scholarly journals SUN-284 Rare Case of Adipsic Diabetes Insipidus Post Astrocytoma Resection: Case Report

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Alanoud Alanazi ◽  
Yasir Elamin ◽  
Zahra AlSaeed ◽  
Fatima Alabdrabalnabi

Abstract 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.

1977 ◽  
Vol 11 (4) ◽  
pp. 433-433 ◽  
Author(s):  
Hulda J Wohltmann ◽  
Perry V Haluahka ◽  
Philip J Privitera ◽  
Harry S Margolius ◽  
Richard G Wagner ◽  
...  

2020 ◽  
Vol 6 (6) ◽  
pp. e295-e299
Author(s):  
Yasir Elamin ◽  
AlAnoud AlAnazi ◽  
Zahra A. AL Saeed ◽  
Fatimah M. Alabdrabalnabi

Objective: We report a case of adipsic diabetes insipidus (ADI) post-astrocytoma resection. Methods: Clinical and laboratory data are presented. Results: A 16-year-old female with a history of incompletely resected hypothalamic astrocytoma was admitted with a headache. Head magnetic resonance imaging showed an interval increase in a suprasellar lesion with extension to the third ventricle. Following a second stage resection, she developed an increased urine output with diluted urine resulting in a negative fluid balance; however, she was unable to sense thirst. Blood tests showed a serum sodium of 155 mEq/dL (normal, 136 to 145 mEq/dL), serum osmolality at 321 mOs/kg (normal, 285 to 295 mOs/kg) and a urine osmolality of 128 mOsm/kg (normal, 300 to 1,600 mOsm/kg). Serum creatinine and potassium were normal. Pituitary hormone profiles were found to be normal: growth hormone 0.171 ng/mL (normal, 0.123 to 8.05 ng/mL), luteinizing hormone 3.44 mIU/mL (normal, 7.59 to 89.08 mIU/mL), follicle-stimulating hormone 5.60 mIU/mL (normal, 2.55 to 16.69 mIU/mL), thyroid-stimulating hormone 2.9 mIU/mL (normal, 0.35 to 4.94 mIU/mL), free thyroxine 0.92 ng/dL (normal, 0.7 to 1.48 ng/dL), adrenocorticotropic hormone 19.56 pg/mL (normal, 7.2 to 63.3 pg/mL), and prolactin 7.25 ng/mL (normal, 5.18 to 26.53 ng/mL). The patient was treated with desmopressin acetate 120 μg tablets twice daily with a fixed fluid intake of 1.5 to 2.0 L/day with close monitoring of fluid intake, output, and body weight. The response was good with a gradual reduction of serum sodium level of around 7 to 9 mEq/L/day. Conclusion: ADI is a rare entity of central diabetes insipidus, where the absence of polydipsia can be challenging in diagnosing and managing the condition. Cases of ADI are likely under reported and clinicians need to be aware of this condition.


2020 ◽  
pp. 201010582097866
Author(s):  
Raja Ezman Raja Shariff ◽  
Sharifah Faradila Wan Muhamad Hatta ◽  
Sazzli Kasim

Suprasellar tuberculomas are uncommon causes of intracranial tumours worldwide, even in areas endemic for tuberculosis. Often, they present with combinations of pituitary hormone involvement, which can lead to various complications due to hypopituitarism. We present a rare case of suprasellar tuberculoma leading to diabetes inspidus.


2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Wei Zhang ◽  
Yimin Shen ◽  
Yuezhong Ren ◽  
Yvbo Xin ◽  
Lijun Wang

Abstract Background Diabetes insipidus (DI) can be a common cause of polydipsia and polyuria. Here, we present a case of congenital nephrogenic diabetes insipidus (CNDI) accompanied with central diabetes insipidus (CDI) secondary to pituitary surgery. Case presentation A 24-year-old Chinese woman came to our hospital with the complaints of polydipsia and polyuria for 6 months. Six months ago, she was detected with pituitary apoplexy, and thereby getting pituitary surgery. However, the water deprivation test demonstrated no significant changes in urine volume and urine gravity in response to fluid depression or AVP administration. In addition, the genetic results confirmed a heterozygous mutation in arginine vasopressin receptor type 2 (AVPR2) genes. Conclusions She was considered with CNDI as well as acquired CDI secondary to pituitary surgery. She was given with hydrochlorothiazide (HCTZ) 25 mg twice a day as well as desmopressin (DDAVP, Minirin) 0.1 mg three times a day. There is no recurrence of polyuria or polydipsia observed for more than 6 months. It can be hard to consider AVPR2 mutation in female carriers, especially in those with subtle clinical presentation. Hence, direct detection of DNA sequencing with AVPR2 is a convenient and accurate method in CNDI diagnosis.


