Low Serum Osmolality Research Articles

6768 A Rare Presentation of Primary Adrenal Insufficiency with Hypertension & Hypokalemia

Abstract Disclosure: A.M. San Hernandez: None. R. Alshantti: None. G. Espinoza Mercado: None. J.L. San Hernandez: None. Introduction: Adrenal Insufficiency is caused by the failure of the adrenal cortex to produce glucocorticoids +/- mineralocorticoids. This can be due to a defect in the adrenal cortex, or in the hypothalamic pituitary axis. The clinical manifestations are usually non-specific, ranging from mild vague symptoms to life threatening crisis. Therefore, diagnosis requires a high level of suspicion by providers. Unusual presentations of primary adrenal insufficiency (PAI) with hypertension and hypokalemia have been rarely described in the literature. We present a rare case of PAI with hypertension and hypokalemia. Case Presentation: A 68 years old female with a medical history of rheumatoid arthritis, hypothyroidism on Levothyroxine, chronic transaminitis, and bicytopenia presented to the hospital with a 6 weeks history of generalized weakness, loss of appetite, weight loss, and dizziness. Patient denied any diuretic or steroid use within the last 2 years. On arrival, she was afebrile, hypertensive (168/84mmHg), with normal oxygenation and pulse. Physical examination was unremarkable with normal volume status. Initial laboratory results showed low sodium 116 mEq/L, low serum osmolality 247 MEQ/kg, normal potassium 3.6 mEq/L, Creatinine 0.3 mg/dL & BUN 9 mg/dL. She was initially started on IVF normal saline. Further workup revealed normal TSH & FT4 levels. Urine study showed urine osmolality (477 MOSM/KG), & urine sodium (127 mEq/L). Given these findings, SIADH was suspected and fluid restriction was started. Sodium level continued to be low with minimal improvement to 120 mEq/L, potassium levels also dropped (3.3-3.2 mEq/L), requiring daily replacement. BP remained elevated ranging from 150s to 160s systolic and 80s to 90s diastolic. Hypertension was controlled with her home medication Amlodipine. Although atypical presentation with hypertension & hypokalemia, the diagnosis of adrenal insufficiency was considered. Laboratory evaluation showed low morning cortisol 5.2 ug/dL, with album level 3.5 g/dL. Cosyntropin stimulation test showed 1.3 ug/dL (at baseline), 9.9 (30 min post administration), and 14.4 (1 hour post administration); results confirming PAI. ACTH, Renin, Aldosterone, & DHEAS levels were normal. CT adrenal was normal. Patient was started on hydrocortisone; some of her symptoms & Na level improved. Further investigation of the etiology of PAI and possible hyperaldosteronism is pending outpatient follow up. Conclusion: Adrenal insufficiency is a life threatening condition with serious consequences if diagnosis is missed. It manifests by a wide spectrum of symptoms and signs, some can be masked by the presence of other comorbid conditions leading to atypical presentations. Our case highlights the importance of maintaining a high level of suspicion of adrenal insufficiency in patients with atypical presentation, including those with hypertension & hypokalemia. Presentation: 6/3/2024

Association between serum osmolality and deteriorating renal function in patients with acute myocardial infarction: analysis of the MIMIC- IV database

BackgroundTo investigate the association between serum osmolality and deteriorating renal function in patients with acute myocardial infarction (AMI).MethodsThree thousand eight hundred eighty-five AMI patients from the Medical Information Mart for Intensive Care IV were enrolled for this study. The primary outcome was deteriorating renal function. Secondary outcomes included the new-onset of acute kidney injury (AKI) and progress of AKI. < 293.2725 mmol/L was defined as low serum osmolality, and ≥ 293.2725 mmol/L as high serum osmolality based on upper quartile. Univariate and multivariate logistic regression models were used to explore the associations between serum osmolality and the development of deteriorating renal function, the new-onset of AKI and progress of AKI among AMI patients. Subgroup analysis was also conducted.ResultsOne thousand three hundred ninety-three AMI patients developed deteriorating renal function. After adjusting all confounding factors, high serum osmolality was associated with increased risk of deteriorating renal function [odds ratio (OR) = 1.47, 95% confidence interval (CI): 1.22–1.78], new-onset of AKI (OR = 1.31, 95% CI: 1.01–1.69), and progress of AKI risk (OR = 1.26, 95% CI: 1.01–1.59) among AMI patients. In addition, when the stratified analysis was performed for age, AMI type, cardiogenic shock, and estimated glomerular filtration rate (eGFR), high serum osmolality was risk factor for the risk of deteriorating renal function among patients aged 65 years or older, without cardiogenic shock, and with an eGFR ≥ 60 mL/min/1.73m2.ConclusionHigher serum osmolality increased the risk of deteriorating renal function among AMI patients.

