PURPOSE OF REVIEWThe COVID-19 pandemic has had unprecedented global effects, yet the rapid emergence of telehealth across the globe has allowed healthcare professionals to connect virtually with ...patients and families while following safe social distancing guidelines. Telehealth has been used relatively well in patients from remote regions with limited access to subspecialty healthcare providers. This article discusses novel ways of using telehealth during the current pandemic and measures that would need to be taken to sustain telehealth and teleconsultations.
RECENT FINDINGSTelehealth has expanded to outpatient pediatric cardiology clinics across the globe during the pandemic. Technological advancements in video conferencing and the abundance of readily available wearable devices have allowed cardiologists to establish a preliminary diagnosis and set forth a treatment plan. Additional support by insurance providers and relaxation of mandatory regulations by the government have allowed telehealth to succeed during the pandemic. Although many subdisciplines within pediatric cardiology can be easily adapted into a sustainable telehealth model, some unique patient interactions, such as fetal cardiology, exercise physiology, and echocardiograms cannot be done remotely. The field of telehealth medicine with HIPAA-compliant programs and both insurance and government support should remain in our armamentarium of available resources for all patients and families.
SUMMARYAlthough not unique to pediatric cardiology, telehealth has emerged as an avenue to perform an initial evaluation and even establish a care pathway for patients. It is well recognized that telehealth visits will not supplant all patient--physician interactions but is a very acceptable first step in the majority of cases and can often steer the patient to subsequently undergo more selective and streamlined care.
Trauma remains a leading cause of death worldwide, and most early preventable deaths in both the civilian and military settings are due to uncontrolled hemorrhage, despite paradigm advances in modern ...trauma care. Combined tissue injury and shock result in hemostatic failure, which has been identified as a multidimensional molecular, physiologic and clinical disorder termed trauma‐induced coagulopathy (TIC). Understanding the biology of TIC is of utmost importance, as it is often responsible for uncontrolled bleeding, organ failure, thromboembolic complications, and death. Investigations have shown that TIC is characterized by multiple phenotypes of impaired hemostasis due to altered biology in clot formation and breakdown. These coagulopathies are attributable to tissue injury and shock, and encompass underlying endothelial, immune and inflammatory perturbations. Despite the recognition and identification of multiple mechanisms and mediators of TIC, and the development of targeted treatments, the mortality rates and associated morbidities due to hemorrhage after injury remain high. The purpose of this review is to examine the past and present understanding of the multiple distinct but highly integrated pathways implicated in TIC, in order to highlight the current knowledge gaps and future needs in this evolving field, with the aim of reducing morbidity and mortality after injury.
Exsanguination due to trauma-induced coagulopathy is a continuing challenge in emergency trauma care. Fibrinogen is a crucial factor for haemostatic competence, and may be the factor that reaches ...critically low levels first. Early fibrinogen substitution is advocated by a number of authors. Little evidence exists regarding the indications for fibrinogen supplementation in the acute phase. This study aims to estimate the prevalence of hypofibrinogenaemia in a multi-center trauma population, and to explore how initial fibrinogen concentration relates to outcome. Also, factors contributing to low fibrinogen levels are identified.
Patients arriving in hospital less than 180 minutes post-injury requiring full trauma team activation in four different centers were included in the study. Time from injury, patient demographics, injury severity scores (ISS) and 28 days outcome status were recorded. Initial blood samples for coagulation and blood gas were analyzed. Generalized additive regression, piecewise linear regression, and multiple linear regression models were used for data analyses.
Out of 1,133 patients we identified a fibrinogen concentration ≤1.5g/L in 8.2%, and <2 g/L in 19.2%. A non-linear relationship between fibrinogen concentration and mortality was detected in the generalized additive and piecewise linear regression models. In the piecewise linear regression model we identified a breakpoint for optimal fibrinogen concentration at 2.29 g/L (95% confidence interval (CI): 1.93 to 2.64). Below this value the odds of death by 28 days was reduced by a factor of 0.08 (95% CI: 0.03 to 0.20) for every unit increase in fibrinogen concentration. Low age, male gender, lengthened time from injury, low base excess and high ISS were unique contributors to low fibrinogen concentrations on arrival.
Hypofibrinogenaemia is common in trauma and strongly associated with poor outcome. Below an estimated critical fibrinogen concentration value of 2.29 g/L a dramatic increase in mortality was detected. This finding indicates that the negative impact of low fibrinogen concentrations may have been previously underestimated. A number of clinically identifiable factors are associated with hypofibrinogenaemia. They should be considered in the management of massively bleeding patients. Interventional trials with fibrinogen substitution in high-risk patients need to be undertaken.
Purpose of review
The purpose of this review is to explore the historical and serendipitous events that led to the creation of modern-day pacemakers. In addition, this review will explore how ...contemporary conduction site-specific pacing has overcome some of the deleterious effects from historical chronic right ventricular apical pacing.
Recent findings
Recently, there have been tremendous advances in not just the lead design but the tools required to promote more physiologic pacing. Although cardiac resynchronization pacing has been around for nearly 2 decades, this review also introduces and discusses the early results of His-bundle pacing and left bundle branch pacing and some of the potential applicability of this technology for our children.
Summary
Pacemakers have evolved significantly in the last 30 years through collaborative partnerships between physicians and engineers. The future of cardiac pacing is bright compared to the field of electrotherapy 50 years ago. Future iterations of pacemakers must consider unusual anatomy and growing children. Pediatric patients contribute to a small percentage of the overall device volume, but the majority of these patients will have a pacemaker for life. We need to be proactive and consider what are the best short and long-term solutions for this cohort.
