bluuebunny/crossref_metadata_2025_split huggingface dataset:
Diabetic Myonecrosis: A Case Study
Authors: Reisner Timothy , Burks James K 
Published: May 2021

Abstract
Background: Diabetic myonecrosis is a rare complication of diabetes mellitus with less than 200 cases reported in the literature since initial description in 19651. Diabetic myonecrosis most commonly affects the thigh and usually presents with acute muscle pain, edema, and erythema in the absence of trauma or fever1. The pathogenesis has yet to be elucidated—atherosclerosis, microangiopathy, vasculitis, and ischemia-reperfusion injury have been theorized. Laboratory findings are relatively nonspecific—of the findings reported in a systematic review, CRP was elevated in 90%, ESR elevated in 83.3%, WBC elevated in 42.5%, and CK elevated in 31.6%1. Definitive diagnosis can be made by muscle biopsy which demonstrates muscle necrosis and edema; however, it is not routinely recommended due to procedural complications. MRI is the diagnostic modality of choice for diabetic myonecrosis which is both sensitive and specific for the diagnosis2.
Clinical Case: 76-year-old male with T2DM presented to regional hospital with severe right lower leg pain in the absence of fever, tachycardia, hypotension, or recent trauma. Physical exam demonstrated discrete erythema of distal 2/3 of posterior right lower leg extending to the ankle distally. Labs demonstrated normal CK, elevated ESR, HgbA1c 8.2%, and negative blood cultures. MRI of the right lower extremity demonstrated abnormal prolongation of T2 relaxation time involving posterior muscle compartment including soleus and gastrocnemius with associated perifacial and subcutaneous edema. These findings were consistent with diabetic myonecrosis without evidence of osteomyelitis or abscess. Rest, optimal glycemic control, and aspirin were recommended and patient improved gradually with complete clinical resolution on outpatient follow-up.
Conclusions: Diabetic myonecrosis is a rare complication of diabetes and should be considered in patients presenting with acute muscle pain. Among cases described in literature, 5.7% have affected the soleus and 5% have affected the gastrocnemius respectively1. The diagnostic modality of choice is contrast enhanced MRI with typical findings including hyperintense signal on T2 weighted images with associated muscular, perifascial, and/or subcutaneous edema3. The optimal treatment is yet unknown, but reasonable strategies based on case series include rest, glycemic control, and NSAID therapy1.
References: 1. Horton WB, Taylor JS, Ragland TJ, Subauste AR. Diabetic muscle infarction: a systematic review. BMJ Open Diabetes Res Care. 2015;3(1):e000082. doi:10.1136/bmjdrc-2015-000082
2. Morcuende JA, Dobbs MB, Crawford H, Buckwalter JA. Diabetic muscle infarction. Iowa Orthop J. 2000;20:65–74.
3. Goswami P, Baruah MP. The Role of MRI in Diagnosis of Diabetic Muscle Infarction : an Underdiagnosed Entity. Int J Endocrinol Metab. 2012;9(2):353–355. doi:10.5812/kowsar.1726913X.1886
Glucose-6-phosphate Dehydrogenase Deficiency Induced Haemolysis in Male With Newly Diagnosed Diabetes During Diabetic Ketoacidosis Treatment: A Case Report
Authors: Albasri Eman Ebrahim 
Published: May 2021

Abstract
Background: Glucose-6-phosphate dehydrogenase (G6PD) deficiency could be a risk factor for diabetes, as suggested by various epidemiological data, but still a matter of debate. The occurrence of haemolysis during diabetes crises was reported in patients with G6PD deficiency, furthermore the fall in glucose level during the treatment of hyperglycemia is suggested as a possible cause for hemolysis in G6PD deficiency. We reviewed the mechanisms that may link the two diseases. Clinical Case: A 19-year-old male, with G6PD deficiency, presented to the emergency department in our institution with history of generalised weakness, epigastric pain, nausea, and vomiting. He gave history of polyuria, polydepsia and weight loss over a period of two weeks. Diagnosis of DM was confirmed by laboratory tests that showed a mild DKA: arterial pH 7.28, HCO3 18 mmol/l, plasma glucose 21 mmol/l, urinary ketones ++, and hemoglobin 16.1 g/dl (12.0–15.0 g/dl). DKA was treated according to DKA guidelines. Ketoacidosis remission was achieved two days after rehydration and treatment with continuous intravenous insulin infusion (0.05–0.1 IU/kg). The patient then started on subcutaneous intensive insulin injection therapy, three times daily