Background and Purpose- The purpose of these guidelines is to provide an up-to-date comprehensive set of recommendations in a single document for clinicians caring for adult patients with acute arterial ischemic stroke. The intended audiences are prehospital care providers, physicians, allied health professionals, and hospital administrators. These guidelines supersede the 2013 Acute Ischemic Stroke (AIS) Guidelines and are an update of the 2018 AIS Guidelines. Methods- Members of the writing group were appointed by the American Heart Association (AHA) Stroke Council's Scientific Statements Oversight Committee, representing various areas of medical expertise. Members were not allowed to participate in discussions or to vote on topics relevant to their relations with industry. An update of the 2013 AIS Guidelines was originally published in January 2018. This guideline was approved by the AHA Science Advisory and Coordinating Committee and the AHA Executive Committee. In April 2018, a revision to these guidelines, deleting some recommendations, was published online by the AHA. The writing group was asked review the original document and revise if appropriate. In June 2018, the writing group submitted a document with minor changes and with inclusion of important newly published randomized controlled trials with >100 participants and clinical outcomes at least 90 days after AIS. The document was sent to 14 peer reviewers. The writing group evaluated the peer reviewers' comments and revised when appropriate. The current final document was approved by all members of the writing group except when relationships with industry precluded members from voting and by the governing bodies of the AHA. These guidelines use the American College of Cardiology/AHA 2015 Class of Recommendations and Level of Evidence and the new AHA guidelines format. Results- These guidelines detail prehospital care, urgent and emergency evaluation and treatment with intravenous and intra-arterial therapies, and in-hospital management, including secondary prevention measures that are appropriately instituted within the first 2 weeks. The guidelines support the overarching concept of stroke systems of care in both the prehospital and hospital settings. Conclusions- These guidelines provide general recommendations based on the currently available evidence to guide clinicians caring for adult patients with acute arterial ischemic stroke. In many instances, however, only limited data exist demonstrating the urgent need for continued research on treatment of acute ischemic stroke.

Guidelines for the Early Management of Patients With Acute Ischemic Stroke: 2019 Update to the 2018 Guidelines for the Early Management of Acute Ischemic Stroke: A Guideline for Healthcare Professionals From the American Heart Association/American Stroke Association.

BackgroundThe effect of endovascular thrombectomy that is performed more than 6 hours after the onset of ischemic stroke is uncertain. Patients with a clinical deficit that is disproportionately severe relative to the infarct volume may benefit from late thrombectomy. MethodsWe enrolled patients with occlusion of the intracranial internal carotid artery or proximal middle cerebral artery who had last been known to be well 6 to 24 hours earlier and who had a mismatch between the severity of the clinical deficit and the infarct volume, with mismatch criteria defined according to age (<80 years or ≥80 years). Patients were randomly assigned to thrombectomy plus standard care (the thrombectomy group) or to standard care alone (the control group). The coprimary end points were the mean score for disability on the utility-weighted modified Rankin scale (which ranges from 0 [death] to 10 [no symptoms or disability]) and the rate of functional independence (a score of 0, 1, or 2 on the modified Rankin scale, whic...

https://www.nejm.org/doi/pdf/10.1056/NEJMoa1706442

Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct.

Based on the proposed criteria, definite PJI exists when:

(1)

There is a sinus tract communicating with the prosthesis; or




(2)

A pathogen is isolated by culture from at least two separate tissue or fluid samples obtained from the affected prosthetic joint; or




(3)

Four of the following six criteria exist:

(a)

Elevated serum erythrocyte sedimentation rate (ESR) and serum C-reactive protein (CRP) concentration,




(b)

Elevated synovial leukocyte count,




(c)

Elevated synovial neutrophil percentage (PMN%),




(d)

Presence of purulence in the affected joint,




(e)

Isolation of a microorganism in one culture of periprosthetic tissue or fluid, or




(f)

Greater than five neutrophils per high-power field in five high-power fields observed from histologic analysis of periprosthetic tissue at ×400 magnification.













PJI may be present if fewer than four of these criteria are met.

New definition for periprosthetic joint infection: from the Workgroup of the Musculoskeletal Infection Society.

