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The Journal of Clinical Endocrinology... Sep 2022Central diabetes insipidus (CDI) is a clinical syndrome which results from loss or impaired function of vasopressinergic neurons in the hypothalamus/posterior pituitary,... (Review)
Review
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.
Topics: Adult; Arginine Vasopressin; Diabetes Insipidus; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Polyuria; Syndrome
PubMed: 35771962
DOI: 10.1210/clinem/dgac381 -
Clinical Journal of the American... May 2019Hypernatremia is common in hospitalized, critically ill patients. Although there are no clear guidelines on sodium correction rate for hypernatremia, some studies...
BACKGROUND AND OBJECTIVES
Hypernatremia is common in hospitalized, critically ill patients. Although there are no clear guidelines on sodium correction rate for hypernatremia, some studies suggest a reduction rate not to exceed 0.5 mmol/L per hour. However, the data supporting this recommendation and the optimal rate of hypernatremia correction in hospitalized adults are unclear.
DESIGN, SETTING, PARTICIPANTS, & MEASUREMENTS
We assessed the association of hypernatremia correction rates with neurologic outcomes and mortality in critically ill patients with hypernatremia at admission and those that developed hypernatremia during hospitalization. We used data from the Medical Information Mart for Intensive Care-III and identified patients with hypernatremia (serum sodium level >155 mmol/L) on admission (=122) and hospital-acquired (=327). We calculated different ranges of rapid correction rates (>0.5 mmol/L per hour overall and >8, >10, and >12 mmol/L per 24 hours) and utilized logistic regression to generate adjusted odds ratios (aOR) with 95% confidence intervals (95% CIs) to examine association with outcomes.
RESULTS
We had complete data on 122 patients with severe hypernatremia on admission and 327 patients who developed hospital-acquired hypernatremia. The difference in in-hospital 30-day mortality proportion between rapid (>0.5 mmol/L per hour) and slower (≤0.5 mmol/L per hour) correction rates were not significant either in patients with hypernatremia at admission with rapid versus slow correction (25% versus 28%; =0.80) or in patients with hospital-acquired hypernatremia with rapid versus slow correction (44% versus 40%; =0.50). There was no difference in aOR of mortality for rapid versus slow correction in either admission (aOR, 1.3; 95% CI, 0.5 to 3.7) or hospital-acquired hypernatremia (aOR, 1.3; 95% CI, 0.8 to 2.3). Manual chart review of all suspected chronic hypernatremia patients, which included all 122 with hypernatremia at admission, 128 of the 327 hospital-acquired hypernatremia, and an additional 28 patients with ICD-9 codes for cerebral edema, seizures and/or alteration of consciousness, did not reveal a single case of cerebral edema attributable to rapid hyprnatremia correction.
CONCLUSIONS
We did not find any evidence that rapid correction of hypernatremia is associated with a higher risk for mortality, seizure, alteration of consciousness, and/or cerebral edema in critically ill adult patients with either admission or hospital-acquired hypernatremia.
Topics: Aged; Aged, 80 and over; Cohort Studies; Critical Illness; Female; Hospital Mortality; Humans; Hypernatremia; Male; Middle Aged; Sodium
PubMed: 30948456
DOI: 10.2215/CJN.10640918 -
JAMA May 2021Fluid therapy is an important component of care for patients with traumatic brain injury, but whether it modulates clinical outcomes remains unclear. (Randomized Controlled Trial)
Randomized Controlled Trial
Effect of Continuous Infusion of Hypertonic Saline vs Standard Care on 6-Month Neurological Outcomes in Patients With Traumatic Brain Injury: The COBI Randomized Clinical Trial.
IMPORTANCE
Fluid therapy is an important component of care for patients with traumatic brain injury, but whether it modulates clinical outcomes remains unclear.
OBJECTIVE
To determine whether continuous infusion of hypertonic saline solution improves neurological outcome at 6 months in patients with traumatic brain injury.