before meals and once before bedtime. Fasting and post-prandial blood glucose levels decreased to 7-8mmol/L, and 10 –13 mmol/l respectively. On day 4, the patient developed dizziness while he was taking a bath, On examination he was pale and had icterus, however, the vital signs and systemic examination were normal, blood tests revealed a hemolytic anemia as follows: (normal values): Hemoglobin 9 g/dl (12.0–15.0 g/dl), reticulocytes 8.5% (0.5–1.5%), total bilirubin 82 umol/l (0–20 umol/l), unconjugated bilirubin 58 umol/l (3–15 umol/l), By the 7th day, hemoglobin levels had fallen to the lowest value of 8.3, then gradually raised to 10.2 g/dl, 2 weeks later, hemoglobin electrophoresis was normal, Coombs test was negative. G6PD activity was below 300 U/L (reduced activit&lt;600) with two separate measurements. The patient had no bacterial infections and had not ingested haemolytic drugs. Hemolysis ceased spontaneously and hemoglobin increased gradually. Conclusion: G6PD deficiency and diabetes mellitus could aggravate each other, and In patients at risk of G6PD deficiency screening of the enzyme activity should be considered following diabetes decompensation, and in case of G6PD deficiency, it is advisable to correct plasma glucose level gradually to avoid the rapid drop in glucose availability, which may cause hemolysis in these patients.
Intravenous Insulin Resistance in a Critically Ill Patient Secondary to Decreased Peripheral Perfusion
Authors: Umadat Deviani , Arudkumaran Dharscika , Eschler Deirdre Cocks 
Published: May 2021

Abstract
Introduction: Intravenous (IV) insulin infusion is the preferred treatment modality for hyperglycemia in the intensive care unit (ICU) due to its short duration of action and easy titratability. However, administration of IV insulin has challenges. These include frequent monitoring, site infiltration, and high insulin dose requirements with other ICU medications such as epinephrine. There are, however, limited reports demonstrating an elevated insulin requirement due to poor peripheral perfusion. Below illustrates such a case, necessitating a change from peripheral to central IV insulin administration.
Case Presentation: A 50 year old male with well controlled type 2 diabetes and previous aortic valve replacement presented to our facility for prosthetic valve endocarditis complicated by aortic root abscess. He was admitted to the ICU, treated with IV antibiotics, abscess washout and aortic valve replacement. Preoperatively, he was started on IV regular insulin via continuous infusion through a central line. During the pre and intraoperative periods, his hourly IV insulin requirement ranged from 2.4 to 5 units/ hour (hr). His blood glucose (BG) ranged from 107-251mg/dL (n 70-99mg/dL). The patient became hypotensive intraoperatively requiring vasopressor support. Dobutamine and norepinephrine infusions were started via central access and were continued postoperatively at steady rates. Vasopressin was added through central access as the patient failed to meet hemodynamic targets. Postoperatively, the propofol infusion was discontinued and the IV regular insulin infusion was moved to the peripheral line where the propofol had previously been administered. BG increased steadily to a maximum of 402 mg/dL despite an increase in the peripheral IV insulin rate to 152.4 units/hr. The site of the IV insulin drip was changed to another solitary peripheral access without success in decreasing the IV insulin infusion rate. The elevated requirements were deemed secondary to the patient’s lack of peripheral perfusion and should decrease with transition to a central line. A preemptive decrease in insulin drip rate to 10% of the peripheral dose was used to avoid hypoglycemia. The insulin drip was changed to a central access with a rate of 15units/ hr. BG values declined to a range of 140 -180 mg/dL. The patient remained on the multiple vasopressors for hemodynamic support, however, the insulin drip was able to be decreased and ultimately, discontinued.
Conclusion: This case illustrates a unique challenge in the treatment of hyperglycemia with multifactorial shock and our approach to management. Elevated IV insulin requirements persisted despite stability in vasopressor dose, change to a solitary peripheral IV site, and lack of interfering medications in the treatment regimen. This is the first case to demonstrate a relationship between high IV insulin requirements and poor peripheral perfusion.
