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BackgroundPatient safety competencies in nursing are essential for the quality of healthcare. To develop practices and collaboration in nursing care, valid instruments that measure competencies in patient safety are needed.ObjectiveTo identify instruments that measure the patient safety competencies of nurses.DesignA scoping review.Data sourcesThe Cochran Library, Epistemonikos, Eric, Ovid Medline, CINAHL, Embase and Web of Science databases were searched for articles reporting on instruments measuring patient safety competence in nursing. The search was limited to English peer-reviewed scientific papers published from January 2010 to April 2021.Review methodA blinded selection of articles fulfilling the inclusion criteria was performed by two researchers based on the Preferred Reporting Items for Systematic Reviews and Meta-Analyses extension for Scoping Reviews. Data were then extracted, synthesised and presented in tables and text.ResultsOur search identified 1,426 papers, of which 32 met the inclusion criteria. The selected papers described nine instruments, of which the ‘Health Professional Education in Patient Safety Survey’ was the most used instrument. The identified instruments comprised domains for patient safety skills, attitudes, knowledge, communication, teamwork and errors. The instruments had been tested for content (face) and construct validity as well as for reliability. However, sensitivity and responsiveness were rarely assessed.ConclusionsOver the last decade, there has been a growing body of instruments aimed at measuring patient safety competencies among nurses. The future development of new instruments should consider including the important dimension of ethics in patient safety as well as evaluating the instrument’s responsiveness to be able to track changes over time.

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Background: Severe hypomagnesemia can result in hypocalcemia as magnesium is a co-factor necessary for PTH production in the parathyroid glands. Calcium replacement alone can prove difficult in the setting of hypomagnesemia, therefore optimal treatment should also include repletion and normalization of magnesium levels. Sodium-glucose cotransporter 2 inhibitors (SGLT-2i) are a class of oral medications used in the treatment of type 2 diabetes and recently in heart failure which inhibit the sodium-glucose transporter in the proximal tubule of the kidney. A lesser known effect of SGLT-2i is renal tubular resorption of magnesium leading to increased serum magnesium levels. We report a case of refractory diuretic-induced hypomagnesemia and subsequent hypocalcemia which was successfully treated with SGLT-2i. Clinical Case: A 74-year-old male with uncontrolled type 2 DM, vitamin D deficiency, NASH cirrhosis, chronic lower extremity edema on furosemide therapy, and CKD stage III presented with unexplained hypocalcemia at 7.4–8.4 mg/dL (n: 8.8 – 10.4 mg/dL) and hypomagnesemia at 1.0–1.3 mg/dL (n: 1.5 – 2.5 mg/dL) for the past two years. He had been followed by his PCP who performed a workup revealing 25-OH vitamin D level 22.6 ng/mL, PTH 43 pg/mL (n: 10–55 pg/mL) with corresponding calcium 8.1 mg/dL. He was started on ergocalciferol 50,000IU, magnesium oxide 400mg daily, titrated up to 400mg BID, and calcium carbonate 400mg BID with no improvement in magnesium or calcium level. Later, he was admitted to the hospital with volume overload. During admission, magnesium was repleted with IV magnesium sulfate to a level of 2.1 mg/dL and serum calcium level normalized to 8.8 mg/dL without supplementation once magnesium level was replete. He was discharged with resumption of oral magnesium sulfate 400mg BID, but within 10 days his serum magnesium level dropped to 1.0 mg/dL. Endocrinology was consulted, and due to the severe hypomagnesemia, empagliflozin 10mg daily was started for the purpose of increasing the serum magnesium level and secondarily for improvement in glucose and edema control. After one week of treatment, the magnesium level increased to 1.4mg/dL and calcium level to 8.7mg/dL. Six months later, magnesium and calcium levels remained stable at 1.7 mg/dL and 9.1 mg/dL, respectively. The patient continues to now remain normocalcemic and normomagnesemic on empagliflozin 12.5mg daily. Conclusion: SGLT-2i represent a potent class of anti-hyperglycemic agents with the secondary effect of renal tubular absorption of magnesium which may help achieve appropriate PTH secretion in cases of treatment refractory hypocalcemia. This is one of the first cases to report the off-label use of SGLT-2i for refractory hypocalcemia due to hypomagnesemia. SGLT-2i should be considered in these cases especially in the setting of suboptimally controlled type 2 DM when other interventions have been unsuccessful.

Introduction Graves’ disease is an autoimmune disorder that causes excess thyroid hormone (T4 and T3). T4 is converted into T3 (active hormone) in the peripheral tissues by the deiodinase enzyme. T3 has an effect on the cardiac electrical system as well as myocyte contractility. Excess T3 can result in cardiac arrythmias as well as ventricular dysfunction (heart failure). Takotsubo cardiomyopathy is a subtype of nonischemic cardiomyopathy related to severe physiologic or mental stress. Excess catecholamine levels have been reported to cause this disease as well. Takotsubo cardiomyopathy has rarely been reported in Graves’-associated thyrotoxicosis. Case report 55-year-old female who presented to the ED with palpitations and difficulty breathing. She had been seen by her PCP within the past two weeks with complaint of recent 30 lb weight. TSH was noted to be < 0.001 and a neck ultrasound revealed a diffusely enlarged, hypervascular thyroid. She was referred for outpatient endocrinology consultation for further workup. Prior to her initial endocrinology appointment, she developed palpitations and shortness of breath. She did not have any known family history of thyroid disease or other autoimmune conditions. She drinks 1-2 glasses of wine per week and quit smoking in 2017. Physical exam on admission revealed a heart rate of 133 bpm and a blood pressure of 145/93, normal temperature, and normal respirations. Thyroid was diffusely enlarged and without nodularity. No evidence of orbitopathy. Heart was tachycardic but without murmur. Lungs clear. Abdomen soft, nontender. No significant peripheral edema or pretibial rash. No neurological dysfunction. Labs revealed TSH < 0.001, Free T4 > 7.77, Free T3 12.0, TRAb 44.4%, TSI 433%, Anti-TPO 614, high-sensitivity troponin of 112. EKG showed nonspecific infero-lateral T wave changes, rate 123. Echocardiogram demonstrated left ventricular apical hypokinesis but preserved basilar contractility. Ejection fraction was estimated at 40-45%. Nuclear stress test did not reveal any indication of myocardial hypoperfusion. Discussion/Conclusion Takotsubo cardiomyopathy can mimic acute myocardial infarction both clinically as well as on EKG/serum biomarkers. Troponin levels are typically elevated as a result of myocardial stretch and subsequent troponin “leak”. Echocardiogram demonstrates apical ballooning of the left ventricle, and by definition coronary arteries will be free of significant occlusive disease. A small number of cases have been reported in association with endocrine conditions including thyrotoxicosis due to Graves’ disease. The majority of cases associated with thyrotoxicosis will resolve spontaneously with 1-3 weeks. Treatment consists of medication to decrease cardiac preload as well as afterload (ACE inhibitor, beta blocker, diuresis as needed), similar to medical treatment of other nonischemic cardiomyopathies.