Heart failure related fatigue: An exploratory analysis of serum osmolality from the national health and nutrition examination survey

BackgroundFatigue is a prominent symptom of heart failure (HF). However, underlying mechanisms remain poorly understood. Fluid volume status has been suggested as a physiologic mechanism of HF-related fatigue. Serum osmolality may fluctuate with changes in volume status associated with neurohormonal dysregulation. The relationship of fatigue to serum osmolality has not been assessed in adults with HF. ObjectivesDescribe the relationship between serum osmolality and fatigue in adults with HF. MethodsWe analyzed two waves of cross-sectional data from the National Health and Nutrition Examination Survey (2015–2016 and 2017–2018). Adults who self-reported having HF without select co-morbid conditions known to contribute to fatigue were included. Data were weighted to provide US national estimates, and complex sample design used for analyses. Sequential logistic regression was used to isolate the effect of serum osmolality on the odds of having fatigue. ResultsData from the sample represented 1.4 million Americans with HF (58.5 % male; median age 68 years), of whom 1,001,589 (67.9 %) reported fatigue. Participants with fatigue had lower serum osmolality compared to those without fatigue (t = -3.04, p = .009). Higher serum osmolality was associated with 8.8 % lower odds of experiencing fatigue when controlling for sex and body mass index (OR = 0.912, p = .007, CI 0.857 - 0.972). ConclusionsHF-related fatigue is associated with lower serum osmolality. Low serum osmolality may indicate excess volume and the presence of a heightened neurohormonal response, both of which may influence fatigue. Alternatively, serum osmolality may directly affect other physiologic changes that may contribute to fatigue.

The U-shaped association between serum osmolality and 28-day mortality in patients with sepsis: a retrospective cohort study

BackgroundSepsis is a recognized global health challenge that places a considerable disease burden on countries. Although there has been some progress in the study of sepsis, the mortality rate of sepsis remains high. The relationship between serum osmolality and the prognosis of patients with sepsis is unclear.MethodPatients with sepsis who met the criteria in the Medical Information Mart for Intensive Care IV database were included in the study. Hazard ratios (HRs) and 95% confidence intervals (CIs) were determined using multivariable Cox regression. The relationship between serum osmolality and the 28-day mortality risk in patients with sepsis was investigated using curve fitting, and inflection points were calculated.ResultsA total of 13,219 patients with sepsis were enrolled in the study; the mean age was 65.1 years, 56.9 % were male, and the 28-day mortality rate was 18.8 %. After adjusting for covariates, the risk of 28-day mortality was elevated by 99% (HR 1.99, 95%CI 1.74-2.28) in the highest quintile of serum osmolality (Q5 >303.21) and by 59% (HR 1.59, 95%CI 1.39-1.83) in the lowest quintile (Q1 ≤285.80), as compared to the reference quintile (Q3 291.38-296.29). The results of the curve fitting showed a U-shaped relationship between serum osmolality and the risk of 28-day mortality, with an inflection point of 286.9 mmol/L.ConclusionThere is a U-shaped relationship between serum osmolality and the 28-day mortality risk in patients with sepsis. Higher or lower serum osmolality is associated with an increased risk of mortality in patients with sepsis. Patients with sepsis have a lower risk of mortality when their osmolality is 285.80-296.29 mmol/L.

Serum osmolality was non-linearly associated with the risk of all-cause and cardiovascular mortality in patients with diabetes

AimsThis study aimed to evaluate the relationship between both low and high osmolarity and the risk of all-cause and cause-specific mortality in diabetic population.MethodsAll participants were included from the National...

FRI358 A Rare Cause Of SIADH: Leptomeningeal Deposits Metastatic From T-cell Proliferative Disorder

