A complex case of post-operative adipsic diabetes insipidus and cognitive impairment

Disclosure: A.U. Kulkarni: None. P. Lekprasert: None. K. Win: None.Arginine Vasopressin (AVP) along with the intact thirst mechanism maintains appropriate sodium levels in the human body, lack of which causes central Diabetes Insipidus (DI). Adipsic DI is a rare entity where the thirst mechanism is disrupted causing lack of compensatory water intake. We present a case of Adipsic DI following ACOM (Anterior Communicating Artery) aneurysmal clipping.Case:A 65yo man with a history of Hypertension presented to the ED with lethargy, headache, blurry and double vision for 5 days. Vitals were notable for elevated BP of 220/110 mmHg with a normal neurological exam. CT head showed 4mm left parafalcine subdural hematoma, and 3cm left ACOM aneurysm. Nicardipine drip for BP management was initiated. Craniotomy with aneurysmal micro-clipping was performed the next day without any immediate intra-operative complications. Post-operatively, during the first night, polyuria was noted with a total urine output of 5.7L, up-trending serum sodium of 139mmol/L (previously 131mmol/L), serum osmolality of 286mOsm/kg, Urine studies showed urine soidum < 20mmol/L, urine potassium of 2.7mmol/L, urine chloride < 20mmol/L, and urine osmolality of 51 (300-1090 mOsm/kg), consistent with DI. On post-op day 2, he suffered multiple acute infarcts causing left-sided hemi-neglect and aphasia. He was treated with as-needed intravenous DDAVP dosing under Endocrinology guidance while monitoring urine output and serum sodium. By post-op day 6 sodium had normalized, and DI was considered resolved. He was discharged to acute rehabilitation, where Adipsia was reported and water intake was monitored. Around post-op day 10, the patient became hyponatremic, likely due to the transition to the SIADH phase. This resolved in 4 weeks from his initial surgery. He was seen in the Endocrinology clinic where he continued to report adipsia. Discussion: Anatomically, the osmoreceptors that regulate thirst overlap with the cell bodies containing AVP in the hypothalamus and share a common blood supply through small branches of the ACOM. Any disruption of this blood supply can lead to Central DI with adipsia. Adipsic DI most commonly occurs as a surgical complication. ACOM clippings account for about 40% of cases followed by resection of large craniopharyngiomas, supra-sellar tumors and infrequently in traumatic brain injury and neurosarcoidosis. Management involves prescribed DDAVP orally or intranasally to target a urine output of 1.5-2L/ day and fixed dose daily fluids to ensure euvolemia. It remains challenging as these patients often experience significant cognitive and memory impairment. Limited information is available about thirst recovery, which could be partial or complete. Recovery can occur over months-to-years with no identified pattern. Thus, we must anticipate and monitor patients undergoing these surgical procedures for adipsic DI to reduce complications of sodium and water balance.Presentation: Sunday, July 13, 2025