Role of Octreotide in Sulfonylurea-Induced Hypoglycemia
Authors: Zafar Sheema , Mahali Lakshmi Priyanka , Ahsan Hamza 
Published: May 2021

Abstract
Introduction: The most common adverse effect associated with sulfonylurea ingestion is hypoglycemia. Sulfonylureas have very narrow therapeutic indices with a prolonged half-life in End-Stage renal Disease (ESRD). As per literature review, insulin and oral sulfonylureas are responsible for 13.9% and 10.7% of emergency hospitalizations respectively. It is, however, not surprising that intentional or unintentional overdose with these agents can lead to prolonged hypoglycemia which can prove to be fatal.
Case Report:76-year-old female presented to the Emergency Department (ED) with complaints of generalized weakness since the past three days. Her past medical history was significant for ESRD, Hypertension and Non-Insulin Dependent Diabetes Mellitus type II (home regimen of glipizide 10 mg daily). On physical exam, she was tachypneic and appeared lethargic. Her neurological exam was intact, and she was oriented to time, place and person. Her labs were significant for BUN of 77 mg/dL (5–20 mg/dL), Creatinine of 9.94 mg/dL (&lt;1.3mg/dL) and blood glucose of 89 mg/dL (70-140mg/dL). Liver and thyroid function tests were normal. Computed Tomography scan of the head was unremarkable. In the ED, she received 5 mg of glipizide after which she became more confused and lethargic. Her blood glucose level was 21mg/dL thus she received seven pushes of intravenous (IV) dextrose (25g each), two doses of intramuscular glucagon (1mg each) and was started on a continuous infusion of dextrose (D10) at 75cc/hour. Her blood glucose levels continued to remain low with a repeat value of 34 mg/dL and her mental status continued to worsen. Labs checked at that time were significant for a C-Peptide level of 22.13ng/ml (1.00–4.00ng/ml) and an insulin level of 43.7uU/ml (&lt;20uU/ml) suggesting it to be sulfonylurea toxicity. Sulfonylurea level could not be checked due to laboratory limitations. She was started on subcutaneous octreotide 30 mcgs every 6 hours as per endocrinology recommendations. Her blood glucose started to improve, and her mental status returned to baseline. Per oral food intake was resumed, she remained euglycemic and octreotide was discontinued.
Conclusion: Octreotide is a synthetic octapeptide analogue of somatostatin which can effectively suppress insulin secretion. Glucose, on the other hand, would stimulate insulin release and cause rebound hypoglycemia. Boyle et al, showed that octreotide was superior to diazoxide and glucose in preventing sulfonylurea-induced hypoglycemia. Therefore, we as clinicians should be able to quickly recognize sulfonylurea toxicity as the cause of hypoglycemia and attempt to administer octreotide as soon as possible. This in turn would help decrease length of hospital stay and avoid the detrimental effects of hypoglycemia like seizures, coma and death especially in older individuals.
SARS-CoV-2 Infection Related Diabetes Mellitus
Authors: Beliard Kara A , Yau Mabel , Wilkes Meredith , Romero Christopher Joseph , Wallach Elizabeth , Rapaport Robert 
Published: May 2021

Abstract
Introduction: SARS-Cov-2 (severe acute respiratory distress syndrome- coronavirus 2) viral infection has a predilection for pancreatic beta cells causing insulin deficiency. Studies from the SARS-CoV outbreak in 2003 highlighted the relationship between SARS-CoV and ACE-2 (angiotensin-converting enzyme 2) receptors in pancreatic islet cells. We describe a pediatric patient who developed Diabetes Mellitus after exposure to the Sars-CoV-2 virus.
Case Report: A previously healthy 13-year-old female of Mexican descent was found to be hyperglycemic at her annual visit. The patient endorsed polyuria and polydipsia for 3 weeks, and weight loss for 3months. 3 months prior to presentation, her mother became ill and tested positive for SARS-CoV-2 by PCR analysis. The patient had no SARS-CoV-2 associated symptoms.
