Altered Mental Status Research Articles

Clinical assessment and short-term mortality prediction of older adults with altered mental status using RASS and 4AT tools

BackgroundAltered mental status (AMS) in older adults is a common reason for admission to emergency departments (EDs) and usually results from delirium, stupor, or coma. It is important to proficiently identify underlying factors and anticipate clinical outcomes for those patients. AimThe primary objective of this study was to reveal and compare the clinical outcomes and etiologic factors of older patients with delirium, stupor, and coma. The secondary objective was to identify the 30-day mortality risk for those patients. MethodThe study was conducted as prospective and observational research. We included patients aged 65 years and older who presented with new-onset neurological and cognitive symptoms or worsening in baseline mental status. Patients who presented no change in their baseline mental status within 48 h and those who needed urgent interventions were excluded. Selected patients were assessed using RASS and 4AT tools and classified into three groups: stupor/coma, delirium, and no stupor/coma or delirium (no-SCD). Appropriate statistical tests were applied to compare these 3 groups. The 30-day mortality risks were identified by Cox survival analysis and Kaplan-Meier curve. ResultsA total of 236 patients were eligible for the study. Based on their RASS and 4AT test scores: 56 (23.7%), 94 (40.6%), and 86 (36.4%) patients formed the stupor/coma, delirium and no-SCD groups, respectively. There was no statistical difference in the three groups for gender, mean age, and medical comorbidities. Neurological (34.7%), infectious (19.4%), and respiratory (19.0%) diseases were the leading factors for AMS. Post-hoc tests showed that CCI scores of the delirium (6, IQR = 3) and stupor/coma (7, IQR = 3) groups were not significantly different. The 30-day mortality rates of stupor/coma, delirium, and no-SCD groups were 42.%, 15.9%, and 12.8%, respectively (p < 0.005). The hazard ratio of the stupor/coma group was 2.79 (CI: 95%, 1.36–5.47, p = 0.005). ConclusionAMS remains a significant clinical challenge in EDs. Using the RASS and 4AT tests provides benefits and advantages for emergency medicine physicians. Neurological, infectious, and respiratory diseases can lead to life-threatening mental deterioration. Our study revealed that long-term mortality predictor CCI scores were quite similar among patients with delirium, stupor, or coma. However, the short-term mortality was significantly increased in the stupor/coma patients and they had 2.8 times higher 30-day mortality risk than others.

Clinical significance of Nosocomiicoccus ampullae isolated from blood cultures.

Nosocomiicoccus species are infrequently isolated from clinical specimens and their clinical significance has not been evaluated. We retrospectively reviewed five cases in which Nosocomiicoccus ampullae was identified in a single blood culture set during routine culture. All patients were admitted for altered mental status and had several comorbidities. Patients improved without antibiotic therapy directed to N. ampullae or their condition declined due to underlying conditions, and N. ampullae isolation was not considered clinically significant in any case. Matrix-assisted laser desorption/ionization-time of flight mass spectrometry and/or 16S rRNA gene Sanger sequencing allowed genus identification, but whole genome sequencing was required for accurate species identification. All strains were susceptible to penicillin, oxacillin, cefoxitin, tetracycline, doxycycline, daptomycin, minocycline, clindamycin, nitrofurantoin, vancomycin, and linezolid; they showed high-level resistance to trimethoprim-sulfamethoxazole and erythromycin, and inducible resistance to clindamycin, applying Clinical and Laboratory Standards Institute Staphylococcus spp. guidelines with an extended incubation. They frequently carry genes associated with macrolide resistance. In conclusion, N. ampullae appears to have low pathogenicity and most probably represents a contaminant when isolated from a single blood culture set.IMPORTANCENosocomiicoccus species are recently described as members of the Staphylococcaceae family. With their inclusion in commercial matrix-assisted laser desorption/ionization-time of flight mass spectrometry databases, Nosocomiicoccus species can now be identified when Gram-positive cocci in clusters are detected in positive blood cultures. However, their clinical significance is not known, making it difficult for the clinical microbiology laboratory to decide the extent of work-up. Based on our study, Nosocomiicoccus species demonstrate low pathogenicity and opportunistic potential. If isolated from a single blood culture set, limited work-up should be performed to an extent similar to other possible blood culture contaminants.

Limitations in the use of automated mental status detection for clinical decision support

BackgroundClinical decision support (CDS) tools improve adherence to evidence-based practices but are dependent upon data quality in the electronic health record (EHR). Mental status is an integral component of many risk stratification scores, but it is not known whether EHR-measures of altered mental status are reliable. The Glasgow Coma Scale (GCS) is a measure of altered mentation that is widely adopted and entered in the EHR in structured format. We sought to determine the accuracy GCS < 15 as an EHR-measure of altered mentation compared to ED provider documentation. MethodsIn patients presenting to an academic Emergency Department (ED) with pneumonia we abstracted GCS values entered by nurses during routine care and in a randomly selected subset manually reviewed provider documentation for evidence of altered mental status. We defined eConfusion as present if GCS < 15 at any point during the ED encounter. We then calculated the CURB-65 score and corresponding suggested disposition using each method. Performance of eConfusion and corresponding CURB-65 compared to manual versions was measured using agreement (Cohen’s K), sensitivity, and specificity. ResultsAmong 300 randomly selected encounters, 47 (16 %) had eConfusion present and 46 (15 %) had evidence of altered mental status in provider documentation with Cohen’s K 0.73. eConfusion had 78 % sensitivity and 96 % specificity for provider documented altered mental status. When input into CURB-65 to recommend inpatient disposition, eConfusion had 95 % sensitivity, and recommended discordant disposition for 3 %. ConclusionsThere was modest agreement between eConfusion and provider documentation of altered mental status. eConfusion had good specificity but low sensitivity which resulted in under-estimation of the CURB-65 score and occasional inappropriate disposition recommendations compared to provider documentation. These data do not support the use of GCS as a measure for altered mentation for use in CDS tools in the ED.

A - 94 A Case of New Onset Refractory Status Epilepticus (NORSE) Associated with COVID-19.

