Does central sensitization correlate with two-year postoperative functional outcome scores following hip arthroscopy?

Background: Central sensitization (CS) involves amplified central nervous system (CNS) signaling and several biochemical changes which lead to pain hypersensitivity. Data on the effects of CS are limited in orthopaedics and has been associated with reported levels of postoperative pain after hip arthroscopy.

Methods: Patients over the age of 18 who underwent hip arthroscopy with preoperative as well as 2-year postoperative functional outcome scores were identified through the Multicenter Arthroscopic Study of the Hip (MASH) database.

Use of Telemedicine Among Hand Surgeons and Their Patients.

Purpose: Initially designed to address geographic obstacles to patient care, reliance on telemedicine rapidly increased during the coronavirus pandemic. The purpose of this study was to analyze the proficiency of computer and mobile device usage among a cohort of surgeons and their patients who either used telemedicine or had in-person visits.

Methods: We retrospectively identified patients who had an outpatient telemedicine visit (T group), or in-person visit (NT group) with a hand and wrist orthopedic surgeon, between March 2020 and July 2020.

Stability of trusses by graphic statics.

This paper presents a graphical method for determining the linearized stiffness and stability of prestressed trusses consisting of rigid bars connected at pinned joints and which possess kinematic freedoms. Key to the construction are the rectangular areas which combine the reciprocal form and force diagrams in the unified Maxwell-Minkowski diagram. The area of each such rectangle is the product of the bar tension and the bar length, and this corresponds to the rotational stiffness of the bar that arises due to the axial force that it carries.

Controversies and unresolved issues in antiphospholipid syndrome pathogenesis and management.

While much is understood concerning the clinical features of patients with antiphospholipid syndrome (APS), many issues remain. The proper designation of patients with "definite" APS and the correct categorization of patients by both laboratory and clinical features are matters of ongoing debate. Recent proposals have identified new subsets of patients who have many typical features of APS but either do not fit the criteria for a "definite" diagnosis or have initially negative laboratory tests for antiphospholipid antibodies.

Treatment options for patients who have antiphospholipid syndromes.

The antiphospholipid thrombosis syndrome, associated with anticardiolipin (aCL) or subgroup antibodies, can be divided into one of six subgroups (I-VI). There is little overlap (about 10% or less) between these subtypes, and patients usually conveniently fit into only one of these clinical types. Although there appears to be no correlation with the type, or titer, of aCL antibody and type of syndrome, the subclassification of thrombosis and aCL antibody patients into these groups is important from the therapy standpoint.

The clinical spectrum of antiphospholipid syndrome.

Antiphospholipid syndrome (APS) is a disorder characterized by a wide variety of clinical manifestations. Virtually any organ system or tissue may be affected by the consequences of large- or small-vessel thrombosis. There is a broad spectrum of disease among individuals with antiphospholipid antibodies (aPL).

Thrombolytic therapy: current clinical practice.

Thrombolytic therapy is an essential tool in the array of therapies designed to reopen arteries and veins occluded with thrombus. As the use of thrombolytic agents has entered mainstream practice, their application has expanded to include a wide variety of indications and settings. Thrombolytic agents are used in patients who have thrombosis of coronary arteries, precerebral and cerebral arteries, the aorta, iliac and mesenteric arteries, and peripheral arteries.

Thrombolytic therapy: clinical applications.

The therapeutic use of thrombolytic agents is the result of the increasing understanding of the pathophysiologic mechanisms underlying normal and deranged thrombosis and fibrinolysis. Plasminogen activators capable of increasing the production of plasmin exhibit considerable efficacy in the treatment of a variety of arterial and venous thrombotic disorders. The ideal thrombolytic agent has not been developed, but the desired clinical result of rapid opening of the thrombosed vessel without reocclusion, without activation of systemic fibrinogenolysis, and without a risk of hemorrhage are defined.

Thrombolytic therapy.

