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BackgroundThe reported incidence of left ventricular (LV) thrombus after ST elevation myocardial infarction (STEMI) varies significantly, with studies reporting incidence from 2% to as high as 20% depending on the patient cohort scanned, the timing of the scan and the modality used. Routine clinical practice in the United Kingdom remains an echocardiogram prior to discharge, usually 24–48 hours post infarct.Current data suggests that the highest risk cohort for LV thrombus formation are anterior STEMI patients, with apical akinesia or dyskinesia and LV ejection fraction (EF) <50%. The time point at which the highest incidence of thrombus formation will have occurred is similarly poorly defined, though 14 days post infarct has been proposed. What is known is that cardiac magnetic resonance (CMR) has a much higher sensitivity than non-contrast echocardiogram to detect LV thrombus. We sought to compare the incidence of LV thrombus formation in this high-risk group at 2- and 14-days post infarct using CMR.MethodsWe recruited 2 cohorts of patients after anterior STEMI with EF <50%, apical akinesia and no thrombus seen on initial post infarct echocardiogram – group 1 underwent CMR at day 2 and group 2 at day 14. All patients underwent CMR on a Phillips Ingenia 1.5T (Phillips, Netherlands) using standard protocols including volumes, early and late gadolinium enhanced imaging.Normally distributed continuous variables were compared with independent sample T test and presented as means with standard deviations. Proportions were compared with χ2 squared. P values of <0.05 were considered significant.ResultsIn total 55 patients were recruited. 29 were scanned on day 2, 26 were scanned at day 14.All patients were prescribed aspirin and prasugrel, with none prescribed anticoagulation before CMR.Overall, 12 (46%) of patients scanned at Day 14 had LV thrombus compared to 4 (14%) scanned at day 2 (p 0.009).Results comparing the two groups are shown in table 1.Abstract 6-001 Table 1[Image Omitted. See PDF.]A comparison of those scanned at day 14 with thrombus and those without is shown in table 2.Abstract 6-001 Table 2[Image Omitted. See PDF.]ConclusionIn this anterior STEMI cohort, we have shown a significantly higher incidence of LV thrombus when scanning with CMR at day 14 than scanning at day 2, with a notably high incidence at day 14 compared to previous studies. Conventional risk factors do not seem to influence LV thrombus incidence, however residual apical akinesia at 2 weeks was significantly more prevalent in those who went on to have thrombus.It is likely that the current routine practice of non-contrast echocardiography before discharge may under diagnose LV thrombus in this cohort, how this corresponds to outcomes remains unclear. Larger studies, ideally with repeat scans in the same patients, is required to confirm the ideal timing of CMR.Abstract 6-001 Figure 1Early gadolinium enhanced 4 chamber showing extensive microvascular obstruction and large apical LV thrombus[Image Omitted. See PDF.]Abstract 6-001 Figure 2Late gadolinium enhanced ventricular long axis showing extensive infarction and large apical LV thrombus[Image Omitted. See PDF.]

Background and aimsSub-Tenon’s block (STB) is increasingly used for cataract surgery to reduce risk of complications related to needle blocks.1 The technique involves making a conjunctival incision with blunt forceps and scissors followed by insertion of a blunt cannula into the sub-Tenon’s space. Recently, a sub-Tenon’s technique has been described in which a small aperture in conjunctiva is made with a lacrimal dilator.2 This technique accelerates block performance, minimize local trauma, improves surgical field and avoids surgical incision of conjunctiva.3 We report preliminary results of a randomized, prospective, non-inferiority study comparing standard vs. lacrimal dilator-facilitated sub-Tenon’s block.MethodsPatients undergoing elective cataract surgery were enrolled into two groups; standard sub-Tenon’s dissected with Westcott scissors (WS) or entry portal obtained with a lacrimal dilator (LD) A 19G, 2.5 cm long sub-Tenon’s curved cannula was used in both groups to deliver 3 mL, 2% lidocaine. No sedation was used. Data collection included demography, procedure duration, chemosis, intraoperative analgesia (Numeric Rating Scale 1–10), akinesia (4-primary gazes) and the quadrant/s of subconjunctival haemorrhage on the first postoperative day.ResultsPatients in both groups were comparable for demographic data, procedure duration, analgesia and akinesia (p>0.05). The incidence of chemosis and subconjunctival hemorrhage were significantly lower in Group LD (n=15) in comparison to Group WS (n=26) (p=0.001 and p<0.001, respectively).Abstract ESRA19-0370 Figure 1Lacrimal dilator-facilitated entry during STB.Abstract ESRA19-0370 Figure 2Subconjunctival haemorrhage following STB in the same patient; with lacrimal dilator in the right eye(a) and with scissors in the left eye(b).ConclusionsIncisionless sub-Tenon’s block with lacrimal dilator is a practical and effective alternative to standard technique with reduced chemosis and subconjunctival hemorrhage.

