Case Of Central Diabetes Insipidus Research Articles

A case of central diabetes insipidus after COVID-19 as a probable diagnosis of lymphocytic infundibulo-neurohypophysitis with positive anti-rabphilin-3A antibodies with review of literature.

Coronavirus disease 2019 (COVID-19) is caused by severe acute respiratory syndrome coronavirus 2, and various complications have been reported. Furthermore, there have been increasing reports of endocrinopathy related to COVID-19 following the pandemic. We report a 49-year-old healthy woman who developed rapid onset of polydipsia and polyuria three weeks after COVID-19. Laboratory tests indicated low urine osmolarity and increased serum osmolarity, and antidiuretic hormone (ADH) was undetectable. Urine osmolality remained low with water deprivation. Similarly, plasma ADH responses to hypertonic-saline infusion were blunted and urine osmolality increased in response to desmopressin. There was no clear evidence of anterior pituitary dysfunction. T1-weighted magnetic resonance imaging (MRI) showed pituitary stalk thickening and absence of posterior pituitary bright signal spots, suggesting the presence of hypophysitis. Based on these results, we made a probable diagnosis of lymphocytic infundibulo-neurohypophysitis (LINH) which have caused central diabetes insipidus. Positive findings for serum anti-rabphilin-3A antibodies, reported as a potential diagnostic marker for LINH, were also noted. Following oral desmopressin administration, polydipsia and polyuria were quickly improved, though treatment with desmopressin was still required over four months. This is the first report of a patient with a probable diagnosis of LINH after COVID-19 who tested positive for anti-rabphilin-3A antibodies. Positive findings for those antibodies suggest that pituitary dysfunction associated with COVID-19 is hypophysitis involving an abnormal immune mechanism. The presence of anti-rabphilin-3A antibodies may be useful as a non-invasive diagnostic marker of LINH and potentially serve as a valuable diagnostic aid in cases of LINH associated with COVID-19.

A case of central diabetes insipidus due to Rathke’s cyst presenting with nocturnal enuresis

A case of central diabetes insipidus due to Rathke’s cyst presenting with nocturnal enuresis

Developing central diabetes insipidus following neurohypophysitis during the convalescent period after recovering from covid-19: presentation of a clinical case and literature review

Currently, there is a substantial body of research dedicated to exploring the impact of SARS-CoV-2 on the endocrine system. However, information regarding pathological changes in the hypothalamo-pituitary system in the context of COVID-19 remains limited. Hypophysitis is a general term encompassing various inflammatory conditions affecting the pituitary gland, leading to structural alterations in the hypothalamo-pituitary axis and various levels of hormonal deficiencies in the anterior and/or posterior pituitary.This paper presents a clinical case of central diabetes insipidus resulting from neurohypophysitis, manifested two months after recovering from the novel coronavirus infection SARS-CoV-2 (COVID-19). Our study contributes to expanding knowledge about a rare but potentially consequential outcome of the novel coronavirus infection, which holds significance given the global prevalence of COVID-19. The unexpected consequences of SARS-CoV-2 infection contribute to maintaining caution among medical professionals and stimulate interest in scientific research.

FRI350 Prolonged Transient Central Diabetes Insipidus Induced By Traumatic Brain Injury

Abstract Disclosure: R. Marques: None. S. Sharma: None. B.S. Flores Chang: None. A. Sajan: None. Introduction: Central diabetes insipidus (CDI) is a rare complication of traumatic brain injury (TBI). Most cases of CDI due to TBI are transient and resolve within 2-5 days. We report a patient with prolonged transient CDI which lasted for 35 days after sustaining a gunshot wound to the head. Case Description: A 17-year-old male with no past medical history presented after gunshot wound in the head. He had comminuted fractures of the right temporal bone, right zygomatic arch, greater and lesser rings of sphenoid bone, right maxillary sinus, right medial orbital wall, right orbital floor and bilateral frontal sinuses. A computerized tomography of head showed subarachnoid haemorrhage of the frontal lobes as well as subdural haemorrhage of right parietal lobe, right falx cerebri and left cerebral hemisphere. On hospital day 2, he had an intracranial pressure monitor placed which was unremarkable. He underwent right hemicraniectomy with debridement and washout on hospital day 3. Shortly afterwards, his urine output increased to >500 cc/hr with serum sodium of 172 mEq/L [135-145], serum osmolality 307 mOsmol/kg [270-295], and urine osmolality of 117 mOsm/kg [300-900]; consistent with CDI. He was acutely treated with intravenous desmopressin with resolution of hypernatremia. During the next five weeks of his 3-month hospitalization, he continued to have polyuria with specific gravity as low as 1.003 [1.005-1.030], and occasional hypernatremia, with a peak serum sodium of 150 mEq/L. Intranasal desmopressin as well as free water supplementation were given daily to alleviate his polyuria and hypernatremia. Evaluation of anterior pituitary function was normal except for decreased gonadotrophins. His polyuria resolved after five weeks, and labs showed urine osmolality of 530 mOsm/kg with serum sodium 138 mEq/L and urine specific gravity 1.010, consistent with resolution of CDI. Intranasal desmopressin was discontinued. His serum sodium remained stable without desmopressin for the next 7 weeks with serum sodium at discharge of 141 mEq/L. Discussion: The damage of the hypothalamic vasopressin-producing neurons, their axons or the posterior pituitary results in permanent post-TBI CDI. In cases of transient CDI, the pathogenesis is likely related to small vessel damage or inflammatory edema rather than direct neuronal damage. In our case, the patient initially developed hypernatremia and polyuria from acute CDI due to hemicraniectomy with debridement and washout. He continued to have prolonged transient CDI due to the extensive intracranial hemorrhage and edema. The CDI resolved with desmopressin (both intravenous and intranasal) and fluid replacement. Transient CDI is a rare complication intracranial haemorrhage. Our case highlights that the severity of TBI may correlate with the duration of transient CDI. Presentation: Friday, June 16, 2023