Abstract Disclosure: S. Bendaram: None. R. Zielinski: None. V. Kantorovich: None. Introduction: Atypical causes of SIADH, though rare, are important to identify and diagnose in order to optimize timely treatment. Case: Patient is a 51-year-old male with history of obesity and pre-diabetes who presented to the ED with symptoms of generalized weakness and severe fatigue with no antecedent events such as nausea, vomiting, diarrhea, fever or recent illness. He denied lightheadedness or a syncopal episode. History was significant for the use of prednisone for a skin rash in the recent past. Labs were significant for mild hyponatremia with sodium level of 130 mmol/L [136-141] with a low serum osmolality at 273 mOsm/kg and a urine osmolality of 287 mOsm/kg. Further evaluation revealed a low cortisol level of 1.9 ug/dL [6.2 - 19.4]. Repeat cortisol was also low at 1.1 ug/dl. Cosyntropin stimulation test resulted in insufficient response, and iatrogenic adrenal insufficiency was suspected due to prior steroid use. Steroid replacement therapy was initiated with Hydrocortisone. The patient’s ACTH was found to be inappropriately normal at 17pg/ml (6-50). For further evaluation, he underwent MRI Pituitary which revealed leptomeningeal lesions concerning for an infectious, inflammatory, or malignant metastatic process. At this time, he was still hyponatremic with sodium of 130 mmol/L and continued to complain of weakness and not feeling well overall, however denied any neurological symptoms. Repeat labs for hyponatremia showed serum osmolality of 283 mOsm/kg and urine osmolality of 573 mOsm/kg while urine sodium was 100 mmol/L, concerning for mild SIADH. This was managed with fluid restriction initially and then with addition of salt tablets. He underwent lumbar puncture with Cerebrospinal fluid analysis, which did not reveal an infectious etiology. A rheumatological work up for inflammatory cause was negative. Imaging of his chest and abdomen in a search for primary malignancy revealed soft tissue lesions in the abdominal subcutaneous fat. Biopsy of the soft tissue lesions were concerning for a T-cell lymphoproliferative disorder with the absence of typical histological features. Repeat biopsy, flow cytometry and cytogenetic studies were inconclusive, which was suspected to be secondary to the patient receiving steroids prior to the biopsy. Conclusion: This case represents SIADH likely caused by a T-cell lymphoproliferative disorder. Although the biopsies have been inclusive, if the patient has Non-Hodgkin’s T cell lymphoma (NHL), leptomeningeal spread is a known complication of this disorder. The underlying mechanism that we propose behind SIADH in our patient is the leptomeningeal lesion located near the hypothalamus enhancing ADH release. Presentation: Friday, June 16, 2023

FRI356 SIADH In Acromegaly And Cerebrovascular Accident

Abstract Disclosure: S. Siddiqui: None. I.A. Guatemala Funes: None. G. Simranpreet: None. T. Zahedi: None. F. Zhang: None. Introduction: Acromegaly is characterized by excess growth hormone secretion with distinctive features of acral overgrowth, soft tissue swelling, arthralgia, jaw prognostication, hyperglycemia, hyperhidrosis, and frontal bone bossing. Hypotonic hyponatremia may occur in patients with syndrome of inappropriate antidiuretic hormone secretion (SIADH), hypothyroidism, hypocortisolism, polydipsia, medications, heart failure, liver disease, or renal dysfunction. We reported a rare case of a patient with acromegaly treated with octreotide (somatostatin analogue) who was admitted for cerebrovascular accident and developed hyponatremia due to SIADH. Case Report: Patient is an 81 year old female with typical clinical features of acromegaly who presented with expressive aphasia and left sided facial droop. MRI and CT head revealed a 26 x 14 x 29 mm densely calcified/ossified extra-axial mass in the posterior fossa, displacing the brainstem and small vessel ischemia. Patient was treated with monthly intramuscular injection of octreotide for more than 20 years before she was switched to oral octreotide formula two weeks ago. Patient had nausea, vomiting, and altered mental status. Labs showed hyponatremia with serum Na 118 mmol/L, low serum osmolality 247 mOsm/kg, high urine osmolality 437 mOsm/kg, and urine Na 104 mmol/L. Serum Na further dropped to 115 mmol/L after IV normal saline which may be related to the desalination phenomenon of SIADH. Tolvaptan and hypertonic saline were initiated followed by treatment with salt tablets and furosemide. After several days, her serum Na level slowly trending up back to normal 135 mmol/L and patient recovered with no focal neurological deficits. Discussion: Treatment for acromegaly involves multiple approaches, such as somatostatin receptor ligands, GH antagonism, surgery, radiotherapy, and dopamine receptor agonists. Life-treating endocrine disorder may result from pituitary infarction or hemorrhage in patient with acromegaly. Although gastrointestinal sodium loss may precipitate hyponatremia in our patient, her elevated urine sodium and urine osmolality were consistent with SIADH. Clinicians should be cautious of the sudden onset of hyponatremia due to SIADH in acromegaly patients and prompt treatment is warranted. Presentation: Friday, June 16, 2023

Serum sodium as a diabetes risk factor?