New Onset Refractory Status Epilepticus (NORSE) is a rare condition of prolonged medication-refractory seizures potentially due to elevated inflammatory molecules in the brain. NORSE can be triggered by a viral infection and is a documented neurologic consequence of COVID-19. A 74-year-old, left-handed, Hispanic male was in his usual state of health until experiencing 1-2weeks of speech decline, which culminated in an episode of altered mental status (disorientation and mumbling speech). He presented to the Emergency Department with drowsiness and complaints of a "funny feeling" on the left side of his head. Upon arrival, he was found to be COVID-19 positive and hyperglycemic with normal CT, MRI, lumbar puncture, and bloodwork. An EEG showed "focal temporal activity" and he was diagnosed with non-convulsant status epilepticus. Hospitalization and medical sedation lasted 2months followed by 8months of inpatient rehabilitation. The patient was discharged shortly before presenting for neuropsychological evaluation. Neuropsychological evaluation showed weaknesses in learning and free recall, visuospatial skills (due to disorganization and poor attention to details), processing speed, and executive functioning. The patient reported elevated anxiety symptoms. Collateral report indicated severe declines in executive organizational abilities, as well as mild memory and divided attention declines. Results suggest frontal cortical and subcortical impairments affecting multiple areas of cognition and functional decline consistent with a diagnosis of major neurocognitive disorder. Similar to the literature, status epilepticus was attributed to inflammatory meningoencephalitis triggered by the prior COVID-19 infection. Interdisciplinary care was an integral factor in this case.

H - 29 Delivering Culturally Sensitive Neuropsychological Assessment Feedback: a Case Study of Atypical Neurosyphilis.

To demonstrate the neuropsychological correlates of atypical neurosyphilis and the importance of delivering assessment results in a culturally sensitive manner. The patient was a 52-year-old African American male with 12years of education who was raised in a rural, southern town and worked as a delivery driver. He was hospitalized after three weeks of altered mental status, memory loss, and seizures. Electroencephalography (EEG) showed left lateralized periodic discharges. Magnetic resonance imaging (MRI) showed hyperintensities in the left hippocampus and amygdala consistent with limbic encephalitis. Cerebrospinal fluid studies revealed lymphocytic pleocytosis and hypoglycorrhachia. Rapid plasma regain and venereal disease tests were positive for syphilis in serum and CSF. He was initially treated with empiric antibiotics and antiseizures medications with modest improvement. His mental status improved after penicillin treatment, and he was discharged after 14days. Repeat MRI showed cortical atrophy in the left medial frontal lobe and left hippocampus. The patient demonstrated executive dysfunction (e.g., set-loss and source memory errors) and poor performance across verbal and visual memory tasks. He also demonstrated an inaccurate understanding of the possible causes of his illness. Feedback was delivered across two sessions: one session to discuss test results and a second session with the patient and his wife to discuss syphilis as a sexually transmitted infection and address the historical context of syphilis among African American men. Neurosyphilis can present as limbic encephalitis and can mimic autoimmune encephalitis and other infectious diseases. Tailoring assessment feedback to a patient's sociocultural context is vital for encouraging continued treatment.

Urine Toxicology Test for Children With Altered Mental Status.

The rate of unintentional ingestion of edible cannabis products in young children is rising rapidly as laws decriminalizing both recreational and medical marijuana in the United States become more widespread.1 Cannabis poisoning in children can lead to a myriad of symptoms, most notably neurologic changes. The abrupt onset and severity of signs and symptoms after ingestion can cause diagnostic uncertainty for practitioners in the emergency department. Here, we present a case series of 5 children, 6 years of age and younger, who initially presented with altered mental status and were ultimately diagnosed with acute δ-9-tetrahydrocannabinol toxicity after cannabis ingestion confirmed by urine toxicology testing. Although urine toxicology testing is not routinely used as a diagnostic tool in pediatrics, the increasing accessibility of edible cannabis products suggests that more widespread urine toxicology testing in children with undifferentiated altered mental status is warranted.

FRI200 Severe Cushing Syndrome Due To An ACTH-producing Pheochromocytoma

Abstract Disclosure: G.A. Stamatiades: None. A. Bikas: None. H.J. Shah: None. K. Wong: None. A. Vaidya: None. M. Nehs: None. S.S. Basaria: None. Background: Pheochromocytomas are rare catecholamine-secreting tumors that arise from sympathetic adrenomedullary chromaffin tissue. Rarely, pheochromocytomas co-secrete ACTH and patients present with Cushing syndrome. Due to its rarity, clinicians may not consider this etiology of Cushing syndrome. We report a case of a man with ACTH-producing pheochromocytoma in whom methodic systematic approach led to its diagnosis and successful treatment. Clinical Case: A 48-year-old man presented with altered mental status. His family confirmed depressed mood, paucity of thought, and occasional blank stares. The patient was diagnosed with type-2 diabetes mellitus and hypertension 3 months ago, which were not controlled despite being on multiple anti-hypertensives and anti-diabetic agents. His EEG, head CT, and brain MRI were normal. On admission, his laboratory tests were notable for hypokalemia (3.0 mmol/L, n&amp;lt;5.3 mmol/L) and metabolic alkalosis (HCO3 33 mmol/L, n&amp;lt;32 mmol/L). Physical examination showed facial plethora, multiple ecchymoses and profound proximal muscle weakness. CT scan of the abdomen showed a 3.4 cm left adrenal nodule with a density of 33 Hounsfield units and a 73% absolute washout. The right adrenal gland was hyperplastic. Plasma and urinary metanephrines were significantly elevated (plasma metanephrines 1.6 nmol/l, n &amp;lt; 0.50 nmol/l, urinary metanephrines 1,685 mcg/24h, n &amp;lt;646 mcg/24h). Midnight salivary cortisol was 11,500 ng/dl (n&amp;lt;100 ng/dl) and 24h urinary free cortisol was 13,099 mcg/24h (n &amp;lt; 45 mcg/24h). ACTH was 450 pg/ml (n&amp;lt;63pg/ml) with a serum cortisol of 93 ug/dl (n&amp;lt;18.4 ug/dl). His serum cortisol after 8 mg Dexamethasone Suppression test was 100 ug/dl. DOTATATE PET CT scan showed uptake in the left adrenal nodule. The workup was suggestive of left-sided pheochromocytoma producing ectopic ACTH. The patient underwent laparoscopic left adrenalectomy. Postoperative ACTH was undetectable, indicating surgical cure. His blood pressure and plasma glucose gradually improved and remained normal after discontinuation of all medications. Surgical pathology was consistent with pheochromocytoma with positive staining for ACTH, confirming the diagnosis of ACTH-producing pheochromocytoma. He was discharged home after successful rehabilitation. Clinical Lessons: Pheochromocytomas are a rare cause of ectopic ACTH production, resulting in clinical Cushing syndrome. Imaging of the contralateral adrenal gland provides a valuable clue in making the diagnosis of ectopic ACTH production (as the gland is enlarged rather than atrophic). Reference: (1) Elliott PF, Berhane T, Ragnarsson O, Falhammar H. Ectopic ACTH- and/or CRH-Producing Pheochromocytomas. J Clin Endocrinol Metab. 2021 Jan 23;106(2):598-608. doi: 10.1210/clinem/dgaa488. PMID: 32710791. Presentation: Friday, June 16, 2023