Prosthetic joint infection (PJI) is a tremendous burden for individual patients as well as the global health care industry. While a small minority of joint arthroplasties will become infected, appropriate recognition and management are critical to preserve or restore adequate function and prevent excess morbidity. In this review, we describe the reported risk factors for and clinical manifestations of PJI. We discuss the pathogenesis of PJI and the numerous microorganisms that can cause this devastating infection. The recently proposed consensus definitions of PJI and approaches to accurate diagnosis are reviewed in detail. An overview of the treatment and prevention of this challenging condition is provided.

/pdf/prosthetic-joint-infection-20eesbrxfa.pdf

Prosthetic Joint Infection

Copyright © 2017 Massachusetts Medical Society. BACKGROUND The effect of endovascular thrombectomy that is performed more than 6 hours after the onset of ischemic stroke is uncertain. Patients with a clinical deficit that is disproportionately severe relative to the infarct volume may benefit from late thrombectomy. METHODS We enrolled patients with occlusion of the intracranial internal carotid artery or proximal middle cerebral artery who had last been known to be well 6 to 24 hours earlier and who had a mismatch between the severity of the clinical deficit and the infarct volume, with mismatch criteria defined according to age (<80 years or ≥80 years). Patients were randomly assigned to thrombectomy plus standard care (the thrombectomy group) or to standard care alone (the control group). The coprimary end points were the mean score for disability on the utility-weighted modified Rankin scale (which ranges from 0 [death] to 10 [no symptoms or disability]) and the rate of functional independence (a score of 0, 1, or 2 on the modified Rankin scale, which ranges from 0 to 6, with higher scores indicating more severe disability) at 90 days. RESULTS A total of 206 patients were enrolled; 107 were assigned to the thrombectomy group and 99 to the control group. At 31 months, enrollment in the trial was stopped because of the results of a prespecified interim analysis. The mean score on the utility-weighted modified Rankin scale at 90 days was 5.5 in the thrombectomy group as compared with 3.4 in the control group (adjusted difference [Bayesian analysis], 2.0 points; 95% credible interval, 1.1 to 3.0; posterior probability of superiority, >0.999), and the rate of functional independence at 90 days was 49% in the thrombectomy group as compared with 13% in the control group (adjusted difference, 33 percentage points; 95% credible interval, 24 to 44; posterior probability of superiority, >0.999). The rate of symptomatic intracranial hemorrhage did not differ significantly between the two groups (6% in the thrombectomy group and 3% in the control group, P = 0.50), nor did 90-day mortality (19% and 18%, respectively; P = 1.00). CONCLUSIONS Among patients with acute stroke who had last been known to be well 6 to 24 hours earlier and who had a mismatch between clinical deficit and infarct, outcomes for disability at 90 days were better with thrombectomy plus standard care than with standard care alone. (Funded by Stryker Neurovascular; DAWN ClinicalTrials.gov number, NCT02142283.) A BS TR AC T Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct

Thrombectomy 6 to 24 Hours after Stroke with a Mismatch between Deficit and Infarct

/pdf/annular-rupture-during-transcatheter-aortic-valve-2upea1mptb.pdf

Annular rupture during transcatheter aortic valve replacement: novel treatment with amplatzer vascular plugs

Previous studies show that total knee replacement (TKR) patients have difficulty performing certain tasks involving deep knee flexion which are part of activities of daily living (ADL). Muslims’ lifestyles heavily depend on the ability to fully flex the knee, and many daily activities, such as praying, social encounters (attending the Sheikh’s majlis), dining or even using the hole bathroom, are carried out on the ground. The LPS Flex implant has been designed to accommodate this by giving up to 165 degrees of flexion. One-thousand and thirty-two (1032) TKRs were performed on patients diagnosed with osteoarthritis using the LPS Flex mobile bearing implant over a five year period with a minimum of 1 year post-operative follow up. The results were then compared to a series obtained from the Zimmer Feedback database which is managed independently by the Audit and Research Office, Department of Orthopaedic and Trauma Surgery, University of Dundee, Dundee, Scotland, United Kingdom. 44% of pre-op cases had full flexion as per our set criteria. There were no apparent differences in patello-femoral pain levels, complications or Knee Society score despite the fact that our patients had, on average, an increase in maximum flexion along with an increase in functional ability. The knee score failed to assess this improved functionality of patients who had full flexion; a new diagnostic method is therefore needed. The results indicate that the implant allows patients to maintain a high degree of flexion and function post-operatively, with few complications.