Her exam was notable for a BMI was in the 78%ile for age with no acanthosis nigricans. She had no family history of diabetes or autoimmune disease.
Initial blood glucose was 729 mg/dL, with bicarbonate of 20.6 mEq/L, pH 7.45, and anion gap of 14 mEq/L. Large ketones were present in the urine. Her concomitant C-peptide level of 1.0 ng/ml was low in the setting of hyperglycemia. Her HbA1c was 14.3%. Diabetes-related autoantibodies, celiac, and thyroid antibodies were negative. Her Sars-CoV-2 antibody titer was positive with a negative PCR.
The patient was treated with a basal-bolus regimen of subcutaneous insulin at a maximal total daily dose of 0.7 u/kg/day. 5 weeks later, her insulin requirement and HbA1C were both lower; at 0.5 u/kg/day and 9.3% respectively.
Discussion: This patient’s symptoms of hyperglycemia started shortly after her exposure to the SARS-CoV-2 virus. She had no features consistent with Type 2 DM. She similarly had no serological evidence of DM related autoimmunity, thus being different from reports of new-onset Type 1 DM with confirmed autoimmunity presenting during the Sars-CoV-2 pandemic. Although Type 1B DM without evidence of humoral islet autoimmunity and monogenic DM could not be fully excluded, we postulate that the patient developed SARS-CoV-2 associated DM given her time course and documented exposure to SARS –CoV-2 with the presence of SARS-CoV antibodies. One similar case has previously been reported By Holstein et al. 1 While we share the lack of direct evidence of causation, we postulate that more patients with similar presentations will be reported during the current pandemic.
Reference: 1.Hollstein, T et al. Autoantibody-negative insulin-dependent diabetes mellitus after SARS-CoV-2 infection: a case report [published online ahead of print, 2020 Sep 2]. Nat Metab. 2020;10.1038/s42255-020-00281-8. doi:10.1038/s42255-020-00281-8
Selecting Patients at Risk of Developing DKA on Gliflozins
Authors: Maletkovic Jelena 
Published: May 2021

Abstract
Background: Since the introduction of gliflozins less than a decade ago we have witnessed how these medications are changing our approach to treating patients with type 2 diabetes mellitus. While recognizing tremendous benefits from these medication we are aware of potentially fatal risks. We present three cases of diabetic keto-acidosis in patients with type 2 diabetes mellitus and no prior history of diabetic emergencies while on SGLT2 inhibitors. Cases: A 58 year old woman with history of type 2 diabetes mellitus for 8 years and history of bulimia was treated with an SGLT2 Inhibitor for 12 months with stable control of diabetes mellitus. After an episode of very low calorie diet for 30 hours the patient was admitted to ICU with findings of diabetic ketoacidosis. She was critically ill but responded to treatment and needed only oral medication for future diabetic control. The second patient was a 49 year old man with type 2 diabetes mellitus and obesity who has been treated with oral antidiabetics for 7 years prior to requiring MDI insulin regimen in the past 3 years. The patient was well controlled in the past one year since introduction of SGLT2 inhibitors to his therapy. After a 2 day episode of eating carb heavy diet and using about 20% of prescribed insulin the patient developed DKA and was admitted to ICU where he needed to be intubated but improved and stabilized over the next few days. The third patient was a 52 year old man with history of type 2 DM for 13 years, well controlled in the past 3 years since SGLT2Is were added to his oral antidiabetic therapy. After one night of binge drinking alcohol with poor calorie intake the patient was diagnosed with DKA. After successful treatment this patient remains on oral antidiabetic medications. Conclusion: SGLT2Is have been prescribed in our clinic with great success since the first introduction of these medications. These are the only three patients who developed DKA on SGLT2 inhibitors in the past 6 years to our knowledge. All three patient had risk factors that were recognized but likely not enough emphasized. The first patient developed DKA during a “starvation phase” of eating disorder, the second one during a short episode of non-compliance with insulin while on a high carb diet and the third one after one episode of binging on alcoholic drinks. When prescribing SGLT2 inhibitors we are turning some patients with classical type 2 DM into ketosis prone diabetics. Eating disorders, extremely low or heavy carbohydrate intake, alcohol consumption and non-compliance with other antidiabetic medications should be subjects that we discuss when starting gliflozins in order to avoid significant risks. While using impressive benefits of these medications we should be aware of their side effects and recognize those that are at risk of serious side effects.