Electrolytes play a key role in controlling fluid status, muscle contraction, neurological function, coagulation, and acid base status, as well as multiple enzymatic reactions. Diabetes is associated with multiple significant electrolyte disorders, predominantly affecting serum sodium (Na), potassium, and magnesium.1 In healthy individuals, serum Na levels range between 135–146 mmol/L. Hyponatremia is defined as a serum Na < 135 mmol/L, typically accompanied by a low serum osmolality (<275 mosm/L). It is the most frequently seen electrolyte disorder, present in about 5% of adults and 35% of hospitalized patients.2, 3 In a New York health system analysis of 10 385 patients hospitalized with COVID-19 in 2020, hyponatremia was present in 37.5% of patients.4 Low serum Na may activate the renin-angiotensin-aldosterone system, may cause increased sympathetic nervous system tone, and may be associated with oxidative stress. Insulin, either administered therapeutically or in the setting of hyperinsulinemia from insulin resistance, increases renal tubular water reabsorption via a presumed vasopressin effect and can result in hyponatremia. Chronic kidney disease and diuretic use in hypertension further increase the risk of hyponatremia as well as other electrolyte imbalances such as hypokalemia and hypomagnesemia.7 Serum Na simply may represent the state of hydration. Might some of these mechanisms contribute to effects of even small deviations in serum Na from normal? Should we look more carefully at Na as a biomarker of outcome? Further analysis of large clinical data sets may give answers to these questions.

Severe hyponatremia as presenting symptom of small cell lung carcinoma

Abstract A 62-year-old female patient was admitted to ICU in our clinic with symptomatic severe hyponatremia with complaints of fatigue, vertigo, paresthesia of upper extremities and three episodes of loss of consciousness in the past month. She had been hospitalized two weeks before in neurology clinic because of the same symptoms. CT of the brain, EEG, ophthalmology examinations were negative. She did not complain of hemoptysis, cough, weight loss, fever, chest pain or dyspnea. Nephrologist was consulted and renal origin of the hyponatremia was excluded, before admission. Initial laboratory tests were glucose:5,47 umol/L,sodium:109 mEq/L,potassium;4.5 mEq/L,urea 3,9 umol/l;creatinine:52,7 mol/l,calcium:1,22umol/L,TSH 5;Cortisol 819nmol/L;ACTH:16,34 pg/ml. Her medical history included hypertension, primary hypothyroidism and history of smoking. Upon laboratory findings of low serum osmolality, high urine osmolality, high urine sodium levels and clinical euvolemia, and in the absence of renal, pituitary disfunction, adrenal insufficiency, inappropriate ADH syndrome was diagnosed and initially was treated with 3% NaCl. Since this treatment had no effect, it was started with fluid restriction, per os sodium intake was increased and therapy with loop diuretic was initiated, which resulted in correction of the hyponatremia. For the etiology consideration of inappropriate ADH syndrome CT of the thorax was performed, which revealed a neo infiltrative process with atelectasis in the poster basal segment of the left lobe. Histopathological sampling from the biopsy of the mass revealed small cell carcinoma of the lung. Metastasis were not detected. Since basal morning cortisol level was above upper range, with inappropriate measurements of ACTH constantly above 15 pg/ml, additional tests for ectopic Cushing syndrome were done. Overnight 1mg dexamethasone suppression test showed absent suppression of the morning cortisol values of 656nmol/L and ACTH of 22,14 pg/ml and absent circadian rhythm of cortisol secretion, with high measurements of midnight serum cortisol of 652 nmol/L. Diagnosis of ectopic Cushing syndrome and SIADH as part of paraneoplastic syndrome in small cell lung carcinoma was made. It is to be noted that patient had no significant symptoms or signs of hypercortisolemia. We report here a case of small cell carcinoma of the lung whose first presentation was with symptomatic hyponatremia as a result of inappropriate ADH syndrome. The most common neoplasms associated with hyponatremia are various forms of lung cancer. Because of the aggressive nature of the disease, the most common manifestation of small cell carcinoma of the lung is a metastatic one. Therefore, identifying the disease in earlier stages is very important. Unfortunately, these patients have low rates of survival and face a very poor prognosis even with treatment. The presence and early identification of paraneoplastic syndromes can be beneficial in this context.

