scholarly journals Vasopressin Bolus Protocol Compared to Desmopressin (DDAVP) for Managing Acute, Postoperative Central Diabetes Insipidus and Hypovolemic Shock

2017 ◽  
Vol 2017 ◽  
pp. 1-4
Author(s):  
Anukrati Shukla ◽  
Syeda Alqadri ◽  
Ashley Ausmus ◽  
Robert Bell ◽  
Premkumar Nattanmai ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Case Report ◽  
Specific Gravity ◽  
Diabetes Insipidus ◽  
Serum Sodium ◽  
Urine Output ◽  
Hypovolemic Shock ◽  
Central Diabetes Insipidus ◽  
Intravenous Fluids ◽  
Decompressive Craniotomy

Introduction. Management of postoperative central diabetes insipidus (DI) can be challenging from changes in volume status and serum sodium levels. We report a case successfully using a dilute vasopressin bolus protocol in managing hypovolemic shock in acute, postoperative, central DI. Case Report. Patient presented after bifrontal decompressive craniotomy for severe traumatic brain injury. He developed increased urine output resulting in hypovolemia and hypernatremia. He was resuscitated with intravenous fluids including a dilute vasopressin bolus protocol. This protocol consisted of 1 unit of vasopressin in 1 liter of 0.45% normal saline. This protocol was given in boluses based on the formula: urine output minus one hundred. Initial serum sodium was 148 mmol/L, and one-hour urine output was 1 liter. After 48 hours, he transitioned to 1-desamino-8-D-arginine vasopressin (DDAVP). Pre-DDAVP serum sodium was 149 mmol/L and one-hour urine output 320 cc. Comparing the bolus protocol to the DDAVP protocol, the average sodium was 143.8 ± 3.2 and 149.6 ± 3.2 mmol/L (p=0.0001), average urine output was 433.2 ± 354.4 and 422.3 ± 276.0 cc/hr (p=0.90), and average specific gravity was 1.019 ± 0.009 and 1.016 ± 0.01 (p=0.42), respectively. Conclusion. A protocol using dilute vasopressin bolus can be an alternative for managing acute, central DI postoperatively, particularly in setting of hypovolemic shock resulting in a consistent control of serum sodium.

scholarly journals Successful Treatment of Transient Central Diabetes Insipidus following Traumatic Brain Injury in a Dog

2019 ◽  
Vol 2019 ◽  
pp. 1-6
Author(s):  
Catriona Croton ◽  
Sarah Purcell ◽  
Andrea Schoep ◽  
Mark Haworth
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Diabetes Insipidus ◽  
Successful Treatment ◽  
Serum Sodium ◽  
Rapid Onset ◽  
Central Diabetes Insipidus ◽  
The Other ◽  
Clinical Progression ◽  
First Report

An 11-year-old female spayed Maltese presented comatose, half an hour after vehicular trauma, and was treated for traumatic brain injury and pulmonary contusions. The dog developed severe hypernatremia within six hours of presentation, which responded poorly to the administration of five percent dextrose in water. As central diabetes insipidus was suspected, desmopressin was trialled and resolution of hypernatremia was achieved six days later. Transient trauma-induced central diabetes insipidus has been described previously in two dogs; in the first, serum sodium concentrations were evaluated three days after injury and the other developed hypernatremia seven days after injury. To the authors’ knowledge, this is the first report of rapid onset, transient, and trauma-induced central diabetes insipidus in a dog that encompasses the complete clinical progression of the syndrome from shortly after injury through to resolution.

scholarly journals Acute Transient Central Diabetes Insipidus: A Rare Case of DI Secondary to Vasopressin Withdrawal

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A571-A571
Author(s):  
Crystal Cobb ◽  
Ibitoro Nnenna Osakwe
Keyword(s):  
Diabetes Insipidus ◽  
Serum Sodium ◽  
Clinical Picture ◽  
Urine Output ◽  
Early Recognition ◽  
Bowel Perforation ◽  
Fluid Management ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Central Diabetes Insipidus