Predictors of the Spontaneous Resolution of Central Diabetes Insipidus Following Endoscopic Endonasal Surgery for Craniopharyngioma.

Central diabetes insipidus (CDI) is the most common complication of endoscopic endonasal surgery (EES) for craniopharyngioma. However, some cases of CDI could spontaneously resolve during the follow-up period. Hence, this study aimed to determine the predictive factors for the spontaneous resolution of CDI. Data of patients with CDI who underwent EES for craniopharyngioma between February 2009 and June 2021 were retrospectively reviewed. All patients were divided into 2 groups based on the resolution of CDI during follow-up: the recovery and no recovery groups. The baseline characteristic, surgical, and follow-up results of patients were compared. We identified 84 patients with CDI (35 in the recovery group and 49 in the no recovery group). A direct comparison showed that retaining the pituitary stalk (57.1% vs. 14.3%, P= 0.000) and no-hypothalamic injury (HI) (68.6% vs. 20.4%, P= 0.000) were more common in the recovery group, whereas hydrocephalus at diagnosis (8.6% vs. 46.9%, P= 0.000) was significantly more common in the no recovery group. Subsequently, we found through univariate and multivariate analysis that the spontaneous resolution of CDI was associated with hydrocephalus at diagnosis (yes vs. no: odds ratio [OR], 0.198; P= 0.045), pituitary stalk injury (retaining vs. sectioning: OR, 7.055; P= 0.004), and the Hong etal HI pattern (mild-HI vs. no-HI: OR, 0.183; P= 0.038; unilateral-HI vs. no-HI: OR, 0.147; P= 0.017; bilateral-HI vs. no-HI: OR, 0.154; P= 0.044). Hydrocephalus at diagnosis, pituitary stalk injury, and the Hong etal HI pattern might be predictors of the spontaneous resolution of CDI following EES for craniopharyngioma.

Central diabetes insipidus: a late sequela of BNT162b2 SARS-CoV-2 mRNA vaccine?

BackgroundThe development of an effective vaccine is a powerful tool to contain the global spread of coronavirus disease 2019 (COVID-19). Still, it raises potential safety concerns about the subsequent enhancement of associated immunopathology. Increasing evidence shows that the endocrine system, including the hypophysis, may be involved in COVID-19. Moreover, occasional but increasing reports of endocrine disorders involving the thyroid have been reported after the severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) vaccine. Among them, a few cases encompass the pituitary. Here we report a rare case of central diabetes insipidus following SARS-CoV-2 vaccination.Case presentationWe report a 59-year-old female patient with a 25-year history of Crohn's disease in long-term remission, who presented with sudden onset of polyuria eight weeks after administration of an mRNA SARS-CoV-2 vaccination. Laboratory evaluation was consistent with isolated central diabetes insipidus. Magnetic resonance imaging displayed involvement of the infundibulum and the posterior hypophysis. Eighteen months after the vaccination, she is still under desmopressin treatment and had stable pituitary stalk thickening on magnetic resonance imaging. Although Crohn's disease-associated hypophysitis has been reported, it is scarce. In the absence of other recognizable causes of hypophysitis, we believe the involvement of the hypophysis in our patient may have been triggered by the SARS-CoV-2 vaccine.ConclusionsWe report a rare case of central diabetes insipidus potentially associated with SARS-CoV-2 mRNA vaccination. Further studies are needed to understand better the mechanisms underlying autoimmune endocrinopathies development in the context of COVID-19 infection and SARS-CoV-2 vaccination.

