Vocal cord dysfunction and wheezing.

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The "2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes" incorporates new evidence since the "2013 ACCF/AHA Guideline for the Management of ST-Elevation Myocardial Infarction" and the corresponding "2014 AHA/ACC Guideline for the Management of Patients With Non-ST-Elevation Acute Coronary Syndromes" and the "2015 ACC/AHA/SCAI Focused Update on Primary Percutaneous Coronary Intervention for Patients With ST-Elevation Myocardial Infarction." The "2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes" and the "2021 ACC/AHA/SCAI Guideline for Coronary Artery Revascularization" retire and replace, respectively, the "2016 ACC/AHA Guideline Focused Update on Duration of Dual Antiplatelet Therapy in Patients With Coronary Artery Disease."

A comprehensive literature search was conducted from July 2023 to April 2024. Clinical studies, systematic reviews and meta-analyses, and other evidence conducted on human participants were identified that were published in English from MEDLINE (through PubMed), EMBASE, the Cochrane Library, Agency for Healthcare Research and Quality, and other selected databases relevant to this guideline.

Many recommendations from previously published guidelines have been updated with new evidence, and new recommendations have been created when supported by published data.

2025 ACC/AHA/ACEP/NAEMSP/SCAI Guideline for the Management of Patients With Acute Coronary Syndromes: A Report of the American College of Cardiology/American Heart Association Joint Committee on Clinical Practice Guidelines.

Journal of the American College of Cardiology

Autoimmune hepatitis (AIH) is a chronic inflammatory liver disease which, if untreated, often leads to cirrhosis, liver failure and death. The last British Society of Gastroenterology (BSG) guideline for the management of AIH was published in 2011. Since then, our understanding of AIH has advanced in many areas. This update to the previous guideline was commissioned by the BSG and developed by a multidisciplinary group. The aim of this guideline is to review and summarise the current evidence, in order to inform and guide diagnosis and management of patients with AIH and its variant syndromes. The main focus is on AIH in adults, but the guidelines should also be relevant to older children and adolescents.

British Society of Gastroenterology guidelines for diagnosis and management of autoimmune hepatitis.

Acute HIV-1 infection (AHI) is a transient period where the virus causes evident damage to the immune system, including an extensive apoptosis of CD4+ T cells associated with a high level of activation and a major cytokine storm to fight the invading virus. HIV infection establishes persistence by integrating the viral genome into host cell DNA in both replicating and non-replicating forms, effectively hiding from immune surveillance within infected lymphocytes as cellular reservoirs. The measurement of total HIV-1 DNA in peripheral blood mononuclear cells (PBMCs) is a reliable reflection of this reservoir. Initiating treatments during AHI with nucleoside reverse transcriptase inhibitors (NRTIs) and/or integrase strand transfer inhibitors (INSTIs) is essential to alter the dynamics of the global reservoir expansion, and to reduce the establishment of long-lived cellular and tissue reservoirs, while preserving and enhancing specific and non-specific immune responses. Furthermore, some of the patients treated at the AHI stage may become post-treatment controllers and should be informative regarding the mechanism of viral control, so patients treated during AHI are undoubtedly the best candidates to test innovative remission strategies toward a functional cure that could play a pivotal role in long-term HIV control. AHI is characterized by high levels of viral replication, with a significant increase in the risk of HIV transmission. Detecting AHI and initiating early treatment following diagnosis provides a window of opportunity to control the epidemic, particularly in high-risk populations.

Acute HIV-1 Infection: Paradigm and Singularity.

Viruses

Cardiac arrest is the loss of functional cardiac activity; emergency clinicians are integral in the management of this condition.

This paper evaluates key evidence-based updates concerning cardiopulmonary resuscitation (CPR).

