The incidence of intentional or accidental valproic acid (VPA) overdose is increasing. Severe VPA toxicity may lead to coma and death. Traditionally the treatment of patients with VPA toxicity has been limited to supportive measures. VPA is highly protein bound and therefore it is considered not to be removable by extracorporeal means. However, studies of VPA toxicokinetics indicate that at blood levels that exceed therapeutic concentrations, VPA protein binding sites become saturated, leading to increased concentration of the free unbound drug. The free unbound drug has a small molecular weight and therefore it is theoretically amenable to removal by extracorporeal means. We present a patient with VPA toxicity who was successfully treated with "in-series" hemodialysis and hemoperfusion followed by continuous venovenous hemodiafiltration (CVVHDF) and review the literature on the management of VPA toxicity using extracorporeal therapies.
Mini‐Abstract The radiological detection of “fibrin sheaths” after removing central catheters is a well‐known delayed complication. “Fibrin sheaths” after implantable cardioverter‐defibrillator (ICD) removal because of infective endocarditis is unusual. We report the case of a 26‐year‐old woman with an ICD who developed infective endocarditis. A transesophageal echocardiography showed an image of “fibrin sleeve” on the superior vena cava (SVC). The patient had no history of SVC central catheter placement. The coexistence of vegetation and “fibrin sheaths” at different moments, as in our case, requires an awareness of this situation for differential diagnosis and treatment.
Introduction During the acute phase of Tako-tsubo syndrome (TTS) electrocardiogram (ECG) features change and myocardial edema is a common finding in Cardiac Magnetic Resonance (CMR). However, the relationship between ECG changes and myocardial edema is still unclear. Purpose To define if the presence and extension of myocardial edema might be predicted by electrocardiographic changes since admission to CMR. Methods Consecutive patients with TTS undergoing CMR during hospitalization were included. All patients underwent serial electrocardiography during the acute phase. Myocardial edema presence and extension was assessed by expert observers using the 17-segments cardiac segmentation model. ECG were analysed by expert observers blinded to the presence of myocardial edema. ECG pattern as predictors of myocardial edema presence and its extension were analysed by a binary regression and Student's t test. Results A total of 42 patients were included. Admission cQT was 472±60 ms. Thirty patients (71%) developed widespread negative T-waves and 55% showed cQT prolongation (cQT 476±58 ms) by the time of CMR. The median (IQR) time from admission to CMR imaging was 5 days (2–7 days). Myocardial edema was found in 30 patients (71%) and mean number of myocardial segments affected by edema was 4.8±2.5. Widespread negative T-wave development at the time of CMR imaging was associated with a smaller number of myocardial segments with edema. However no significant correlation was found between extension of myocardial edema and QT prolongation. No ECG pattern predicted a full recovery of myocardial edema (Table). Conclusions Development of widespread negative T-wave at the time of CMR predicts smaller myocardial edema extension. However, no other ECG features by the time of CMR were able to predict the full recovery of myocardial edema. Funding Acknowledgement Type of funding source: None
A 50-year-old woman without remarkable medical history was admitted at the Emergency Department for acute dyspnoea. The patient had been recently submitted to C5-C6 microdiscectomy. She was tachypneic and oxygen saturation was 88%. CT angiography showed bilateral pulmonary embolism (PE) (Figure 1A, yellow arrowheads) with signs of right ventricle overload. Bilateral deep vein thrombosis was also confirmed. The patient was admitted at the Intensive Care Unit, clinically stable. Few hours later, she presented sudden hemodynamic and respiratory deterioration, requiring invasive mechanical ventilation and vasopressors. Due to recent cervical surgery, systemic fibrinolysis was ruled out. Decision for percutaneous thrombectomy and inferior vena cava filter placement was made. Nevertheless, percutaneous thrombectomy was unsuccessful due to the impossibility to catheterize pulmonary artery. Contrast injection demonstrated that the guiding catheter was located in the left atrium (Figure 1B), suggesting a patent foramen ovale (PFO). Transoesophageal echocardiogram confirmed the presence of a 5x6 mm PFO with right-to-left shunt (Figures 1C – yellow arrows, and 1D). In addition, a 4 cm mobile mass attached to the aortic valve and protruding throughout the left ventricle outflow tract was visualized, suggesting paradoxical embolism (Figure 1E – white arrows). Accordingly, open surgical approach with pulmonary thrombectomy, PFO closure and removal of the left-sided thrombus was decided. Unfortunately, despite careful cannulation, thrombus was not found when aortic valve was inspected. Worst suspicions were confirmed, when the patient presented non-reactive mydriatic pupils. A brain CT showed signs of an extensive bihemisferic ischemic stroke (Figure 1F) presumably related to cerebral embolization of aortic thrombus. The patient finally died. Autopsy study was not consented. PFO has been associated with paradoxical embolisms and risk of stroke in PE. This case strikingly illustrates that treatment of these patients may be challenging in spite of an adequate diagnosis and management. Abstract P845 Figure.
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