Sudden Vision Loss During Hemodialysis

Introduction Catheter-related blood stream infections (CRBSIs) are a common and unfortunate consequence of prolonged vascular access in hemodialysis patients. Metastatic infections are feared sequelae of bacteremia, and include endocarditis, osteomyelitis, septic arthritis, epidural abscess, and endophthalmitis.1 The following is a case of Serratia endophthalmitis originating from a tunneled-dialysis catheter. Case Presentation A 47 year-old Caucasian female with a history of end stage renal disease on hemodialysis, Type 2 diabetes mellitus, and hypertension was undergoing her routinely scheduled hemodialysis session when she experienced “flashes of hot pink” in her left eye. The hemodialysis session was terminated, and the patient returned home. When she awoke the next morning she noticed a large black spot obscuring vision in her left eye as well as pain in the affected eye. The patient presented to Wills Eye Emergency Department that day. She denied any recent fevers, chills, pain, or erythema at the catheter site. She did, however, report that her left-sided chest wall tunneled dialysis catheter had been manipulated and tubing had been exchanged the day prior because of concerns that it was clogged. The patient was transferred to Thomas Jefferson University Hospital (TJUH) for further care. Initial vital signs revealed a temperature of 98.6 degrees Fahrenheit, heart rate of 88 beats per minute, respiratory rate of 21 per minute, blood pressure of 160/94 mmHg, and 95% oxygen saturation on room air. Physical exam was significant for a diffusely erythematous left sclera with a hazy cornea and a small hypopion occupying the bottom third of the pupil (Figure 1). Her left pupil was sluggishly reactive to light. The patient’s visual acuity exam of the left eye revealed 20/60 vision (20/20 in right eye). Her left chest wall port site was non-erythematous with no palpable fluctuance or drainage. There was no tenderness to palpation in this area. Cardiac exam revealed a grade II/VI systolic ejection murmur most prominent at the right upper sternal border. There were crackles at both lung bases and bilateral 2+ lower extremity pitting edema to the shins. There were no splinter hemorrhages or other skin changes. The patient’s admission laboratory values were notable for a white blood cell count of 16,200 cells/microliter (normal range 4,000-11,000) with 92% neutrophils (normal range 40-73%) and a hemoglobin of 7.5 g/dl (normal 12.5-15) decreased from a baseline of 9 g/dl. A chest x-ray was normal

To Fib or Not to Fib: Misdiagnosis of Atrial Fibrillation on Telemetry Case Presentation and Root Cause Analysis

Case presentation, current practices of telemetry management, root cause analysis, goals for improvement, proposed intervention and next steps

Squamous Cell Carcinoma Metastatic to the Heart Mimicking ST-Elevation Myocardial Infarction

INTRODUCTION Heart disease remains the leading cause of mortality in the United States, accounting for about one quarter of all deaths in 20131. Acute ischemic heart disease is a major subpopulation of this group, and typically presents with characteristic electrocardiographic (EKG) changes. The most concerning of these findings are ST-elevations, as ST Elevation Myocardial Infarction (STEMI) typically indicates the need for emergent reperfusion therapy because 30-day mortality of untreated STEMI is approximately 10-15% versus 5% in treated cases2. As a result, clinicians are taught to recognize the symptoms and signs of myocardial ischemia and STEMI in order to achieve timely reperfusion either via thrombolytic therapy within 30 minutes or percutaneous coronary intervention within 90 minutes. However, ST-elevations may result from etiologies other than acute ischemia, and can be secondary to other acutely life-threatening pathologies or relatively benign, subacute causes. For example, ventricular aneurysms resulting from prior myocardial infarction and pericarditis can result in ST-elevation on EKG. Intracranial hemorrhage or stress (takotsubo) cardiomyopathy can also present with ST-elevations, theorized to be the result of increased catecholamines. Left ventricular hypertrophy, a sequela of poorly controlled hypertension, can also lead to J point elevations mimicking STEMI3,4. Here we review a case of unusual ST-elevation in a patient with oropharyngeal squamous cell carcinoma metastatic to the heart

Balloon aortic valvuloplasty: Treatment of rapid deployment aortic valve replacement complicated by a paravalvular leak