Abstract 81

Background: The diagnosis of central Diabetes insipidus (DI) requires intact renal function to manifest polyuria. Therefore, it may not become evident in patients with oliguric or anuric renal failure such as in chronic kidney disease (CKD) or end stage renal disease (ESRD). This might get manifested after renal transplantation, however there are only 5 cases reported so far of Central DI post renal transplantation. Here we report a case of central DI that was unmasked in a patient with CKD after kidney transplantation leading to polyuria. Case Report: RV, 26-year-old male had one episode of febrile illness with hematuria at age of 20 years and was diagnosed IgA nephropathy by renal biopsy following which he recovered completely. Hypertension was detected in Feb 2021, and he has been on Cilnidipine 10 mg OD, Clonidine 0.1 mg TDS, Metoprolol XL 40 mg OD. At age of 25 years, he had covid illness and his kidney function deteriorated to ESRD for which he was started on twice weekly hemodialysis for 8 months and then underwent live donor renal transplantation in October 2021. Two months later, he was admitted for polyuria, polydipsia, and nocturia. After renal transplantation, his urine volume increased to 9-10 L/ d, while it had been less than 500 mL/day before the transplantation. His serum creatinine level improved from 3.2 mg/dL prior to transplant to 0.8 mg/dL after transplant. He had not been diagnosed with diabetes before, and his blood glucose levels were within the normal range. He showed no symptoms of polyuria or polydipsia before transplantation and had no history of head trauma or neurosurgery. Diagnosed to have primary hypothyroidism in Feb 2021 during pre-transplant workup, for which he was started on levothyroxine 50 ug and was euthyroid. The patient received prednisolone, tacrolimus, mycophenolate mofetil, and sulfamethoxazole/trimethoprim after the transplantation. During evaluation for polyuria, urine volume was >100 ml/kg in 24 Hour. Serum osmolality of 295 mOsm/kg, urine osmolality of 101 mOsm/kg, and serum sodium of 138 mEq/L, RBS 86 mg/dl, Urea 24 mg/dl. Anterior pituitary hormone profile workup was normal. To evaluate the cause of polyuria, water deprivation test was performed which confirmed complete central diabetes insipidus. He was started on oral desmopressin 120 ug in divided doses. His urine output subsequently decreased to about 2.5 L/d with resolution of excessive thirst and nocturia. MRI sella revealed normal anterior pituitary, infundibulum and diminished posterior pituitary bright spot in the T1-weighted image. Patient is continued on desmopressin therapy at 6 months with marked improvement in symptoms. Conclusion: In this case, the water deprivation test and diminished posterior pituitary bright spot-on MRI and the responsiveness to desmopressin therapy confirm the diagnosis of central DI. Hence, any case of polyuria after renal transplantation must be evaluated for Central Diabetes Insipidus.

LBMON140 Central Diabetes Insipidus Manifesting After Vasopressin Withdrawal In A Critically Ill Patient

Abstract Introduction Central diabetes insipidus is a rare clinical entity characterized by a lack of vasopressin secretion from the posterior pituitary. We present a case of central diabetes insipidus manifesting after the withdrawal of vasopressin in a critically ill patient. Case presentation A 19 year old female with a history of Hodgkin's Lymphoma treated with chemotherapy was transferred from another medical facility while intubated and sedated for management of severe ARDS. She had undergone extensive infectious workup and the etiology was attributed to COVID-19 pneumonia and or bleomycin toxicity. She was started on Methylprednisolone for management of bleomycin toxicity and suspected organizing pneumonia. During her hospitalization, she developed septic shock for which she received broad spectrum antibiotics and pressor support. On day 12 of her hospitalization, vasopressin was discontinued and within 12 hours, there was a rise in serum sodium from 134 to 146 along with polyuria with dilute urine (daily urine output of ∼6-7 liters, urine osmolality decreased from 771 to 279 and urine specific gravity decreased from 1. 037 to 1. 026). No diuretics were administered and serum glucose was without excursions. With administration of 2 mcg DDAVP, urine osmolality increased by more than 50% from 279 to 497, serum sodium decreased from 146 to 141 and urine specific gravity increased from 1. 004 to 1. 026 confirming the diagnosis of central DI. CT head was negative. MRI brain could not be done due to hemodynamic instability. Endocrinology was consulted and concomitant adrenal insufficiency testing was not sought due to chronic steroid therapy. The dose of DDAVP was titrated to ∼1-2 mcg per day based on serum sodium levels and daily urine output. Approximately 10 days later, Vasopressin was restarted due to hemodynamic instability and with ongoing DDAVP therapy, hyponatremia was noted. Thus, DDAVP was discontinued while on vasopressin. She was continued on vasopressin for the remainder of her hospitalization ∼ 11 more days until she unfortunately passed away. Discussion Our patient developed central diabetes insipidus after withdrawal of vasopressin. She continued to require DDAVP for ∼10 days before Vasopressin had to be restarted due to hemodynamic instability, after which DDAVP had to be discontinued due to concern of SIADH. Central diabetes has been linked to critical illness in a transient state driven by depletion of endogenous stores, negative feedback repression and posterior pituitary hypoperfusion. However, our patient continued to require exogenous supplementation. More research is needed in this regard to elucidate the differing etiologies and characteristics of transient versus permanent DI. Critical illness is a rare but extremely important cause of central DI and can quickly prove to be life threatening without timely diagnosis and treatment. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