Cardiac arrest includes shockable rhythms (i.e., pulseless ventricular tachycardia and ventricular fibrillation) and non-shockable rhythms (i.e., asystole and pulseless electrical activity). The goal of cardiac arrest management is to achieve survival with a good neurologic outcome, in part by restoring systemic perfusion and obtaining return of spontaneous circulation (ROSC), while seeking to diagnose and treat the underlying etiology of the arrest. CPR includes high-quality chest compressions to optimize coronary and cerebral perfusion pressure. Chest compressions should be centered over the mid-sternum, with the compressor's body weight over the middle of the chest. A compression depth of 5-6&#xa0;cm is recommended at a rate of 100-120 compressions per minute, while allowing the chest to fully recoil between each compression. Clinicians should seek to minimize any interruptions in compressions. When performed by bystanders, compression-only CPR may be associated with improved survival to hospital discharge when compared to conventional CPR with ventilations. However, in trained personnel, there is likely no difference with compression-only versus conventional CPR. Mechanical approaches for CPR are not associated with improved patient outcomes, including ROSC or survival with good neurologic function, but mechanical compression devices may be beneficial in select circumstances (e.g., few rescuers available, prolonged arrest/transport). Monitoring of chest compressions is not associated with improved ROSC, survival, or neurologic outcomes, but it can improve guideline adherence. Types of monitoring include real-time feedback, a CPR coach, end tidal CO2 , arterial line monitoring, regional cerebral tissue oxygenation, and point-of-care ultrasound.

An understanding of CPR literature updates can improve the ED care of patients in cardiac arrest.

Emergency medicine updates: Cardiopulmonary resuscitation.

American Journal of Emergency Medicine

To review the key updates in the 2024 KDIGO clinical practice guideline for the evaluation and management of chronic kidney disease (CKD) and highlight the essential role of pharmacists in implementing these recommendations.

The updated guideline introduces significant changes in CKD management, including the use of validated equations for estimating glomerular filtration rate (GFR) for drug dosing, with incorporation of serum cystatin C into GFR estimates for specific patient populations, and an emphasis on a comprehensive approach to delay disease progression. The guideline recommends sodium-glucose cotransporter 2 inhibitor (SGLT2i) therapy for kidney disease with proteinuria, with or without diabetes, renin-angiotensin-aldosterone system inhibitors (RAASi) blood pressure control and proteinuria management, and statins to reduce the risk of atherosclerotic cardiovascular disease. New evidence supports the use of finerenone in patients with type 2 diabetes and CKD, and GLP-1 receptor agonists for their kidney-protective effects. The guidelines also emphasize the importance of nephrotoxin stewardship and prevention of acute kidney injury through patient education on sick day medication management.

Pharmacists play a crucial role in implementing these updated guidelines through comprehensive medication management, nephrotoxin stewardship, drug dosing adjustments, and patient education. Their involvement in interprofessional care teams is essential for optimizing health outcomes in patients with CKD.

KDIGO 2024 clinical practice guideline on evaluation and management of chronic kidney disease: A primer on what pharmacists need to know.

American Journal of Health-system Pharmacy : AJHP

Despite the widespread adoption of lung-protective ventilation strategies, mortality among patients on invasive mechanical ventilation (IMV) remains high. Mechanical power (MP) integrates various variables responsible for ventilator-induced lung injury and has been associated with mortality in patients with acute respiratory distress syndrome (ARDS). However, the impact of MP on intensive care unit (ICU) mortality in the larger group of patients with acute hypoxemic respiratory failure (AHRF) has not been well established, and previous studies have reported inconsistent thresholds for predicting outcomes.

Is high MP (&gt; 17 J/min) within the first 24 hours of IMV, calculated using dynamic driving pressure, associated with ICU mortality in patients with AHRF? Additionally, does a threshold exist below which IMV is considered "safe"?

In this multicenter cohort study, we included adult patients with AHRF who received IMV. Patients were excluded if they received IMV for &gt; 24 hours before inclusion or were on extracorporeal life support. We applied multivariable logistic regression models with inverse probability of treatment weighting and used change-point regression models with restricted cubic splines.

Of the 21,714 patients in our registry, 9,031 (42%) met the inclusion criteria. After adjusting for baseline characteristics, high MP was associated with increased ICU mortality (odds ratio 1.58 [95% CI: 1.44, 1.72]), with a non-linear dose-response relationship. No consistent "safe" MP threshold was identified. High MP was also associated with lower extubation rates and fewer ventilator-free days.

Exposure to high MP within the first 24 hours of IMV was associated with increased ICU mortality in patients with AHRF. The absence of a consistent "safe" threshold suggests that reducing MP at IMV initiation may be a potential strategy to improve outcomes, warranting exploration in clinical trials.

The association between mechanical power within the first 24 hours and ICU mortality in mechanically ventilated adult patients with acute hypoxemic respiratory failure: A registry-based cohort study.

Chest

Clinical practice guidelines recommend initiation of anticoagulation within 2 weeks after stroke with atrial fibrillation. It is unknown whether there is an optimal starting day within the 14-day period that balances the risks of recurrent embolic events against serious hemorrhagic events.