Intractable hyponatremia complicated by a reset osmostat: a case report

BackgroundHyponatremia associated with a low serum osmolality is a common and confounding electrolyte disorder. Correcting hyponatremia is also complicated, especially in the setting of chronic hyponatremia. Here, we provide a rational approach to accurately detecting and safely treating acute on chronic euvolemic hyponatremia in the setting of acute polydipsia with a chronic reset osmostat.Case presentationA 71-year-old hispanic gentleman with chronic hyponatremia presented with hiccups, polydipsia, and a serum sodium concentration of 120 mEq/L associated with diffuse weakness, inattentiveness, and suicidal ideation. Symptomatic euvolemic hyponatremia warranted hypertonic saline treatment in the acute phase and water restriction in the chronic phase. Both interventions resulted in improvement in symptoms and/or the serum sodium concentration, but to a serum sodium level that persistently remained below the normal range. Remarkably, the urine osmolality appropriately fell when the serum sodium concentration fell below 126 mEq/L. Also remarkable was the appropriate increase in urine osmolality when the serum sodium concentration exceeded 126 mEq/L. The preservation of both concentration and dilution, albeit at a lower-than-normal serum osmolality, shows that the osmostat regulating antidiuretic hormone release had been “reset.” Both physiologic and pharmacologic resetting of the osmostat are discussed.ConclusionsPreservation of urinary concentrating and diluting ability at a lower-than-normal serum sodium concentration, especially in the setting of chronic hyponatremia, is diagnostic of a reset osmostat. The presence of a reset osmostat often confounds the treatment of concomitant acute hyponatremia. Early recognition of a reset osmostat avoids the need to normalize serum sodium concentration, expedites hospital discharge, and limits potential harm from overcorrecting acute hyponatremia.

PMON318 Nephrogenic syndrome of inappropriate antidiuresis in a 19 months old child with gross developmental delay

Abstract Case report 19 months old African American boy with nonsignificant past medical history presented with inability to walk, hypotonia chewing difficulties and speech delay. Initial laboratory evaluations demonstrated serum hyponatremia of 120-129 mEq/dl, low serum osmolality 261 mosm/kg (normal serum osmolality 275-295 mosm/kg) with inappropriately high urine osmolality 445 mosm/kg) (normal urine osmolality 300-1000 mosm/kg). Blood work for thyroid, adrenal, and pituitary function was unremarkable. Vasopressin level of 2.4 pg/ml (normal 0.0 - 4.7 pg/mL) did not support the diagnosis of Syndrome of Inappropriate Antidiuretic Hormone Secretion (SIADH). Fludrocortisone challenge test ruled out aldosterone deficiency with insufficient decrease in urine sodium and no response in serum sodium. Renal ultrasound and brain MRI were normal. Genetic testing revealed AVPR2 X-linked mutation c.409C&amp;gt;T p.R137C, consistent with nephrogenic syndrome of inappropriate antidiuresis (NSIAD). The patient was discharged on sodium chloride tablets 2g every 8 hours and remained stable, asymptomatic. One month after discharge patient showed significant neurological improvement. Discussion Sodium is known to play a significant role in growth and maturation of the whole body, especially of the nervous system. Moderate (120-129 mEq/L) to severe (&amp;lt;120 mEq/L) hyponatremia can present with nausea, malaise, headache, lethargy, motor and speech delay, seizures and even death due to brain herniation. Normal fluid and electrolyte balance is achieved by the thirst mechanism and free water excretion in kidneys. This is mediated by Vasopressin, which acts through V2R receptor in distal renal collecting duct. Syndrome of inappropriate antidiuretic hormone secretion (SIADH) is the most common cause of hyponatremia. Reset osmostat syndrome with a congenitally low serum osmolality threshold is one of the rare disorders on the differential. Hereditary nephrogenic syndrome of inappropriate antidiuresis is very rare mutation in vasopressin receptor, which clinically resembles SIADH except for normal/low vasopressin levels in set of hyponatremia. It causes gain of function and inappropriately high water retention. Presentation: Monday, June 13, 2022 12:30 p.m. - 2:30 p.m.

LBODP013 Hypophysitis And Adrenalitis Associated With The Use Of Immunotherapy "clinical Case Report"

