Aphasic status epilepticus is a rare neurological complication of the hyperosmolar hyperglycaemic state, a severe metabolic emergency in diabetes mellitus. Symptoms include language disturbance without significantly impaired consciousness. The diagnosis is complex, and management of the aphasic status epilepticus involves metabolic correction and antiseizure medications. We describe a 66-year-old man with type 2 diabetes who presented with progressive speech decline and impaired coordination following a fall. EEG confirmed non-convulsive status epilepticus, and MR brain scan showed transient left temporal changes with later hippocampal atrophy. Initial treatment with insulin and levetiracetam led to significant recovery. This case underscores hyperosmolar hyperglycaemic states as a reversible cause of aphasic status epilepticus and highlights the varied neurological presentations of uncontrolled diabetes. We include a review of the literature to contextualise this under-recognised clinical entity.

ABSTRACTWolfram syndrome is a rare autosomal recessive disorder characterized by diabetes insipidus, diabetes mellitus, optic atrophy, and deafness (DIDMOAD). We present the case of a 19‐year‐old male with a history of juvenile‐onset non‐autoimmune diabetes mellitus who presented with fever, chills, seizures, altered sensorium, vomiting, and abdominal pain. The patient was treated for a hyperosmolar hyperglycemic state precipitated by gastrointestinal infection with intravenous fluids, antibiotics, and insulin therapy. Physical examination revealed short stature, delayed secondary sexual characteristics, neck rigidity, and bilateral upward plantar reflexes. Further neuroimaging revealed pontine atrophy, partial central diabetes insipidus, and bilateral optic atrophy. Fundoscopy confirmed optic disc pallor and generalized visual field loss. Pure tone audiometry indicated profound bilateral high‐frequency sensorineural hearing loss, and magnetic resonance (MR) urography findings were consistent with a neurogenic bladder. His sensorium and neurological deficits improved within 3 days, and he was later discharged with close follow‐up by a multidisciplinary team. This case highlights the classic presentation of Wolfram syndrome in a young male with diabetes and neurological complications, emphasizing the need for early recognition and multidisciplinary management. Wolfram syndrome poses significant diagnostic challenges due to its varied and progressive symptoms, and this report aims to contribute to the existing knowledge base and create awareness about the condition, its clinical presentation, and the need for a multidisciplinary management approach.

Aims/introductionGlucagon plays a pivotal role in the development of hyperglycemia in diabetes mellitus. The purpose of this study was to investigate the hypothesis that hyperglucagonemia based on measurements of pancreas-specific glucagon is present in diabetic ketosis/ketoacidosis (DK/DKA) and hyperosmolar hyperglycemic state (HHS), and if so, to explore factors contributing to that hyperglucagonemia.Materials and methodsA total of 109 patients (92 with DK/DKA, and 17 with HHS) were investigated. Pancreas-specific glucagon levels were measured with a sandwich enzyme-linked immunosorbent assay at treatment initiation. The relationships of plasma glucagon levels, serum ketone bodies levels, and endogenous insulin secretion were assessed. The change in plasma glucagon levels after treatment was also assessed.ResultsThe median plasma glucagon level was significantly higher in the HHS group (142.9 pg/mL) than in the DK/DKA group (63.6 pg/mL). In the DK/DKA group, the plasma glucagon level was positively correlated with the serum ketone bodies level (ρ = 0.55, P < 0.0001), but there was no correlation in the HHS group. In the DK/DKA group, a negative correlation was seen between the plasma glucagon level and the serum C-peptide immunoreactivity (CPR)/plasma glucose ratio in type 1 diabetes patients (n = 26) (ρ = − 0.67, P = 0.0002). In the HHS group, a positive correlation was seen between the plasma glucagon level and the serum CPR/plasma glucose ratio (ρ = 0.71, P = 0.0013). The plasma glucagon level was significantly lower after treatment in both the DK/DKA and HHS groups.ConclusionsHyperglucagonemia was found in DK/DKA and HHS with pancreas-specific glucagon measurements. The results suggest that the causes of hyperglucagonemia differ in DK/DKA due to type 1 diabetes mellitus and HHS.Supplementary InformationThe online version contains supplementary material available at 10.1007/s13340-025-00852-8.