To determine if there is an optimal delay time to initiate treatment with a direct oral anticoagulant after atrial fibrillation-related stroke that minimizes the risk of a composite outcome of ischemic or hemorrhagic events.

This phase 2, pragmatic, response-adaptive randomized clinical trial was conducted between June 2017 and June 2023 at acute care hospitals in Texas and included patients who had a mild to moderate ischemic stroke (minimum lesion diameter of 1.5 cm) with atrial fibrillation and were prescribed a direct oral anticoagulant within 2 weeks from stroke onset.

Within 3 to 4 days after atrial fibrillation-associated ischemic stroke, patients were randomized to a group for treatment start date (group 1 was day 3 or 4 after stoke onset; group 2 was day 6; group 3 was day 10; and group 4 was day 14) with a direct oral anticoagulant for secondary stroke prevention.

The composite primary outcome was an ischemic (stroke or systemic embolism) or hemorrhagic (symptomatic intracranial hemorrhage or major systemic hemorrhage) event observed within 30 days from the index stroke time of onset. Posterior probabilities were used to estimate which timing groups were optimal for treatment initiation and were recalculated at predefined intervals. The randomization allocations were adjusted to favor the groups with higher probabilities.

The trial enrolled and randomized 200 patients (50% were female; the median age was 75 years [IQR, 65-81 years]; 17.5% were Asian, Black, or &gt;1 race; 16.5% were Hispanic; the median National Institutes of Health Stroke Scale score was 6.5 [IQR, 4-14]; and the median lesion diameter was 3.1 cm [IQR, 2.0-4.4 cm]). No ischemic events were observed for group 1, 3 events were observed for group 2, 2 events were observed for group 3, and 2 events were observed for group 4. One hemorrhagic event was observed for group 1, 1 event was observed for group 2, 1 event was observed for group 3, and 0 events were observed for group 4. Group 1 had a posterior probability of 0.41 for being the optimal day for treatment initiation and it was 0.26 for group 2, 0.17 for group 3, and 0.15 for group 4. The use of response-adaptive randomization was feasible and favored groups with earlier initiation times for use of a direct oral anticoagulant.

A clearly superior day to initiate use of a direct oral anticoagulant for secondary stroke prevention in patients with atrial fibrillation was not identified, but the evidence suggests that initiating use of a direct oral anticoagulant earlier is better than at later times within the first 2 weeks after stroke onset.

ClinicalTrials.gov Identifier: NCT03021928.

Optimal Delay Time to Initiate Anticoagulation After Ischemic Stroke in Atrial Fibrillation: A Pragmatic, Response-Adaptive Randomized Clinical Trial.

JAMA Neurology

Accurate measurements of the platelet count are necessary to diagnose thrombocytosis or thrombocytopenia correctly, gauge the severity of the clinical risk and identify the most appropriate therapeutic intervention. Despite increased diagnostic accuracy with the electronic counters, it is still unsatisfactory in rare situations. Conditions causing spurious thrombocytopenia include the following. 1) Pre-analytical errors, such as difficult venipunctures, over-/under-filling of blood collection tubes, insufficient mixing of blood with the anticoagulant (EDTA), which may cause fibrin formation; 2) EDTA-induced, temperature- and time-dependent, antibody-mediated in vitro platelet agglutination, with consequent reduction in the number of single platelets in the sample; the condition, referred to as Pseudothrombocytopenia, is benign and does not need follow-up or medical interventions; the use of alternative in vitro anticoagulants does not prevent agglutinates formation in all samples; accurate platelet counts could be obtained by testing EDTAsamples immediately after blood collection. 3) EDTA-induced in vitro platelet adherence to leukocytes (Platelet Satellitism), caused by bridging IgG antibodies binding to GPIIb-IIIa on platelets and the Fc receptor-III on leukocytes; occasionally, leukocytes may phagocytose platelets and/or form platelets/leukocytes clumps. 4) Presence of large/giant platelets (commonly from patients with congenital or acquired thrombocytopenia) that are not recognized as such by electronic counters, which distinguish platelets from other cells based on their smaller size. 5) Blood from patients with type 2B von Willebrand Disease, which may display large/giant platelets and platelet agglutinates. All the above conditions are easily identifiable by microscopic examination of anticoagulated peripheral blood smears, which is an indispensable diagnostic procedure in hematology.

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