Abstract Introduction: Transient Central Diabetes Insipidus (tCDI) induced by vasopressin withdrawal is a rare condition which is possibly under recognized. It occurs in very sick, often critically ill patients and usually complicates an already complex clinical picture, so early recognition and treatment are critical to reduce morbidity. Case Description: A 47-y/o male with a PMH of Coffin Lowry syndrome, atrial fibrillation, and GERD presented with abdominal pain and flu like symptoms. His home medications were metoprolol, loratadine and colestipol. Work up revealed bowel perforation for which he was taken to the OR for repair. Intraoperatively he developed septic shock requiring pressor support with norepinephrine and vasopressin. He was weaned off norepinephrine on post-op day (POD)1, and vasopressin on POD 2. Approximately three hours after withdrawal of vasopressin support his urine output increased dramatically up to a peak of 350 cc/hour with a recorded 24hr urine volume of >5L. Concurrently, his serum sodium was found to have increased from 147 mmol/L to 173 mmol/L (n 135-145) over the course of 13 hours. Clinically, he became increasingly lethargic with abnormal eye movements. His sodium did not improve with fluid management with D5W. His other laboratory values included a urine osmolality of 141 mOsm/kg, urine sodium of 60 mmol/L and a peak serum sodium of 177mmol/L. He was administered 1mcg desmopressin and his D5W rate was increased. His urine output dropped gradually to ~150cc/hr, his serum sodium level started to trend down to 168 mmol/L and his urine osmolality increased to 439 mOsm/kg five hours after desmopressin administration, with improvement in mental status. The patient received a total of two doses of desmopressin and continued support with IV fluids. His sodium eventually normalized, and his polyuria did not return. Discussion: This patient’s clinical picture is consistent with tCDI secondary to discontinuation of vasopressin. Transient Central diabetes insipidus due to vasopressin withdrawal is a phenomenon that is not well understood, but there is a strong male preponderance, and it tends to occur more commonly in patients with underlying neurological conditions, as did our patient. Current proposed mechanisms include decreased production and release of exogenous ADH due to negative feedback, down regulation of the V2 receptors, and hypoperfusion to the posterior pituitary. This condition deserves more investigation to better understand the incidence, risk factors and pathophysiological mechanisms.

scholarly journals SAT-235 Young Male with Persistent Central Diabetes Insipidus After a Car Accident

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Liudmila Yesaulava ◽  
Caroline Houston ◽  
Sanjeda Sultana
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Specific Gravity ◽  
Diabetes Insipidus ◽  
Intracranial Hypertension ◽  
Serum Sodium ◽  
Mass Effect ◽  
Midline Shift ◽  
Pituitary Dysfunction ◽  
Ct Head

Abstract BACKGROUND: Central diabetes insipidus (CDI) occurs in 20% of cases of traumatic brain injury (TBI). Most cases of post-TBI CDI resolve within 2–5 days. Only 6% of long-term survivors of TBI have evidence of persistent CDI.1 We report a patient with persistent CDI after TBI. Clinical Case: A 27 year old male was referred for polyuria. Three months prior he was in a rollover motor vehicle accident. At that time, CT head revealed frontal and occipital contusions with scattered subarachnoid, subdural, and intraventricular blood. There was no evidence of skull fracture, mass-effect, or midline shift. On hospital day 4, his urine output increased to > 3L/day, with serum sodium of 146 mEq/L (n 135–145) and urine specific gravity of 1.015 (n 1.005–1.030). Repeat head CT revealed bilateral subdural hematomas causing mild mass effect. During the rest of his 2-month hospitalization, he continued to have polyuria with specific gravity as low as 1.005, and occasional hypernatremia, with a peak serum sodium of 149 mEq/L. Serum sodium on discharge was 144 mEq/L. On presentation to our clinic, his family and caretakers reported polydipsia, polyuria and nocturia. He had no history of diabetes mellitus or lithium use. On exam he was tachycardic but normotensive with no signs of dehydration. Neurologic exam was normal except for distractibility and impaired long- and short-term memory. After 3 hours of water deprivation, laboratory testing revealed serum sodium 150 mEq/L, serum osmolality 307 mOsmol/kg (n 270–295), urine osmolality 119 mOsmol/kg (n 300–900), and ADH 3 pmol/L (n </= 14); consistent with CDI. Oral desmopressin led to resolution of polydipsia and polyuria. Evaluation of anterior pituitary function was normal. Six months post TBI, CT head revealed increased left frontal subdural hematoma with effacement of the right lateral ventricle and 1cm left-to-right midline shift. A burr hole procedure was performed but CDI persisted. Conclusion: Animal studies have shown that neurohypophyseal apoptosis occurs by inducing intracranial hypertension lasting 12 hours or more.2 Persistent DI may herald rising intracranial pressure (ICP), as reflected by our patient’s case.1 Clinicians should be aware of the reciprocal association between increased ICP and persistent CDI following TBI. References: (1) Tudor R. M., Thompson C. J. Posterior pituitary dysfunction following traumatic brain injury: review. Pituitary. 2019 Jun; 22(3):296–304. (2) Tan H., et al. Assessment of the role of intracranial hypertension and stress on hippocampal cell apoptosis and hypothalamic-pituitary dysfunction after TBI. Sci Rep. 2017 Jun; 7(1):3805.

