deamino-arginine-vasopressin and Coma

The authors report permanent central diabetes insipidus (CDI) in a patient after severe traumatic brain injury (TBI) in traffic accident. A 16-year-old boy entered to a medical facility in coma (GCS score 6) with the following diagnosis: acute TBI, severe cerebral contusion, subarachnoid hemorrhage, depressed comminuted cranial vault fracture, basilar skull fracture, visceral contusion. CDI was diagnosed in 3 days after injury considering polyuria and hypernatremia (155 mmol/l). Desmopressin therapy was initiated through a feeding tube. Thirst appeared when a patient came out of the coma after 21 days despite ongoing desmopressin therapy. Considering persistent thirst and polyuria, we continued desmopressin therapy in a spray form. Under this therapy, polyuria reduced to 3-3.5 liters per a day. Symptoms of CDI persisted in long-term period (2 years after TBI) while function of adenohypophysis was intact. This case demonstrates a rare development of permanent diabetes insipidus after TBI. CDI manifested only as polyuria and hypernatremia in coma. Thirst joined after recovery of consciousness. Probable causes of CDI were damage to neurohypophysis and partially injury of pituitary stalk because of extended basilar skull fracture and/or irreversible secondary lesion of hypothalamus following diffuse axonal damage after TBI.. В статье представлен клинический случай развития постоянной формы центрального несахарного диабета (ЦНД) у пациента после тяжелой черепно-мозговой травмы (ТЧМТ) в результате дорожно-транспортного происшествия. Подросток 16 лет поступил в лечебное учреждение в состоянии комы (6 баллов по шкале комы Глазго) с диагнозом: сочетанная травма; острая ТЧМТ; ушиб головного мозга тяжелой степени; субарахноидальное кровоизлияние; вдавленный многооскольчатый перелом свода черепа справа; протяженный перелом основания черепа; ушиб внутренних органов. На 3-и сутки развились полиурия и гипернатриемия (155 ммоль/л); диагностирован ЦНД и начата терапия десмопрессином в таблетированной форме через зонд. При выходе из комы (21-е сутки) отмечено появление жажды на фоне продолжения терапии. В связи с сохраняющейся жаждой и полиурией произведен перевод на терапию десмопрессином в виде спрея, на этом фоне отмечено уменьшение выделения мочи до 3—3,5 л в сутки. Симптоматика ЦНД наблюдалась и через 2 года после ТЧМТ, при этом функция аденогипофиза оставалась сохранной. Представленный случай является примером развития постоянного несахарного диабета у подростка с ТЧМТ, находившегося под длительным наблюдением. Клиническая картина ЦНД в состоянии комы проявлялась только полиурией и гипернатриемией, а по мере повышения уровня сознания присоединилась жажда. Вероятными причинами развития ЦНД явились повреждение нейрогипофиза и частичное повреждение стебля гипофиза в результате протяженного перелома основания черепа и/или необратимого вторичного повреждения гипоталамуса вследствие диффузного аксонального повреждения головного мозга после ТЧМТ.

Topics: Adolescent; Brain Injuries, Traumatic; Coma; Deamino Arginine Vasopressin; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hypernatremia; Male; Polyuria

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: Antidiuretic Agents; Coma; Deamino Arginine Vasopressin; Female; Humans; Hyponatremia; Infusions, Intravenous; Middle Aged; von Willebrand Disease, Type 2

Enuresis nocturna is regularly treated by desmopressin, a vasopressin analog. Its side effects, notably neurological, are fortunately rare. We comment on 5 enuretic children on desmopressin who suffered from hyponatremic encephalopathy (natremia 115-127, median 117 mmol/l).. Side effects appeared at therapeutic doses (10-40 mg/d intranasal). An excessive fluid intake at night was often noted, leading to a dilutional hyponatremia. This may be due to a lack of correct information to the parents. These children presented after a period of warning symptoms, such as headache, vomiting and altered consciousness. Parents could have sought earlier medical attention if they had been informed about these symptoms.. In the absence of fluid restriction, severe hyponatremia can occur in enuretic children on desmopressin. It is therefore mandatory for the prescribing doctor to adequately inform patients and parents to limit fluids at night when desmopressin is used, and seek medical help quickly if any sign of intracranial hypertension appears.

Topics: Administration, Intranasal; Antidiuretic Agents; Child; Child, Preschool; Coma; Confusion; Deamino Arginine Vasopressin; Drinking; Enuresis; Female; Glasgow Coma Scale; Humans; Hyponatremia; Intracranial Hypertension; Male; Seizures; Time Factors

A 30-year-old man known to have a factor-IX deficiency was presented at the emergency department with unexplained coma. After immediate treatment with factor IX, a CT-scan of the brain revealed no intracerebral haemorrhage. However, blood tests showed severe hyponatraemia, low serum osmolarity and high urine-sodium excretion consistent with the Syndrome of Inappropriate Antiduretic Hormone Secretion (SIADH). Therapy with hypertonic saline was instituted resulting in a gradual rise in the serum-sodium concentration. The cause of the hyponatraemia however remained unclear. After repeat history taking the patient mentioned the use of desmopressin for nocturia. Hyponatraemia as a complication of desmopressin use occurs in 8% of adult patients treated for nocturia. Direct availability of a patient's drug history, by means of an electronic record for instance, could avoid unnecessary tests and delay in diagnosis.

Topics: Adult; Coma; Deamino Arginine Vasopressin; Humans; Hyponatremia; Inappropriate ADH Syndrome; Male; Saline Solution, Hypertonic; Urination Disorders

Topics: Antidiuretic Agents; Child; Coma; Deamino Arginine Vasopressin; Enuresis; Female; Humans; Hyponatremia; Seizures

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.

Topics: Anti-Inflammatory Agents, Non-Steroidal; Coma; Deamino Arginine Vasopressin; Drug Therapy, Combination; Female; Humans; Hyponatremia; Ibuprofen; Middle Aged; Renal Agents; von Willebrand Diseases

Desmopressin, a synthetic analogue of the antidiuretic hormone, is an effective medication for primary nocturnal enuresis for both children and adults. Its safety is well established. Although it has a favorable side effect profile, because of its pharmacological effect, intranasal desmopressin can rarely induce water intoxication with profound hyponatremia if given without adequate restriction of water intake. The authors describe an adult patient with water intoxication and severe hyponatremia accompanied by loss of consciousness and seizures after 2-day intranasal administration of desmopressin. The present and the previously reported cases emphasize the need for greater awareness of the development of this serious and potentiallyfatal complication. In addition, to adjust the drug to the lowest required dosage, adequate restriction of water intake is recommended, and serum levels of sodium should be measured periodically to allow for early detection of water intoxication and hyponatremia.

Topics: Administration, Intranasal; Adult; Coma; Deamino Arginine Vasopressin; Drinking; Enuresis; Female; Humans; Hyponatremia; Seizures; Water Intoxication

Topics: Child; Coma; Deamino Arginine Vasopressin; Drug Therapy, Combination; Enuresis; Humans; Hyponatremia; Male; Seizures

Topics: Administration, Intranasal; Adolescent; Coma; Cystic Fibrosis; Deamino Arginine Vasopressin; Female; Humans; Seizures