Background: Hemichorea is a rare hyperkinetic movement disorder that may occur as a complication of ischemic stroke or metabolic disturbances, particularly non-ketotic hyperglycemic hyperosmolar state (NKHHS). Case Series: We present two female patients with uncontrolled type II diabetes mellitus who developed hemichorea associated with ischemic stroke. The first case showed severe hyperglycemia (&gt;500 mg/dL) without radiological abnormalities on non-contrast CT scan. The second case presented with hyperglycemia (375 mg/dL) and a hyperdense lesion in the left caudate nucleus. Both patients received aspirin and insulin, while symptomatic management included haloperidol and, in the second case, additional valproic acid. Both patients demonstrated gradual clinical improvement. Discussion: Post-stroke hemichorea is reported in only 1–4% of cases. The underlying mechanism involves disruption of the striato-thalamo-cortical pathway and, in hyperglycemia, impairment of GABA metabolism. Most cases respond well to glycemic control, although neuroleptics or antiepileptics may be necessary to control symptoms. Conclusion: This case series highlights that hemichorea can be a rare manifestation of ischemic stroke, either with or without radiological evidence, and may be aggravated by uncontrolled hyperglycemia. Early diagnosis, strict glycemic regulation, and appropriate symptomatic treatment are crucial for favorable outcomes. Keywords: Ischemic stroke, hemichorea, hyperglycemia

Rates of diabetic ketoacidosis (DKA) and hyperglycaemic hyperosmolar state (HHS) have been rising in the US and Europe, but drivers remain unclear. Asian data are limited. This study examines trends and risk factors for DKA and HHS admissions among patients with type 2 diabetes (T2D) in Singapore. We analysed 47,489 adults (≥18 years) with T2D from a tertiary hospital in Singapore (2013-2022). DKA and HHS admissions were identified via diagnostic codes. Trends in standardized admission rates, HbA1c, and medication use were described. A nested case-control logistic regression model (1:2 incidence-density matched) was used to estimate the effect of HbA1c on the odds of admission for DKA and/or HHS. DKA and HHS admissions increased from 2013 to 2022 despite declining mean HbA1c, though DKA rates decreased after 2020. Higher HbA1c was significantly associated with admission odds (OR 1.18, 95% CI 1.13-1.23). Other independent risk factors included younger age (OR 0.72, 95% CI 0.70-0.74), lower BMI (OR 0.96, 95% CI 0.95-0.98), social housing (OR 1.50, 95% CI 1.13-1.98), diabetes duration >10 years (OR 1.58, 95% CI 1.14-2.21) and CKD stage ≥3A, with the highest odds in stage 4 (OR 5.81, 95% CI 4.13-8.17). DKA and HHS admission rates rose despite improving HbA1c. High-risk groups may require closer monitoring and targeted interventions.

Diabetic striatopathy is a rare, acute neurological complication of diabetes mellitus which presents with non-ketotic hyperglycemia and involuntary movements, specifically hemichorea or hemiballismus. Striatal abnormalities on neuroimaging have been reported in most, but not all cases. This case report aims to increase awareness that diabetic striatopathy can be a presenting symptom of diabetes mellitus.A 92-year-old Filipino female with no history of diabetes presented with acute onset of focal clonic flexion of the left upper extremity for a few hours, which progressed to right hemifacial spasm. She was diagnosed with a hyperosmolar hyperglycemic state and was treated accordingly. Cranial CT scan findings were unremarkable. There was an immediate resolution of her neurologic symptoms after the correction of hyperglycemia.The diagnosis of diabetic striatopathy highlights the importance of increasing awareness and understanding of this condition among clinicians to prevent delayed diagnosis and treatment. Screening for hyperglycemia is advisable for patients with involuntary movements. The prognosis for diabetic striatopathy is good with prompt glycemic control in most cases.

