Contemporary evaluation of the causes of cardiac tamponade: Acute and long-term outcomes

Background: Cardiac tamponade is a life-threatening state that complicates various medical conditions. The contemporary interventional era may have led to changes in clinical characteristics, causes and outcomes of cardiac tamponade. Methods: We investigated all patients diagnosed with cardiac tamponade, based on clinical and echocardiographic findings, at a single medical center between the years 2000 and 2013. Data on medical history, index hospitalizations, pericardial fluid etiologies, and acute and long-term outcomes were collected. Results: Cardiac tamponade was observed in 83 patients (52% females). Major etiologies included complications of percutaneous cardiac interventions (36%) and malignancies (primarily lung cancer; 23%), infectious/inflammatory causes (15%) and mechanical complications of myocardial infarction (12%). Sixteen (19%) patients died during the index hospitalization. Acute presentation of symptoms and lower quantity of effusion were associated with in-hospital mortality (p = 0.045 and p = 0.007). Tamponade secondary to malignancy was associated with the most substantial increment in post-discharge mortality (from 16% in-hospital to 68% 1-year mortality). During the mean follow-up of 45 months, 39 (45%) patients died. Malignancies, mechanical complications of myocardial infarction and bleeding/coagulation abnormalities were etiologies associated with poor survival (80% mortality during follow-up). Tamponade secondary to complications of percutaneous cardiac interventions or infectious/inflammatory causes were associated with significantly lower mortality (28% and 17%; log rank p < 0.001). Conclusions: In a contemporary cohort, complications of percutaneous cardiac intervention replaced malignant diseases as the leading cause of cardiac tamponade. Nevertheless, these iatrogenic complications were associated with a relatively favorable outcome compared to tamponade induced by complications of myocardial infarction, coagulation abnormalities and malignant diseases.

El video digital como sistema de adquisición de datos. Una aplicación particular: la medición de variables cinemáticas en la marcha humana

La marcha humana es una de las áreas de estudio de la asignatura Biomecánica de 4° Año de la Carrera de Ingeniería Biomédica de la Facultad de Ciencias Exactas, Físicas y Naturales de la Universidad Nacional de Córdoba. Podemos describir la marcha humana normal (locomoción) como “una serie de movimientos alternantes, rítmicos, de las extremidades y del tronco que determinan un desplazamiento hacia delante del centro de gravedad” (Luna, 1999). En el estudio de la marcha, el ciclo comienza cuando un pie hace contacto con el suelo y termina con el siguiente contacto del mismo pie; a la distancia entre estos dos puntos de contacto del pie con el suelo se la llama un paso completo. El ciclo de la marcha se divide en dos componentes principales: la fase de apoyo y la fase de balanceo. Una pierna está en fase de apoyo cuando está en contacto con el suelo y en fase de balanceo cuando no hace contacto con el suelo. Estas dos fases se van alternando de una pierna a la otra durante la marcha.Fil: Martín, Javier. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales; Argentina.Fil: Martinez, Marcela. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales; Argentina.Fil: Micolo, Martín. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales; Argentina.Fil: Schliamser, Federico. Universidad Nacional de Córdoba. Facultad de Ciencias Exactas, Físicas y Naturales; Argentina.Otras Ingeniería Médic

Cerebrospinal fluid biomarkers of brain injury, inflammation and synaptic autoimmunity predict long-term neurocognitive outcome in herpes simplex encephalitis