scholarly journals MON-242 A Hidden Thirst: Unmasking of Central Diabetes Insipidus

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Ellen Dauterive ◽  
Jose Subauste
Keyword(s):  
Diabetes Insipidus ◽  
Serum Sodium ◽  
Urine Output ◽  
Fluid Intake ◽  
Case Reports ◽  
Free Water ◽  
Altered Mental Status ◽  
Central Diabetes Insipidus ◽  
Shunt Revision ◽  
Shunt Occlusion

Abstract Introduction: Central diabetes insipidus (CDI) is a common pathology following traumatic brain injury, intracranial operations, medication use, and some infections. This case highlights how CDI can be unmasked when access to free water is restricted. Case Description: A 50 yo AAM with history of Down syndrome, hydrocephalus with ventriculo-atrial shunt, and seizure disorder treated with phenytoin, was brought in from home after three back-to-back seizures. EMS was called and intubated the patient in the field. Medical history was significant for ventriculo-peritonal shunt placed shortly after birth with revisions in 2011 and 2016. Revision in 2016 was complicated by infection with klebsiella pneumoniae. He was admitted to NSICU. Shunt evaluation showed no abnormality or obstruction. Lab work on admission at 5 am was significant for low potassium and sodium was normal. Patient was stabilized and extubated later that day. Repeat labs, at 4 pm, showed a sodium of 155 mEq/L with a normal potassium. Urine output was reviewed and significant for greater than 400 cc’s per hour for at least 2 hours. Urine osmoles (264 mOsm/kg, n 50-1200) and serum osmoles (314 mOsm/kg, n 280-295) were consistent with diabetes insipidus (DI). His IV fluid intake during this time was 3 liters bolused on admission followed by continuous fluids at 125 cc’s per hour. On review of systems, patient admitted to polydipsia and polyuria throughout the day for last several years. He reported urinating 2-3 times at night. During an admission 3 years prior for ventriculo-peritoneal shunt revision, serum sodium had risen to 159 mEq/L following his surgery and returned to normal prior to discharge. MRI pituitary during admission was negative for pituitary abnormality. To treat as well as differentiate central versus nephrogenic DI, desmopressin 1mcg IV was given. The patient was allowed to drink to thirst. Urine osmolarity increased from 159 mOsm/kg to 494 mOsm/kg after 2 hours and serum sodium slowly trended down. His urine output and thirst decreased with continued administration of desmopressin. He was discharged on a maintenance dose of 0.1 mg desmopressin twice a day. On follow up in clinic, his sodium has been maintained between 140-145. Discussion: This patient with CDI was compensating with large fluid intake daily as an outpatient for at least three years. His risk factors included phenytoin use as well as previous VP shunt occlusion complicated by infection which has been reported to contribute to CDI in other case reports. This case highlighted how CDI can be unmasked when a patient loses access to free water such as with altered mental status or intubation for surgery. References 1.Central diabetes insipidus: A complication of ventriculoperitoneal shunt malfunction during pregnancy. Goolsby, Lynn et al. American Journal of Obstetrics & Gynecology, Volume 174, Issue 5, 1655-7

scholarly journals Use of Chlorothiazide in the Management of Central Diabetes Insipidus in Early Infancy

2017 ◽  
Vol 2017 ◽  
pp. 1-5
Author(s):  
Manish Raisingani ◽  
Resmy Palliyil Gopi ◽  
Bina Shah
Keyword(s):  
Diabetes Insipidus ◽  
Serum Sodium ◽  
Urine Output ◽  
Cleft Lip ◽  
Fluid Intake ◽  
Cleft Lip And Palate ◽  
Early Infancy ◽  
Central Diabetes Insipidus ◽  
Biochemical Tests ◽  
Duration Of Action