FRI494 Ischemic Stroke After Radioactive Iodine Therapy In Graves Disease

Abstract Disclosure: T. Rave: None. J. Giunta: None. Hyperthyroidism is defined as excess thyroid hormone, most commonly due to Graves Disease. Thiomides are first line therapy, however more definitive options are radioactive iodine (RAI) or thyroidectomy. RAI enters thyroid follicular cells and destroys the thyroid tissue with beta ray emissions. Patients with Graves disease, toxic multinodular goiter, and thyroid cancer can benefit from RAI, but it is contraindicated in pregnancy, breast feeding, and severely uncontrolled thyrotoxicosis. Early side effects are pancytopenia, thyrotoxicosis, and later complications are bone marrow suppression and cancer. There are several reports of cerebral vascular accidents (CVA) after RAI therapy, however, there is limited research demonstrating whether CVA is a direct consequence of RAI or secondary to thyrotoxicosis. This case describes a possible RAI-induced CVA. A 60-year-old female with a past medical history of type 2 Diabetes Mellitus, hypertension, obesity, and Graves disease presented with altered mental status and gait instability for 1 day. She received RAI therapy 1 day prior to symptom onset for uncontrolled Graves disease. She was previously on Methimazole and PTU, however, both were discontinued due to an intolerable rash. As a result, she was maintained on a beta blocker prior to RAI. On presentation, she was afebrile, normotensive with a heart rate of 79. She was oriented only to person and place and had an unbalanced gait. Her Burch-Wartofsky score was 30, which was concerning for thyrotoxicosis. Her TSH was undetectable and EKG showed normal sinus rhythm. She was placed on atenolol, PTU and hydrocortisone. Her CT head was negative for acute disease, however, her MRI brain diagnosed an acute ischemic stroke. During admission, she had episodes of atrial fibrillation with rapid ventricular response. This patient presented with thyrotoxicosis after RAI therapy complicated by a CVA. It is important to note that on presentation she was reliably taking a beta blocker outpatient and her EKG was normal sinus rhythm making atrial fibrillation a less likely culprit of her CVA. Research has found that hyperthyroidism alone can lead to a prothrombotic state, however, additional literature reports that both hyperthyroid and euthyroid patients have an increased risk of CVA following RAI. Whether a CVA is secondary to thyrotoxicosis or a direct effect of RAI, this potentially life-threatening complication should be discussed with patients prior to treatment. Presentation: Friday, June 16, 2023

FRI502 Myxedema Coma With An Unusual Pattern Of Thyroid Function Tests Due To Amiodarone-induced Hypothyroidism

Abstract Disclosure: S. Nguyen: None. B. Force: None. R. Schneider Aguirre: None. Introduction: Myxedema coma is an endocrine emergency characterized by severe hypothyroidism resulting in altered mental status or coma, hypothermia, cardiovascular compromise, pulmonary edema or pleural effusions, and/or gastrointestinal hypomotility, classically in the context of an elevated TSH and low thyroxine levels. Amiodarone use is associated with alteration of thyroid function tests and could cloud the laboratory presentation of myxedema coma. Here we present a case of myxedema coma in a patient with amiodarone-induced hypothyroidism with an elevated free T4 (FT4) and low total T3 (TT3). Clinical Case: A 64-year-old female with a history of chronic systolic heart failure, persistent atrial flutter treated with amiodarone, cerebrovascular accident, hypertension, chronic kidney disease stage 4, but not hypothyroidism, presented with constipation, confusion and lethargy worsening over 3 days. On initial evaluation, she was minimally responsive, hypothermic to 95.6 °F and bradycardic to low 50s. She was intubated for airway protection and vasopressors were started due to concern for cardiogenic shock. Exam was notable for coarse facial features, edema and cold extremities. A bedside echocardiogram showed reduced cardiac function from baseline. Her TSH was 40.65 uIU/mL (RR, 0.45-5.33 uIU/mL), FT4 1.79 ng/dL (RR 0.64-1.42 ng/dL), total T4 14.30 mcg/dL (RR 6.09-12.23 mcg/dL), TT3 70 ng/dL (RR 87-178 70 ng/dL). Sodium was 135 mmol/L (RR 136-145 mmol/L), serum glucose was 42 mg/dL, (RR 70-110 mg/dL), and eGFR was 18 mL/min/1.73 m2 (baseline eGFR 28 mL/min/1.73 m2). Evaluations for myocardial infarction and infectious etiology were initiated and ultimately negative. While elevated FT4 is not characteristic of myxedema coma, the overall constellation of stupor, constipation, bradycardia, hyponatremia, hypoglycemia, decreased eGFR and decreased cardiac function, in the setting of an elevated TSH and low TT3, made the diagnosis of myxedema coma extremely likely. The patient was started on levothyroxine 200 mcg IV daily and hydrocortisone 100 mg IV every 8 hours. After 16-20 hours on this regimen, the patient was weaned off sedation and vasopressors, extubated, and recovered baseline mental status. Hydrocortisone was stopped and on day 3 of hospitalization, she was transitioned to oral levothyroxine 88 mcg daily. Due to premature ventricular contractions her dose was decreased to 50 mcg orally daily five days after her initial presentation to the hospital. During this time, the TSH decreased to 3.59 uIU/mL and the FT4 rose to 2.83 ng/dL. Conclusion: We conclude that in patients treated with amiodarone, myxedema coma can still occur even if T4 levels are normal or elevated, likely due to decreased T4 to T3 conversion. In these cases, elevated TSH and a clinical picture consistent with severe hypothyroidism are more reliable indicators if the (free) T4 levels are unexpectedly elevated. Presentation: Friday, June 16, 2023