The Edwards Intuity Elite valve system was designed to facilitate minimally invasive surgery and streamline complex aortic valve replacements and has since gained more popularity. Despite the superior results shown with rapid deployment aortic valve replacement (RDAVR) utilizing this valve system, paravalvular leaks (PVL), as a complication, remains a concern. Currently, there is no universally agreed single treatment option. A 53-year-old male with a history of well-controlled diabetes mellitus and hypertension presented to the emergency room with a 1-month history of angina, syncope on exertion and dyspnea. On further workup, he was found to have severe aortic stenosis in the setting of a bicuspid aortic valve, with non-obstructive coronary artery disease. He proceeded to urgent RDAVR with a 23 mm Edwards Intuity Valve. Six months post-RDAVR he re-presented with dyspnea on exertion and near syncopal episodes. Postoperative transthoracic and transesophageal echocardiography revealed moderate to severe PVL posterior to the prosthetic aortic valve. Balloon valvuloplasty with a 25 mm True Balloon was performed. Resolution of the PVL was confirmed postprocedure both by angiography and echocardiography. The patient was followed for 1 year and remained symptom-free with evidence of mild PVL on surveillance echocardiography. In conclusion, multiple treatment options for RDAVR complicated by PVL exist; however mid to long-term outcome data are lacking. We presented one such case successfully treated with balloon aortic valvuloplasty

Unsuspected pheochromocytoma incidentally found on chest CT

A 51-year-old woman with history of migraine headaches and intermittent nausea, vomiting, palpitations, and diaphoresis presented to the emergency department with hypertensive emergency 1 month after starting a beta blocker for migraine prophylaxis. Contrast-enhanced computed tomography of the chest incidentally revealed a large abdominal mass in the area of the left adrenal gland. Iodine-123 metaiodobenzylguanidine scan imaging showed localized uptake into the left adrenal gland. Along with imaging results, laboratory testing confirmed the diagnosis of pheochromocytoma. The patient was treated with blood pressure control, specifically alpha blockade, and surgical excision of the mass. This case displays a typical clinical presentation of pheochromocytoma coupled with atypical radiographic size and appearance

The Use of Midodrine as an Adjunctive Therapy to Liberate Patients from Intravenous Vasopressors: A Systematic Review and Meta-analysis of Randomized Controlled Studies

Background: Studies evaluating the role of midodrine as an adjunctive therapy to liberate patients with shock from intravenous (IV) vasopressors have yielded mixed results. The aim of our study was to evaluate the efficacy and safety of midodrine as an adjunctive therapy to liberate patients with shock from IV vasopressors. Methods: Electronic searches of the MEDLINE, EMBASE, and Cochrane databases through April 2022 for randomized controlled trials (RCTs) that evaluated the use of midodrine versus control in patients with shock and a low dose of IV vasopressors. The primary outcome was total IV vasopressor time, while the secondary outcomes included time-to-IV vasopressor discontinuation, IV vasopressor restart, intensive care unit (ICU) length of stay (LOS), hospital LOS, and incidence of bradycardia. Results: The final analysis included four RCTs with a total of 314 patients: 158 in the midodrine group and 156 in the control group, with a weighted mean age of 64 years (54.2% men). There was no significant difference in the total IV vasopressor time between the midodrine and control groups (standardized mean difference [SMD] - 0.53; 95% confidence interval [CI] - 1.38 to 0.32, p = 0.22; I2 = 92%). Also, there were no significant differences between the two groups in the time-to-IV vasopressor discontinuation (SMD - 0.05; 95% CI - 0.57 to 0.47, p = 0.09), IV vasopressor restart (19.3 vs. 28.3%; risk ratio [RR] 0.74; 95% 0.25-2.20, p = 0.59), ICU LOS (SMD - 0.49; 95% CI - 1.30 to 0.33, p = 0.24), and hospital LOS (SMD 0.01; 95% CI - 0.27 to 0.29, p = 0.92). However, compared with the control group, the midodrine group had a higher risk of bradycardia (15.3 vs. 2.1% RR 5.56; 95% CI 1.54-20.05, p = 0.01). Conclusions: Among patients with vasopressor-dependent shock, midodrine was not associated with early liberation of vasopressor support or shorter ICU or hospital length of stay. Adding midodrine increased the risk of bradycardia. Further large RCTs are needed to better evaluate the efficacy and safety of midodrine in liberating patients from IV vasopressors