DESIGN, SETTING, AND PARTICIPANTS
Multicenter randomized clinical trial conducted in 9 intensive care units in France, including 370 patients with moderate to severe traumatic brain injury who were recruited from October 2017 to August 2019. Follow-up was completed in February 2020.
INTERVENTIONS
Adult patients with moderate to severe traumatic brain injury were randomly assigned to receive continuous infusion of 20% hypertonic saline solution plus standard care (n = 185) or standard care alone (controls; n = 185). The 20% hypertonic saline solution was administered for 48 hours or longer if patients remained at risk of intracranial hypertension.
MAIN OUTCOMES AND MEASURES
The primary outcome was Extended Glasgow Outcome Scale (GOS-E) score (range, 1-8, with lower scores indicating worse functional outcome) at 6 months, obtained centrally by blinded assessors and analyzed with ordinal logistic regression adjusted for prespecified prognostic factors (with a common odds ratio [OR] >1.0 favoring intervention). There were 12 secondary outcomes measured at multiple time points, including development of intracranial hypertension and 6-month mortality.
RESULTS
Among 370 patients who were randomized (median age, 44 [interquartile range, 27-59] years; 77 [20.2%] women), 359 (97%) completed the trial. The adjusted common OR for the GOS-E score at 6 months was 1.02 (95% CI, 0.71-1.47; P = .92). Of the 12 secondary outcomes, 10 were not significantly different. Intracranial hypertension developed in 62 (33.7%) patients in the intervention group and 66 (36.3%) patients in the control group (absolute difference, -2.6% [95% CI, -12.3% to 7.2%]; OR, 0.80 [95% CI, 0.51-1.26]). There was no significant difference in 6-month mortality (29 [15.9%] in the intervention group vs 37 [20.8%] in the control group; absolute difference, -4.9% [95% CI, -12.8% to 3.1%]; hazard ratio, 0.79 [95% CI, 0.48-1.28]).
CONCLUSIONS AND RELEVANCE
Among patients with moderate to severe traumatic brain injury, treatment with continuous infusion of 20% hypertonic saline compared with standard care did not result in a significantly better neurological status at 6 months. However, confidence intervals for the findings were wide, and the study may have had limited power to detect a clinically important difference.
TRIAL REGISTRATION
ClinicalTrials.gov Identifier: NCT03143751.
Topics: Adult; Brain Injuries, Traumatic; Combined Modality Therapy; Female; Fluid Therapy; Glasgow Outcome Scale; Humans; Hypernatremia; Hypnotics and Sedatives; Infusions, Intravenous; Intracranial Hypertension; Kaplan-Meier Estimate; Male; Middle Aged; Saline Solution, Hypertonic
PubMed: 34032829
DOI: 10.1001/jama.2021.5561 -
The American Journal of Case Reports Dec 2021BACKGROUND Diabetes insipidus (DI) is a clinical syndrome characterized by polyuria and polydipsia that result from a deficiency of antidiuretic hormone (ADH), central...
BACKGROUND Diabetes insipidus (DI) is a clinical syndrome characterized by polyuria and polydipsia that result from a deficiency of antidiuretic hormone (ADH), central DI, or resistance to ADH, nephrogenic DI. In otherwise healthy patients with DI, normal thirst mechanism, and free access to water, the thirst system can maintain plasma osmolality in the near-normal range. However, in cases where DI presents with adipsia, cognitive impairment, or restricted access to water, true hypernatremia may occur, leading to severe morbidity and mortality. CASE REPORT We report a case of a 2-year-old boy who had global developmental delay and post-brain debulking surgery involving the hypothalamic region, which resulted in central DI and thirst center dysfunction. We describe the clinical presentation, the current understanding of adipsic DI, and a new practical approach for management. The main guidelines of treatment include (1) fixed desmopressin dosing that allows minimal urinary breakthroughs in-between the doses; (2) timely diaper weight-based replacement of water; (3) bodyweight-based fluid correction 2 times a day, and (4) providing the nutritional and water requirements in a way similar to any healthy child but at fixed time intervals. CONCLUSIONS This plan of management showed good effectiveness in controlling plasma sodium level and volume status of a child with adipsic DI without interfering with his average growth. This home treatment method is practical and readily available, provided that the family remains very adherent.