Abstract Background we present a case of hypophysitis with gonadotropic and somatotropic axis compromise and adrenalitis secondary to the use of nivolumab and ipilimumab. Clinical Case A 74-year-old woman with a history of metastatic renal cell carcinoma treated with ipilimumab and nivolumab for 10 months, suspended treatment due to pneumonitis. Three months later, she consulted the emergency department due to limitations in daily activities, asthenia, and drowsiness. physical examination was unremarkable except for hypotension. Laboratory studies showed profound hyponatremia (106 mEq/l, n: 135 a 145 mEq/l), low serum osmolality (236 mmol/kg n: 275 - 295 mmol/kg) and a basal cortisol (5 μg/dL n: 3.7 - 19.4 μg/dL). Hypophysitis was suspected and a pituitary profile revealed low somatomedin C (25 ng/ml n: 54 204 ng/ml), FSH (20.6 UI/L n: 26.7 -133.4 UI/L), and strikingly elevated ACTH (91.9 pg/mL n: 4.7 - 48.5 pg/mL). Pituitary MRI had no structural anomaly. A diagnosis of hypophysitis and primary adrenal insufficiency secondary to adrenalitis due to the use of immunotherapy was made. The compromise of the gonadotropic and somatotropic axis with a normal image can occur in up to 23% of patients with this clinical entity. The patient had significant clinical improvement with glucocorticoid and mineralocorticoid replacement. Conclusions To our knowledge this is the first reported case of hypophysitis and adrenalitis secondary to immunotherapy. Hypophysitis has a prevalence up to 8% with the combination of ipilimumab plus nivolumab. It should be considered despite a normal pituitary MRI. However, adrenalitis associated with the use of these drugs has only been reported in 2.6% and the coexistence of both entities is even rarer Presentation: No date and time listed

ODP332 Maternal Central Diabetes Insipidus Immediately after Delivery, Owing to Vasospasm of the Internal Carotid Artery

Abstract Background Sheehan's syndrome is a cause of hypopituitarism during the postpartum period, but it rarely manifests immediately after birth. Clinical Case We report the case of a 30-year-old woman who delivered her second child, lost 1,050 mL of blood in the process, but did not receive a blood transfusion. A few hours after delivery, the patient complained of headache, nausea, and thirst, and her urine production increased to 9 L/day. No menstrual irregularities or abnormalities during pregnancy or childbirth had been reported. None of hypotension, external eye muscle paralysis, or visual impairment were identified on physical examination. The laboratory findings were low urine osmolality and high serum osmolality and sodium concentration. The concentrations of thyroid hormones, growth hormone (GH), and anti-diuretic hormone (ADH) were found to be low. The IgG4 concentration was not high (4.7 mg/dL; normal &amp;lt;105 mg/dL) and the patient was negative for anti rabphilin-3A antibody. Pituitary magnetic resonance imaging (MRI) on the day of admission showed enlargement of the pituitary gland and stalk, and magnetic resonance angiography showed stenosis of the left internal carotid artery. The patient showed a poor response to GH-releasing peptide 2 and thyroid releasing hormone stimulation. Hypertonic saline administration did not cause an increase in ADH concentration. We diagnosed adult growth hormone deficiency (aGHD), central hypothyroidism, and central diabetes insipidus (DI). The enlargement of the pituitary gland was slightly less marked and the stenosis of the left internal carotid artery improved 7 days after admission. After 6 months, the pituitary gland was almost normal in size, although the aGHD, central hypothyroidism, and central DI remained. Sheehan's syndrome or lymphocytic hypophysitis could have been responsible for the postpartum hypopituitarism. This case was not typical of lymphocytic hypophysitis with respect to the hormone deficiency pattern, the MRI findings, and the lack of anti rabphilin-3A antibody. Sheehan's syndrome is caused by ischemic necrosis of the anterior pituitary gland after severe postpartum hemorrhage. The prevalence of central DI is estimated to be 2%–3%. Typically, pituitary dysfunction progresses slowly and develops several years after childbirth. In contrast, in the present patient, stenosis of the left internal carotid artery developed and improved during short periods of time. The vasospasm of the internal carotid artery caused reductions in flow through the superior and inferior hypophysial arteries, which resulted in ischemia and necrosis of the pituitary gland, similar to Sheehan's syndrome. Clinical Lesson: Although rare, maternal central DI can be caused by ischemia and vasospasm immediately after the delivery of a child. The possibility of a pituitary stroke in the presence of neoplastic disease should not be ruled out, and imaging and pituitary gland function should be followed over the long term. Presentation: No date and time listed

WATER INTOXICATION: A CASE OF HYPONATREMIA AND ACUTE RENAL FAILURE

WATER INTOXICATION: A CASE OF HYPONATREMIA AND ACUTE RENAL FAILURE

Association Between Serum Osmolality and Acute Kidney Injury in Critically Ill Patients: A Retrospective Cohort Study.