OBJECTIVES: To investigate the correlation between biomarkers of brain injury and long-term neurocognitive outcome, and the interplay with intrathecal inflammation and neuronal autoimmunity, in patients with herpes simplex encephalitis (HSE). METHODS: A total of 53 adult/adolescent HSE patients were included from a prospective cohort in a randomized placebo-controlled trial investigating the effect of a 3-month follow-up treatment with valaciclovir. Study subjects underwent repeated serum/CSF sampling and brain MRI the first 3 months along with cognitive assessment by Mattis Dementia Rating Scale (MDRS) during 24 months. CSF samples were analyzed for biomarkers of brain injury, inflammation and synaptic autoimmunity. The pre-defined primary analysis was the correlation between peak CSF neurofilament protein (NFL), a biomarker of neuronal damage, and MDRS at 24 months. RESULTS: Impaired cognitive performance significantly correlated with NFL levels (rho = -0.36, p = 0.020). Development of IgG anti-N-methyl-D-aspartate receptor (NDMAR) antibodies was associated with a broad and prolonged proinflammatory CSF response. In a linear regression model, lower MDRS at 24 months was associated with previous development of IgG anti-NMDAR (beta = -0.6249, p = 0.024) and age (z-score beta = -0.2784, p = 0.024), but not CSF NFL, which however significantly correlated with subsequent NMDAR autoimmunization (p = 0.006). CONCLUSIONS: Our findings show that NFL levels are predictive of long-term neurocognitive outcome in HSE, and suggest a causative chain of events where brain tissue damage increases the risk of NMDAR autoimmunisation and subsequent prolongation of CSF inflammation. The data provides guidance for a future intervention study of immunosuppressive therapy administered in the recovery phase of HSE

MyD88 expression by CNS-resident cells is pivotal for eliciting protective immunity in brain abscesses

MyD88 KO (knockout) mice are exquisitely sensitive to CNS (central nervous system) infection with Staphylococcus aureus, a common aetiological agent of brain abscess, exhibiting global defects in innate immunity and exacerbated tissue damage. However, since brain abscesses are typified by the involvement of both activated CNS-resident and infiltrating immune cells, in our previous studies it has been impossible to determine the relative contribution of MyD88-dependent signalling in the CNS compared with the peripheral immune cell compartments. In the present study we addressed this by examining the course of S. aureus infection in MyD88 bone marrow chimaera mice. Interestingly, chimaeras where MyD88 was present in the CNS, but not bone marrow-derived cells, mounted pro-inflammatory mediator expression profiles and neutrophil recruitment equivalent to or exceeding that detected in WT (wild-type) mice. These results implicate CNS MyD88 as essential in eliciting the initial wave of inflammation during the acute response to parenchymal infection. Microarray analysis of infected MyD88 KO compared with WT mice revealed a preponderance of differentially regulated genes involved in apoptotic pathways, suggesting that the extensive tissue damage characteristic of brain abscesses from MyD88 KO mice could result from dysregulated apoptosis. Collectively, the findings of the present study highlight a novel mechanism for CNS-resident cells in initiating a protective innate immune response in the infected brain and, in the absence of MyD88 in this compartment, immunity is compromised

Brain abscess in Korean children: A 15-year single center study

PurposeA brain abscess is a serious disease of the central nerve system. We conducted this study to summarize the clinical manifestations and outcomes of brain abscesses.MethodsA retrospective chart review of pediatric patients diagnosed with brain abscesses from November 1994 to June 2009 was performed at Samsung Medical Center, Seoul, Korea.ResultsTwenty-five patients were included in this study. On average, 1.67 cases per year were identified and the median age was 4.3 years. The common presenting clinical manifestations were fever (18/25, 72%), seizure (12/25, 48%), altered mental status (11/25, 44%), and signs of increased intracranial pressure (9/25, 36%). A total of 14 (56%) patients had underlying illnesses, with congenital heart disease (8/25, 32%) as the most common cause. Predisposing factors were identified in 15 patients (60%). The common predisposing factors were otogenic infection (3/25, 12%) and penetrating head trauma (3/25, 12%). Causative organisms were identified in 64% of patients (16/25). The causative agents were S. intermedius (n=3), S. aureus (n=3), S. pneumoniae (n=1), Group B streptococcus (n=2), E. coli (n=1), P. aeruginosa (n=1), and suspected fungal infection (n=5). Seven patients received medical treatment only while the other 18 patients also required surgical intervention. The overall fatality rate was 16% and 20% of patients had neurologic sequelae. There was no statistical association between outcomes and the factors studied.ConclusionAlthough uncommon, a brain abscess is a serious disease. A high level of suspicion is very important for early diagnosis and to prevent serious consequences