Please confirm that an ethics committee approval has been applied for or granted: Not relevant (see information at the bottom of this page)Background and Aims Endophthalmitis is a severe intraocular inflammation that can occur following surgery or eye trauma. Wound infection has been described as a primary foci of infection in endogenous endophthalmitis. We present a case of purulent endophthalmitis treated with immediate pars plana vitrectomy (PPV) under peribulbar block and conscious sedation.MethodsA 75-year-old male patient, with multiple cardiovascular risk factors, underwent open aortic valve replacement, and was readmitted one month later with sternal wound infection. He received antimicrobial treatment. Four months later, the patient presented with purulent endophthalmitis. PPV ensued under peribulbar block and conscious sedation with a propofol perfusion. Peribulbar block was performed with two injections of Ropivacaine 1%: inferior-temporal (5mL) and superior-nasal (3mL), to ensure adequate spread within the intraconal and extraconal spaces.ResultsPeribulbar anaesthesia allowed akinesia and good surgical conditions with respiratory and hemodynamic stability. The surgical procedure was performed successfully without perioperative complications.ConclusionsPeribulbar anaesthesia is a feasible anaesthetic technique for PPV, as it allows akinesia during surgery, better hemodynamic stability, and fewer postoperative complications, especially in older fragile patients with comorbidities. PPV performed under peribulbar block can be considered a reliable approach in managing purulent endophthalmitis, offering a safe alternative to general anaesthesia.

Continuous imaging of cardiac functions is highly desirable for the assessment of long-term cardiovascular health, detection of acute cardiac dysfunction and clinical management of critically ill or surgical patients 1 – 4 . However, conventional non-invasive approaches to image the cardiac function cannot provide continuous measurements owing to device bulkiness 5 – 11 , and existing wearable cardiac devices can only capture signals on the skin 12 – 16 . Here we report a wearable ultrasonic device for continuous, real-time and direct cardiac function assessment. We introduce innovations in device design and material fabrication that improve the mechanical coupling between the device and human skin, allowing the left ventricle to be examined from different views during motion. We also develop a deep learning model that automatically extracts the left ventricular volume from the continuous image recording, yielding waveforms of key cardiac performance indices such as stroke volume, cardiac output and ejection fraction. This technology enables dynamic wearable monitoring of cardiac performance with substantially improved accuracy in various environments. Innovations in device design, material fabrication and deep learning are described, leading to a wearable ultrasound transducer capable of dynamic cardiac imaging in various environments and under different conditions.

Early-morning off periods, causing early-morning akinesia, can lead to significant motor and nonmotor morbidity in levodopa-treated fluctuating Parkinson’s disease (PD) cases. Despite validated bedside scales in clinical practice, such early-morning off periods may remain undetected unless specific wearable technologies, such as the Parkinson’s KinetiGraph™ (PKG) watch, are used. We report five PD cases for whom the PKG detected early-morning off periods that were initially clinically undetected and as such, untreated. These five cases serve as exemplars of this clinical gap in care. Post-PKG assessment, clinicians were alerted and targeted therapies helped abolish the early-morning off periods.