Hyperglycemic hyperosmolar nonketotic syndrome (HHNS) is a complication of type 2 diabetes mellitus that can progress to coma and death if left untreated. Focal hyperglycemic seizures are still an uncommon but noteworthy association of HHNS and most commonly involve the occipital and parietal lobes. Gerstmann syndrome, also called angular gyrus syndrome, consists of a tetrad of finger agnosia, acalculia, left-right disorientation, and agraphia that is usually accompanied by aphasia and most commonly presents in parietal lobe pathology. Here we report a case of a 50-year-old right-handed male with complaints of focal right-sided upper limb and facial seizures and findings of acalculia, finger agnosia, left-right disorientation, semantic aphasia, and loss of comprehension. Laboratory reports suggested HHNS seizures that presented clinically as Gerstmann syndrome. Magnetic resonance imaging (MRI) of the brain revealed dominant (left in our case) parietal lobe pathology. Although it is understood that HHNS is linked with focal neurological deficits, the exact mechanism by which this happens is still unknown, and Gerstmann syndrome associated with hyperglycemic seizures is still underreported, necessitating additional research.

Introduction: Diabetes Mellitus (DM) constitutes a group of metabolic disorders characterized by hyperglycemia resulting from different etiopathogenic mechanisms. Among the main complications that can lead to emergency admissions, diabetic ketoacidosis (DKA) and hyperglycemic hyperosmolar state (HHS) stand out. Objective: To analyze the epidemiological profile of adult patients with diabetes admitted urgently in the southern region of Brazil, for morbidities classified under ICD-10 codes: E10–E14, from January 2021 to December 2023. Methods: Data from the Hospital Information System (SIH) of DATASUS were used. The evaluated variables included sex, age group, color/race, and number of hospitalizations. Results: A total of 35,024 hospitalizations were recorded during the analyzed period. Rio Grande do Sul reported the highest number of cases (38.97%), followed by Paraná (37.51%) and Santa Catarina (23.51%). The most prevalent age group was 60 to 69 years (30.35%), followed by 70 to 79 years (24.24%). The male sex represented 53.72% of the admissions. Regarding color/race, 81.96% of the patients were white, 12.27% were brown, and 4.8% were black. Discussion: A growing trend in hospitalizations was observed between 2021 and 2022, maintained only in Rio Grande do Sul between 2022 and 2023. The predominance of the male sex corroborates studies conducted in Alagoas (2016), but diverges from findings in Bahia (2012) and Rio Grande do Sul (2019). The most affected age group (60 to 69 years) and the predominance of the white population also coincide with previous studies in AL and RS. Conclusion: Diabetes Mellitus represents a significant public health problem in the southern region of Brazil, with a high frequency of emergency hospitalizations and specific demographic patterns, highlighting the need for regionalstrategies for prevention, clinical management, and targeted public policies.

To minimize the risk of cerebral edema in the management of hyperglycemic emergencies, guidelines recommend gradually decreasing serum glucose levels, but there is limited literature validating these reduction goals or evaluating outcomes associated with different correction rates. This study evaluated cerebral edema rates associated with 2 different serum glucose correction rates in adults with hyperglycemic emergencies. This retrospective study's primary endpoint was the incidence of cerebral edema. Secondary endpoints included average hourly changes in sodium, potassium, chloride, bicarbonate, anion gap, glucose, blood urea nitrogen, creatinine, and calculated osmolality, over the treatment course. Patients were divided into 2 groups based on their average hourly serum glucose correction rate (> 75 mg/dL and ≤ 75 mg/dL), and their outcomes were compared. Patients were included if they were ≥18 years old, received the institutions' diabetic ketoacidosis or hyperglycemic hyperosmolar state insulin infusion order set within 12 hours of presenting to the hospital, and had a pre-insulin infusion glucose > 600 mg/dL. One hundred thirty-four patients had a slow correction rate, and 51 had a rapid correction rate. The median time from starting the insulin infusion to achieving a glucose < 300 mg/dL in the slow and rapid correction rate groups was 9.9 and 6.1 hours, respectively (p < 0.001). In the total population, 2 (1.5%) cerebral edema events occurred. Both patients were in the slow correction rate group and had radiographic evidence of cerebral edema on post-return of spontaneous circulation imaging. There were significantly larger decreases in glucose and osmolality levels in the rapid correction rate group at several time points during treatment. Rapid serum glucose correction rates were not associated with increased cerebral edema events. Our findings suggest glucose and osmolality levels can be corrected faster than what is currently recommended.

