Comparison and combination of a hemodynamics/biomarkers-based model with simplified PESI score for prognostic stratification of acute pulmonary embolism: findings from a real world study.

Background: Prognostic stratification is of utmost importance for management of acute Pulmonary Embolism (PE) in clinical practice. Many prognostic models have been proposed, but which is the best prognosticator in real life remains unclear. The aim of our study was to compare and combine the predictive values of the hemodynamics/biomarkers based prognostic model proposed by European Society of Cardiology (ESC) in 2008 and simplified PESI score (sPESI). Methods: Data records of 452 patients discharged for acute PE from Internal Medicine wards of Tuscany (Italy) were analysed. The ESC model and sPESI were retrospectively calculated and compared by using Areas under Receiver Operating Characteristics (ROC) Curves (AUCs) and finally the combination of the two models was tested in hemodinamically stable patients. All cause and PE-related in-hospital mortality and fatal or major bleedings were the analyzed endpoints Results: All cause in-hospital mortality was 25% (16.6% PE related) in high risk, 8.7% (4.7%) in intermediate risk and 3.8% (1.2%) in low risk patients according to ESC model. All cause in-hospital mortality was 10.95% (5.75% PE related) in patients with sPESI score ≥1 and 0% (0%) in sPESI score 0. Predictive performance of sPESI was not significantly different compared with 2008 ESC model both for all cause (AUC sPESI 0.711, 95% CI: 0.661-0.758 versus ESC 0.619, 95% CI: 0.567-0.670, difference between AUCs 0.0916, p=0.084) and for PE-related mortality (AUC sPESI 0.764, 95% CI: 0.717-0.808 versus ESC 0.650, 95% CI: 0.598-0.700, difference between AUCs 0.114, p=0.11). Fatal or major bleedings occurred in 4.30% of high risk, 1.60% of intermediate risk and 2.50% of low risk patients according to 2008 ESC model, whereas these occurred in 1.80% of high risk and 1.45% of low risk patients according to sPESI, respectively. Predictive performance for fatal or major bleeding between two models was not significantly different (AUC sPESI 0.658, 95% CI: 0.606-0.707 versus ESC 0.512, 95% CI: 0.459-0.565, difference between AUCs 0.145, p=0.34). In hemodynamically stable patients, the combined endpoint in-hospital PE-related mortality and/or fatal or major bleeding (adverse events) occurred in 0% of patients with low risk ESC model and sPESI score 0, whilst it occurred in 5.5% of patients with low-risk ESC model but sPESI ≥1. In intermediate risk patients according to ESC model, adverse events occurred in 3.6% of patients with sPESI score 0 and 6.65% of patients with sPESI score ≥1. Conclusions: In real world, predictive performance of sPESI and the hemodynamic/biomarkers-based ESC model as prognosticator of in-hospital mortality and bleedings is similar. Combination of sPESI 0 with low risk ESC model may identify patients with very low risk of adverse events and candidate for early hospital discharge or home treatment.

Bilateral thalamic infarct in two unresponsive octogenarians.

Bilateral thalamic infarct (BTI) represents an uncommon stroke presentation. Pathophysiology recognizes the occlusion of an anatomic variant of the thalamic blood supply from perforating branches of posterior cerebral arteries. Presentation could be nonspecific and dramatic in the same time, being coma or stupor the possible clinical scenario encountered. Diagnosis is performed by neuroradiological imaging showing the typical bilateral paramedian thalamic infarcts. Literature lacks of evidence in very old patients, therefore we describe two cases of BTI occurred in octogenarians presenting unresponsive. BTI in very old patients presenting comatose should be taken in account as diagnostic possibility.

Menorrhagia, Tranexamic Acid and False Negative D-Dimer in Patients with Venous Thromboembolism Case Report and Systematic Literature Review.

A 56 years-old woman came to our attention for abrupt onset of shortness of breath. Pulmonary embolism was firstly ruled out due to negative D-Dimer and unlikely probability. On second day, the patient presented with heavy menorrhagia and treated with tranexamic acid (TA). She informed that similar episode happened some months ago, so she had been treated with cycles of TA, discontinued the last time few days before the hospital admission. After three days from oral intake of TA, the patient suffered from abrupt painful left calf without any cardiac or respiratory sign. Urgent legs ultrasonography showed distal deep vein thrombosis and this time a new D-Dimer assay showed a mild positivity. The patient underwent to computer tomography pulmonary angiography which revealed bilateral segmental pulmonary embolism. Other three case reports referred to patients with acute venous thromboembolism after taking TA for menorrhagia emergedfrom systematic review of literature. Two of them presented with false negative D-Dimer. In another one D-Dimer assay was positive but performed after cardiopulmonary resuscitation. TA could link with venous thromboembolism both influencing D-Dimer value, proving false negativity, and increasing the thrombotic risk in young-adult females suffering from menorrhagia. These possibilities should be taken into account in this population.

