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The left internal jugular vein may be an alternative route for the placement of a pulmonary artery catheter when the right jugular vein is not available. Although the placement through the left internal jugular vein is expected to be more difficult, little has been written regarding difficulties in achieving proper placement of the catheter through the left internal jugular vein.
This prospective and observational study includes patients undergoing cardiac surgery with the catheter placement by monitoring the pressure waveform for 2 years. We measured the time required for the catheter to pass through the tricuspid and pulmonary valves, respectively. The data were analyzed by Mann-Whitney. P < 0.05 was considered significant.
The catheter placement through the right and left internal jugular vein was done in 285 (group R) and 10 patients (group L), respectively. The time duration through the tricuspid valve in group L was significantly longer than that in group P (8 [5-14] s vs 70 [19.8-138] s, median [range], P < 0.01), whereas the time duration through the pulmonary valve was comparable between the two groups (15 [10-27.75] s vs 15 [10.25-19] s, median [range], P = 0.62).
These results indicate that the difficulty in the catheter placement through the left jugular vein may be to pass through the tricuspid valve, not the pulmonary valve.
These results indicate that the difficulty in the catheter placement through the left jugular vein may be to pass through the tricuspid valve, not the pulmonary valve.
Alteration of the mechanisms of cerebral blood flow (CBF) regulation might contribute to the pathophysiology of sepsis-associated encephalopathy (SAE). selleck kinase inhibitor However, previous clinical studies on dynamic cerebral autoregulation (dCA) in sepsis had several cofounders. Furthermore, little is known on the potential impairment of neurovascular coupling (NVC) in sepsis. The aim of our study was to determine the presence and time course of dCA and NVC alterations in a clinically relevant animal model and their potential impact on the development of SAE.
Thirty-six anesthetized, mechanically ventilated female sheep were randomized to sham procedures (sham, n = 15), sepsis (n = 14), or septic shock (n = 7). Blood pressure, CBF, and electrocorticography were continuously recorded. Pearson's correlation coefficient Lxa and transfer function analysis were used to estimate dCA. NVC was assessed by the analysis of CBF variations induced by cortical gamma activity (Eγ) peaks and by the magnitude-squared coherence (MSC) betweatients' comorbidities or other confounders. Furthermore, a mean arterial pressure targeting therapy aiming to optimize dCA might not be sufficient to prevent neuronal dysfunction in sepsis since it would not improve NVC.
A progressive loss of dCA and NVC occurs during septic shock and is associated with cortical dysfunction. These findings indicate that the alteration of mechanisms controlling cortical perfusion plays a late role in the pathophysiology of SAE and suggest that alterations of CBF regulation mechanisms in less severe phases of sepsis reported in clinical studies might be due to patients' comorbidities or other confounders. Furthermore, a mean arterial pressure targeting therapy aiming to optimize dCA might not be sufficient to prevent neuronal dysfunction in sepsis since it would not improve NVC.
Transcranial direct current stimulation (tDCS) has been investigated as a tool for dysphagia recovery after stroke in several single-center randomized controlled trials (RCT).
The aim of this investigation was to quantitatively evaluate the effect of tDCS on dysphagia recovery after a stroke utilizing a systematic review and meta-analysis.
Major databases were searched through October 2019 using a pre-defined set of criteria. Any RCT investigating the efficacy of tDCS in post-stroke dysphagia using a standardized dysphagia scale as outcome measure was included. Studies were assessed for risk of bias and quality using the Physiotherapy Evidence Database (PEDro) scale. Effect sizes were calculated from extracted data and entered into a random effects analysis to obtain pooled estimates of the effect.
Seven RCTs with a total sample size of 217 patients fulfilled the criteria and were included in the analysis. The overall results revealed a small but statistically significant pooled effect size (0.31; CI 0.03, 0.59; p = 0.03). The subgroup which explored the stimulation intensity yielded a moderately significant effect size for the low-intensity stimulation group (g = 0.44; CI = 0.08, 0.81 vs. g = 0.15, CI -0.30, 0.61). For the other subgroup analyses, neither comparisons of affected vs. unaffected hemisphere or acute vs. chronic stroke phase revealed a significant result.
This meta-analysis demonstrates a modest but significant beneficial effect of tDCS on improving post-stroke dysphagia. Whether benefits from this intervention are more pronounced in certain patient subgroups and with specific stimulation protocols requires further investigation.
This meta-analysis demonstrates a modest but significant beneficial effect of tDCS on improving post-stroke dysphagia. Whether benefits from this intervention are more pronounced in certain patient subgroups and with specific stimulation protocols requires further investigation.
Acute diplopia is a diagnostic challenge for clinicians, in particular in the emergency department. The most common cause of acute diplopia are ocular motor nerve palsies (OMP). In this prospective study, we focused on identifying the most crucial signs and symptoms for differentiating between peripheral and central OMP.
We prospectively evaluated 56 non-consecutive patients who presented at our emergency department with acute binocular diplopia (≤ 10days). The patient history was taken using a standardized questionnaire and patients underwent a neurological, neuro-ophthalmological and neuro-otological examination, including measurement of the subjective visual vertical (SVV), Harms tangent screen test, and cranial MRI.
Forty-six out of 56 patients were diagnosed with an ocular motor cranial nerve palsy (OMP), 21 of peripheral and 23 of central origin; in two patients, the etiology remained unknown. The following features were different in peripheral and central OMP (1) the presence of vertigo/dizziness was more frequent in central (43.
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