Abstract Langerhans cell histiocytosis (LCH) is a rare disorder, affecting approximately 1 in 560 000 adults, and is characterized by a wide spectrum of clinical presentations. Early disease onset involving concurrent multiple endocrine dysfunctions is exceptionally uncommon (Mendoza ES, Lopez AA, Valdez VAU et al. Adult-onset Langerhans cell histiocytosis presenting with adipsic diabetes insipidus, diabetes mellitus and hypopituitarism: a case report and review of literature. J Clin Transl Endocrinol Case Rep 2015; 1: 1–5). We report a rare case of multisystem LCH in a 24-year-old man who presented with an ulcerated plaque over the axilla and orange papules over the scalp. The patient had a recent diagnosis of diabetes insipidus, thyrotropin deficiency and gonadotropin deficiency, indicative of panhypopituitarism. A diagnostic skin biopsy was performed to further investigate these dermatological manifestations. Histopathological analysis revealed parakeratosis in the epidermis and sheets of medium-sized ovoid cells permeating the dermis. These cells exhibited nuclear grooves, with a small collection of lymphocytes observed adjacent to the infiltrates. Immunohistochemical staining confirmed the ovoid cells were positive for S100, CD1a and CD68, but negative for CD20, CD3, melan-A, p63 and CD30. Most of the cells also demonstrated positivity for cyclin D1. The lymphocytes consisted of a mixed population of B cells and T cells, with T cells predominating. These findings were diagnostic of LCH. Further imaging confirmed multisystem involvement, including the skin, lymph nodes, pituitary gland and temporal bone. The management of his condition was coordinated through a multidisciplinary team approach, including close collaboration with the endocrinology and haematology teams. The patient was initiated on replacement therapy for panhypopituitarism, including hydrocortisone, desmopressin, thyroxine and gonadotropin. Treatment with 12 cycles of single-agent cytarabine achieved complete remission. However, during follow-up, the patient experienced a limited recurrence of cutaneous lesions, which was managed effectively with cycles of high-dose methotrexate. This case highlights the dermatological manifestations and multiorgan involvement of LCH, along with its potential to cause severe endocrine dysfunction. The complexity of this rare condition emphasizes the need for a multidisciplinary approach to manage its aggressive course. Early diagnosis and treatment are crucial, especially in cases affecting high-risk end organs.

Home capillary monitoring of sodium in a patient with adipsic diabetes insipidus

Abstract Disclosure: P. Sargin: None. J. Montoya: None. Several complications have been reported during the postoperative phase following craniopharyngioma resection, with electrolyte disturbances and hormonal imbalances as two of the most common during the early postoperative period. Central diabetes insipidus (DI) occurs commonly in these patients. In rare cases, patients lose their thirst response to hyperosmolarity, resulting in adipsic diabetes insipidus (ADI). Patients with ADI may develop permanent DI that is often difficult to manage even with proper treatment, leading to multiple hospitalizations, numerous comorbidities including severe hypernatremia and deep vein thrombosis (DVT), high morbidity and mortality. Panhypopituitarism is another common post-operative complication of any suprasellar mass. It is associated with multiple systemic, often life-threatening comorbidities; some are poorly understood. The intricate interplay of hormones in the pituitary gland and their diverse effects on various body systems has hindered our complete comprehension of their synergistic effects and the resulting complications. An otherwise healthy 29-year-old man with craniopharyngioma underwent resection 4 months ago at another facility. His postoperative course was complicated with central DI and panhypopituitarism and he was discharged with desmopressin, levothyroxine, and steroids. He also had a pacemaker placed due to unexplained sick sinus syndrome (SSS) that developed following surgery. He was admitted with lethargy and altered mental status, then was diagnosed with hypovolemic shock in the setting of DI with possible contributing adrenal insufficiency. Laboratory work-up showed hypernatremia (156mEq/L), thrombocytopenia (92k/uL), and macrocytic anemia (7.0g/dL) with normal coagulation factors. Further studies showed extensive occlusive DVT in both legs. A comprehensive work-up was unable to identify the source of cytopenias. After appropriate management, he was discharged home in stable condition. Two weeks later, he presented for the third time with unresponsiveness and worsening severe hypernatremia (170mEq/L). Per the family, he was refusing to drink anything at home. During this admission, the hospital course was prolonged with widely fluctuating Na levels. The diagnosis was concluded as ADI. Eventually, his Na level stabilized, family was educated on adequate water intake. In this complex case with multiple comorbidities, we are highlighting the relationship between panhypopituitarism and its association with SSS and cytopenias with no other identifiable cause. Although it is difficult to prove the causation in our case, some case reports have reported the association between ADI and DVT. The case presented highlights the complex challenges in managing these complications, emphasizing the need for comprehensive care and continuous patient education to mitigate potential adverse outcomes. Presentation: 6/1/2024

