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Traumatic elbow instability is a difficult condition to manage. Many surgeons consider the elbow a perplexing black box and evaluating damaged structures in the setting of pain and swelling a diagnostic challenge. Injury most commonly occurs from a fall onto an outstretched hand but also results from elbow dislocation, direct trauma, and sporting activities. The injury can initiate on the medial or lateral side, depending on forearm position at the time of injury, and usually follows a predictable pattern, with progressive instability caused by soft-tissue disruption and fractures of the medial or lateral column. Primary medial instability, lateral instability, and 
combined injury patterns have been described and discussed. Simple elbow dislocations and certain fractures can be managed nonsurgically, whereas complex patterns of instability and fracture-dislocations routinely require surgery. Stiffness and nerve injury are the most common complications and occur from both surgical and nonsurgical management. This chapter describes the diagnosis and management of traumatic elbow instability and the management of its sequela.Shoulder arthroplasty was first introduced through the developments of Dr. Charles Neer and over the past decade has seen several advancements. Improved recognition and training have heightened the awareness of arthroplasty as a treatment alternative both for surgeons and patients. The addition of reverse shoulder arthroplasty has been the driving force behind the explosive growth of arthroplasty and is now performed more often than anatomic shoulder arthroplasty. Although revision shoulder arthroplasty is primarily of interest to the subspecialist, it is a skill sought by the general orthopaedic surgeon. It is important for the orthopaedic surgeon to be knowledgeable about the planning, necessary skills, and management of basic shoulder arthroplasty.Glenohumeral instability is one of the most common conditions of the upper extremity, especially in athletes and active individuals. Over the past two decades, there has been a transformation of surgical treatment from traditionally open repair/reconstruction to arthroscopic management. This has especially been true with management of both anterior and posterior instability without significant bone loss. In this setting, and in certain patient populations (eg, contact/collision athletes), arthroscopic treatment may not be sufficient. Therefore, open techniques, such as coracoid bone transfer, also occupy an important role in management of glenohumeral instability. The goal of this review is to provide technical "pearls" in management of glenohumeral instability. Specifically, the review will highlight treatments such as arthroscopic anterior and posterior instability repair, posterior glenoid bone augmentation, and open coracoid transfer (Latarjet) for anterior instability with bone loss. We will also review management of complications related to coracoid transfer.Anterior glenohumeral instability remains a common clinical problem in the athletic and working patient populations, and further, recurrence rates following stabilization surgery continue to be problematic. Over the past 5 years, there have been substantial improvements in the understanding of anterior shoulder instability. To better counsel and treat patients, it is imperative for surgeons to have a comprehensive understanding of the epidemiology of shoulder instability, the anatomy of the glenohumeral joint particularly as it relates to glenoid and humeral head bone loss, surgical indications, and surgical techniques. These critical topics are summarized in an effort to provide a complete guide to managing anterior shoulder instability in 2020.

To define, characterize, and classify hyperreflectivity on optical coherence tomography and report its prevalence in macular telangiectasia Type 2.

In a primary cross-sectional analysis, multimodal imaging data were retrospectively analyzed. The definition of hyperreflectivity and neovascularization on optical coherence tomography followed optical coherence tomography angiography-based criteria. Eyes were graded for the presence of hyperreflectivity and neovascularization and further categorized into three classes based on position and extent of hyperreflectivity. In a secondary analysis, eyes were reviewed for ≥24 months using optical coherence tomography imaging.

Three hundred and twenty-two eyes from 161 patients were analyzed in the cross-sectional analysis. Hyperreflectivity was found in 177 (55%) and neovascular membranes in 49 (15%) eyes. Hyperreflectivity correlated significantly with parameters indicative of disease progression. In the longitudinal analysis, 206 eyes from 103 patients were reviewed over a mean of 35.6 months. 17/86 eyes (20%) showed a de novo development of hyperreflectivity. 8/29 eyes (28%) with preexistent intraretinal hyperreflectivity developed outer retinal hyperreflectivity. A high proportion of eyes with outer retinal hyperreflectivity (17/52 [33%]) developed neovascular membranes.

Hyperreflectivity represents a common finding in macular telangiectasia Type 2 but lacks a uniform definition. PT2385 price We propose a hyperreflectivity grading scale that may help to estimate disease progression and identify eyes at risk for developing neovascular membranes.

Hyperreflectivity represents a common finding in macular telangiectasia Type 2 but lacks a uniform definition. We propose a hyperreflectivity grading scale that may help to estimate disease progression and identify eyes at risk for developing neovascular membranes.

To quantify retinal vasculature changes in Stargardt disease1 (STGD1) with volume-rendered optical coherence tomography angiography.

Optical coherence tomography angiography volumes from healthy subjects and two subgroups of patients with STGD1 with the presence/absence of definitely decreased autofluorescence areas were compared. Optical coherence tomography angiography vessel surface area and vessel volume were measured in central zones (Z) of 1-, 2-, and 3-mm diameter.

Twenty nine eyes of 15 patients with STGD1 (20/9 eyes with/without definitely decreased autofluorescence) and 30 eyes of 15 controls contributed data. An enlarged foveal avascular zone was found in patients with STGD1 without and even more with definitely decreased autofluorescence associated with a vessel rarefication in central and also paracentral zones with unnoticeable autofluorescence. Vessel surface area and vessel volume were reduced in both STGD1 subgroups for all zones (P < 0.0001). Stargardt disease 1 eyes when compared to without definitely decreased autofluorescence showed reduced vessel surface area and vessel volume in Z2+3 (both P < 0.