Purposes: Acute kidney injury (AKI) is a common complication in critically ill patients and is usually associated with poor outcomes. Serum osmolality has been validated in predicting critically ill patient mortality. However, data about the association between serum osmolality and AKI is still lacking in ICU. Therefore, the purpose of the present study was to investigate the association between early serum osmolality and the development of AKI in critically ill patients.Methods: The present study was a retrospective cohort analysis based on the medical information mart for intensive care III (MIMIC-III) database. 20,160 patients were involved in this study and divided into six subgroups according to causes for ICU admission. The primary outcome was the incidence of AKI after ICU admission. The association between early serum osmolality and AKI was explored using univariate and multivariate logistic regression analyses.Results: The normal range of serum osmolality was 285–300 mmol/L. High serum osmolality was defined as serum osmolality >300 mmol/L and low serum osmolality was defined as serum osmolality <285 mmol/L. Multivariate logistic regression indicated that high serum osmolality was independently associated with increased development of AKI with OR = 1.198 (95% CL = 1.199–1.479, P < 0.001) and low serum osmolality was also independently associated with increased development of AKI with OR = 1.332 (95% CL = 1.199–1.479, P < 0.001), compared with normal serum osmolality, respectively.Conclusions: In critically ill patients, early high serum osmolality and low serum osmolality were both independently associated with an increased risk of development of AKI.

The Association of Salivary Conductivity with Cardiomegaly in Hemodialysis Patients

Patients on maintenance hemodialysis are at high risk for cardiovascular morbidity and mortality. Fluid overload is generally regarded as the main cause of cardiovascular death among them. Cardiothoracic ratio (CTR) by chest plain film is routinely performed to evaluate their volumetric states and cardiac conditions. We recently reported that salivary conductivity is a reliable marker for assessing fluid status in healthy adults. This cross-sectional study aims to explore the association between salivary conductivity and CTR. Cardiomegaly is defined as a CTR greater than 0.5. A total of 129 hemodialysis patients were enrolled, 42 of whom (32.6%) had cardiomegaly. Patients with cardiomegaly had significantly lower serum osmolality, lower serum sodium, and lower salivary conductivity, but a higher percentage of underlying atrial fibrillation. In the multiple linear regression analysis, CTR was negatively associated with salivary conductivity or to the serum sodium level and positively correlated with older age. We further divided patients into low, medium, and high salivary conductivity groups according to the tertials of conductivity levels. There was a significant trend for the increment of cardiomegaly from high to low salivary conductivity groups (p for trend: 0.021). The receiver operating characteristic curves for the diagnostic ability of salivary conductivity on cardiomegaly reported the area under the curve equal to 0.626 (95% CI: 0.521–0.730, p = 0.02). Moreover, older age and higher serum osmolality were independent determinants for salivary conductivity by multiple linear regression analysis. This work has presented that salivary conductivity is a novel approach to uncover fluid overload and cardiomegaly among chronic hemodialysis patients.

Hyponatremia as the Initial Presentation of Evolving Pituitary Apoplexy

Pituitary apoplexy (PA) is a known, often under-recognized medical emergency and is characterized by ischemic or hemorrhagic necrosis of the pituitary gland. It is a rare clinical syndrome that occurs in 2-12% of pituitary tumors. Hyponatremia can occur secondary to hypocortisolism (12-40%) or, rarely, to the syndrome inappropriate antidiuretic hormone (ADH) secretion.We present the case of a 69-year-old man who presented with altered mental status on post-operative day 3 from total knee replacement surgery. Initial testing revealed hyponatremia of 124 mmol/L, low serum osmolality of 266 mOsm/kg, and high urine osmolality of 664 mOsm/kg with urine sodium of 179 mmol/L. Head computerized tomography revealed a sellar mass of 1.8 x 2.4 cm. Initial testing revealed low prolactin (0.7 ng/mL), normal TSH (0.458 mcIU/mL) with borderline low free T4 of 0.72 ng/dL. Morning cortisol was 12.7 mcg/dL with ACTH of 8.5 pg/mL. Cosyntropin stimulation test was done revealing baseline cortisol of 5.8 mcg/dL (at midnight), increasing to 25.8 mcg/dL after 30 minutes and to 30.9 mcg/dL 60 minutes after cosyntropin administration. His sodium and mental status initially improved with fluid restriction and salt tablets, for the assumed syndrome of inappropriate ADH secretion. The patient remained hemodynamically stable. On the fourth day, however, his mental status deteriorated. Magnetic resonance imaging revealed expansion of sella with hyperintense mass 2.2 x 2.0 x 2.8 cm with compression of the optic chiasm. He was given stress dose hydrocortisone and levothyroxine and underwent emergency transsphenoidal resection. Biopsy revealed acute hemorrhage within infarcted adenoma. Postoperatively, both the patient’s sodium and mental status improved significantly and he was discharged to home on hydrocortisone and levothyroxine.The main clinical concern in the management of PA remains under-diagnosis at presentation. Prognosis is dependent on management during the acute phase. PA can present as hyponatremia even in the absence of overt hypocortisolism, presumably due to inappropriate ADH secretion. Therefore, PA should be considered as one of the differential diagnoses in hemodynamically stable patients with altered mental status and hyponatremia.