Abstract Disclosure: J. Chippior: None. L. Ghalib: None. A 44 year-old female with a PMH of primary hypothyroidism, and a pituitary macroadenoma that was lost to follow up, presented to the ED with a chief complaint of an acute headache and decreased visual acuity involving the right eye over the past year. Patient was found to have a large, homogenous suprasellar mass with the largest dimension measuring 6.3 cm in size, and causing displacement of the optic chiasm. Initial hormonal workup was most notable for elevated prolactin at 128 ng/ml (3.3-26.7 ng/ml), which was slightly lower than when it was previously measured 10 years ago. The patient was taken to the OR for transsphenoidal endoscopic partial resection, but within 24 hours of post-op, she developed hypernatremia at 153 mmol/dL (135-145 mmol/dL) that was suspected to be secondary to diabetes insipidus (DI). In addition, she also suffered several small strokes involving her right midbrain and basal ganglia. She required multiple doses of DDAVP throughout her stay and this was ultimately continued upon discharge. Unfortunately, as follow up MRI had shown residual tumor within the third ventricle, she returned for a 2nd resection but once again suffered additional post-operative complications. The patient experienced additional strokes involving the right frontal and parietal lobes, and her DI became more labile than before, with her serum sodium peaking at 172 mmol/dL. Despite such a high degree of hypernatremia, she did not demonstrate any signs of thirst or any desire to access free water, even after her post-stroke encephalopathy had largely resolved. With less than 100 severe cases documented over the past four decades, it was suspected that the patient had a rare form of DI known as “adipsic DI”. Osmoreceptors within the hypothalamus can trigger the release of ADH or stimulate thirst, with the former requiring a smaller change in serum osmolality to generate such a response. Pituitary surgery involves manipulation of the infundibulum and any inadvertent severing can prevent ADH’s ability to travel from the hypothalamus to the posterior pituitary, subsequently leading to DI. The majority of patients with post-op DI increase their free water intake and subsequently do not develop hypernatremia. Those with adipsic DI lack this compensatory mechanism which leads to the electrolyte disturbance, and carries a higher risk of morbidity and mortality than those with typical DI. Following her second surgery, our patient was discharged with DDAVP once again but this time with a higher dose and frequency. She’s had numerous hospital readmissions since then for altered mental status in the setting of hypernatremia as she still struggles to meet her free water intake and continuously relies on her family for reminders. Though her case is certainly not typical, it highlights the added complexity of managing adipsic DI as it relies not only on DDAVP replacement, but replicating what is supposed to be an innate behavior. Presentation: 6/3/2024

Double trouble: adipsic diabetes insipidus and panhypopituitarism in isolated hypothalamo-pituitary langerhans cell histiocytosis

Introduction: Even though rare, Adipsic Diabetes Insipidus (ADI) is a potentially life-threatening complication of craniopharyngioma: due to the mass effect of the tumor or perioperative consequences leading to severe hypernatremic dehydration. Even in expert hands, management of water balance, in the absence of thirst is extremely challenging. Case Description: A 25-year-old gentleman, an electrician presented to the neurosurgical casualty with worsening headaches, impaired vision, and features of raised intracranial pressure over 2 months. He was found to have a large cystic suprasellar mass with well-defined margins measuring 2.7cm x 2.7cm x 3cm with chiasmal compression, suggestive of craniopharyngioma, complicating with bitemporal hemianopia, hypogonadotropic hypogonadism (LH 0.78IU/L, FSH 1.2IU/L, Testosterone 33ng/dL), secondary hypothyroidism, cranial diabetes insipidus, prediabetes sparing the cortisol axis. He underwent transcranial resection of the tumor, revealing WHO grade1 adamantinomatous craniopharyngioma followed by radiotherapy. The post-operative period was complicated with severe hypernatremia despite escalating doses and changing dosage forms of desmopressin from parenteral to nasal spray to oral tablets. Two weeks following discharge, he presented with severe hypernatremia (176mEq/L), polyuria, weight loss, hypotension, and altered sensorium where his lack of thirst was appreciated. Conclusions: In those with ADI, for the management of water balance, a “personalized approach” with the involvement of both patient and family is of paramount importance. With appropriate dose titration of desmopressin, careful fluid prescription, and frequent monitoring of electrolytes even at best centers, it is a battle that is hard to win.

