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 Central Diabetes Insipidus Due to Acute Myeloid Leukemia

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A575-A576
Author(s):  
Dakota J Boston ◽  
Steven N Levine ◽  
Rajini Kanth Reddy Yatavelli
Keyword(s):  
Acute Myeloid Leukemia ◽  
Diabetes Insipidus ◽  
Myeloid Leukemia ◽  
Hematopoietic Cell Transplantation ◽  
Case Reports ◽  
Free Water ◽  
Central Diabetes Insipidus ◽  
Chromosome 3 ◽  
Monosomy 7 ◽  
Acute Myeloid

Abstract Central diabetes insipidus (CDI) is a condition characterized by decreased secretion of antidiuretic hormone (ADH) and is commonly seen with pathology involving the hypothalamic/pituitary area. Common etiologies include congenital disorders, neurosurgery or trauma, infiltrative disorders, primary or secondary cancers, and idiopathic causes. CDI associated with acute myeloid leukemia (AML) is extremely rare, with about 100 published case reports, and typically occurs in patients with chromosome 3 or 7 abnormalities. A 49-year-old woman was admitted to the inpatient oncology service for chemotherapy with gemtuzumab with a goal of inducing remission of her AML prior to allogeneic hematopoietic cell transplantation. She had been diagnosed with AML 7 months prior to this admission and was considered high risk for poor clinical outcome due to cytogenetics demonstrating deletion of chromosome 7 and inversion of chromosome 3. She was noted to have increasing serum sodium and endocrine was consulted for evaluation of hypernatremia. Patient had a peak sodium of 154 meq/L which improved with free water replacement. She reported excessive thirst with associated polyuria and nocturia. Laboratory tests demonstrated inappropriately dilute urine for the degree of serum osmolality, consistent with a low ADH tone. A water deprivation test was performed which resulted in plasma and urine osmolalities of 311 mosm/kg and 103 mosm/kg, respectively. After the administration of desmopressin the Uosm increased to 345 mosm/kg at 2 hours and 484 mosm/kg at 5 hours, confirming a diagnosis of Central DI. Evaluation of other pituitary axes showed normal TSH and FT4 with a normal cortisol response on a cosyntropin stimulation test. She had low-normal LH and FSH plus a mildly elevated prolactin level (38.7 ng/mL) which were attributed to stress. An MRI of the brain done to rule out any hypothalamic/pituitary metastasis or hypophysitis was normal. AML associated with Central DI occurs rarely, is associated with a poor prognosis, and the pathogenesis is unclear. The most commonly reported cytogenetic aberrations in patients with AML and CDI are monosomy 7 and 3q alterations. Our patient had monosomy 7 and chromosome 3 inversion. Proposed pathogenic mechanisms include leukemic infiltration of the pituitary, overexpression of ectopic virus integration (EVI-1) site interfering with hypothalamic neuroendocrine secretion, and abnormal thrombopoiesis interfering with ADH levels in blood. This case illustrates a lesser-known cause for central diabetes insipidus. While other more common etiologies of CDI should still be considered first, recognition of this association can provide clarity to the origin of DI in select patients.

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.

The effects of water deprivation and water loading during treatment with 1-deamino-8-D-arginine vasopressin in central diabetes insipidus in childhood

1981 ◽  
Vol 97 (3) ◽  
pp. 358-360 ◽  
Author(s):  
Dorothy J. Becker ◽  
Thomas P. Foley
Keyword(s):  
Diabetes Insipidus ◽  
Water Intake ◽  
Arginine Vasopressin ◽  
Urine Output ◽  
Water Deprivation ◽  
Fluid Intake ◽  
Marked Decrease ◽  
Central Diabetes Insipidus ◽  
Water Loading ◽  
Serum Osmolarity

Abstract. Nine children aged 72/12 to 179/12 years with central diabetes insipidus were subjected to water deprivation and water loading during treatment with 1-deamino-8-D-arginine vasopressin (DDVAP). Urine output remained unchanged despite the large differences in water intake. Serum osmolarity was not significantly affected by water deprivation. However, there was a marked decrease in serum osmolarity during water loading. This was not accompanied by any symptoms of haemodilution. Thus patients apparently tolerate large variations in fluid intake during therapy with DDVAP.

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 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.