88. New onset central diabetes insipidus in pediatric scoliosis fusions utilizing tranexamic acid

<h3>BACKGROUND CONTEXT</h3> Central diabetes insipidus (CDI) is a polyuric disease characterized by renal excretion of large volumes of dilute urine, plasma volume contraction, hypernatremia and serum hyperosmolality. CDI occurs frequently after pituitary surgery and traumatic brain injury, and has been rarely reported after significant spinal cord trauma. CDI occurring in pediatric surgery during spinal fusion has only been sporadically reported and, to date, we found only one reported case of CDI with a documented suppressed vasopressin level that developed during spine fusion for idiopathic scoliosis in a pediatric patient. CDI presenting during anesthesia has been related to medications commonly used in anesthesia such as propofol, dexmedetomidine, sevoflurane, ketamine and opioids. Our scoliosis surgery protocol uses total intravenous anesthesia (TIVA) with infusions of remifentanil, propofol, ketamine and tranexamic acid (TXA) (loading dose 10 mg/kg, maintenance at 1 mg/kg/hour, later increased to 5 mg/kg/hour). Since increasing the TXA dosing, we have documented 9 cases of intraoperative CDI marked by sudden development of polyuria. We did not have any documented cases of CDI prior to TXA use or at the lower dose of 1mg/kg/hour. <h3>PURPOSE</h3> To document the incidence of CDI in pediatric patients undergoing posterior scoliosis utilizing TXA. <h3>STUDY DESIGN/SETTING</h3> Retrospective chart review. <h3>PATIENT SAMPLE</h3> The study included 599 posterior scoliosis surgery cases performed by three different surgeons between March 2012 and November 2017 at a tertiary pediatric hospital. <h3>OUTCOME MEASURES</h3> Cessation of polyuria and correction of sodium elevation. There were no cases of CDI postoperatively. <h3>METHODS</h3> Retrospective chart review. <h3>RESULTS</h3> Of 599 posterior spine fusions, 9 cases were diagnosed with introperative CDI. Five of nine of there curves were idiopathic and females predominanted. Mean urine output prior to TXA infusion was 1.1 ml/kg/hour and increased to 4.2 ml/kg/hour within 1-3.5 hours of the start of TXA infusion. Concomitantly, mean plasma sodium increased from 137 ± 3.2 mEq/L to 142 ± 3.5 mEq/L. All responded to vasopressin infusion with TXA continuation orcessation of TXA alone. No cases of postoperative CDI were seen. Group 1 (TXA at 1 mg/kg/hr) had 0/363 cases. Group 2 (TXA at 2-5mg/kg/hr) had 9/236 cases. A Fisher's exact test for comparing the Group 1 rate (0%) vs Group 2 rate (3.8%) had a significant p-value of <0.001. <h3>CONCLUSIONS</h3> This is the first reported series of intraoperative CDI development in pediatric deformity correction surgery utilizing TXA infusion. The evidence suggests a dose-dependent association between TXA and CDI. Surgeons and anesthesiologists need to be aware that TXA in pediatric scoliosis surgery can lead to intraoperative CDI. Rapid treatment with vasopressin or cessation of infusion can prevent potential sequelae. <h3>FDA DEVICE/DRUG STATUS</h3> Tranexamic Acid (Approved for this indication)

Immune Checkpoint Inhibitors as a Threat to the Hypothalamus-Pituitary Axis: A Completed Puzzle.