Topics: Child; Child, Preschool; Diabetes Insipidus; Diabetes Insipidus, Nephrogenic; Diabetes Insipidus, Neurogenic; Diabetes Mellitus; Humans; Hypernatremia; Male; Thirst
PubMed: 34898594
DOI: 10.12659/AJCR.934193 -
Cureus Aug 2023Sarcoidosis is an inflammatory condition that can impact multiple organs in the body such as the lungs, skin, eyes, and, occasionally, the central nervous system. When...
Sarcoidosis is an inflammatory condition that can impact multiple organs in the body such as the lungs, skin, eyes, and, occasionally, the central nervous system. When sarcoidosis affects the nervous system, it is referred to as neurosarcoidosis and is estimated to occur in approximately 5%-15% of sarcoid patients. When neurosarcoidosis affects the pituitary gland, it can result in panhypopituitarism, which can be life-threatening. A 35-year-old male with a known diagnosis of sarcoidosis by skin biopsies presented to the hospital with altered mental status, hypernatremia, hypotension, and hypothermia. He reported symptoms of polyuria and polydipsia for several weeks before admission. Laboratory workup revealed elevated serum sodium at 167 mmol/L, high serum osmolality at 381 mOsm/kg, and low urine osmolality at 381 mOsm/kg, consistent with diabetes insipidus. Anterior pituitary hormone profile workup revealed low 8 am serum cortisol (1.9 mcg/dL) and inappropriately normal adrenocorticotropic hormone (ACTH) (34 pg/ml), low serum free testosterone (<2.5 ng/dL), low luteinizing hormone (0.7 mIU/ml), low follicular stimulating hormone (< 2.6 mIU/ml), low free T4 at 0.4 ng/dL. and inappropriately normal thyroid-stimulating hormone (TSH) at 2.77 uIU/mL. Serum prolactin was mildly elevated at 86.8 ng/mL. Angiotensin-converting enzyme level was within the normal range at 33 U/L. A diagnosis of panhypopituitarism was made. Brain MRI revealed a 3 cm mass in the suprasellar region involving the hypothalamus and bilateral optic tracts with a mass effect on the anterior third ventricle. No discrete pituitary or stalk lesion was identified. A ventriculostomy tube was placed for developing hydrocephalus. A biopsy of the suprasellar mass revealed non-caseating granuloma, confirming neurosarcoidosis. Treatment was initiated with high-dose IV corticosteroids to manage secondary adrenal insufficiency and neurosarcoidosis. He was also started on IV desmopressin and IV levothyroxine to manage his diabetes insipidus and central hypothyroidism. He was transitioned to oral therapy upon discharge. Panhypopituitarism secondary to neurosarcoidosis is a rare presentation that can occur due to the infiltration of the pituitary gland or the infiltration of the hypothalamus affecting the hypothalamic-pituitary axis. Neurosarcoidosis should be considered a differential when evaluating patients with symptoms consistent with panhypopituitarism. Prompt diagnosis and initiation of corticosteroids and deficient hormones can be lifesaving.
PubMed: 37692696
DOI: 10.7759/cureus.43169 -
Frontiers in Medicine 2022The primary solute of the is sodium and accompanying anions. The solvent is water. The kidneys acutely regulate homeostasis in filtration, secretion, and resorption of... (Review)
Review
The primary solute of the is sodium and accompanying anions. The solvent is water. The kidneys acutely regulate homeostasis in filtration, secretion, and resorption of electrolytes, non-electrolytes, and minerals while balancing water retention and clearance. The gastrointestinal absorptive and secretory functions enable food digestion and water absorption needed to sustain life. Gastrointestinal perturbations including vomiting and diarrhea can lead to significant volume and electrolyte losses, overwhelming the renal homeostatic compensatory mechanisms. Dysnatremia, potassium and acid-base disturbances can result from gastrointestinal pathophysiologic processes. Understanding the renal and gastrointestinal contributions to homeostatis are important for the clinical evaluation of perturbed volume disturbances.