EFFECTS OF ADRENALECTOMY AND HYPOPHYSECTOMY ON WATER AND ELECTROLYTE METABOLISM IN MALE AND FEMALE RATS WITH INHERITED HYPOTHALAMIC DIABETES INSIPIDUS (BRATTLEBORO STRAIN)

1976 ◽  
Vol 71 (2) ◽  
pp. 193-217 ◽  
Author(s):  
R. J. BALMENT ◽  
I. CHESTER JONES ◽  
I. W. HENDERSON ◽  
J. ANN OLIVER
Keyword(s):  
Diabetes Insipidus ◽  
Water Intake ◽  
Urine Output ◽  
Free Water ◽  
Female Rats ◽  
Plasma Osmolarity ◽  
Electrolyte Metabolism ◽  
Male And Female ◽  
Male And Female Rats ◽  
Solute Excretion

SUMMARY Observations on water and electrolyte metabolism after hypophysectomy or adrenalectomy, in male and female rats with hereditary hypothalamic diabetes insipidus (Brattleboro strain) are confirmed and extended. The diabetic (homozygous, DI) state relative to the non-diabetic (heterozygous, non-DI) state was characterized by (1) water intake of 55–120% body weight; (2) copious urine hypo-osmotic to plasma; (3) greater excretory rates of total solute, Na, Ca and Mg; (4) similar plasma composition except that in male DI rats, K concentration was less, and in female DI rats osmolarity was higher; (5) glomerular filtration rates (GFR) were similar with close correlations between: food and water intakes, water intake and output, urinary Na and K, Na and CI, K and Cl, and Ca and Mg; (6) both female DI and non-DI rats had lower urinary Na: K ratios and lower plasma Na concentrations than males; (7) female DI rats excreted relatively larger amounts of K and Cl, and had higher plasma Ca concentrations than other groups. Hypophysectomized DI rats had decreased water intake and urine output, decreased solute excretion, decreased loss of osmotically free water, lower excretory rates of Na, K and Cl, and increased urinary osmolarity and K concentrations. Hypophysectomized non-DI rats had increased urinary excretory rates, decreased solute excretion (by 60–70%), decreased osmotically free water absorption, decreased urinary osmolarity, Na and K concentrations, and increased excretory rates of Ca and Mg. Hypophysectomized DI and non-DI rats had increased plasma osmolarity and Na concentration. Plasma renin activities (PRA) were higher in DI than in non-DI rats with female values lower than those of males; values for both sexes of DI and non-DI rats were reduced after hypophysectomy. Adrenalectomized DI rats had about a 50% reduction in water intake, urine output and free water clearance, increased urinary concentration of electrolytes and total solute by day 4 after operation; their Na balance (dietary:urine) did not change significantly in contrast to adrenalectomized non-DI rats in which a greater percentage of dietary Na appeared in the urine. GFR was similarly reduced in adrenalectomized DI and non-DI rats. Plasma osmolarity increased in adrenalectomized male DI, decreased in female DI and non-DI, and did not change in male non-DI rats. Plasma K concentrations increased after adrenalectomy in all groups, only non-DI rats had a significantly decreased plasma Na concentration. There was no sex difference in pituitary oxytocic activity but it was consistently reduced in DI rats; there was little change after adrenalectomy in male DI and non-DI rats; but there was an increase in DI and non-DI females. Pituitaries of DI rats had no measurable ADH activity (except the inherent activity of oxytocin). Pituitary ADH values for male and female non-DI rats were similar and were unaffected by adrenalectomy.

scholarly journals Five cases with central diabetes insipidus and hypogonadism as first presentation of neurosarcoidosis

2000 ◽  
Vol 142 (4) ◽  
pp. 365-372 ◽  
Author(s):  
C Bullmann ◽  
M Faust ◽  
A Hoffmann ◽  
C Heppner ◽  
F Jockenhovel ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Case Reports ◽  
Lymphocytic Hypophysitis ◽  
Central Diabetes Insipidus ◽  
Presenting Symptoms ◽  
Pituitary Dysfunction ◽  
Mri Scans ◽  
Primary Evaluation ◽  
Therapy Result

OBJECTIVES: We retrospectively reviewed 5 patients with neurosarcoidosis, who all presented with central diabetes insipidus and hypogonadism. DESIGN: This was a single-centre, retrospective analysis of 5 cases with a minimum follow-up of 2 years. METHODS: Case analysis included clinical, biochemical, and endocrinological evaluation and frequent CT/MRI scans of involved organs as primary evaluation and in response to immunosuppressive therapy. RESULT: Neurosarcoidosis was diagnosed in all patients. Two patients had no proven extracerebral manifestation and had a stable disease over 3 and 5 years. One patient showed deterioration with corticosteroids alone but partial remission after additional cyclophosphamide. Pituitary dysfunction remained unchanged in all patients, despite total clinical and radiological remission in two patients. However, one of these patients died of acute granulomatous meningoencephalitis after two years of follow-up. CONCLUSION: Although the presenting symptoms of neurosarcoidosis may vary, the occurrence of central diabetes insipidus associated with typical radiological features is suggestive of neurosarcoidosis. However, there is an increasing number of case reports on lymphocytic hypophysitis. Without the bioptic diagnosis, the differentiation between potentially lethal isolated neurosarcoidosis and lymphocytic hypophysitis is difficult. These cases demonstrate the difficulties in diagnosing neurosarcoidosis and reflect experiences with follow-up parameters.