Simple SummaryEndocrine dysfunctions are among the most frequent toxicities induced by immune checkpoint inhibitors (ICI). Recent evidence suggests that each tract of the hypothalamic–pituitary axis can be injured by ICI, though at different frequencies. According to the limited literature, ICI agents modulating the PD-1/PD-L1 axis rarely cause posterior pituitary/hypothalamic dysfunction. In comparison, anti-CTLA4 agents seemed to affect the function of the posterior pituitary only through the extension of inflammation/autoimmunity reactions primarily triggered in the anterior pituitary (panhypophysitis). Waiting for more extensive data, oncologists need to be aware of the rare possibility that patients on ICI may manifest signs and symptoms attributable to dysfunction of the hypothalamic–pituitary axis. This knowledge is essential in order to preserve cancer patients from complications due to late diagnosis or misdiagnosis. Indeed, if promptly suspected, the hypothalamic–pituitary dysfunction may be successfully treated once endocrinological consultation is rapidly requested and provided.Immune checkpoint inhibitors (ICI) prolong the survival in an increasing number of patients affected by several malignancies, but at the cost of new toxicities related to their mechanisms of action, autoimmunity. Endocrine toxicity frequently occurs in patients on ICI, but endocrine dysfunctions differ based on the ICI-subclass, as follows: agents targeting the CTLA4-receptor often induce hypophysitis and rarely thyroid dysfunction, which is the opposite for agents targeting the PD-1/PD-L1 axis. Recently, few cases of central diabetes insipidus have been reported as an adverse event induced by both ICI-subclasses, either in the context of anterior hypophysitis or as selective damage to the posterior pituitary or in the context of hypothalamitis. These new occurrences demonstrate, for the first time, that ICI-induced autoimmunity may involve any tract of the hypothalamic–pituitary axis. However, the related pathogenic mechanisms remain to be fully elucidated. Similarly, the data explaining the endocrine system susceptibility to primary and ICI-induced autoimmunity are still scarce. Since ICI clinical indications are expected to expand in the near future, ICI-induced autoimmunity to the hypothalamic–pituitary axis presents as a unique in vivo model that could help to clarify the pathogenic mechanisms underlying both the dysfunction induced by ICI to the hypothalamus–pituitary axis and primary autoimmune diseases affecting the same axis.

EARLY-ONSET CENTRAL DIABETES INSIPIDUS IN A NEWBORN WITH HOLOPROSENCEPHALY

Holoprosencephaly is a complex brain malformation caused by the inability of the prosencephalon to divide to form the cerebral hemispheres. Central diabetes insipidus (CDI), as a result of a defect in vasopressin release, may be seen due to the abnormal hypothalamic infundibular region. CDI developing secondary to holoprosencephaly in the early neonatal period has rarely been reported in the literature. A case of early-onset CDI with holoprosencephaly and 13q deletion is presented.

Abstract #1003638: Diabetes Insipidus and Third Cranial Nerve Palsy Associated with a Pituitary Macroadenoma

We present a case of central diabetes insipidus uncovered during the work up of a non-functional pituitary macroadenoma. This case is unique due to the rarity of the association of diabetes insipidus with a relatively small pituitary macroadenoma and the absence of nocturnal polyuria.

Interesting and Rare Case of Central Diabetes Insipidus in a Patient With Acute Myeloid Leukemia

Introduction: Central Diabetes Insipidus (CDI) is the lack of antidiuretic hormone (ADH) leading to impaired urinary concentration and manifests with extreme thirst and excessive urination. Patients unable to drink fluids are at risk of severe dehydration and hypernatremia. CDI can be a rare complication of acute myeloid leukemia (AML). The occurrence of AML with CDI is extremely rare with only few case reports published. This combination of AML with CDI has been reported to be associated with monosomy 7 and inversion (3) (q21q26) and portends an overall a very poor treatment response resulting in poor outcomes.Case Presentation: 66-year-old female with hypertension, polycythemia vera diagnosed in 2006 with transformation to AML in 2020. FISH studies revealed monosomy 7. Cytogenetic studies showed inv (3)(q21q26.2). Remission induction chemotherapy was initiated. Subsequently, neutropenic fever and sepsis secondary to Clostridium difficile colitis lead to hospitalization. Her sodium (Na) level gradually trended up and reached a peak of 157 mmol/l (range 136-145) and elevated serum osmolality at 311 mOsm/K with low urine osmolality 135 mOsm/K, low urine sodium at 13 and low urine specific gravity 1.006 concerning for CDI. She developed polyuria and received desmopressin (DDAVP) leading to improvements in urine osmolality to 267 mOsm/K, 30 minutes indicating CDI diagnosis. Her Na gradually normalized to 144 mmol/l, urine osmolality improved to 580 mOsm/K and urine specific gravity to 1.025. She is now on DDAVP 0.05 mg oral twice daily and her Na is in normal range. MRI pituitary did not show any evidence of metastatic lesion with intact pituitary bright spot. Her other pituitary hormonal workup was normal except for hypogonadotropic hypogonadism.Discussion: The pathophysiology of AML and CDI is unclear. Leukemic cells infiltration of the neurohypophysis; thrombosis of small vessels in hypothalamic nuclei and the posterior pituitary; alterations of the neutrophil migration placed on the chromosome 7 leading to glycoprotein gp 130 production, a cell surface marker on granulocytes are some of hypothesis suggested. CDI has a variable onset in the course of myeloid malignancies. MRI pituitary can be normal in most of the cases.