Neuroaxonal Dystrophies (NAD) are neurodegenerative diseases characterized by axonal “spheroids” occurring in different age groups. The identification of mutations delineated new molecular entities in these disorders. We report neuropathological data of a new form of NAD, characterized by a precocious prenatal onset, different from classical and connatal Infantile Neuroaxonal Dystrophy (INAD). We studied 5 fetuses examined after pregnancy termination and 2 term neonates deceased just after birth, 4/7 from consanguineous parents. All subjects presented severe fetal akinesia sequence with microcephaly. In 4/7 cases, a molecular study was performed. In all cases, “spheroids” with typical immunohistochemical features were identified, with variable spreading in the central and peripheral nervous system. Basal ganglia, brainstem, cerebellum and spinal cord involvement was constant. Associated CNS malformations, unusual in INAD, were associated including hydrocephalus (2), callosal agenesis/hypoplasia (2), olfactory agenesis (1), cortical (3) and retinal (1) anomalies. None cases demonstrated mutations in PLA2G6, found in INAD. The clinical and neuropathological features of these fetal cases are different from those of “classical” INAD. The absence of mutations of PLA2G6, in addition, suggests that the fetal NAD is a new entity, distinct from INAD, with different molecular basis. Associated malformations suggest a wide phenotypic spectrum and probable genetic heterogeneity. Finally, fetal NAD is an additional etiology of fetal akinesia.

Wallerian degeneration is a widespread mechanism of programmed axon degeneration. In the three decades since the discovery of the Wallerian degeneration slow (WldS) mouse, research has generated extensive knowledge of the molecular mechanisms underlying Wallerian degeneration, demonstrated its involvement in non-injury disorders and found multiple ways to block it. Recent developments have included: the detection of NMNAT2 mutations that implicate Wallerian degeneration in rare human diseases; the capacity for lifelong rescue of a lethal condition related to Wallerian degeneration in mice; the discovery of ‘druggable’ enzymes, including SARM1 and MYCBP2 (also known as PHR1), in Wallerian pathways; and the elucidation of protein structures to drive further understanding of the underlying mechanisms and drug development. Additionally, new data have indicated the potential of these advances to alleviate a number of common disorders, including chemotherapy-induced and diabetic peripheral neuropathies, traumatic brain injury, and amyotrophic lateral sclerosis.In recent decades, our understanding of the molecules and pathways involved in the classical axon degeneration pathway, Wallerian degeneration, has been transformed. Coleman and Höke synthesize the recent developments in the field and discuss how the findings might be translated to aid the treatment of human disease.

Huntington’s disease (HD) is a debilitating neurodegenerative genetic disorder caused by an expanded polyglutamine-coding (CAG) trinucleotide repeat in the huntingtin (HTT) gene. HD behaves as a highly penetrant dominant disorder likely acting through a toxic gain of function by the mutant huntingtin protein. Widespread cellular degeneration of the medium spiny neurons of the caudate nucleus and putamen are responsible for the onset of symptomology that encompasses motor, cognitive, and behavioural abnormalities. Over the past 150 years of HD research since George Huntington published his description, a plethora of pathogenic mechanisms have been proposed with key themes including excitotoxicity, dopaminergic imbalance, mitochondrial dysfunction, metabolic defects, disruption of proteostasis, transcriptional dysregulation, and neuroinflammation. Despite the identification and characterisation of the causative gene and mutation and significant advances in our understanding of the cellular pathology in recent years, a disease-modifying intervention has not yet been clinically approved. This review includes an overview of Huntington’s disease, from its genetic aetiology to clinical presentation and its pathogenic manifestation. An updated view of molecular mechanisms and the latest therapeutic developments will also be discussed.

This case study describes the antenatal care, birth, and subsequent management of a baby boy born via elective lower segment Caesarean section. The pregnancy, initially uneventful, revealed multiple congenital anomalies during the second trimester. Despite extensive efforts, including respiratory support and antibiotic treatment for late-onset sepsis, the neonate's condition deteriorated rapidly, leading to a cardiac arrest on day 25 of life. Palliative care was provided, consistent with the parents' wishes for a do-not-resuscitate (DNR) approach due to the severity of the congenital anomalies. This case underscores the complexities of managing neonates with profound congenital anomalies, and the importance of respectful and supportive care for families facing such challenges.