scholarly journals Perplexing Polyuria Caused by a Rare Disorder

2021 ◽  
Vol 5 (Supplement_1) ◽  
pp. A597-A598
Author(s):  
Jennifer Ann Wittwer
Keyword(s):  
Diabetes Insipidus ◽  
Urine Output ◽  
Central Diabetes Insipidus ◽  
Rare Disorder ◽  
Focal Lesion ◽  
Bone Lesions ◽  
Erdheim Chester Disease ◽  
The Right ◽  
Erdheim Chester ◽  
Chester Disease

Abstract Background: Central diabetes insipidus is an uncommon condition characterized by polyuria and polydipsia. In adults, central diabetes insipidus is most commonly caused by a primary brain tumor, followed by idiopathic causes, head trauma, and neurosurgery. The presence of diabetes insipidus is often discovered prior to the underlying culprit and detection may reveal further pituitary dysfunction. Herein an unusual cause of central diabetes insipidus is presented. Case: A 35-year-old male was seen in consultation for polyuria. He initially presented with fevers, cloudy urine, and excess urine output. He indicated frequent water consumption, craving cold water and feeling persistently dehydrated with poor energy levels. During hospitalization, the patient had up to 9 liters of urine output daily, with low urine osmolality and intermittent hypernatremia. As patients’ labs were consistent with central diabetes insipidus a brain MRI was completed and showed a thickened enhancing infundibulum and some fullness of the right pituitary without a focal lesion noted, concerning for autoimmune or inflammatory hypophysitis. Other pituitary axes were evaluated, and patient was noted to have a low morning total testosterone and low IGF-1. Concurrently, the patient was discovered to have multiple bone lesions on an MRI abdomen and pelvis, which prompted a bone scan showing diffuse uptake in osseous structures. A PET scan was then obtained demonstrating mandibular uptake as well as hypermetabolic activity in both adrenal glands, the right iliac bone, bilateral femurs and humeri. Biopsy of the mandibular lesion was performed, and the specimen revealed chronic xanthogranulomatous and lymphocytic inflammation consistent with a diagnosis of Erdheim-Chester disease. The patient was discharged on desmopressin and a biologic agent for treatment of Erdheim-Chester disease. Clinical Lesson: Erdheim-Chester disease is a rare non-Langerhans histiocytic multisystem disorder that often presents with skeletal, neurologic, endocrine, cutaneous, cardiac and renal abnormalities. There is a slight male predominance of the disorder and diagnosis occurs between the 5th and 7th decade of life. Erdheim-Chester disease is a form of histiocytosis with a histologic hallmark of xanthomatous infiltration of tissues by CD68-positive foamy histiocytes. This case reflects the diagnostic delay often associated with the condition. Early identification is essential to organize a multidisciplinary team to ensure accurate diagnosis and to initiate appropriate therapy. Presently interferon-alpha is the first line treatment, but other biologics are often used and provide promising outcomes. The presented case highlights many of the idiosyncrasies associated with this rare disorder and calls attention to the possibility of Erdheim-Chester disease when an initial cause of central diabetes insipidus is not obvious.

scholarly journals Changes in copeptin levels before and 3 months after transsphenoidal surgery according to the presence of postoperative central diabetes insipidus

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yoo Hyung Kim ◽  
Yong Hwy Kim ◽  
Young Soo Je ◽  
Kyoung Ryul Lee ◽  
Hwan Sub Lim ◽  
...  
Keyword(s):  
Diabetes Insipidus ◽  
Serum Sodium ◽  
Transsphenoidal Surgery ◽  
Pituitary Surgery ◽  
Diagnostic Value ◽  
Normal Serum ◽  
Central Diabetes Insipidus ◽  
Copeptin Level ◽  
Percentage Difference ◽  
Normal Serum Sodium

AbstractCopeptin levels reflect arginine vasopressin (AVP) release from the hypothalamus. Pituitary surgery often impairs AVP release and results in central diabetes insipidus (CDI). Here, we aimed to investigate how serum copeptin level changes 3 months after pituitary surgery and whether it has a diagnostic value for postoperative permanent CDI. Consecutive patients who underwent endoscopic transsphenoidal surgery at a single tertiary hospital were recruited. Serum copeptin levels were measured preoperatively and 3 months postoperatively. Among 88 patients, transient and permanent CDI occurred in 17 (19.3%) and 23 (26.1%), respectively. Three-month postoperative copeptin levels significantly declined from preoperative levels in permanent CDI group (P < 0.001, percentage difference =  − 42.2%) and also in the transient CDI group (P = 0.002, − 27.2%). Three months postoperative copeptin level < 1.9 pmol/L under normal serum sodium levels was the optimal cutoff value for diagnosing permanent CDI with an accuracy of 81.8%, while 3-month postoperative copeptin level ≥ 3.5 pmol/L excluded the CDI with a negative predictive value of 100%. Conclusively, 3 months postoperative copeptin levels significantly decreased from preoperative levels in the transient CDI group as well as the permanent CDI group. Three-month postoperative copeptin levels ≥ 3.5 pmol/L under normal serum sodium levels may be diagnostic for excluding postoperative CDI.

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