Disclosure: F.O. Asemota: None. L. Sangurima: None. A. Sajan: None.Introduction: Rhabdomyolysis is a rare sequelae of hyperosmolar hyperglycemic state (HHS). We present a case of HHS complicated by rhabdomyolysis resulting in mortality. Case: A 73-year-old Hispanic male with hypertension and diabetes mellitus presented with lethargy after being found unconscious at home. On admission, he had tachycardia (106 beats per minute) and tachypnea (25 breaths per minute). He was unresponsive to pain or verbal commands and had dry mucous membranes. Initial investigations revealed an elevated anion gap metabolic acidosis (pH 6.938 [7.300-7.400], bicarbonate level 7.1 mEq/L [24 - 30], serum glucose 1647 mg/dL [70-99], and anion gap 37 mEq/L [7-16]. Further evaluation showed serum lactate 16 mmol/L [0.5 - 2.2], a small amount of urine ketones, and serum osmolality 422 mOsm/kg [290 - 300], establishing the diagnosis of severe diabetic ketoacidosis with hyperosmolar hyperglycemic state. Initial potassium level was normal. The patient was started on intravenous fluids and insulin drip. The electrolytes were replaced as needed. Additionally, initial blood culture showed growth of Streptococcus and Klebsiella pneumoniae for which empiric antibiotics were initiated. An electrocardiogram showed ST elevation in anterior leads, which was deemed related to demand ischemia by the cardiology team and was treated empirically with heparin. The patient had a cardiac arrest the next day and passed. A careful review of labs drawn a few hours before the arrest revealed creatine kinase of 15,432 IU/L [38 - 174], potassium 6.3 mEq/L [3.5-5.3], and phosphorus of 5.0 mg/dL [2.7 - 4.5] consistent with rhabdomyolysis which was missed. Discussion: Rhabdomyolysis is a known, rare, and usually subclinical complication of HHS precipitated by hyperosmolarity and electrolyte abnormalities. Low insulin or insulin resistance leads to decreased glucose inside the muscle cells and attenuates Na+/K+ ATPase activity. This causes accumulation of intracellular sodium and calcium due to the reduced exchange of calcium and sodium. The intracellular calcium accumulation results in the dissolution of muscle fibers causing myoglobin to be released into the bloodstream. The myoglobin in turn blocks the tubules within the nephrons, leading to severe kidney damage. In addition, insulin infusion causes a rapid shift of electrolytes into the cell, leading to hypokalemia and hypophosphatemia, which can also contribute to the development of rhabdomyolysis. Conclusion: Although most cases of rhabdomyolysis are subclinical in HHS, it has the potential to be fatal in unrecognized cases as in our patient. The early recognition of rhabdomyolysis is needed for electrolyte monitoring and careful fluid resuscitation to prevent morbidity and mortality.Presentation: Monday, July 14, 2025