Author(s):  
Aaron R. Caldwell ◽  
Megan E. Rosa-Caldwell ◽  
Carson Keeter ◽  
Evan C. Johnson ◽  
François Péronnet ◽  
...  

<b><i>Background:</i></b> Debate continues over whether or not individuals with low total water intake (TWI) are in a chronic fluid deficit (i.e., low total body water) [<xref ref-type="bibr" rid="ref1">1</xref>]. When women with habitually low TWI (1.6 ± 0.5 L/day) increased their fluid intake (3.5 ± 0.1 L/day) for 4 days 24-h urine osmolality decreased, but there was no change in body weight, a proxy for total body water (TBW) [<xref ref-type="bibr" rid="ref2">2</xref>]. In a small (<i>n</i> = 5) study of adult men, there were no observable changes in TBW, as measured by bioelectrical impedance, after increasing TWI for 4 weeks [<xref ref-type="bibr" rid="ref3">3</xref>]. However, body weight increased and salivary osmolality decreased indicating that the study may have been underpowered to detect changes in TBW. Further, no studies to date have measured changes in blood volume (BV) when TWI is increased. <b><i>Objectives:</i></b> Therefore, the purpose of this study was to identify individuals with habitually low fluid intake and determine if increasing TWI, for 14 days, resulted in changes in TBW or BV. <b><i>Methods:</i></b> In order to identify individuals with low TWI, 889 healthy adults were screened. Participants with a self-reported TWI less than 1.8 L/day (men) or 1.2 L/day (women), and a 24-h urine osmolality greater than 800 mOsm were included in the intervention phase of the study. For the intervention phase, 15 participants were assigned to the experimental group and 8 participants were assigned to the control group. The intervention period lasted for 14 days and consisted of 2 visits to our laboratory: one before the intervention (baseline) and 14 days into the intervention (14-day follow-up). At these visits, BV was measured using a CO-rebreathe procedure and deuterium oxide (D<sub>2</sub>O) was administered to measure TBW. Urine samples were collected immediately prior, and 3–8 h after the D<sub>2</sub>O dose to allow for equilibration. Prior to each visit, participants collected 24-h urine to measure 24-h hydration status. After the baseline visit, the experimental group increased their TWI to 3.7 L for males and 2.7 L for females in order to meet the current Institute of Medicine recommendations for TWI. <b><i>Results:</i></b> Twenty-four-hour urine osmolality decreased (−438.7 ± 362.1 mOsm; <i>p</i> &#x3c; 0.001) and urine volume increased (1,526 ± 869 mL; <i>p</i> &#x3c; 0.001) in the experimental group from baseline, while there were no differences in osmolality (−74.7 ± 572 mOsm; <i>p</i> = 0.45), or urine volume (−32 ± 1,376 mL; <i>p</i> = 0.89) in the control group. However, there were no changes in BV (Fig. <xref ref-type="fig" rid="f01">1</xref>a) or changes in TBW (Fig. <xref ref-type="fig" rid="f01">1</xref>b) in either group. <b><i>Conclusions:</i></b> Increasing fluid intake in individuals with habitually low TWI increases 24-h urine volume and decreases urine osmolality but does not result in changes in TBW or BV. These findings are in agreement with previous work indicating that TWI interventions lasting 3 days [<xref ref-type="bibr" rid="ref2">2</xref>] to 4 weeks [<xref ref-type="bibr" rid="ref3">3</xref>] do not result in changes in TBW. Current evidence would suggest that the benefits of increasing TWI are not related changes in TBW.