FRI360 A Protracted Course Of Worsening Adrenergic And Neuroglycopenic Symptoms Due To Delay In Diagnosis Of Insulinoma

Abstract Disclosure: A. Karca: None. W. Lai: None. S. Naidoo: None. L.N. Saladi: None. B.C. Jameson: None. A 33-year-old Hispanic male presented with altered mental status, witnessed seizure and hypoglycemia (capillary BG 40mg/dL). Patient and family reported multiple episodes of symptomatic hypoglycemia and progressively worsening adrenergic and neuroglycopenic episodes with altered mental status requiring hospital admissions and evaluation for endogenous hyperinsulinemia in the past several months prior to admission. Patient was admitted to the ICU. Laboratory workup revealed documented hypoglycemia (venous BG 45mg/dL) and inappropriate insulin (17uU/mL, n3-25uU/mL), c-peptide (2.7ng/mL, n0.8-4.2 ng/mL) and pro-insulin (38.3 pmol/L, n&amp;lt;18.8 pmol/L) levels. Sulfonylurea and meglitinide screens were negative. Patient required continuous dextrose infusion as well as octreotide, with enteral feeding, to maintain BG &amp;gt;70mg/dL. Abdominal US, multiple CT scans, endoscopic US failed to locate source of endogenous hyperinsulinemia. Multi-discipline discussion among ICU team, Endocrinology, Interventional Radiology (IR), and Surgery considered MRI versus IR-guided selective arterial calcium stimulation (SACS) vs PET-CT NETSPOT with Ga-68 Dotatate, which had been ordered, but unable to be arranged prior to this admission. Ultimately, MRI with pancreatic protocol revealed 3.5cm exophytic solid mass arising from the tail of the pancreas and patient underwent laparoscopic hand-assisted distal pancreatectomy and splenectomy, with intraoperative ultrasound to confirm the location of the mass. Histologic examination revealed a well-differentiated neuroendocrine tumor. Chart review revealed documented hypoglycemia as far back as eight years prior to this admission, although no further results were available from that time to confirm endogenous source. Possible explanations for delay in diagnosis include patient health literacy, inaccessibility of outpatient testing, limitations of testing modalities, and access to staff skilled in more specialized testing, like PET-CT NETSPOT and SACS. Localizing techniques are divided into pre-operative and intra-operative, with pre-operative techniques further divided into non-invasive and invasive modalities. First line pre-operative testing includes US and CT, which have widely varying sensitivity depending on size and location of the tumor. MRI can have better sensitivity for smaller and distal tumors. PET-CT NETSPOT with Ga-68 Dotatate, has very high sensitivity and specificity in limited studies. If not localized with non-invasive modalities, SACS is an invasive modality with high sensitivity and specificity. Although insulinomas are a rare neuroendocrine tumor with challenging diagnostic workup, higher clinical suspicion with early biochemical workup, patient education, referral to endocrinology, better accessibility of diagnostic testing will help lead to timely diagnosis and management. Presentation: Friday, June 16, 2023

SAT156 Two Cases Of Hypoglycemia From Inhalation Of Heroin Adulterated With A Sulfonylurea

Abstract Disclosure: K. Kim: None. J. Hwang: None. S. Sam: None. Context: Hypoglycemic disorders in non-diabetic patients are rare. In the setting of concomitant illicit opioid abuse, hypoglycemia is highly unusual and an underlying cause should be systematically investigated. Objective: We report two separate cases of non-diabetic women both admitted to our intensive care unit for critical hypoglycemia secondary to inhaled heroin containing sulfonylureas. Case 1—A 51 year old female with a history of heroin addiction (on methadone) was brought to the emergency department with altered mental status. She was found to have refractory hypoglycemia and was transferred to the medical intensive care unit (MICU) for monitoring. She reported poor appetite and food intake in the past week and endorsed consuming one alcoholic beverage the night before. Case 2—A 61 year old female with a history of heroin and cocaine abuse was found by the paramedics at home with a decreased level of responsiveness and blood sugar of &amp;lt;30 mg/dL who also required MICU admission. She endorsed using heroin, cocaine and substantial alcohol 2 days prior to admission at a party. She reported 2 episodes of hypoglycemia in the past requiring hospitalization, with no known cause. Kidney and liver disease were ruled out in both subjects. A thorough history including illicit drug use and critical blood samples at the time of hypoglycemia including drug toxicity screen, sulfonylurea screen were obtained. Labs demonstrated an insulin-mediated hypoglycemia and positive sulfonylurea screen for glipizide in both patients. Results: Because of their non-diabetic status, their compelling history and the results of their comprehensive laboratory work-up, we conclude that these subjects had a common exposure- insufflation of heroin contaminated with an oral hypoglycemic agent shortly before their admissions with critical hypoglycemia and clinical instability. Conclusions: This is the first report of hypoglycemia related to inhalation of heroin adulterated with the sulfonylurea glipizide. Frequently heroin is intentionally mixed with other agents (diphenhydramine) to increase the volume for sale, optimize the drug uptake or to ease the side effects. These cases highlight the importance of obtaining a thorough clinical history including potential illicit drug use, acquiring timely and appropriate laboratory samples for toxicologic analysis, and interpreting the findings to curb a potentially deadly epidemic. Presentation: Saturday, June 17, 2023

FRI244 Autoimmune Polyglandular Syndrome Type 2 And Peripartum Cardiomyopathy: A Case Report