Importance of Full Flexion After Total Knee Replacement in Muslims' Daily Lifestyle

A 35-year-old male who underwent surgical closure of an aortopulmonary window (APW) defect at 6 weeks of age, presented with increasing dyspnea on exertion, and recurrent episodes of symptomatic atrial arrhythmias. Echocardiography suggested left to right shunting at the level of the pulmonary artery (PA) (Video S1). Cardiac computed tomography confirmed the presence of an aortopulmonary fistula (Figure 1). A cardiac catheterization revealed a PA pressure of 48mmHg, amean pulmonarywedge pressure of 14mmHg, pulmonary vascular resistance of 2.3 wood units, and a shunt fraction (QP/QS) of 2.3. Intracardiac echocardiography (ICE) confirmed the presence of a

Transcatheter closure of a residual aortopulmonary window defect.

CD163 is a scavenger receptor expressed on innate immune cell populations which can be shed from the plasma membrane via the metalloprotease ADAM17 to generate a soluble peptide with lympho-inhibitory properties. The purpose of this study was to investigate CD163 as a possible effector of stroke-induced adaptive immune system suppression. Liquid biopsies were collected from ischemic stroke patients (n=39), neurologically asymptomatic controls (n=20), and stroke mimics (n=20) within 24 hours of symptom onset. Peripheral blood ADAM17 activity and soluble CD163 levels were elevated in stroke patients relative to non-stroke control groups, and negatively associated with post-stroke lymphocyte counts. Subsequent in vitro experiments suggested that this stroke-induced elevation in circulating soluble CD163 likely originates from activated monocytic cells, as serum from stroke patients stimulated ADAM17-dependant CD163 shedding from healthy donor-derived monocytes. Additional in vitro experiments demonstrated that stroke-induced elevations in circulating soluble CD163 can elicit direct suppressive effects on the adaptive immune system, as serum from stroke patients inhibited the proliferation of healthy donor-derived lymphocytes, an effect which was attenuated following serum CD163 depletion. Collectively, these observations provide novel evidence that the innate immune system employs protective mechanisms aimed at mitigating the risk of post-stroke autoimmune complications driven by adaptive immune system overactivation, and that CD163 is key mediator of this phenomenon.

/pdf/monocyte-lymphocyte-cross-communication-via-soluble-cd163-2zldow8svl.pdf

Monocyte-Lymphocyte Cross-Communication Via Soluble CD163 Directly Links Innate Immune System Activation And Adaptive Immune System Suppression Following Ischemic Stroke

Minimally invasive transcatheter closure using Amplatzer occluders have been used to treat myocardial and aortic fistulas following surgical procedures. We present images demonstrating the use of an Amplatzer plug to treat a left ventricular (LV) pseudoaneurysm following a surgical procedure in which an LV vent was inserted. A 72-year old female with severe tricuspid regurgitation, history of patent foramen ovale closure, and pacemaker implantation was evaluated for recurrent heart failure and constrictive pericarditis and underwent a pericardiectomy, tricuspid valve ring repair, and bypass grafting of the right coronary artery. During cardiopulmonary bypass, a 15-French DLP vent cannula (Medtronic, Minneapolis, MN) was advanced into the LV via the right superior pulmonary vein. After a

Abdul R Tarabishy

Papers

Annular rupture during transcatheter aortic valve replacement: novel treatment with amplatzer vascular plugs

Importance of Full Flexion After Total Knee Replacement in Muslims' Daily Lifestyle

Transcatheter closure of a residual aortopulmonary window defect.

Monocyte-Lymphocyte Cross-Communication Via Soluble CD163 Directly Links Innate Immune System Activation And Adaptive Immune System Suppression Following Ischemic Stroke

Percutaneous closure of left ventricular pseudoaneurysm caused by a central venting cannula.