Disclosure: R. Maini: None. K. Oguntuyo: None. D. Alban: None. P.D. Greenberg: None.Background: Leptospirosis, a zoonotic infection caused by spirochetes, can present as Weil’s disease, characterized by fever, jaundice, renal failure, and conjugated hyperbilirubinemia. There is minimal evidence of an association between leptospirosis infection and diabetic emergencies. To date, only one pediatric case from India documented a patient with type 1 diabetes who presented with DKA induced by leptospirosis. Clinical Case: A 49-year-old male with history of type 2 diabetes, obesity, and MASLD presented with altered mental status and jaundice. Laboratory evaluation revealed hyperosmolar hyperglycemic state (HHS), direct hyperbilirubinemia, and renal failure. Initial labs showed glucose of 858 mg/dL with elevated serum osmolality, normal pH, HbA1c 9.7%, creatinine 5.5 mg/dL, AST 68 U/L, ALT 115 U/L, alkaline phosphatase 101 U/L, total bilirubin 10 mg/dL, and direct bilirubin 7.1 mg/dL. The patient had recently started Ozempic 0.25mg weekly and completed 3 doses so far. He also took Metformin daily and did not use insulin at home. During the admission, the total bilirubin peaked at 27.2 mg/dL, direct bilirubin at 21.9 mg/dL, and creatinine at 6.4 mg/dL. Imaging, including CT scan and RUQ ultrasound, ruled out an obstruction, and a HIDA scan revealed delayed tracer clearance and gall bladder dyskinesia. Social history revealed that the patient worked in sanitation, so an infectious disease panel was sent. The patient tested positive for leptospirosis IgM. The patient was initially treated with an insulin drip, normal saline intravenous fluids, and bridged to basal/bolus subcutaneous insulin. He was treated with courses of Zosyn and Doxycycline with improvement in both renal function and bilirubin levels. He was discharged on insulin and Ozempic was discontinued. Conclusion: This is the first case documenting a presentation of HHS in the setting of leptospirosis infection. The clinical course was complicated by isolated direct hyperbilirubinemia and gall bladder dyskinesia, potentially exacerbated by recent Ozempic use.Presentation: Monday, July 14, 2025

Disclosure: A.J. Zaidi: None. W. Akhter: None. M. Fathima: None. J. Gilden: Novartis Pharmaceuticals. A. Khan: None.Background: Atypical forms of Diabetes Mellitus (DM) may present with unusual clinical features, challenging diagnosis and management. LADA (Latent Autoimmune DM in Adults), idiopathic, forms associated with beta-cell dysfunction, or ketosis-prone DM can present in adulthood with features that resemble type 1 DM but without a clear autoimmune etiology. We present the case of a young man who developed significant hyperglycemia but did not meet the typical criteria for either type 1 or type 2 DM, with significant retinopathy. Case Report: A 38-year-old African male with no known past medical history presented to the emergency room for malaise and was found to have a blood glucose (BG) level >700 mg/dL. The patient had no known prior or family history of DM. Over the preceding weeks, he noted polyuria, polydipsia, and fatigue. His clinical presentation raised concerns for Diabetic Ketoacidosis (DKA)/Hyperosmolar Hyperglycemic State (HHS), leading to ICU admission and initiation of insulin infusion. Laboratory showed normal bicarbonate levels, anion gap, and initial serum osmolarity of 309, negative blood ketones, although urine ketones were positive; HbA1c of 15%. He was discharged with insulin (Lantus 8 units and Novolog 2 units TID) and metformin (METF) 1000 mg BID.Two weeks later when he was evaluated in clinic he was only taking METF with small doses of short-acting insulin, as needed. Autoimmune testing was negative for GAD, IA-2, Zn transporter, and islet cell antibodies, which ruled out typical Type 1 diabetes; low c-peptide (0.18 units)(normal range 0.81-3.85 ng/ml) with low BG of 53 mg/dl. Continuous Glucose Monitoring (CGM) revealed episodes of hypoglycemia (HYPO). The METF dose was then decreased and eventually stopped. CGM continued to show premeal and exercise HYPO with 50s before dinner. He was also found to have advanced Diabetic retinopathy and proteinuria with Ur Albumin 4.4 mg/dl (normal 0.3-2.0) Clinical Course and Management: Off any antihyperglycemic agents, fasting BG average increased to around 200 mg/dl. with higher post meal BG. Patient was trialed with acarbose with no effect on BG, then a dipeptidyl peptidase-4 (DDP-4) inhibitor. However, BG increased to the 300’s. Insulin therapy was reintroduced. The final diagnosis for type of DM remains unclear. Conclusion: This case highlights the complexity involved in diagnosing and managing atypical forms of DM, including LADA, monogenic, and ketosis-prone DM. It is a spectrum, which may present with features of both type 1 and type 2 DM but lacks definitive biomarkers. Clinicians should consider the atypical forms in adult patients with new-onset diabetes and atypical presentations, especially when there is an absence of typical autoimmune markers. Management remains challenging.Presentation: Saturday, July 12, 2025