Acute Myeloid Leukemia Leading to Central Diabetes Insipidus

Background: Central diabetes insipidus (CDI) as a complication of acute myeloid leukemia (AML) is rare, occurring in less than 0.6% of AML cases. The mechanism is thought to involve leukemic infiltration in or around the pituitary gland, not always seen on imaging. In one study, as many as 61.4% of patients with CDI due to AML had no abnormalities on MRI, and at autopsy 46% of AML patients had perihypohyseal leukemic infiltration in the absence of overt CDI. CDI is also associated with AML in cases that involve monosomy 7 and inversion 3q21q26, both of which result in ectopic viral integration site 1 (EVI-1) overexpression. It is postulated that EVI-1 overexpression interferes with hypothalamic secretion of antidiuretic hormone (ADH) or may lead to its inactivation. We present a case of adipsic CDI due to AML in a patient with monosomy 7. Case: A 70-year-old female presented for routine follow-up and was found to have a white blood cell count of 2.6 K/µL with 29% blasts, anemia (Hgb 10.3 g/dL) and normal platelets (300 K/µL). She was diagnosed with AML and molecular evaluation showed del (3)(q21),-7,add(17(p13) consistent with monosomy 7. She was admitted for induction chemotherapy with cytarabine, daunorubicin and intrathecal methotrexate. She denied thirst. On physical exam she was euvolemic and visual fields were full on confrontation. Her admission sodium was 146 mmol/L, urine osmolality was 149 mOsm/kg H2O, urine sodium 14 mmol/L. Urine output was 5.1 L over the first 24 hours. She underwent a 6 hour water deprivation test, during which her urine output averaged 250 cc/hr. Her sodium increased to 158 mmol/L, serum osmolality 331 mOsm/kg H2O, urine osmolality 146 mOsm/kg H2O. She was then administered 100 µg of DDAVP PO and her serum sodium and osmolality decreased to 155 mmol/L and 326 mOsm/kg H2O, respectively, while her urine osmolality nearly doubled to 292 mOsm/kg H2O. Urine output decreased to 50-100 cc/hr. At no point during her testing did she report thirst. The patient’s pituitary laboratory profile did not show any other abnormalities. Her pituitary MRI revealed subtle thickening of the proximal infundibulum and hypothalamus but no definitive intra-sellar pathology. She was discharged on twice daily DDAVP with a sodium of 142. Unfortunately, her AML was refractory to treatment. She was transitioned to comfort care and died peacefully. Conclusion: CDI as a complication of AML is very rare and is a poor prognostic marker. Based on her MRI findings, the most likely mechanism in this case was infundibular/hypothalamic infiltration. Her adypsia is interesting and may point to more generalized hypothalamic involvement including thirst center. Her monosomy 7 mutation may have also played a role. We present this case to bring awareness to this etiology of DI and its proposed mechanisms.

A Case of Central Diabetes Insipidus due to Pituitary Adenoma Complicated by Amphotericin-Induced Nephrogenic Diabetes Insipidus

A Case of Central Diabetes Insipidus due to Pituitary Adenoma Complicated by Amphotericin-Induced Nephrogenic Diabetes Insipidus