Neurotoxicity of β-lactam antibiotics : experimental kinetic and neurophysiological studies

The neurotoxic potential of intravenous administered benzylpenicillin (BPC) was studied in rabbits with intact blood-CNS barriers and rabbits with experimental E. coli meningitis. At onset of epileptogenic EEG activity or seizures, serum, CSF and brain tissue were collected for assay of BPC. Based on the fact that, in tissues, BPC seems to remain extracellularly, brain concentrations of BPC were expressed as brain tissue fluid (BTF) levels, calculated as lOx the concentration in whole brain tissue. Neurotoxicity could be precipitated in all rabbits. In normal rabbits BTF levels of BPC were considerably higher than those in CSF indicating a better penetration across the blood-brain barrier (BBB). BPC penetrated better to CSF and BTF in meningitic rabbits than in normal controls, suggesting some degree of damage of the BBB concomitant with meningeal inflammation. E. coli meningitis did not increase the neurotoxicity of BPC. In control rabbits the intracistemal injection of saline resulted in some degree of pleocytosis. Unmanipulated animals are therefore preferable as controls. Epileptogenic EEG-changes was the most precise of the two variables used for demonstration of neurotoxicity. EEG-changes were therefore used as neurotoxicity criterion in the following rabbit experiments. To evaluate the effect of uraemia alone and uraemia plus meningitis on the neurotoxity of BPC in rabbits, cephaloridine was used to induce uraemia. Meningitis was induced by intracistemal inoculation of a cephalosporinresistant strain of E. cloacae. Untreated  rabbits were used as controls. Uraemia resulted in increased BTF penetration of BPC, possibly explained by permeability changes in the BBB and/or decreased binding of BPC to albumin. Uraemia did not result in increased penetration of BPC into the CSF of non-meningitic rabbits. Uraemic non-meningitic rabbits had the highest BTF levels of BPC at the criterion, indicating that cephaloridine-induced renal failure increased the epileptogenic threshold in these rabbits. The combination of uraemia and meningitis increased the neurotoxicity of BPC since the criterion was reached at considerably lower BTF levels of BPC. Meningitis, either alone or together with uraemia, did not increase the neurotoxicity in comparison to control rabbits. Higher BTF levels of BPC were found in meningitic rabbits than in controls with intact blood-CNS barriers at onset of EEG-changes. In all groups of rabbits there was a pronounced variability of BPC levels in the CSF while the intra-group variations in BTF levels were much smaller. Thus, BTF and not CSF levels were decisive for the neurotoxicity of BPC. Using   the same EEG-model, the neurotoxic potential of imipenem/cilastatin (I) and a new penem derivative, FCE 22101 were compared in a cross-over study. Both I and FCE 22101 were significantly more neurotoxic than BPC. While BTF levels of the three antibiotics could be detected in all tested rabbits, detectable CSF levels were only found in one of twelve rabbits treated with I or FCE 22101, indicating that BTF concentrations rather than CSF ones are decisive for neurotoxicity of ß-lactam antibiotics. The EEG-model used was found to be a suitable model for cross-over studies of intravenously administered antibiotics. Using the "silent-second" as EEG-threshold, a CNS interaction between intraperitoneally administered BPC and intravenous thiopental was demonstrated in rats. The most probably site for this interaction is the organic acid transport system out of the CNS. Thiopental distribution in the rat brain seemed to depend not only on its lipid solubility.Diss. (sammanfattning) Umeå : Umeå universitet, 1988, härtill 5 uppsatser.digitalisering@um