Abstract #1404147: Adipsic Diabetes Insipidus in a Patient with Aggressive Suprasellar Mature Teratoma

IntroductionAdipsic diabetes insipidus (ADI) is a rare hypothalamic disorder consisting of central diabetes insipidus (CDI) and loss of thirst. In hyperosmolar state, signals from osmosensors integrate in the central thirst center resulting in stimulatory signals between subfornical-oragan, organum-vasculosm of lamina terminalis and median preoptic nucleus increasing thirst and release of vasopressin. Disruption in this mechanism leads to adipsia.Case presentation27 yr old male with history of prediabetes, 4.6cm third ventricular epidermoid cyst s/p endoscopic ventriculosmoy, hypogonadotropic hypogonadism, central hypothyroidism, and CDI underwent right frontal craniotomy for residual third ventricular cyst. Developed worsening DI, new onset hyperglycemia, and secondary adrenal insufficiency. Discharged with oral DDAVP 300mcg oral twice daily for CDI. 1 week later presented to ED with weakness. BP 132/112, HR 139, RR 38, SPO2 94%. Labs significant for corrected sodium of 172 (136-145mmol/L), glucose 699 (70-99mg/dl), calcium 11.8 (8.3-10.6 mg/dl). Discharged after 3 weeks with intranasal DDAVP 10mcg twice daily (BID). Again presented 1 week after for weakness. Vitals BP 105/64, HR 134, F 37.3 C, RR 31, SPO2 96%. Corrected sodium of 174 (136-145mmol/L) and glucose 708 (70-99mg/dl). Denied missing medication. Reported no increased water intake. Patient was diagnosed with adipsic DI based on subjective lack of thirst during period of significant hyperosmolar hypernatremia state. Overtime switched to 10mcg BID intranasal DDAVP and started on 4L fixed water intake. Had 5L urine output daily. Sodium levels ranged from 132-137. Discharged on intranasal DDAVP 10mcg AM/20mcg PM, 4L daily fixed water intake, and twice weekly sodium checks as outpatient. Goal sodium 135-140. DDAVP adjusted after sodium rose to 145. At recent clinic visit continued fixed 4L fluid intake with extra 500-1L intake for increased sweating/exercise, and sodium level 134. A1c 10% on insulin, and weight gain of 70lbs since surgery (8mon piror), BMI of 45. Started on GLP-1RA and sleep study. Learning points: Less than 100 cases of ADI reported worldwide and associated with increased morbidity/mortality1. This patient likely developed ADI due to disruption of central thirst center from epidermoid cyst and trans frontal craniotomy. We must be hypervigilant for ADI in patients with third ventricular tumors who undergo frontal craniotomy. Management is complex and requires patients are followed closely with weekly labs, either fixed water intake or fixed DDAVP dose and adjustment depending on labs. Important to screen these patients for obesity and sleep apnea given increased likelihood of hypothalamic dysfunction1. Reference: Cuesta, M., Hannon, M. J. & Thompson, C. J. Adipsic diabetes insipidus in adult patients. Pituitary 20, 372-380 (2017). https://doi.org/10.1007/s11102-016-0784-4Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