Diabetes mellitus and dementia are common chronic diseases affecting older people in the community and in hospitals. Even though both diseases have been independently well-characterized, comorbid diabetes and dementia/cognitive impairment are much less understood. In particular, cognitive impairment can make glucose monitoring much more challenging and can more readily lead to diabetes-related emergencies such as hypoglycemia, hyperosmolar hyperglycemic state, or diabetic ketoacidosis. Based on this, improving diabetes management in the community and in the hospital settings via glucose monitoring is essential in older people with T2DM and particularly those with comorbid diabetes and dementia. The use of continuous glucose monitoring (CGM) holds promise for greater glycemic management in older patients with diabetes and those at high risk for dementia. In this brief review, we will review the few existing studies for CGM use in the community and the hospital in this population, as well as the link between hospital admissions. Existing studies show high feasibility and good adherence with using CGM among older people. In addition, diabetes technologies can improve risk factors associated with hospitalization, leading to decreased hospitalization rates. We illustrate how the current studies highlight the need for studies in the hospital in this frail population, who potentially will benefit most from CGM systems. Although existing feasibility studies show high promise in this frail population, more data are needed on CGM for older people living with diabetes and memory problems in the hospital setting.

Pulmonary mucormycosis and achromobacter xylosoxidans co-infection in an immunocompromised host: a case report

This report highlights a rare case of a man in his 50s with central pontine myelinolysis who initially presented with dysphagia and dysarthria. The patient also exhibited unsteady gait, dizziness, and weakness in all extremities. Imaging studies revealed a typical “bat-wing” lesion at the base of the pons. The patient was diagnosed with central pontine myelinolysis secondary to a diabetic hyperglycemic hyperosmolar state complicated with hypernatremia. Following insulin therapy and rehydration, his symptoms were resolved within 1 week, while the imaging-detected lesions persisted. In most cases, central pontine myelinolysis develops due to the rapid correction of chronic hyponatremia; central pontine myelinolysis resulting from a hyperglycemic hyperosmolar state combined with hypernatremia is extremely rare. This case suggests that the coexistence of a hyperglycemic hyperosmolar state and hypernatremia can lead to central pontine myelinolysis, with a synergistic interaction between their pathogenic mechanisms. It emphasizes that in diabetic patients with poor glycemic control presenting with neurological symptoms, the possibility of central pontine myelinolysis should be vigilantly considered. Furthermore, this case supplements the understanding of the etiology and pathogenesis of central pontine myelinolysis, reminding clinicians to pay attention to central pontine myelinolysis caused by nontraditional factors.

Extrapontine Myelinolysis in the Context of Hypernatremia and Hyperosmolar Hyperglycemic State

Predictors and Outcomes of Hospitalized Patients with Diabetic Ketoacidosis versus Hyperosmolar Hyperglycemic State (HHS): Insights from National In-patient Sample 2016–2021

