with caution in severe cases of COVID-19 because of the risk of pulmonary oedema.

Topics: Antidiuretic Agents; Brain Injuries; Coronavirus Infections; COVID-19; Deamino Arginine Vasopressin; Dehydration; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Disease Management; Fluid Therapy; Humans; Hypernatremia; Hyponatremia; Hypotonic Solutions; Inappropriate ADH Syndrome; Neurosurgical Procedures; Pandemics; Pneumonia, Viral; Postoperative Complications; Practice Guidelines as Topic; Saline Solution; Shock

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

Diabetes insipidus (DI) is a well documented complication observed after traumatic head injuries. We report a case of hyperacute onset DI in a 19-year-old male who sustained a hypothalamic-pituitary injury when he was stabbed in the head with a 30-cm long thin-bladed knife. At CT, our patient showed significant hemorrhagic contusions of the lower hypothalamus. He developed polydipsia, polyuria, and mild hypernatremia in the Emergency Department. Diagnostic digital subtraction angiography showed a hypervascular congestive pituitary gland with prominent draining veins. On the third day his hypernatremia became severe (183mEq/L). He was managed with parenteral fluids and a regimen of intranasal DDAVP (1-desamino 8-d-arginine vasopressin), leading to improved plasmatic sodium levels, urine output, and urinary specific gravity. In patients presenting with hyperacute posttraumatic DI, emergency room physicians and neurosurgeons should rule out direct injury to the hypothalamus and/or the posterior lobe of the pituitary, and initiate early pharmacological treatment.

Topics: Acute Disease; Brain Injuries; Confusion; Craniocerebral Trauma; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Humans; Hypernatremia; Hypoglycemic Agents; Hypothalamo-Hypophyseal System; Hypothalamus; Magnetic Resonance Angiography; Magnetic Resonance Imaging; Male; Polyuria; Tomography, X-Ray Computed; Wounds, Stab; Young Adult

The study was aimed at verifying whether the occurrence of hypernatremia during the intensive care unit (ICU) stay increases the risk of death in patients with severe traumatic brain injury (TBI). We performed a retrospective study on a prospectively collected database including all patients consecutively admitted over a 3-year period with a diagnosis of TBI (post-resuscitation Glasgow Coma Score < or = 8) to a general/neurotrauma ICU of a university hospital, providing critical care services in a catchment area of about 1,200,000 inhabitants.. Demographic, clinical, and ICU laboratory data were prospectively collected; serum sodium was assessed an average of three times per day. Hypernatremia was defined as two daily values of serum sodium above 145 mmol/l. The major outcome was death in the ICU after 14 days. Cox proportional-hazards regression models were used, with time-dependent variates designed to reflect exposure over time during the ICU stay: hypernatremia, desmopressin acetate (DDAVP) administration as a surrogate marker for the presence of central diabetes insipidus, and urinary output. The same models were adjusted for potential confounding factors.. We included in the study 130 TBI patients (mean age 52 years (standard deviation 23); males 74%; median Glasgow Coma Score 3 (range 3 to 8); mean Simplified Acute Physiology Score II 50 (standard deviation 15)); all were mechanically ventilated; 35 (26.9%) died within 14 days after ICU admission. Hypernatremia was detected in 51.5% of the patients and in 15.9% of the 1,103 patient-day ICU follow-up. In most instances hypernatremia was mild (mean 150 mmol/l, interquartile range 148 to 152). The occurrence of hypernatremia was highest (P = 0.003) in patients with suspected central diabetes insipidus (25/130, 19.2%), a condition that was associated with increased severity of brain injury and ICU mortality. After adjustment for the baseline risk, the incidence of hypernatremia over the course of the ICU stay was significantly related with increased mortality (hazard ratio 3.00 (95% confidence interval: 1.34 to 6.51; P = 0.003)). However, DDAVP use modified this relation (P = 0.06), hypernatremia providing no additional prognostic information in the instances of suspected central diabetes insipidus.. Mild hypernatremia is associated with an increased risk of death in patients with severe TBI. In a proportion of the patients the association between hypernatremia and death is accounted for by the presence of central diabetes insipidus.

Topics: Brain Injuries; Deamino Arginine Vasopressin; Female; Hospitals, University; Humans; Hypernatremia; Incidence; Intensive Care Units; Male; Middle Aged; Proportional Hazards Models; Retrospective Studies; Severity of Illness Index

Recovery of the pituitary function from post-traumatic hypopituitarism is an exceptional event. We present the case of a 32 year-old man who was involved in a road traffic accident in which he suffered a severe head injury. Four days following the trauma the patient developed post-traumatic central diabetes insipidus and desmopressin was started. At discharge of the intensive care unit, the patient was referred to us for endocrine assessment. Three months after the head injury, the hormonal evaluation of the hypothalamic-pituitary axis by means of insulin stress test with the simultaneous administration of TRH and GnRH resulted in reduced responses of GH, cortisol, TSH, FSH, and LH with low baseline serum concentrations of free T4 and testosterone. Both serum basal and stimulated PRL concentrations were normal. Magnetic resonance imaging demonstrated deformity of the sella turcica with displacement of the pituitary gland by a post-traumatic retention cyst. A new evaluation of the pituitary function performed 6 months after the trauma showed spontaneous recovery of the gonadal, thyroid and adrenal function. However, GH response was reduced both to insulin-induced hypoglycemia, clonidine and GHRH tests. Presence of normal serum PRL levels, normal PRL response to TRH and reduced GH responses to pituitary and hypothalamic stimuli suggests both hypothalamic and pituitary damage. The present case shows an unusual case of partial spontaneous resolution of a post-traumatic hypopituitarism. Based on this clinical observation we recommend periodic evaluation of the pituitary function in these kind of patients.

Topics: Accidents, Traffic; Adult; Brain Injuries; Deamino Arginine Vasopressin; Diabetes Insipidus; Follicle Stimulating Hormone; Gonadotropin-Releasing Hormone; Human Growth Hormone; Humans; Hydrocortisone; Hypopituitarism; Hypothalamus; Insulin; Luteinizing Hormone; Magnetic Resonance Imaging; Male; Pituitary Gland; Prolactin; Thyrotropin; Thyrotropin-Releasing Hormone

Topics: Adolescent; Adult; Brain Injuries; Brain Neoplasms; Child; Child, Preschool; Deamino Arginine Vasopressin; Diabetes Insipidus; Diuresis; Female; Humans; Kidney Diseases; Male; Vasopressins