Hartford Hospital is an 938-bed acute care teaching hospital located in the South End of Hartford, Connecticut. Hartford Hospital was established in 1854. The hospital campus is located on Seymour Street in Hartford and is directly adjacent to the main campus of the Connecticut Children's Medical Center. Hartford Hospital was ranked #2 in Connecticut by U.S. News Best Hospitals and ranked #1 in the Hartford, Connecticut metro region by the same source. The hospital is a major tertiary care facility for the statewide region and is state designated as a Level I Trauma Center, able to care for the most critically injured of patients. It has 45 operating rooms and one of the largest surgical caseloads in the United States. The emergency room receives over 100,000 visits per year.
Tandem occlusions (TOs)-concurrent extracranial large artery steno-occlusion and intracranial artery occlusion-represent a challenging clinical predicament. Stroke due to TOs is associated with high mortality and morbidity. Because of increased clot burden compared with single occlusions and impaired anterograde flow, intravenous thrombolysis may be less effective, and outcomes are poor without timely intervention. Endovascular thrombectomy (EVT) has become the cornerstone of intracranial revascularization, but the optimal management of the extracranial carotid lesion remains undefined. Evidence from observational studies and early-phase randomized controlled trials (RCTs) is mixed. Currently, no standardized treatment approach is widely accepted, and practice patterns are guided by personal preference and expert opinion. Ongoing RCTs seek to determine whether there is an optimal approach to EVT in the setting of TO with respect to (a) technique and (b) the order of treatment. Even on completion of active RCTs, a dearth of evidence will remain on the optimal antithrombotic therapy, exact device selection, and EVT in dissection-associated TOs and posterior circulation TOs. In the present narrative review, we critically appraise the literature on the endovascular management of TOs and offer considerations for practice that may help to reduce the burden of tandem occlusion strokes.
The β-lactam/β-lactamase inhibitor (BL/BLI) combination drugs, ceftazidime/avibactam, meropenem/vaborbactam, and imipenem/relebactam, have proven especially useful for treating carbapenemase-producing, carbapenem-resistant organisms (CRO), specifically Klebsiella pneumoniae carbapenemases (KPCs). However, non-KPC mechanisms of resistance are rising in prevalence among Gram-negatives and are increasingly challenging to treat. These newer BL/BLIs, including sulbactam/durlobactam, have an array of activity against mechanisms of carbapenem resistance beyond KPC and therefore play an important role in the treatment of non-KPC carbapenem-resistant organisms. This review, the second in a 2-part series, lays out the non-KPC attributes of the newer BL/BLIs with a focus on clinical utility against Burkholderia cepacia complex, Stenotrophomonas maltophilia, Acinetobacter baumannii, and other rare pathogens.
Lymphoceles (LCs) are one of the most common complications after robot-assisted radical prostatectomy (RARP). Peritoneal flaps (PF) have shown to possibly decrease the incidence of LCs. This individual patient data meta-analysis (IPD-MA) investigates the efficacy of PF on rates of symptomatic lymphoceles (sLCs) requiring intervention, sLCs, overall lymphoceles and perioperative complications. We conducted a prespecified systematic review and IPD-MA (PROSPERO CRD42024519284). A database search via Medline, Web of Science, Embase, Central, ClinicalTrials.gov and the International Clinical Trials Registry Platform was performed up to December 2023. Six randomized controlled trials (RCTs) comparing PF vs. no PF during RARP with PLND were included and five RCTs provided IPD. MA was conducted using a random-effects model (two-stage model). PF significantly reduced sLCs requiring intervention as well as the rates of sLCs and overall lymphoceles. Additionally, PF significantly reduced overall complications, most likely driven by fewer lymphoceles and associated interventions. Furthermore, BMI and the presence of lymphoceles at discharge were identified as risk factors for sLCs. Subgroup analyses suggested that the protective effect of PF diminishes with increasing BMI, indicating limited benefit in patients with severe obesity. The creation of PF after RARP significantly reduces sLCs without affecting the complication rate or meaningfully prolonging operative time. LCs at the time of discharge represent significant risk factors for occurrence of sLCs, indicating a possibility for closer observation for this subgroup. With the evidence provided by this IPD-MA, creation of PF should be the new standard of care to reduce LC-related morbidity.