Abstract Disclosure: A.G. Jimenez: None. J.D. Christensen: None. P. Surampudi: None. S. Phatak: None. J. Yoon: None. Background: Peripartum cardiomyopathy (PPCM) is a diagnosis of exclusion with evolving understanding of pathophysiology. There is limited consideration of the autoimmune processes contributing to PPCM. Case Presentation: A 20-year-old female had a recent delivery complicated by placenta previa, hemorrhage requiring transfusion, and pelvic infection. She presented 2 weeks postpartum with altered mental status and abdominal pain, found to be in septic shock, acute respiratory failure, acute liver injury initially thought to be secondary to retained products of conception. Subsequently, she was diagnosed with moderate-to-severe PPCM as she developed signs of heart failure, low ejection fraction &amp;lt;35%, mild ventricular dilatation, cardiogenic shock, hemorrhagic pericardial effusion with tamponade. She had no other prior cardiovascular history. She was briefly started on bromocriptine for treatment of suspected prolactin-mediated PPCM, in addition to digoxin, as her blood pressure was unable to sustain other treatments for PPCM. However, she hemodynamically decompensated and required persistent pressor support, leading to evaluation for other causes. Due to her prior history of hypothyroidism, an adrenal evaluation with a cosyntropin stimulation test was done. It demonstrated an undetectable cortisol at 0, 30, 60 minutes, with an elevated ACTH (1256, n=7-63 ng/dL), consistent with primary adrenal insufficiency (PAI). Workup for PAI did not reveal any infectious, infiltrative, vascular, pharmacological, or neoplastic etiology. Lab workup for concomitant hypophysitis was significant for low IGF-1 (Z-score -5.8, n= -2.0 to +2.0), but otherwise had expected elevated prolactin (121 ng/mL, n=5.2-26.5 ng/mL), suppressed LH (0.3 mIU/mL) and FSH (2.4 mIU/mL), and normal TSH (3.87 mIU/mL, n=0.27-4.20 mIU/mL) on levothyroxine 100 mcg. She had normal parathyroid hormone and hemoglobin A1c levels with no history of chronic candidiasis. Further workup showed positive antibodies to adrenal 21-hydroxylase enzyme, thyroid peroxidase, and glutamic acid decarboxylase 65, suggestive of autoimmune polyglandular syndrome (APS) type 2. She was started on glucocorticoids and mineralocorticoids for adrenal insufficiency resulting in a significant clinical improvement. She was subsequently discharged in stable condition. Conclusion: Due to increased rates of mortality in PPCM (4-11%), thought should be given to nontraditional etiologies of cardiac failure. Although rare, adrenal insufficiency must be considered in those with moderate-to-severe PPCM who continue to decompensate despite treatments. Untreated adrenal insufficiency can result in fatal consequences if not immediately treated. APS type 2 should be considered even in those without any confirmed family history of autoimmune disease. Those with autoimmune tendencies may be at higher risk of PPCM. Presentation: Friday, June 16, 2023

THU379 A Case Of Hyperglycemia With Severe Anion Gap Metabolic Acidosis: HHS Vs DKA

Abstract Disclosure: M. Shrivastava: None. B.J. Armendariz: None. U. Asija: None. A. Shah: None. M. Levy-kern: None. D. Klamp: None. Background: DKA is more profoundly associated with metabolic acidosis secondary to excessive ketones production in the setting of low insulin. Whereas HHS is associated with hyperglycemia with mild acidemia because ketone production is not as severe, as insulin is high/normal. We present a case of hyperglycemic state which challenged this stereotype. Clinical Case: 57 YO male with no prior history of DM or CKD presented with altered mental status, abdominal pain, 15lbs weight loss. As per wife, patient had URI and his condition had been deteriorating since then. Initial labs revealed leukocytosis, BUN 105, serum creatinine 5.8, Anion gap 37, and blood glucose (BG) 1433mg/dl. Blood Gas significant for pH 7.1, PCO2 20, PO2 138, bicarbonate 7.8, and Lactic acid 1.5. Further testing revealed Urine ketone 15, Serum beta-hydroxybutyrate 0.5 mmol/l, HbA1c 13%, serum Osmolarity 391mOsm/kg. Treatment was initiated with 0.9% NS, electrolyte replacement, and IV insulin infusion. Serum glucose corrected at 50-75mg/dl/hr unmasked underlying hypernatremia. Fluid was switched to 0.45% NS with dextrose 5%. Despite BG correction, patient’s mentation remained altered. Further imaging including MRI brain was negative for osmotic demyelination syndrome. Eventually, BG came below 200mg/dl, and acidemia resolved. Pt was transitioned to subcutaneous insulin. Mentation started improving. Clinical Lesson: T1DM and T2DM are Insulin deficient vs insulin resistant states respectively[1]. Insulin deficiency causes decreased intracellular consumption of glucose, triggering intracellular starvation, promoting lipolysis in presence of stress hormones like glucagon, Norepinephrine, and cortisol[2]. Free fatty acids, produced from lipolysis undergo beta-hydroxylation forming ketones. Hence, metabolic acidosis in DKA is secondary to ketoacidosis. HHS is seen in insulin-resistant states, with normal/high serum insulin. Insulin promotes lipogenesis, hence HHS has minimal ketoacidosis, and is rarely associated with AGMA. Both DKA and HHS are hyperosmolar states most commonly triggered by infections[3], but in HHS, osmolarity generally exceeds 320mmol/l, free water deficit is more profound. This reflects severe dehydration, decreased intravascular volume, tissue hypoperfusion, possibly end organ damage including AKI[4], and in severe cases present as Acute renal failure(ARF)[4][5][6]. Hyperosmolarity can itself induce rhabdomyolysis and thus AKI[5][6]. In our case, ARF caused elevated BUN, decreased acid secretion from renal tubule, worsened acidosis, and presented as AGMA, mimicking DKA. In such situations measuring serum beta-hydroxybutyrate and C-Peptide can differentiate the two conditions. Hypernatremia and dysregulated osmolarity pose risk of osmotic demyelination syndrome. It is pertinent to correct AGMA, osmolarity, and hyperglycemia concurrently. Presentation: Thursday, June 15, 2023

SAT174 Doege-Potter Syndrome In A Patient With Solitary Fibrous Tumor Of The Lung