Non-pharmacological Prophylaxis of Venous Thromboembolism in Acutely Ill Medical Patients.

Venous thromboembolism (VTE) represents one of the leading causes of mortality and morbidity in acutely ill medical patients. VTE prophylaxis can be assured by pharmacological strategies and, when contraindicated, by non pharmacological measures, such as early mobilization, graduated compression stockings (GCS), intermittent pneumatic compression (IPC) or inferior vena caval filters. Literature evidence on non pharmacological VTE prophylaxis lacks and guidelines are not standardized for hospitalized ill medical patients. Much recently randomized clinical trials in patients with stroke and other medical diseases, seem to increase doubts and reduce certainties in this context. In this review we provide information about non pharmacological thromboprophylaxis in acutely hospitalized ill medical patients.

The myasthenic patient in crisis: an update of the management in Neurointensive Care Unit / Pacientes miastenicos em crise: uma melhora de conduta na unidade de terapia intensiva

Myasthenia gravis (MG) is an autoimmune disorder affecting neuromuscular transmission leading to generalized or localized muscle weakness due most frequently to the presence of autoantibodies against acetylcholine receptors in the postsynaptic motor end-plate. Myasthenic crisis (MC) is a complication of MG characterized by worsening muscle weakness, resulting in respiratory failure that requires intubation and mechanical ventilation. It also includes postsurgical patients, in whom exacerbation of muscle weakness from MG causes a delay in extubation. MC is a very important, serious, and reversible neurological emergency that affects 20–30% of the myasthenic patients, usually within the first year of illness and maybe the debut form of the disease. Most patients have a predisposing factor that triggers the crisis, generally an infection of the respiratory tract. Immunoglobulins, plasma exchange, and steroids are the cornerstones of immunotherapy. Today with the modern neurocritical care, mortality rate of MC is less than 5%.

Miastenia grave (MG) é um distúbio autoimune que afeta principalmente a transmissão neuromuscular, levando a fraqueza muscular generalizada ou localizada. É devida mais frequentemente à presença de auto-anticorpos anti-receptores de acetilcolina na fenda pós-sináptica da placa motora. A crise miastênica (CM) é uma complicação da MG caracterizada por piora da fraqueza muscular, resultando en falência respiratória, o que requer entubação endotraqueal e ventilação mecânica. Isto ocorre também em pacientes pós-cirúrgicos, em que há piora da fraqueza muscular devido à MG, causando um atraso na extubação. MC é uma emergência neurológica importante, séria e reversível que afeta 20–30% dos pacientes miastênicos, usualmente duranteo primeiro ano de enfermidade, podendo a crise miastênica ser a manifestação inicial da MG. A maioria dos pacientes tem fatores predisponentes que desencadeiam a crise, geralmente uma infecção do trato respiratório. Imunoglobulina, plasmaférese e esteróides são a pedra angular da imunoterapia. Hoje, dentro da terapia neurocrítica, a taxa de mortalidade na CM é menor que 5%.

Enfoque práctico para el diagnóstico y tratamiento de los estados poliúricos en pacientes con injuria cerebral aguda / Diagnosis and therapy of polyuric states in patients with acute cerebral injury

In patients with acute cerebral injury, polyuric states can potentially trigger, maintain and aggravate the primary neurological damage, due to hypovolemia, arterial hypotension and alterations of osmolarity. The true incidence of the condition in this population is unknown. A widely validated definition of polyuric state is lacking and its etiology is multifactorial. There are two principal classes of polyuria: a) aqueous polyuria with diabetes insipidus as the main cause; and b) osmotic polyuria in which sodium, glucose or ureaplay the main role. Polyuric states are in close association with disorders of water and sodium metabolism and with alterations in acid-base balance. A detailed analysis of the history, clinical picture and simple laboratory determinations in blood and urine, are required for an adequate assessment of these polyuric states. The problem must be faced with pathophysiological reasoning and a systematic and sequential approach, because each disorder needs a specific therapy.