Hyponatremia and Isolated Free T4 Elevation in a Patient With Acute Intermittent Porphyria

Background: Porphyrias represent a spectrum of diseases that stem from dysfunction within the heme biosynthetic pathway. Acute intermittent porphyria (AIP) is the most common type of porphyria due to a genetic deficiency of porphobilinogen deaminase which results in a wide range of neurovisceral symptoms. Hyponatremia and abnormalities with thyroid function have been found in AIP but the mechanisms behind these processes are unclear. Clinical Case: A 26-year-old male with a history of chronic, recurrent abdominal pain presented with 10 days of progressively worsening periumbilical abdominal pain and constipation. He describes that preceding the onset of symptoms he had been binging 5-10 standard alcoholic drinks each day for a few days. Initial laboratory workup demonstrated hyponatremia with Na 114 mmol/L (n: 134 – 137 mmol/L), hypochloremia with Cl 76 mmol/L (n: 95 – 108 mmol/L), and hyperbilirubinemia with total bilirubin 2.5 mg/dL (n: 0.2 – 1.3 mg/dL). CT abdomen/pelvis was negative for any concerning pathology. Further studies showed low serum osmolality at 243 mOsm/kg (n: 275 – 295 mOsm/kg), urine Na 62 mmol/L (n > 20mmol/L), and urine osmolality at 394 mOsm/kg (n: 300 – 900 mOsm/kg) consistent with SIADH. The patient was treated with 3% NaCl and free water restriction to 1.2L/day with improvement in Na levels. Further laboratory workup demonstrated normal TSH, but persistently elevated free T4 with maximum free T4 of 2.77 ng/dL (n: 0.80 – 1.70 ng/dL) which downtrended to 1.99 ng/dL by discharge. Thyroid ultrasound was unremarkable. Pituitary evaluation via hormonal workup and MRI brain was negative for any abnormalities. Given the symptomatology and laboratory findings, the patient was evaluated for porphyria. Laboratory evaluation demonstrated severe elevations in urine porphyrins, urine delta aminolevulinic acid (56.8 mg/24h, n < 4.5 mg/24h), and urine porphobilinogen (82.5 mg/g, n < 2.3 mg/g) consistent with AIP. The patient was treated with four days of hematin infusions which resolved his abdominal pain and was discharged in an improved state. Conclusion: AIP is a rare entity brought out by a deficiency in porphobilinogen deaminase, a key enzyme in the heme biosynthesis pathway. Various metabolic disturbances have been described in AIP including hyponatremia and alterations in thyroid function tests suggestive of thyrotoxicosis. Hyponatremia in our patient was likely due to SIADH from neurovisceral pain. Our patient displayed isolated free T4 elevation as well. We hypothesize this developed due to his acute illness causing a greater decrease in D2 deiodinase activity compared to any concomitant increase in D3 deiodinase activity. This was supported by his free T4 level downtrending following treatment of his AIP attack. More research is needed to further elucidate the mechanism behind these derangements in biochemical markers and their impact on patient prognosis.

Development of diagnostic criteria and severity scale for polydipsia: A systematic literature review and well-experienced clinicians’ consensus

Despite the clinical importance of polydipsia, no diagnostic criteria or severity scales that comprehensively assess this condition are available. Thus, we aimed to develop diagnostic criteria and a severity scale for polydipsia based on a systematic review and well-experienced clinicians’ consensus. We performed a systematic review, identified 27 studies related to diagnostic criteria or severity classification for polydipsia, and extracted items used to assess polydipsia in these studies. Ten well-experienced clinicians—5 psychiatrists and 5 nurses—participated in the Delphi method. They evaluated 39 items extracted based on the results of the systematic review regarding (1) their necessity in diagnosing and assessing the severity of polydipsia, and (2) their relative importance rated on 7-point scale among the items included in the severity scale. The Polydipsia Diagnostic Criteria (PDC) included 4 essential items—excessive drinking, low serum sodium level or low serum osmolality, abnormal normalized diurnal weight gain, and low urine specific gravity—based on consensus reached using the Delphi method. The Polydipsia Severity Scale (PSS) included 13 items with a maximum score of 59. The first diagnostic criteria and symptom scale for polydipsia were developed based on the findings of a systematic review and well-experienced clinicians’ consensus.

Isolated Hyponatremic Dehydration in the Setting of COVID-19–Associated Gastroenteritis in a Toddler

Isolated Hyponatremic Dehydration in the Setting of COVID-19–Associated Gastroenteritis in a Toddler