Abstract Disclosure: N. Mon: None. S.S. Krishnasamy: None. Doege-Potter Syndrome is a non-islet cell tumor hypoglycemia (NICTH) due to a solitary fibrous tumor (SFT) with overexpression of Insulin-like growth factor 2 (IGF2). We report a case of refractory hypoglycemia in a patient with SFT of the lung. Case presentation: A 67-year-old homeless male with hypertension, chronic smoker presented with altered mental status after his blood glucose was found 34mg/dl by EMS. His confusion improved after D50W. He could not recall the event but he reported that he missed his dinner prior to the event. He denied taking any antidiabetic medications. He was diagnosed with left lung solitary fibrous tumor without metastases a week ago after he presented to ER with dyspnea, cough and wheezing. CT chest reported a 21x15.6x18.7 cm lesion with mass effect on the left hemidiaphragm, mediastinum shift to the right and occluded left lower lobe bronchi. Core needle biopsy of the mass revealed SFT with necrosis. He was discharged with Medrol dosepak 4mg daily for presumptive treatment of COPD exacerbation and a plan for elective surgery. While in the ER his BG improved to 136mg/dl after D50W. Few hours later BG dropped to 42mg/dl and D10W infusion was started. Physical exam was unremarkable except bilateral pedal edema. Work up showed BG 42mg/dl, Insulin 3.3 (2.6-24.9 uIU/mL), C peptide 0.39 (1.1-4.4ng/mL), Proinsulin 4.7 (&amp;lt;18.8pmol/L), beta-hydroxybutyrate &amp;lt;0.05 (0.02-0.27mmol/l), 8AM cortisol 10.7 (7.0-25.0 ug/dl), albumin 3.2mg/dl, HbA1c 5.8%, IGF1 53ng/mL (34-245ng/mL), IGF2 203ng/mL (267-616ng/mL) with a IGF2:IGF1 ratio of 3.8. In our patient, the IGF2:IGF1 ratio was not &amp;gt;10 since his IGF 2 was suppressed by the recent steroid use. The rest of the clinical and biochemical features strongly suggested NICTH. His preoperative evaluation showed new onset HFrEF with volume overload. He underwent staged percutaneous coronary interventions with stents placement. He was given hydrocortisone 50mg q6H then to q8H during hospitalization and discharged home with hydrocortisone 40mg TID. He underwent radical resection of lung tumor after optimization of his cardiac condition. He was on stress dose of steroid during surgery. Since he was on high dose steroid for &amp;gt; 3months, hydrocortisone dose was tapered slowly after the surgery. Final biopsy reported solitary fibrous tumor extending to parenchymal staple line. Tumor cells are positive for CD34 and STAT6, and negative for desmin, SMA, and SOX10. He recovered uneventfully and was discharged home with prednisone 5mg daily and follow up in endocrine clinic. Conclusion: NICTH is a rare paraneoplastic syndrome characterized by low levels of insulin, C-peptide, proinsulin, and beta-hydroxybutyrate. A ratio of IGF-2/IGF-1 more than 10 confirms NICTH; however, normal ratio cannot exclude the diagnosis and factors such as low IGFBP 3 or steroid therapy for other conditions need to be considered. Surgery is the mainstay of treatment. Presentation: Saturday, June 17, 2023

FRI333 Neurosarcoidosis Induced Panhypopituitarism​

Abstract Disclosure: K. Alfares: None. H. Jeong Han: None. S. Athimulam: None. Introduction: We hereby present a rare case of neurosarcoidosis causing panhypopituitarism. According to Martin-Grace et al who conducted a literature search for the timeframe of 2002 to 2014, there were only 8 cases of neurosarcoidosis associated pan hypopituitarism. Case Report: A 35-year-old male with a known diagnosis of sarcoidosis on skin biopsies presented to the hospital for altered mental status, hypernatremia, hypotension and hypothermia. He reported symptoms of polyuria and polydipsia for several weeks prior to admission. MRI of the brain revealed a 3cm mass in the suprasellar region involving the hypothalamus and bilateral optic tracts with mass effect on the anterior third ventricle. No discrete pituitary or stalk lesion was identified. A ventriculostomy tube was placed for developing hydrocephalus. Biopsy of the suprasellar mass revealed non-caseating granuloma, confirming neurosarcoidosis. Laboratory work up 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 work up revealed low 8am serum cortisol (1.9 mcg/dL) and inappropriately normal ACTH (34 pg/ml), low serum free testosterone (&amp;lt;2.5 ng/dL) and low Luteinizing hormone (0.7 mIU/ml) and low follicular stimulating hormone (&amp;lt; 2.6 mIU/ml), low free T4 at 0.4 ng/dL and inappropriately normal TSH at 2.77 uIU/mL. Serum prolactin was mildly elevated at 86.8ng/mL. Angiotensin converting enzyme level was within normal range at 33 U/L. A diagnosis of panhypopituitarism was made. Treatment was initiated with high dose IV corticosteroids for management of secondary adrenal insufficiency and neurosarcoidosis. He was also started on IV desmopressin and IV levothyroxine for management of his panhypopituitarism. He was transitioned to oral therapy on discharge. Discussion: Panhypopituitarism secondary to neurosarcoidosis is a rare presentation. Panhypopituitarism from sarcoidosis can occur due to infiltration of the pituitary gland or infiltration of the hypothalamus affecting the hypothalamic-pituitary axis. Sarcoidosis 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. Presentation: Friday, June 16, 2023

SAT157 Management Of Spontaneous Hypoglycemia In Dialysis-dependent Chronic Kidney Disease Using Diazoxide

Abstract Disclosure: A. Schledwitz: None. S.S. Habbsa: None. F. Sotomayor Villanueva: None. Y. Kim: None. Background: Patients with end-stage renal disease (ESRD) are at increased risk of spontaneous hypoglycemia due to decreased renal insulin clearance. Due to its inhibitory effect on pancreatic beta cell insulin secretion, oral diazoxide has been used to treat hypoglycemia due to insulinoma or congenital hyperinsulinemic hypoglycemia, but few cases detail the use of diazoxide in the ESRD population. Here, we present 4 cases of spontaneous hyperinsulinemic hypoglycemia in ESRD successfully treated with diazoxide. Clinical Cases: A 66-year-old man with ESRD presented with altered mental status secondary to severe hypoglycemia despite continuous IV 20% dextrose. Labs revealed glucose 50 mg/dL, insulin 7 (0-3 mcIU/mL), C-peptide 7.8 (0-0.6 ng/mL), proinsulin 35.7 (0-5 pmol/L), beta-hydroxybutyrate [bOH] 0.4 (0-2.7 mg/dL), negative sulfonylurea panel, normal cosyntropin stimulation test and undetectable insulin antibodies, without radiographic evidence of insulinoma. He was started on diazoxide 50 mg TID and remained euglycemic for the remainder of his course. On similar readmission 3 months later, he was restarted on diazoxide with resolution of hypoglycemia within 1 day. A 66-year-old male with ESRD and T1DM treated with pancreas transplant presented with toe gangrene and persistent hypoglycemia. Fasting labs revealed insulin 4, C-peptide 4.5, proinsulin 4.5, and bOH 4.5, without radiographic evidence of insulinoma. He maintained euglycemia 4 days after diazoxide 70 mg BID was started. A 67-year-old male with T2DM and ESRD was admitted for osteomyelitis and 2 years of episodic symptomatic hypoglycemia despite dietary adjustments. Labs showed glucose 59, insulin 7, C-peptide 5.2, proinsulin 7.5, bOH 0.04, and unremarkable imaging. Within 1 day of starting diazoxide 100 mg daily, his blood glucose stabilized, and he was discharged. Finally, a 42-year-old male with ESRD presented with 4 years of persistent episodic hypoglycemia, now refractory to continuous IV dextrose. He was found to have glucose 64, insulin 15, C-peptide 11.5, proinsulin 29, and bOH 0.1, with imaging revealing bulky pancreas without a discrete mass. His hypoglycemic episodes resolved within 1 day of starting diazoxide 100 mg daily. He was readmitted 3 months later for catheter site infection and had no episodes of hypoglycemia with continuation of diazoxide. Conclusion: Diazoxide may be a viable option for the treatment of refractory spontaneous hypoglycemia in patients with dialysis dependent ESRD. Presentation: Saturday, June 17, 2023