ObjectiveTo investigate the relationship between postoperative hypothalamo–hypophyseal injury (HHI) and postoperative water and sodium disturbances in patients with craniopharyngioma.MethodsThe medical records, radiological data, and laboratory results of 178 patients (44 children and 134 adults) who underwent microsurgery for craniopharyngioma in a single center were reviewed. Postoperative HHI was assessed using magnetic resonance imaging. Structural defects of the hypothalamo–hypophyseal system (pituitary, pituitary stalk, floor and lateral wall of the third ventricle) were assessed in four standard T1-weighted images. The defect of each structure was assigned 1 score (0.5 for the unilateral injury of the third ventricle wall), and a HHI score was calculated.ResultsThe number of patients with HHI scores of 0-1, 2, 2.5-3, and >3 was 35, 49, 61, and 33, respectively. Diabetes insipidus (DI) worsened in 56 (31.5%) patients with preoperative DI, while 119 (66.9%) patients were diagnosed with new-onset DI. Hypernatremia and hyponatremia developed in 127 (71.3%) and 128 (71.9%) patients after surgery, respectively. Syndrome of inappropriate antidiuresis occurred in 97(54.5%) patients. During hospitalization, hypernatremia recurred in 33 (18.5%) patients and in 54 (35.7%) during follow-up, of which 18 (11.9%) were severe. DI persisted in 140 (78.7%) patients before discharge. No relationship was found between the HHI score and incidence of early DI, hyponatremia, syndrome of inappropriate diuretic hormone, or prolonged DI. Compared with patients with a score of 0–1, those with scores =2.5-3 (OR = 5.289, 95% CI:1.098-25.477, P = 0.038) and >3 (OR = 10.815, 95% CI:2.148-54.457, P = 0.004) had higher risk of developing recurrent hypernatremia. Patients with a score >3 had higher risk of developing severe hypernatremia during hospitalization (OR = 15.487, 95% CI:1.852-129.539, P = 0.011) and at follow-up (OR = 28.637, 95% CI:3.060-267.981, P = 0.003).ConclusionsThe neuroimaging scoring scale is a simple tool to semi-quantify HHI after surgery. Recurrent and severe hypernatremia should be considered in patients with a high HHI score (>2.5). An HHI score >3 is a potential predictor of adipsic DI development. Preventive efforts should be implemented in the perioperative period to reduce the incidence of potentially catastrophic complications.

Central diabetes insipidus (CDI) is a clinical syndrome which results from loss or impaired function of vasopressinergic neurons in the hypothalamus/posterior pituitary, resulting in impaired synthesis and/or secretion of arginine vasopressin (AVP). AVP deficiency leads to the inability to concentrate urine and excessive renal water losses, resulting in a clinical syndrome of hypotonic polyuria with compensatory thirst. CDI is caused by diverse etiologies, although it typically develops due to neoplastic, traumatic, or autoimmune destruction of AVP-synthesizing/secreting neurons. This review focuses on the diagnosis and management of CDI, providing insights into the physiological disturbances underpinning the syndrome. Recent developments in diagnostic techniques, particularly the development of the copeptin assay, have improved accuracy and acceptability of the diagnostic approach to the hypotonic polyuria syndrome. We discuss the management of CDI with particular emphasis on management of fluid intake and pharmacological replacement of AVP. Specific clinical syndromes such as adipsic diabetes insipidus and diabetes insipidus in pregnancy as well as management of the perioperative patient with diabetes insipidus are also discussed.

Представленный клинический случай демонстрирует редкую патологию диэнцефальной области — адипсический несахарный диабет (АНД) с развитием тяжелой гипернатриемии у женщины 58 лет после эндоскопического трансназального транссфеноидального удаления стебельно-интравентрикулярной краниофарингиомы. АНД у пациентки диагностирован на основании гипернатриемии (150–155 ммоль/л), полиурии (до 4 л в сутки) и отсутствия чувства жажды. На фоне терапии десмопрессином и адекватного восполнения жидкости в послеоперационном периоде отмечена нормализация водно-электролитного баланса. Однако самостоятельное прекращение пациенткой терапии десмопрессином после выписки из стационара и отсутствие адекватного потребления жидкости на фоне полиурии привели к выраженной гипернатриемии (155–160 ммоль/л) и грубым психическим нарушениям.Пациенты с АДН нуждаются в строгом мониторинге клинического состояния и параметров водно-электролитного баланса, в назначении фиксированных доз десмопрессина, а также в адекватном восполнении жидкости.

A 70-year-old man with poorly controlled type 2 diabetes mellitus (DM), hypertension, hypercholesterolemia and alcohol dependence presented intoxicated, with occipital scalp lacerations after a fall. A brain computerised tomography (CT) revealed occipital skull fracture with bilateral subarachnoid haemorrhages, subdural haemorrhages and parenchymal contusions. He was admitted for close observation in the neurosurgical unit. His regular medications consisted of glipizide, empagliflozin, losartan and simvastatin.