PubMed: 35646996
DOI: 10.3389/fmed.2022.892265 -
Clinical and Experimental Emergency... Jun 2023Hyponatremia and hypernatremia are common electrolyte disorders. Few studies to date have focused on patients presenting to the emergency department (ED) with sodium...
OBJECTIVE
Hyponatremia and hypernatremia are common electrolyte disorders. Few studies to date have focused on patients presenting to the emergency department (ED) with sodium (Na) disorders. Our objective was to determine the incidence and outcomes of hyponatremia and hypernatremia in ED patients.
METHODS
This study was a retrospective, single-center review of electronic medical records at an academic suburban ED with approximately 100,000 annual visits. Subjects included consecutive adult ED patients with Na levels measured while in the ED in 2019. Demographic, clinical, and laboratory data were recorded. Outcomes data, including hospital admission, intensive care unit (ICU) admission, mortality, and length of stay (LOS), were recorded. The primary outcome was inhospital death. Secondary outcomes were hospital admission, ICU admission, ED LOS, and hospital LOS. Univariable and multivariable linear and logistic regression analyses were performed to explore the association of candidate predictor variables and outcomes.
RESULTS
Na was measured in 57,427 adults (54%) among a total of 106,764 assessed ED visits in 2019. The mean±standard deviation age was 54±21 years, and 47% of participants were male. Mild, moderate, and severe hyponatremia and hypernatremia occurred in 8%, 2%, and 0.1% of patients and 1%, 0.2%, and <0.1% of patients, respectively. Hospital and ICU admission and mortality rates increased as Na levels increased or decreased further from normal. Adjusted odds ratio (95% confidence interval) values for hospital mortality were 2.39 (1.97-2.90) for mild hyponatremia, 3.93 (2.95-5.24) for moderate hyponatremia, 6.98 (2.87-16.40) for severe hyponatremia, 3.65 (2.47-5.40) for mild hypernatremia, 8.58 (4.92-14.94) for moderate hypernatremia, and 55.75 (11.37-273.30) for severe hypernatremia. Hypernatremia was associated with a greater risk of death than hyponatremia. Patients with hyponatremia and hypernatremia had increased LOS times compared to those with normal Na levels.
CONCLUSION
Hyponatremia and hypernatremia were associated with greater rates of hospital admission, ICU admission, mortality, and prolonged hospital LOS times.
PubMed: 36718485
DOI: 10.15441/ceem.22.380 -
World Journal of Nephrology Jan 2017Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical... (Review)
Review
Hypertonicity causes severe clinical manifestations and is associated with mortality and severe short-term and long-term neurological sequelae. The main clinical syndromes of hypertonicity are hypernatremia and hyperglycemia. Hypernatremia results from relative excess of body sodium over body water. Loss of water in excess of intake, gain of sodium salts in excess of losses or a combination of the two are the main mechanisms of hypernatremia. Hypernatremia can be hypervolemic, euvolemic or hypovolemic. The management of hypernatremia addresses both a quantitative replacement of water and, if present, sodium deficit, and correction of the underlying pathophysiologic process that led to hypernatremia. Hypertonicity in hyperglycemia has two components, solute gain secondary to glucose accumulation in the extracellular compartment and water loss through hyperglycemic osmotic diuresis in excess of the losses of sodium and potassium. Differentiating between these two components of hypertonicity has major therapeutic implications because the first component will be reversed simply by normalization of serum glucose concentration while the second component will require hypotonic fluid replacement. An estimate of the magnitude of the relative water deficit secondary to osmotic diuresis is obtained by the corrected sodium concentration, which represents a calculated value of the serum sodium concentration that would result from reduction of the serum glucose concentration to a normal level.
PubMed: 28101446
DOI: 10.5527/wjn.v6.i1.1