SAT228 Denosumab Associated Severe Hypocalcemia Due To Vitamin D Deficiency In A Patient With Undiagnosed Primary Hyperparathyroidism

Abstract Disclosure: S. Bendaram: None. P.J. Bhatt: None. V. Kantorovich: None. Background: The Human monoclonal antibody, Denosumab is a widely used antiresorptive therapy for Osteoporosis, which in the presence of risk factors can lead to hypocalcemia. We present an interesting case of severe and prolonged hypocalcemia due to Denosumab therapy, due to Vitamin D deficiency from malabsorption, despite the presence of undiagnosed Primary Hyperparathyroidism (PHPT). Case Presentation: 74-year old white female with a history of Crohn’s disease s/p ileostomy, Osteoporosis on Denosumab, Seizure disorder on Divalproex, and Parkinson’s disease presented to the ED for worsening altered mental status and decreased oral intake for at least 2 weeks prior to admission. On presentation, she was alert, oriented to person only, complaining of body aches. She was on no vitamin D supplements. Vital signs were unremarkable except for low BMI of 17.05 kg/m2. Physical exam revealed a chronic upper extremity tremor and a new facial mouth tremor associated with bruxism. Chvostek and Trousseau signs were negative, however this was after 1 dose of IV calcium gluconate in the ED. On presentation, initial labs revealed total calcium of 5.3 mg/dL [8.7-10.5], Albumin 4.7 g/dL [3.4-4.8], Magnesium 1.2 mg/dL [1.6-2.7], creatinine 1.5 mg/dL [04-1.1] (baseline 1.0). Further testing showed ionized calcium of 0.56 mmol/L [1.17-1.33], 25 Hydroxy Vitamin D 9 ng/mL [30-100], PTH 777 pg/mL [15-65] and phosphorus 3.6 mg/dL [2.7-4.5]. She was treated with IV calcium gluconate, 50,000 IU weekly vitamin D3 and calcium citrate 950mg oral BID, followed by which her total calcium went up to 12 mg/dl, with ionized calcium elevated at 1.36 mmol/L, while herPTH levels stayed inappropriately normal at 55 pg/ml. On the day of discharge, 25-OH-Vitamin D was 15 ng/dl, PTH 222 pg/ml and ionized calcium 1.07 mmol/L, when she was alert, oriented, with resolution of bone pains. Conclusion: Hypercalcemia in PHPT is from activation of osteoclasts and when these cells are inhibited by antiresorptive therapy, intestinal absorption will remain the primary source of plasma calcium levels. This explains the severe and prolonged hypocalcemia caused by Denosumab owing to its mechanism of action and long elimination half life, in our patient with Vitamin D deficiency on the background of malabsorption, despite a combination of primary and secondary elevation of PTH. Careful baseline assessment of calcium and Vitamin D levels, along with adequate supplementation and regular monitoring should be undertaken in all patients treated with Denosumab to avoid this. Presentation: Saturday, June 17, 2023

FRI693 Pthrp Mediated Hypercalcemia In A Patient With Recurrent Hepatocellular Carcinoma

Abstract Disclosure: D. Bondarenko: None. M. Ahmad: None. M. Mack: None. P. Ucciferro: None. Background: Humoral hypercalcemia is seen in 30 percent of cancer patients, most commonly driven by parathyroid hormone related peptide (PTHrP) production, osteolytic cytokine production, and 1,25-OH vitamin D production. The most common malignancies associated with PTHrP mediated hypercalcemia are squamous cell carcinomas and breast cancer. Less often hepatocellular cancer presents with hypercalcemia. We describe the case of a patient presenting with hepatocellular carcinoma presenting with recurrent episodes of severe hypercalcemia due to excessive PTHrP production. Clinical Case: The patient was a 68-year-old male with a past medical history of recurrent hepatocellular carcinoma with liver transplant in the past and type 2 diabetes mellitus who presented to the emergency department (ED) for one day of altered mental status. The patient was noted to be extremely agitated and confused by his home health aide and EMS was called. In the ED the patient’s vital signs were as follows: blood pressure of 196/80 mmHg, heart rate of 82 beats per minute, respiratory rate of 18 breaths per minute and temperature of 36.6 degrees Celsius. Initial lab work showed: calcium 13.5 mg/dL, albumin 4.2 g/dL, ionized calcium of 1.63 mmol/L, creatinine 0.99 mg/dL (baseline 0.5 mg/dL), glucose of 438 mg/dL, bicarbonate 23 mmol/L, anion gap 19, and beta hydroxybutyrate 51 mg/dL. Hypercalcemia workup revealed a suppressed PTH of 5 pg/mL (normal 11-67 pg), normal 25-OH vitamin D 43.6 ng/ml (normal 30-100 ng/ml), normal 1,25-OH vitamin D 38 pg/ml (normal 18-72 pg/ml), and elevated PTHrp 36 pg/ml (normal 11-20 pg/ml). The patient was started on aggressive IV fluid resuscitation with normal saline, administered a one-time dose of zoledronic acid and administered a three-day course of calcitonin. For his significant hyperglycemia the patient was started on an insulin infusion and was eventually transitioned to his home basal bolus insulin regimen. On discharge, the patient was scheduled with his oncologist to begin denosumab as an outpatient; however, he chose a palliative approach due to the terminal nature of his disease and recurrent hospitalizations for hypercalcemia. Conclusion: Hypercalcemia of malignancy is common in many different carcinomas with squamous cell cancer, renal cell cancer, breast cancer and multiple myeloma being commonly associated with this phenomenon. Reports of hepatocellular carcinoma associated with hypercalcemia are less common and occur in only 4-8 % of cases. With this case report, we hope to highlight PTHrP as a potential mechanism of humoral hypercalcemia in patients with hepatocellular carcinoma and propose denosumab as a possible treatment for patients with refractory hypercalcemia of malignancy. Presentation: Friday, June 16, 2023