DIABETES INSIPIDUS AS A SYMPTOM OF COVID-19 INFECTION: CASE REPORT

SESSION TITLE: Medical Student/Resident Critical Care Posters SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: October 18-21, 2020 INTRODUCTION: COVID-19 disease usually presents as a respiratory infection which can progress to pneumonia, acute respiratory distress syndrome (ARDS) and multi organ dysfunction. The more severe cases occur in older adults, with chronic conditions such as cardiovascular and cerebrovascular diseases and diabetes[1,2]. We present a case of COVID-19 infection complicated by central diabetes insipidus (DI). CASE PRESENTATION: A 68 y/o man with history of HTN, HLD, DM- 2, A flutter presented with fever, headache, diarrhea and productive cough for 10 days. In the ED he was hypoxemic with O2 sat of 70% on room air and had diffuse wheezing throughout the lung fields. Covid PCR was positive. He was started on Lopinavir/Ritonavir x 2 days, which was aborted due to transaminitis. He was then started on Hydroxychloroquine and steroids. His hypoxemia worsened and on hospital day #15 he was intubated. On day #23 his mentation changed, he became nonresponsive to noxious stimuli, gag reflex was absent and he was polyuric. Over 24 hours his urine output increased to 7 L, serum Na increased from 136 to 153 mEq/L, urine osm was 152, specific gravity 1.005, urine specific gravity Na 43, MRI of the head showed no acute infarction, intracranial hemorrhage or mass, no abnormal intracranial enhancement. He was diagnosed with Central Diabetes Insipidus (DI) He was given DDAVP which lead to decreased urine output, increased urine Na, increased urine osm and specific gravity. His mentation returned to baseline, with a good gag reflex. He subsequently required tracheotomy, had a prolonged ICU course, and died due to worsening hypoxic respiratory failure. DISCUSSION: Multiple electrolyte derangements were described in the COVID positive patients; hyponatremia was the most frequent sodium abnormality[2]. Our patient demonstrated rapid and adequate response to DDAVP administration. Central DI can be produced by many entities like idiopathic, autoimmune, trauma or malignancy. He did not have a history of head trauma, cancer or brain surgery. The patient was briefly placed on Ketamine for sedation which was described as a cause of the central DI in some cases[3]. However,Ketamine's half life is 160 min. Patient was placed on Ketamine during the subsequent hospital stay without repeated electrolyte derangements. Hypothalamus and hypophysis infarct was less likely given negative imaging results and continuous AC. No other infectious causes were identified at that time. CONCLUSIONS: Critically ill patients with COVID pneumonia may develop central DI. We assume possible mechanism of central DI can be hypoxic encephalopathy which can occur in the setting of severe ARDS, or some more specific mechanism like autoimmune dysregulation leading to autonomic and neuroendocrine derangements. It can also be a sign of poor prognosis. We believe further studies and data analysis regarding this novel and complex viral infection will give more answers. Reference #1: Harapan H, Itoh N, Yufika A, et al. Coronavirus disease 2019 (COVID-19): A literature review. J Infect Public Health. 2020;13(5):667-673. https://doi.org/10.1016/j.jiph.2020.03.019 Reference #2: Zhang X, Cai H, Hu J, et al. Epidemiological, clinical characteristics of cases of SARS-CoV-2 infection with abnormal imaging findings. Int J Infect Dis. 2020;94:81-87. https://doi.org/10.1016/j.ijid.2020.03.040 Reference #3: Gaffar S, Eskander JP, Beakley BD, McClure BP, Amenta P, Pierre N. A case of central diabetes insipidus after ketamine infusion during an external to internal carotid artery bypass. J Clin Anesth. 2017;36:72-75. https://doi.org/10.1016/j.jclinane.2016.09.024 DISCLOSURES: No relevant relationships by Moses Bachan, source=Web Response No relevant relationships by Zinobia Khan, source=Web Response No relevant relationships by Hana Rajevac, source=Web Response

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

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.

Central diabetes insipidus related to anti-programmed cell-death 1 protein active immunotherapy

Cancer immunotherapy is a breakthrough strategy entwined with toxicity. Immune-related hypophysitis is conventionally considered distinctive of cytotoxic T-lymphocyte antigen 4 (CTLA-4) inhibitors. Immune-related central diabetes insipidus (CDI) is exceptional. CDI rarely manifests as hypernatremia, which is almost always euvolemic. We report a 71-years-old male patient with advanced lung cancer who experienced severe chronic hypernatremia presented as alterations in mental status five months after initiation of treatment with the anti-PD-1 checkpoint inhibitor nivolumab. Combination of persistenthypernatremia, polyuria, high plasma osmolality and hyposthenuria raised suspicion of diabetes insipidus, prompting measurement of serum concentration of arginine vasopressin(AVP). The inappropriately undetectable serum levels of AVP confirmed central diabetes insipidus (CDI). Nivolumab-related hypophysitis was recognized as possible cause of CDI. Further hormonal assessment excluded any endocrinopathy indicating disorder of posterior pituitary. Pituitary MRI was normal with persistence of hyperintensity of posterior pituitary on T1-weighted images (bright spot). The patient was scheduled to receive 1-deamino-8-D-arginine vasopressin (DDAVP), but he died suddenly due to cardiac arrest before initiation of treatment. Our report describes the first case of nivolumab related CDI, building on existing literature through: (I) underscoring hypovolemic hypernatremia as CDI manifestation; (ii) bringing into spotlight the rare anti-PD-1 treatment related hypophysitis; (iii) enriching the limited evidence on immune-related CDI. Increased awareness of nivolumab related CDI will enable prompt recognition and therapeutic intervention.