The therapeutic use of thrombolytic agents is the natural result of the increasing understanding of the pathophysiologic mechanisms underlying normal and deranged thrombosis and fibrinolysis. Plasminogen activators capable of increasing the production of plasmin exhibit considerable efficacy in the treatment of a variety of arterial and venous thrombotic disorders. The ideal thrombolytic agent has yet to be developed but the desired clinical result of rapid opening of the thrombosed vessel without reocclusion, without activation of systemic fibrinogenolysis, and without a risk of hemorrhage is well defined.

Iron deficiency in pregnancy, obstetrics, and gynecology.

Iron deficiency remains a major health risk in the United States, despite the apparent availability of a high-quality diet. In the United States, at least 7.8 million adolescent girls and premenopausal women are iron-deficient.

Treatment of hereditary and acquired thrombophilic disorders.

The treatment of hereditary and acquired thrombophilic disorders is based on an understanding of the disease pathophysiology, prevalence, associated morbidity and mortality, and available therapeutic options. Genetic mutations are identified that result in activated protein C (APC) resistance and hyperhomocyst(e)inemia. The underlying etiologies are less well-defined; however, the disorders of factor XII deficiency, dysfibrinogenemia, Wien-Penzing platelet defect, and sticky platelet syndrome (SPS) are treatable inherited thrombophilias.

Antiphospholipid syndrome and thrombosis.

Antiphospholipid antibodies [such as anticardiolipin antibodies (ACLA)] are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The most common thrombotic events associated with ACLA are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome) or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome).

Diagnosis of deep venous thrombosis and pulmonary embolism.

Diagnostic evaluation in the patient with suspected deep vein thrombosis (DVT) and pulmonary embolism (PE) includes a clear correlation between clinical probability, test selection and test interpretation. Real-time B-mode ultrasound with color Doppler remains the imaging technique of choice in suspected DVT. The ventilation/perfusion (V/Q) lung scan is the preferred diagnostic modality in suspected PE.

Deep vein thrombosis. Diagnosis and management.

In at least 50% of patients with suspected deep vein thrombosis, the diagnosis is not confirmed by objective testing. The addition of impedance plethysmography and real-time B-mode ultrasound with color-enhanced Doppler imaging to the available diagnostic modalities has altered the approach to clinical evaluation. Pharmacologic treatment has evolved to place emphasis on the use of subcutaneous heparins of greater efficacy and the reduction of hemorrhagic risk with the use of the INR system when warfarin is recommended for long-term therapy.

The antiphospholipid and thrombosis syndromes.

Anticardiolipin antibodies and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories have been advanced. The commonest thrombotic events associated with anticardiolipin antibodies are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome).

Antiphospholipid and thrombosis syndromes.

ACAs and the lupus anticoagulant are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism or mechanisms whereby antiphospholipid antibodies alter hemostasis to induce a hypercoagulable state remain unclear, several theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACAs are DVT and PE (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), cerebrovascular or retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome).

Antiphospholipid antibodies in coronary artery disease: a review.

APAs present a clinical problem that is now recognized to be a significant causative factor of both fatal and nonfatal myocardial infarction as well as other coronary syndromes. Similar to the thrombotic complications of APAs in the cerebrovascular system, the result can be life-threatening or fatal. Correct diagnosis requires a high index of suspicion, especially in patients with known prior thrombotic events and in those who present with myocardial ischemia or infarction without underlying risk factors and at a young age.

Anticardiolipin antibodies and thrombosis.

Anticardiolipin antibodies (ACLAs) are strongly associated with thrombosis and appear to be the most common of the acquired blood protein defects causing thrombosis. Although the precise mechanism(s) whereby ACLAs alter hemostasis to induce a hypercoagulable state remain unclear, several theories, as previously discussed, have been advanced. The most common thrombotic events associated with ACLAs are deep vein thrombosis and pulmonary embolus (type I syndrome), coronary or peripheral artery thrombosis (type II syndrome), or cerebrovascular/retinal vessel thrombosis (type III syndrome), and occasionally patients present with mixtures (type IV syndrome).