Management of central diabetes insipidus in infancy is challenging. The various forms of desmopressin, oral, subcutaneous, and intranasal, have variability in the duration of action. Infants consume most of their calories as liquids which with desmopressin puts them at risk for hyponatremia and seizures. There are few cases reporting chlorothiazide as a temporizing measure for central diabetes insipidus in infancy. A male infant presented on day of life 30 with holoprosencephaly, cleft lip and palate, and poor weight gain to endocrine clinic. Biochemical tests and urine output were consistent with central diabetes insipidus. The patient required approximately 2.5 times the normal fluid intake to keep up with the urine output. Patient was started on low renal solute load formula and oral chlorothiazide. There were normalization of serum sodium, decrease in fluid intake close to 1.3 times the normal, and improved urine output. There were no episodes of hyponatremia/hypernatremia inpatient. The patient had 2 episodes of hypernatremia in the first year of life resolving with few hours of hydration. Oral chlorothiazide is a potential bridging agent for treatment of central DI along with low renal solute load formula in early infancy. It can help achieve adequate control of DI without wide serum sodium fluctuations.

scholarly journals Pengelolaan Central Diabetes Insipidus Pasca Cedera Kepala Berat

2019 ◽  
Vol 8 (2) ◽  
pp. 99-104
Author(s):  
Bona Akhmad Fithrah ◽  
Marsudi Rasman ◽  
Siti Chasnak Saleh
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Diabetes Insipidus ◽  
Antidiuretic Hormone ◽  
Central Diabetes Insipidus ◽  
Young Generation ◽  
Posterior Pituitary ◽  
Challenging Problem ◽  
Mortality And Morbidity ◽  
Post Traumatic

Cedera otak traumatika adalah salah satu penyebab kematian dan kesakitan tersering pada kelompok masyarakat muda. Hasil akhir dari cedera kepala berat dapat menyebabkan gangguan kognitif, perilaku, psikologi dan sosial. Salah satu konsekuensi dari cedera kepala berat adalah terjadinya disfungsi hormonal baik dari hipofise anterior maupun posterior. Angka kejadian disfungsi hormonal ini sekitar 20-50%. Salah satu yang paling menantang dan sering terjadi adalah diabetes insipidus (DI) dan Syndrome inappropriate antidiuretic hormone (SIADH). Angka kejadian diabetes insipidus pasca cedera kepala diduga sebesar 1-2,9% dengan berbagai tingkatannya. Pada beberapa kasus bersifat sementara tapi beberapa kasus terjadi bersifat menetap. Pada laporan kasus ini akan dibawakan sebuah kasus diabetes insipidus pasca cedera kepala berat. Pasien mengalami cedera kepala berat, hingga dilakukan decompressive craniectomi dan trakeostomi. Untuk perawatan lanjutan pasien dirujuk ke Jakarta. Saat menjalani terapi lanjutan ini pasien terdiagnosis diabetes insipidus Pada kasus ini diabetes insipidus tidak timbul langsung setelah cedera kepala tetapi baru timbul lebih kurang satu bulan setelah cedera kepala. Diabetes insipidus dikelola dengan menggunakan desmopressin spray dan oral disamping mengganti cairan yang hilang. Pada kasus ini desmopressin sempat di stop sebelum akhirnya diberikan terus menerus dan pasien diterapi sebagai diabetes insipidus yang menetap. Managing Central Diabetes Insipidus in Post Severe Head Injury PatientAbstractTraumatic brain injury is the cause of mortality and morbidity in society mostly in male-young generation. The last outcome of traumatic brain injury might be deficit in cognitive, behavioral, psychological and social. the consequences of traumatic brain injury might be hormonal disfunction from anterior and posterior pituitary. The incidence around 20-50%. The most challenging problem is diabetes insipidus (DI) and syndrome of inappropriate antidiuretic hormone (SIADH). The incident of post traumatic diabetes insipidus around 1-2,9% with several degree. In certain case its only occurred transiently but some report it could be permanent. In this case report will find one case post traumatic diabetes insipidus. This pasien had severe traumatic brain injury and underwent decompressive craniectomy and tracheostomy. For further therapy patient was referred to Jakarta. In this further treatment patient diagnosed with diabetes insipidus. Diabetes insipidus doesn’t occurred since the first day of injury but occurred almost one month after. Diabetes insipidus managed with desmopressin spray and oral beside replace water loss. For a few days desmopressin stop but diabetes insipidus occurred again so desmopressin given daily both spray and oral and the patient had therapy as diabetes insipidus permanent. 

Central diabetes insipidus in neonate born at 24 weeks of pregnancy – Case report and review of literature

2017 ◽  
Vol 92 (2) ◽  
pp. 205-209
Author(s):  
Dawid Szpecht ◽  
Irmina Nowak ◽  
Agnieszka Ciesielska ◽  
Marta Szymankiewicz ◽  
Janusz Gadzinowski
Keyword(s):  
Case Report ◽  
Diabetes Insipidus ◽  
Central Diabetes Insipidus ◽  
Review Of Literature
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