Central Diabetes Insipidus in a Young Feline

Background: Central diabetes insipidus (CDI) is an endocrine disorder caused by the failure to produce, transport, or release ADH. This disease may show a primary etiology (idiopathic or congenital) or a secondary one (trauma or neoplasms). It is characterized by signs such as polyuria and polydipsia. The definitive diagnosis is obtained by the two-step water deprivation test; the absence of adequate urinary concentration in the first stage confirms the diagnosis of diabetes insipidus and, in the second stage, the response to the application of synthetic desmopressin confirms a central origin. Because CDI is rare in felines, the aim of this study was to report the occurrence of a case of CDI, probably of congenital primary origin, in an 8-month-old kitten.Case: An 8-month-old male feline, castrated, 3.2 kg, was brought to consultation with a report of polydipsia, polyuria, smaller size and weight, and lower activity when compared to his brother, for several months. On physical examination, lethargy, body score 2/5, and mild dehydration were noted, as well as deciduous teeth that should have already been replaced. Abdominal ultrasound and laboratory tests were requested, which ruled out chronic kidney disease (CKD), diabetes mellitus (DM), hyperadrenocorticism (HAC), and hyperthyroidism. Due to the fact that urinalysis evidenced hyposthenuria (urinary density [UD] 1.004), CDI was suspected. The patient underwent a water deprivation test and, after 7.5 h, lost 4.7% of his initial weight, while UD was 1.012, confirming the diagnosis of DI. The investigation then proceeded to the evaluation of the response to synthetic desmopressin by the application of 5 U IM. Two h later, UD was 1.019, confirming the diagnosis of CDI. The prescribed treatment was oral desmopressin at a dose of 100 μg BID. Upon return after 30 days, the feline had gained weight, was well hydrated, and the tutor reported higher activity. A new urinalysis showed a UD of 1.004 and inactive sediment. The tutor was asked to start administering the drug three times a day. However, noting that the patient’s quality of life had significantly improved, and wishing to spare the animal from the stress of taking medication once more a day, she chose not to modify the therapy and not to perform additional tests, due to financial limitation.Discussion: First, CKD, DM, HAC, and hyperthyroidism, more common conditions, were ruled out, and the investigation then proceeded to a water deprivation test. The feline lost 3% to 5% of the initial weight and UD was on the borderlinebetween hypo- and isosthenuria, as described in the literature for the diagnosis of DI. In the second stage of the test, slight urinary concentration was observed after the application of synthetic desmopressin, which confirmed the diagnosis of CDI. The dose of desmopressin prescribed for home treatment, 100 μg BID, was effective to relieve the clinical signs, but urine remained in hyposthenuria in the interval between administrations, suggesting that, for this patient, treatment would be more effective by administering the medication three times a day, in order to maintain an adequate serum concentration. Due to the diagnosis of CDI and the feline being young, the condition’s primary origin is believed to be congenital. It is also suspected that the patient may still have congenital hypothyroidism, due to the clinical signs of late tooth exchange and constant lethargy, in addition to laboratory results of thyroid hormones below reference levels. However, because thyroid tests were made by chemiluminescence, a repetition by radioimmunoassay is indicated. If hypothyroidism is confirmed,it would be possible to assume a common etiological factor between CDI and hypothyroidism, such as hypothalamicpituitary malformation.

Early Copeptin Determination Allows Prompt Diagnosis of Post-Neurosurgical Central Diabetes Insipidus

Introduction: Central diabetes insipidus (CDI) is a frequent complication of pituitary surgery, but its diagnosis lacks standardized criteria. Copeptin, a surrogate marker of arginine vasopressin release, is triggered by psycho-physical stresses such as pituitary surgery. Low postoperative copeptin could predict CDI onset. The aims of this study were the validation of copeptin as a predictor of post-neurosurgical CDI and the identification of the optimal timing for its determination. Methods: Sixty-six consecutive patients operated for a hypothalamic-pituitary lesion were evaluated. Copeptin was determined preoperatively and at 1, 6, 12, 24 and 48 h post-extubation. Fifty-eight patients were reassessed after 3–6 months post-surgery to confirm transient (3 cases) or permanent CDI (5 cases) diagnosis. Results: A marked copeptin peak was identified at 1 h after extubation, when a value below or equal to 12.8 pmol/L had a good accuracy in identifying CDI cases (AUC 0.866, 95% CI 0.751–0.941). Moreover, a copeptin peak above 4.2 pmol/L excluded permanent forms (AUC 1, 95% CI 0.629–1). Regression analysis identified copeptin as the only significant predictor of CDI (OR 0.86, 95% CI 0.75–0.98, p = 0.02). A copeptin T1/T0 ratio below or equal to 1.47 identified patients at risk of isolated biochemical alterations even in the absence of an overt CDI. Conclusions: A prompt increase of copeptin is expected at 1 h after extubation. The absence of this peak is a reliable predictor of post-neurosurgical CDI.