BackgroundHyperglycemic crisis events (HCEs)—encompassing diabetic ketoacidosis (DKA) and hyperosmolar hyperglycemic state (HHS)—constitute lethal determinants for patients with diabetic mellitus (DM) in intensive care. The triglyceride-glucose (TyG) index, an emergent insulin resistance surrogate, lacks rigorous investigation regarding HCE occurrence trajectories and prognostic sequelae among critically ill diabetics. This study aims to evaluate the relationship between the TyG index and HCE incidence/clinical outcomes in critically ill patients with DM and to construct a risk prediction model using machine-learning algorithms.MethodsThis multi-center retrospective investigation leveraged clinical repositories from Medical Information Mart for Intensive Care IV (MIMIC-IV) and eICU Collaborative Research Database (eICU-CRD). Inclusion criteria encompassed critically ill subjects with diabetes possessing computable TyG indices within 24 h post-admission. The main study endpoints included death occurring during hospitalization and death within the intensive care unit. TyG index-outcome interrelationships underwent interrogation via logistic regression, restricted cubic spline (RCS), correlation, and linear analytical methodologies. Overlap weighting (OW), inverse probability treatment weighting (IPTW), and propensity score matching (PSM) mitigated confounding influences. Stratified examinations occurred per determinant factors. Five machine-learning architectures constructed mortality prognostication frameworks, with SHapley Additive exPlanations (SHAP) delineating pivotal predictors.ResultsAmong 4,098 critically ill patients with DM, 328 developed HCE. Patients with HCE had significantly higher TyG levels [10.2 (9.6–11.0) vs. 9.4 (8.9–9.9)] than non-HCE patients, demonstrating TyG’s discriminative ability for HCE. Through multivariate logistic regression, TyG was pinpointed as a separate risk element for both in-hospital (OR 1.956) and ICU death (OR 2.260), linked to extended hospital stays. RCS established a direct positive correlation between increased TyG levels and death rates (nonlinear p = 0.161 and 0.457), continuing even after adjusting for PSM, OW, and IPTW. Subgroup analyses reinforced TyG’s consistent mortality correlation. Machine-learning models, particularly XGBoost, achieved higher predictive accuracy, with TyG as a key component.ConclusionElevated TyG index shows a notable correlation with the occurrence of HCE and negative results in critically ill patients with DM. Advanced multivariate machine-learning models are adept at pinpointing patients at high risk, thereby facilitating prompt clinical action.

Is Our Understanding of Hyperosmolar Hyperglycemic State Accurate?

Identifying predictors of increased healthcare utilization for hyperglycemia may have important implications for designing interventions to improve patient outcomes and reduce costs. Studies examining predictors of 30-day recurrent ED hyperglycemia visits have been limited due to their retrospective nature. This study's objective was to prospectively identify predictors of 30-day recurrent ED visits for hyperglycemia in patients with diabetes. We conducted a multicentre, prospective cohort study of adults ≥ 18 years at one of four Canadian tertiary care, academic EDs with a diagnosis of hyperglycemia, diabetic ketoacidosis, or hyperosmolar hyperglycemic state. Multivariable logistic regression analysis was used to identify variables independently associated with recurrent 30-day ED visits for hyperglycemia. We enrolled 594 patients; 80 (13.5%) had a recurrent ED visit for hyperglycemia within 30 days. Independently associated predictors of 30-day recurrent visits on complete case analysis include substance abuse history (odds ratio [OR] 2.32, 95% confidence interval [CI]: 1.23-4.38) and initial laboratory blood glucose (OR 1.04, 95% CI: 1.01-1.07), while a new diabetes diagnosis was negatively associated (OR 0.29, 95% CI: 0.09-0.94). Sensitivity analysis using multiple imputation for missing data found the following independently associated variables: substance abuse history (OR 2.55, 95% CI: 1.34-4.85), previous ED visit within the past 14 days (OR 2.14, 95% CI: 1.02-4.48), and initial laboratory blood glucose (OR 1.04, 95% CI: 1.01-1.07). Two variables were negatively associated: recent hospitalization within the past 30 days (OR 0.40, 95% CI: 0.19-0.98) and new diabetes diagnosis (OR 0.37, 95% CI: 0.14-0.97). This multicentre prospective study reports predictors independently associated with 30-day recurrent ED visits for hyperglycemia. These predictors should be considered by ED clinicians when making disposition and follow-up plans for this important patient population, and future interventions should explore the interaction between hyperglycemia and substance use to prevent recurrent ED visits and reduce healthcare system costs and utilization.