PEDIATRICS ◽  
1970 ◽  
Vol 45 (2) ◽  
pp. 236-245
Author(s):  
Robert M. Ehrlich ◽  
Sang Whay Kooh

Oral chlorpropamide was administered to 17 children with diabetes insipidus (D.I.). The cause of the D.I. was idiopathic, six; histiocytosis, five; craniopharyngioma, three; pinealoma, two, and post-traumatic, one. Twenty-four-hour urine volume and measurements of serum and urine osmolality at the beginning and end of a 7-hour water deprivation test were used to evaluatechlorpropamide therapy. Administration of 150 to 400 mg of chlorpropamide per day by mouth caused a reduction in urine volume in all patients (range 8 to 67%). No change in aldosterone, 17-hydroxycorticoids, or electrolyte excretion was noted. Serum electrolytes and glomerular filtration rate were not affected by therapy. Glucose tolerance and plasma insulin response remained normal in those patients tested. Mild leucine sensitivity without significant change in plasma insulin was induced in four children. During water deprivation, seven patients with secondary D.I. but only one with idiopathic D.I. produced hypertonic urine. Hypoglycemia developed in seven children and is the major hazard of treatment. Long-term management of D.I. has been possible in nine children. Oral chlorpropamide is a useful drug in children with vasopressin-sensitive diabetes insipidus.


PEDIATRICS ◽  
1960 ◽  
Vol 25 (3) ◽  
pp. 409-418
Author(s):  
S. A. Kaplan ◽  
J. Strauss ◽  
A. M. Yuceoglu

The observations during treatment of three children with acute renal failure by a conservative regimen of therapy are presented. One patient died. The regimen has also been applied to six adults with renal failure; one died. The urine in the early stages of renal failure may be iso-osmotic with plasma and may represent unmodified fluid from the proximal tubules. Cardiac failure associated with hyperkalemia or administration of excessive quantities of fluids is the most frequent cause of death in this disorder. A regimen of therapy is described which embodies the following principles: a) Limitation of daily fluid intake to insensible loss plus the urine volume of the previous day. b) Restriction of sodium intake from the beginning to anticipate the development of acidosis. c) Use of cation exchange resins to prevent excessive increase in the concentration of potassium in the serum. d) Provision of adequate caloric intake through the administration of emulsified fat intravenously. e) Treatment of hyperphosphatemia and hypocalcemia when they occur. f) Continuation of careful supervision and therapy, even after the diuretic phase begins, since renal function continues to be severely restricted for several days afterwards.


Author(s):  
Frances Hampson ◽  
Waleed Salih ◽  
Jennifer Helm Jennifer Helm

A 39-year-old man presented with severe COVID-19 pneumonitis requiring hospital admission. He represented three days following discharge with sudden onset breathlessness and chest pain. Initial imaging suggested the presence of a left pneumothorax. Following further clinical decline a plan was made to insert a CT guided chest drain. However, imaging in the prone position for the procedure unexpectedly revealed a large left lower lobe pneumatocele with only a very small pneumothorax. Events and appearances suggest that this is a rare case of delayed COVID-19 pneumonitis-related pneumatocele formation. We will discuss the clinical significance of this entity.


1996 ◽  
Vol 7 (12) ◽  
pp. 2527-2532
Author(s):  
S Laredo ◽  
K Yuen ◽  
B Sonnenberg ◽  
M L Halperin

Both central diabetes insipidus (DI) and a high rate of excretion of sodium (Na) and chloride (Cl) contributed to the development of polyuria and dysnatremia in two patients during the acute postoperative period after neurosurgery. To minimize difficulties in diagnosis and projections for therapy, two available (but not often used) clinical tools were helpful. First, the osmole excretion rate early on revealed the co-existence of central DI and an osmotic diuresis. The osmoles excreted were largely Na salts; after antidiuretic hormone acted, this electrolyte diuresis caused the urine flow rate to be much higher than otherwise anticipated. Interestingly, part of this saline diuresis occurred when the extracellular fluid volume was contracted. The tool to explain the basis for the dysnatremias was a tonicity balance. Hypernatremia, which developed before treatment of central DI, was primarily a result of a positive balance for Na rather than a large negative balance for water. Moreover, hyponatremia that developed once antidiuretic hormone acted was primarily a result of a negative balance for Na; the urine volume was large and its Na concentration was hypertonic. To prevent a further decline in the plasma Na concentration, either the Na concentration in the urine should be decreased by provision of urea or a loop diuretic while replacing all unwanted water and electrolyte losses; alternatively, the fluid infused should have a similar Na concentration and volume as the urine (infuse hypertonic saline).


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