Sudden Onset Diplopia Associated With Better Diabetes Control - Too Fast Is Not Too Good
Authors: Vemparala Pranathi , Bekele Yididiya , Krishnamurthy Mahesh 
Published: May 2021

Abstract
Introduction: Treatment-induced neuropathy of diabetes (TIND) presenting as a new-onset peripheral neuropathy usually associated with autonomic dysfunction has been documented in literature. It can occur when there is a drop of more than 2% in HbA1C in a three month period. Worsening of existing peripheral neuropathy and retinopathy has also been observed suggesting a common pathophysiological mechanism. However, the onset of a cranial neuropathy temporally linked to intensified glycemic control has not been well reported.
Case Report: A 32-year-old male patient presented to the emergency department with double vision, preceded by headache, and increased burning in his feet. No other neurologic symptoms were reported. Past medical history was significant for poorly controlled, labile type 1 diabetes mellitus. His home medications included gabapentin for peripheral neuropathy, long-acting and short-acting meal time insulin regimen. Physical examination was unremarkable except for a neurological exam which showed pupil-sparing third cranial nerve palsy. CT angiography of the head and neck revealed no acute ischemia, hemodynamically significant stenosis, aneurysm or dissection. MRI of the brain also showed no abnormality. Review of his prior HbA1c values showed a decrease of 3.6 % (14% to 10.4%) over 3 months. The patient was diagnosed with TIND presenting with simultaneous worsening of peripheral neuropathy and new onset right oculomotor nerve palsy. He was discharged on reduced doses of insulin, targeting a gradual decline in HbA1c after initial stabilization. The patient was also asked to liberalize his diet and was given an eye patch. While his peripheral neuropathy improved, there was not much improvement in his diplopia at a two week follow-up visit.
Discussion: Our patient presented with worsening of peripheral neuropathy and pupil sparing oculomotor palsy. Secondary causes including CVA and aneurysm were excluded with brain imaging. Diabetes related microvascular disease presenting with pupil sparing oculomotor palsy is commonly seen in patients older than 50 years of age with uncontrolled diabetes and other vascular risk factors like hypertension and dyslipidemia. Absence of hypertension and hyperlipidemia, sudden onset of presentation and an intense control of DM as evidenced by rapid decline of A1C make TIND the likely cause for his presentation. The paradoxical worsening of his peripheral neuropathy also supports the diagnosis of TIND. Through this case, we highlight the importance of recognizing this entity as management differs significantly. Quality improvement metrics for practitioners in various institutions often include HbA1c target ranges in diabetic patients. Our case highlights the issues associated with rapid corrections of HbA1c and thus we advocate for a gradual decrease of 2 % every 3 months till target goals are reached.
The Mystery of Acidosis
Authors: Naqvi Syeda , Prasad Apurwa , Syed Sabah 
Published: May 2021

Abstract
We present a case of 30-year-old female with past medical history of Type 2 DM, Thyroid nodule and asymptomatic cholelithiasis who presented to ED with abdominal pain, vomiting and sinus tachycardia of 120’s for past one day. She had generalized abdominal pain, not relieved by pain killers. Her lab test includes normal blood count, glucose 150mg/dl, anion gap of 20, metabolic acidosis. Her ultrasound abdomen showed cholelithiasis with no biliary sludge formation. Given her acidosis and severe abdominal pain she was started on Zosyn and underwent cholecystectomy. Her abdominal pain and sinus tachycardia did not resolve till day 3 of admission. Urine was positive for ketones. On chart review, it was found that she started taking sodium glucose transporter 2 inhibitor (SGLT-2 inhibitor), Canagliflozin. She was given IV fluids and insulin. She improved and her tachycardia resolved. Euglycemic acidosis is a rare phenomenon but frequently misdiagnosed. This case emphasizes on importance of side effects of oral glucose lowering agents. SGLT-2 inhibitors can cause lipolysis and ketosis while maintaining euglycemia. Prompt clinical judgement is needed to prevent misdiagnosis. Also, patients should be educated about aggravating factors like stress, dehydration or other severe illnesses.