Background Ischemic stroke accounts for 85–90% of all strokes and currently has very limited therapeutic options. Recent studies of β-adrenergic antagonists suggest they may have neuroprotective effects that lead to improved functional outcomes in rodent models of ischemic stroke, however there is limited data in patients. We aimed to determine whether there was an improvement in mortality rates among patients who were taking β-blockers during the acute phase of their ischemic stroke. Methods A retrospective analysis of a prospectively collected database of ischemic stroke patients was performed. Patients who were on β-adrenergic antagonists both at home and during the first three days of hospitalization were compared to patients who were not on β-adrenergic antagonists to determine the association with patient mortality rates. Results The study included a patient population of 2804 patients. In univariate analysis, use of β-adrenergic antagonists was associated with older age, atrial fibrillation, hypertension and more severe initial stroke presentation. Despite this, multivariable analysis revealed a reduction in in-hospital mortality among patients who were treated with β-adrenergic antagonists (odds ratio 0.657; 95% confidence interval 0.655–0.658). Conclusions The continuation of home β-adrenergic antagonist medication during the first three days of hospitalization after an ischemic stroke is associated with a decrease in patient mortality. This supports the work done in rodent models suggesting neuroprotective effects of β-blockers after ischemic stroke.

Diabetic striatopathy is a rare neurologic complication of uncontrolled diabetes, specifically associated with non-ketotic hyperglycemia. Though the exact pathophysiology is unclear, patients with this syndrome typically present with hemichorea-hemiballismus, but other sensorimotor disturbances may also be present. The diagnosis is made through unique radiographic findings on imaging of the basal ganglia, which may be misconstrued as an alternative diagnosis. The following is a case of diabetic striatopathy in patient with uncontrolled diabetes who was initially thought to have an intracerebral hemorrhage (ICH). A 45-year-old gentleman with a prior history of uncontrolled type 2 diabetes mellitus due to non-compliance, hypertension, and hyperlipidemia presented to the emergency department of an outside hospital with the chief complaint of left arm numbness and weakness, as well as left-sided tinnitus, for one week. His physical exam was significant for lateral strabismus of the left eye. His blood work on evaluation revealed profound hyperglycemia of 700 mg/dL. A computerized topography (CT) scan of the head revealed enhancement of the right basal ganglia. Due to initial concern for an ICH, he was subsequently transferred to a tertiary care center for further evaluation. However, upon a second review of imaging by radiology and neurology, it was determined that this was less likely to be an ICH given his otherwise normal neurologic exam. There was additionally no vasogenic edema on the CT scan. Given his profound hyperglycemia and his symptoms, the working diagnosis of diabetic striatopathy was established. With correction of his blood sugars, his symptoms improved and on follow-up magnetic resonance imaging (MRI) of the brain, his initial basal ganglia enhancement had resolved. This case highlights a rare but significant complication of hyperglycemia that is important to diagnose early to prevent possible permanent structural change and continuous symptoms. This syndrome should especially be considered in diabetic patients with hyperglycemia and abnormal findings on neuroimaging, to facilitate timely treatment via correction of hyperglycemia which can lead to resolution of symptoms.

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Introduction: Hormonal Milieu of pregnancy is known to create a state of “accelerated starvation”, which is exceptionally pathological in a diabetic pregnant patient. Our case presents a diabetic mother with severe chest pain and premature labor in the setting of mixed anion gap metabolic acidosis. Initial diagnosis was diabetic ketoacidosis (DKA), however starvation ketoacidosis (SKA) became more questionable. To our knowledge, this is the first case to report acute coronary syndrome (ACS) as a presentation of SKA with pregnancy. Case Presentation: A 40-year-old woman, gravida 3 para 2 with the diagnosis of Gestational Diabetes at the 9 th week of pregnancy, was transferred to our university hospital at 36 weeks of gestation due to concern for ACS. Patient endorsed intense central chest pain with the start of early labor contractions. Three weeks prior, she followed a low carbohydrate and severely calorie deficient diet to reduce her insulin requirements because of the history of fetal macrosomia noted on ultrasound. Cervix was 80% effaced on pelvic examination with blood chemistry remarkable for glucose level of 174 mg/dL, anion gap (AG) of 18 mEq/L and bicarbonate level of 5 mEq/L. Lactic acid level was 0.7 mEq/L, beta-hydroxybutyrate level 5.30 mmol/L and a positive urine dipstick for ketones. Delta ratio was 0.3, explained as combined high AG and normal AG metabolic acidosis. Electrocardiogram showed transient minimal 1mm elevation in the inferior leads with otherwise negative serial Troponin levels. Pulmonary embolism was ruled out by contrast imaging. She was admitted to the Coronary Care Unit and was started on Heparin drip for the initial diagnosis of STEMI. Delivery was accelerated with artificial membrane rupture, after which she was started on insulin and dextrose drips until the closure of the AG. Further cardiac workup was then deferred to outpatient management due to the clinical stability and resolution of chest pain. Discussion: Although similar in physiology and management, both DKA and SKA are 2 distinct entities and a special attention should be paid for both in the state of pregnancy. DKA tends to be more in type 1 diabetes due to absolute insulin deficiency and can be exacerbated by infection, and noncompliance with insulin or diet. SKA however presents with improper diet that is not meeting the high energy demand, creating a “demand more than supply” state. We believe that concomitant use of insulin while being on a low carbohydrate/calorie diet has caused the opposition of lipolysis, the sole remaining source of energy, which has caused more stress hormones production to override that state. This explains the euglycemia as well as the morbid symptoms the patient presented with. Carbohydrate consistent diet in addition to watchful insulin monitoring are advised in diabetic mothers to avoid starvation and its subsequent complications as preterm delivery and severe maternal morbidity. ...