Chapter 19 - Adipsic diabetes insipidus

Adipsic diabetes insipidus is a rare condition secondary to injury to osmoreceptors in the anterior hypothalamic area. Only two cases have been published secondary to pituitary tumor surgery. A 43-year-old man, postoperative of a non-functioning pituitary macroadenoma invading the third ventricle and compressing the hypothalamus. Reoperated for headache and rhinorrhachia, developing diabetes insipidus in the postoperative period was discharged with 20 μg/day nasal desmopressin. He came again due to sensorial disorder and hypernatremia, managing to control with intravenous hydration and desmopressin. It presents with recurrence of hypernatremia every time intravenous hydration is suspended and taken orally. With high sodium levels, there is an absence of thirst. A diagnosis of adipsic diabetes insipidus is made, indicating supervised administration of water orally with favorable evolution. Adipsic diabetes insipidus is a rare variant of central diabetes insipidus caused by damage to osmoreceptors in the hypothalamus. It manifests with absence of perception of thirst, hypernatremia and polyuria. Its management is complex and requires strict control of the water balance and adherence to treatment.

Background:Adipsic diabetes insipidus (ADI) is a rare disorder triggered by injury to the hypothalamus impairing thirst osmoreceptors and the antidiuretic hormone syntheses leading to absence of thirst.We are reporting a rare case of ADI Post astrocytoma resection who presented with a severe hypernatremia postoperatively.Clinical Case:A 16-year-old female known to have hypothalamic pilocystic astrocytoma post incomplete resection in 2014.She presented in 2018 with one week history of sudden onset heachache, progressively worsen overtime, worst in the morning, there were no relieving factors. On examination she was conscious alert oriented GCS 15/15, Vital signs were normal, fundus exam within normal, pupil equal bilateral reactive to light, there was no focal neurological deficit. Systemic examination was unremarkable. Radiological imaging revealed interval size progression of previously seen suprasella region with extension into the floor of the third ventricle. Investigations: Renal profile & pituitary hormonal profile were normal. She underwent second stage resection.Postoperatively, she developed asymptomatic hypernatremia with inability to sense thirst. On examination: Conscious, alert, BP:100/65, no postural drop, Pulse:95, Fluid balance negative 1L. Systemic examination was unremarkable. Laboratory investigations: Creat 0.77mg/dl (0.6–1), Na 173mEq/dl(136–145), K 3.3mEq/dl(3.5–5.1), Cl 134mEq/dl(98–107), Serum osmolality 363mOs/kg(285 -295), Urine osmolality 468mOs/kg(300 -1600), Urine Na 29mEq/L(20- 110) & Urine volume 1900. Diagnosis of ADI was made where she was treated with desmopressin. Her response was good with reduction in Na level of around 7- 9 mEq/L/Day. She was maintained on twice daily vasopressin, instructed to maintain her fluid intake 1–1.5 L/day and good urine output.Conclusions:Astrocytoma rarely linked with development of central diabetes insipidus and even fewer with adipsia. The absence of polydipsia and polyuria can be misleading. Long-term therapy should consider the benefits of vasopressin and fluid therapy against the risk of brain edema/herniation. Body weight and electrolytes monitoring essential & should be maintained a long with strict fluid intake.

Abstract #805605: Adipsic Diabetes Insipidus in a Patient with a Non-Functioning Pituitary Macroadenoma