Blood Brain Barrier (BBB) breakdown is a secondary form of brain injury which has yet to be fully elucidated mechanistically. Existing research suggests that breakdown of tight junction proteins ...between endothelial cells is a primary driver of increased BBB permeability following injury, and intercellular signaling between primary cells of the neurovascular unit: endothelial cells, astrocytes, and pericytes; contribute to tight junction restoration. To expound upon this body of research, we analyzed the effects of severely injured patient plasma on each of the cell types in monoculture and together in a triculture model for the transcriptional and translational expression of the tight junction proteins Claudins 3 and 5, (CLDN3, CLDN5) and Zona Occludens 1 (ZO-1). Conditioned media transfer studies were performed to illuminate the cell type responsible for differential tight junction expression. Our data show that incubation with 5% human ex vivo severely injured patient plasma is sufficient to produce a differential response in endothelial cell tight junction mRNA and protein expression. Endothelial cells in monoculture produced a significant increase of CLDN3 and CLDN5 mRNA expression, (3.98 and 3.51 fold increase vs. control respectively, p<0.01) and CLDN5 protein expression, (2.58 fold change vs. control, p<0.01), whereas in triculture, this increase was attenuated. Our triculture model and conditioned media experiments suggest that conditioned media from astrocytes and pericytes and a triculture of astrocytes, pericytes and endothelial cells are sufficient in attenuating the transcriptional increases of tight junction proteins CLDN3 and CLDN5 observed in endothelial monocultures following incubation with severely injured trauma plasma. This data suggests that inhibitory molecular signals from astrocytes and pericytes contributes to prolonged BBB breakdown following injury via tight junction transcriptional and translational downregulation of CLDN5.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
8.
An Update on the Coagulopathy of Trauma Maegele, Marc; Schöchl, Herbert; Cohen, Mitchell J
Shock (Augusta, Ga.)
41 Suppl 1, Številka:
Supplement 1
Journal Article
Recenzirano
Odprti dostop
ABSTRACTTrauma remains the leading cause of death with bleeding as the primary cause of preventable mortality during the first 24 h following trauma. When death occurs, it happens quickly, typically ...within the first 6 h after injury. One of four patients to arrive in the emergency department after trauma is already in the state of acute traumatic coagulopathy and shock. The principal drivers of acute traumatic coagulopathy have been characterized by tissue hypoperfusion, inflammation, and the acute activation of the neurohumoral system. Hypoperfusion leads to an activation of protein C with cleavage of activated factors V and VIII and the inhibition of plasminogen activator inhibitor 1 with subsequent hyperfibrinolysis. Endothelial damage and activation result in Weibel-Palade body degradation and glycocalyx shedding associated with autoheparinization. In contrast, there is an iatrogenic coagulopathy that occurs secondary to uncritical volume therapy leading to acidosis, hypothermia, and hemodilution. This coagulopathy then may be an integral part of the “vicious cycle” when combined with acidosis and hypothermia. The present article summarizes an update on the principal mechanisms and triggers of the coagulopathy of trauma including traumatic brain injury.
PURPOSE OF REVIEWPremature ventricular beats (PVCs) are frequently identified in healthy children with structurally normal hearts and generally have a benign clinical course often disappearing ...spontaneously. However, a small percentage of children may develop a cardiomyopathy. The purpose of this review is to understand which children may be at risk of development of left ventricular (LV) dysfunction with idiopathic PVCs.
RECENT FINDINGSThere is increasing evidence that a ventricular ectopic burden more than 24% in adults may lead to LV dysfunction. Most of the pediatric studies to date are retrospective, small case series from single institutions and have conflicting results regarding a direct correlation of the PVC burden to LV dysfunction. Development of a cardiomyopathy from frequent PVCs in children is likely multifactorial relating to the burden itself, presence of higher levels of ectopy (couplets and runs of ventricular tachycardia) as well as the duration of ventricular ectopy. Understanding the duration of ectopy is often unknown as patients are asymptomatic and the irregular heart beat was identified at a well-child examination.
SUMMARYAsymptomatic children with normal ventricular function and a low ectopy burden can be followed without any intervention and generally reassured. Children with an ectopy burden more than 30% are at some risk of developing LV dysfunction and should be more closely followed with noninvasive imaging. Development of symptoms attributed to the ectopy or signs of increasing LV dimensions or LV dysfunction should be treated with medication or catheter ablation.
Review the current state of the art of arrhythmogenic right ventricular cardiomyopathy (ARVC) diagnosis and risk stratification in the pediatric population.
ARVC is an inherited cardiomyopathy ...characterized by progressive myocyte loss and fibrofatty replacement of predominantly the right ventricle and high risk of ventricular arrhythmias and sudden cardiac death (SCD). ARVC is one of the leading causes of arrhythmic cardiac arrest in young people. Early diagnosis and accurate risk assessment are challenging, especially in children who often exhibit little to no phenotype, even if genotype positive. Multimodal imaging provides more detailed assessment of the right ventricle and has been shown in pediatric patients to identify earlier preclinical disease expression. Identification of patients with ARVC allows the clinician to intervene early with appropriate exercise restrictions, even if genotype positive only without phenotypic expression. Emphasis should be placed on stratifying the patient's risk of ventricular arrhythmias and SCD.
ARVC is a challenging diagnosis to make in adolescents who often do not exhibit clinical symptoms. Newer multimodal imaging techniques and improvements in genetic testing and biomarkers should help improve early diagnosis. Exercise restriction for children with ARVC has been shown to reduce disease advancement and decreases the risk of a life-threatening event.
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