The incidence of sudden cardiac arrest in athletes varies according to age, race and ethnic group, sex, sport, and social determinants of health. The common causes of sudden cardiac arrest include cardiomyopathies, electrical disorders, coronary-artery anomalies, and other cardiac structural abnormalities. There has not been an increase in the incidence of sudden cardiac arrest in athletes during the time frame of the coronavirus disease 2019 (Covid-19) pandemic. Primary prevention is based on cardiovascular screening before participation, and secondary prevention on implementation of emergency action plans. Diagnostic evaluation of athletes who survive sudden cardiac arrest should mirror that of age-matched nonathletes, with additional sport-specific considerations, and should be performed by medical professionals with expertise in the interpretation of test results in the context of athletic adaptation. An increasing body of evidence indicates that many athletes can return to play after disease-specific treatment, without an increase in risk, and professional societies now consider return to participation in sports to be reasonable or appropriate through shared decision making for numerous cardiac conditions.
Peripheral T-cell lymphoma, not otherwise specified (PTCL, NOS) rarely occurs in pediatric and young adult populations, where little is known about its clinicopathologic and molecular features. We characterized 16 cases of PTCL, NOS diagnosed in patients ≤21 years old. Seven (44%) cases demonstrated SMARCB1/INI1 loss by immunohistochemistry and SMARCB1/INI1 alterations by next-generation sequencing, including biallelic SMARCB1/INI1 deletion (n = 4), stop codon variant with 1-copy deletion (n = 1) or copy-neutral loss-of-heterozygosity (n = 1), and frameshift variant (n = 1). One case demonstrated biallelic SMARCE1 alterations (a nonsense variant and copy-neutral loss-of-heterozygosity), which, to our knowledge, has not been previously described in a hematopoietic neoplasm. The SWI/SNF-intact group harbored pathogenic TET2, PTEN, EZH2, or TP53 variants. CDKN2A deletions were present in 3 of 7 SWI/SNF-deficient and 0 of 4 SWI/SNF-intact cases. Chromosome 22q11.2 alterations were present on karyotype in 2 of 3 SMARCB1/INI1-deficient cases. SWI/SNF deficiency was associated with intermediate-to-large cell cytomorphology, frequent mitotic (88%; P = .041) and apoptotic (88%) activity, Reed-Sternberg-like cells (63%), necrosis (50%), and fibrosis (50%). All cases expressed CD45 and CD43 at initial diagnosis. SWI/SNF-deficient cases predominantly demonstrated a CD4+/CD8-, TCRab, and PTCL-GATA3 phenotype, whereas SWI/SNF-intact cases predominantly demonstrated a CD8+/CD4-, TCRgd, and PTCL-TBX21 phenotype. A PTCL-TBX21 phenotype was more common in SWI/SNF-intact than in SWI/SNF-deficient cases (P = .041). Cytotoxic markers were expressed in 71% of SWI/SNF-deficient and 88% of SWI/SNF-intact cases. Decreased or absent CD3 expression characterized 88% of SWI/SNF-deficient and 13% of SWI/SNF-intact cases (P = .01). Moreover, 63% of SWI/SNF-deficient cases demonstrated decreased or absent expression of ≥3 pan-T-cell antigens, compared with 13% of SWI/SNF-intact cases. Treatment was heterogeneous. Primary treatment failure or relapse occurred in 4 of 8 SWI/SNF-deficient and 4 of 7 SWI/SNF-intact cases. The median overall survival and event-free survival were 48.7 and 47.5 months for the SWI/SNF-deficient group, and 16.4 and 8.9 months for the SWI/SNF-intact group (P = nonsignificant). Death due to disease or therapy-related complications occurred in 4 of 8 (50%) cases in the SWI/SNF-deficient group and 6 of 7 (86%) of cases in the SWI/SNF-intact group. Our findings expand the knowledge of the clinicopathologic and molecular features of pediatric PTCL and highlight SWI/SNF-deficient T-cell lymphoma as a biologically distinct type of PTCL that is associated with characteristic clinicopathologic features.