Background: Adipsic diabetes insipidus (ADI) is a rare condition with approximately 100 reported cases word wide. Inpatient management can be challenging as patients are predisposed to dysnatremia during this time. Societal guidelines offer little guidance in management of this complex disease. Case: A 62-year-old woman with a history of acromegaly with transphenoidal resection more than 20 years ago, complicated by post-operative hypothyroidism, adrenal insufficiency and adipsic diabetes insipidus presented for admission for a planned cycle on of chemotherapy for her recently diagnosed diffuse large B-cell lymphoma. At admission her initial serum sodium was 130 mmol/L (reference 135-145 mmol/L) near her baseline level. During her 8 day stay she experienced significant fluctuations of serum sodium with a peak level of 151 mmol/L and a nadir of 123 mmol/L. Despite these shifts she experienced no adverse neurological symptoms. 3 weeks later she was again admitted for planned chemotherapy. During this admission she received the same medication treatment protocol as her prior stay, however, the management principles for ADI suggested by Cuesta et al. were applied. The result was a more stable serum sodium with a range of 130-145 mmol/L and no change in concentration by more than 5 mmol/L in a single 24 hour period. Patient was clinically stable and asymptomatic throughout her hospital stayDiscussion:When compared to diabetes insipidus with intact thirst sensation, patients with ADI have been shown to be at increased risk for both hypernatremia and hyponatremia during inpatient admission. The risk is further increased when the admission is for an illness not related to pituitary dysfunction. This case represents an important clinical lesson in ADI where simple management principles led to a drastic change in the patient’s serum sodium. Fortunately, this patient tolerated the sodium shifts well, and did not require critical care interventions to correct her dysnatremia. Among the most important principles were transition from intranasal to oral DDAVP for a more predictable treatment response and the use of oral fluids instead of IV whenever possible. Applying these principles at the time of admission allowed for a better understanding of the treatment goals by the multidisciplinary healthcare team. Although ADI is rare, applying these simple interventions at the time of admission is likely to benefit all patients with diabetes insipidus.

Background Craniopharyngioma is a rare embryonic sellar malformation, that can present with headache, motor and cranial nerve palsies. Treatment of large masses involves surgical excision followed by radiation therapy. Hypopituitarism and diabetes insipidus are some of the post-operative complications. Rarely, patients may develop inability to appreciate fluid losses, resulting in marked hypernatremia and dehydration associated with life-threatening lower extremity thrombosis and pulmonary embolism. We present a patient developing cerebral venous thrombosis resulting from transient adipsic diabetes insipidus accompanied by new-onset pituitary microadenoma. Clinical A 39-year-old female post-excision and radiation therapy for craniopharyngioma developed hypopituitarism and diabetes insipidus. Three months after initiating radiotherapy, she presented with headache and inability to sense thirst. She took desmopressin 100 mcg tablet only three times for the past month. There was hypernatremia at 154 meq/L (Normal Value 135-145 meq/L) and hyperprolactinemia at 235 ng/mL (NV 5.11-26.19 ng/ml). Contrast-enhanced MRI revealed cerebral venous thrombosis and a pituitary microadenoma. Thrombosis has been attributed to plasma volume contraction and consequent plasma hyperviscosity. She was started on enoxaparin, hydration with hypotonic solution, desmopressin 100 mcg tablet and bromocriptine 2.5 mg tablet for the possibility of new-onset prolactin secreting pituitary microadenoma. There was decrease in headache severity and normalization of sodium level. She was discharged on apixaban 2.5 mg tablet twice a day, bromocriptine, levothyroxine 100 mcg tab daily, desmopressin daily or at least twice a week and hydrocortisone 20 mg tab daily. After three months, she had increased ability to sense thirst but still had occasional headaches. Imaging showed partial resolution of thrombosis. Prolactin decreased to 0.925 ng/mL (NV 3-20 ng/ml). In general, prolactinomas have serum prolactin that parallel tumor size. Rarely, minimal prolactin elevations may be consistent with a prolactinoma, but a non-prolactin secreting mass should first be considered in the presence of a microadenoma. The initially elevated prolactin has been attributed to disruption of dopamine inhibition to the pituitary lactotrophs. Serial imaging of the pituitary microadenoma appears to be a reasonable follow-up. Prompt evaluation must be done should there be any signs and symptoms of hormonal hypersecretion or if there is increase in size of the microadenoma. Conclusion This is the first case to demonstrate cerebral venous thrombosis and new-onset pituitary microadenoma in a patient developing transient adipsic diabetes insipidus after treatment for craniopharyngioma. These entities must be included in the workup of patients presenting with headache. No relevant disclosures.