THU147 Peritoneal Dialysis To Improve Hyperglycemic Hyperosmolar State In Child With Renal Failure

Abstract Disclosure: P. Choudhari: None. S. Mootha: None. Background: Hyperglycemic hyperosmolar state (HHS) without ketosis is rare in children. While the crux of management of HHS is extensive hydration followed by insulin, this management can be difficult for children with kidney failure. Clinical Case: A 6-year-old female with complex medical history including Jeune syndrome (asphyxiating thoracic dystrophy), end stage renal disease status post kidney transplant, currently with rejection, now on peritoneal dialysis (PD), and history of steroid induced hyperglycemia was admitted for altered mental status. Several days prior to the current admission, she was admitted for an upper respiratory infection and found to have hyponatremia, which improved with fluid restriction and sodium supplementation. Subsequent worsening of hyponatremia led to adjustments in her PD to include higher amounts of dextrose in the dialysate (1.5% to 2.5%). At the current admission, she was found to have a blood glucose of 2096 mg/dL, uncorrected sodium of 121 mg/dL, corrected to 153 mg/dL, serum osmolality of 406 mOsm/kg, and hemoglobin A1c of 11.3%. She had mild acidemia and beta-hydroxybutyrate of 0.5 mmol/L. She was transferred to the Pediatric Intensive Care Unit (PICU) and intubated given her waxing and waning mental status and complex history. Since she was anuric, fluid resuscitation was carefully managed. She received a total of 14 mL/kg normal saline boluses, which lowered blood glucose by about 240 mg/dL. Multidisciplinary conversations between PICU, Endocrinology, and Nephrology culminated with a plan to attempt to slowly reduce blood glucose levels via PD prior to using regular insulin infusion. 24-hour PD was restarted with lower dextrose in the dialysate (1.5%). Due to persistent hypotension, she required norepinephrine infusion and stress dose hydrocortisone. With PD, blood glucose levels decreased by 20-30 mL/kg/hr in the first day. Regular insulin infusion was started, while continuing 24-hour PD, after blood glucoses stagnated at 1400-1500 mg/dL. After 4-5 days of PD and insulin infusion, the child’s blood glucoses decreased to 300-400 mg/dL. After tolerating her g-tube feeds, she was transitioned to an insulin pump as she was requiring high doses of insulin (1.8 units/kg/hr). Conclusion: We present a child with complex medical history, including history of steroid induced hyperglycemia, end stage renal disease status post renal transplant, anuria, currently on PD, who developed hyperglycemic hyperosmolar state (HHS). PD helped to lower her significant hyperglycemia, initially without insulin. There are few case reports on the use of PD or hemodialysis to improve hyperglycemia or hypernatremia in children with renal failure. This case demonstrates dialysis can be an effective strategy to attempt for children in a hyperosmolar state in whom aggressive fluid management can be detrimental. Presentation: Thursday, June 15, 2023

THU404 Classical Symptoms Masquerading As A Surprising Clinical Picture

Abstract Disclosure: A. Syal: None. Y. Arya: None. S. Teja Sathi: None. J. Prater: None. Introduction: Primary hyperparathyroidism commonly presents in the setting of a parathyroid adenoma or hyperplasia, although it can rarely be caused parathyroid carcinoma, often accounting for &amp;lt;1% of cases. Markedly elevated PTH levels, along with predominant uniglandular involvement should increase the suspicion of an underlying parathyroid carcinoma, given that multiglandular involvement is rarely encountered. Surgical resection with histopathological confirmation remains the mainstay of diagnosis. Case presentation: We describe the case of a female in her late 50s who was brought to the emergency department by her family with complaints of altered mental status, hallucinations, delusions, anxiety, increased urination, constipation, and decreased appetite for the past month. Her laboratory evaluation was significant for hypercalcemia with a corrected calcium of 13.4 mg/dL. She was started on intravenous fluids and calcitonin, with improvement in her clinical condition. Further workup for her hypercalcemia revealed that the serum parathyroid hormone (PTH) was significantly elevated at 1846.4 pg/mL (normal low: 9, normal high: 73). Her serum phosphorus was low, and 25-hydroxy vitamin D was high-normal. This was consistent with a picture of primary hyperparathyroidism. The severely elevated PTH raised concern for parathyroid carcinoma, a rare clinical entity. The patient underwent a nuclear medicine parathyroid scan (technetium 99m sestamibi), which revealed abnormal focal uptake in the inferior right thyroid bed. Ultrasound of the neck revealed a hypoechoic avascular nodule inferior to the right thyroid lobe corresponding to the area of increased sestamibi activity on nuclear medicine scan. After much discussion with the patient’s family, surgical intervention was deferred to a later date, with a focus on stabilization in the acute setting. The patient was started on cinacalcet for her hypercalcemia. Bisphosphonates were initially held in anticipation for surgery but were eventually started. Discussion: Parathyroid carcinoma is a rare malignancy, which can occur both sporadically and as part of the hereditary hyperparathyroidism-jaw tumor syndrome. In clinical practice, subtle clues which increase the suspicion for a parathyroid carcinoma include severely elevated PTH, sometimes up to 10 times the upper limit of normal, increasing adenoma size, and a presentation outside of the commonly inherited MEN-1 syndromes.[1] We rely solely on post-operative pathology to establish the diagnosis of parathyroid carcinoma, given that there are no well-defined features or criteria that can establish the diagnosis on imaging.