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The Use of a Novel Quantitative Marker of Echogenicity of Pleural Fluid in Parapneumonic Pleural Effusions

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Συγγραφέας
Varsamas C., Kalkanis A., Gourgoulianis K.I., Malli F.
Ημερομηνία
2020
Γλώσσα
en
DOI
10.1155/2020/1283590
Λέξη-κλειδί
albumin
glucose
lactate dehydrogenase
glucose
lactate dehydrogenase
adult
aged
antibiotic therapy
Article
biochemical analysis
cell count
clinical article
echogenicity
echography
female
follow up
hospital admission
hospitalization
human
hypoechogenicity index
male
middle aged
parapneumonic pleural effusion
pH measurement
physical parameters
pleura effusion
pleura fluid
pleurisy
polymorphonuclear cell
priority journal
prospective study
septic shock
thoracocentesis
thorax radiography
chest tube
complication
cytology
diagnostic imaging
exudate
inflammation
length of stay
metabolism
neutrophil
pH
pleura effusion
pneumonia
treatment duration
very elderly
Adult
Aged
Aged, 80 and over
Chest Tubes
Duration of Therapy
Exudates and Transudates
Female
Glucose
Humans
Hydrogen-Ion Concentration
Inflammation
L-Lactate Dehydrogenase
Length of Stay
Male
Middle Aged
Neutrophils
Pleural Effusion
Pneumonia
Thoracentesis
Ultrasonography
Hindawi Limited
Εμφάνιση Μεταδεδομένων
Επιτομή
Background. Thoracic ultrasound is an essential tool in the daily clinical care of pleural effusions and especially parapneumonic pleural effusions (PPEs), in terms of diagnosis, management, and follow-up. Hypoechogenicity index (HI) is a quantitative marker of pleural fluid echogenicity. We aimed to examine associations of HI with pleural inflammation in patients with PPE. Methods. All patients included underwent a thoracic ultrasound with HI determination at the first day of their admission for a PPE. Thoracentesis was performed in all patients. Demographics, laboratory measurements, and clinical data were collected prospectively and recorded in all subjects. Results. Twenty-four patients with PPE were included in the study. HI was statistically significantly correlated with intensity of inflammation as suggested by pleural fluid LDH (p<0.001, r = -0.831), pleural fluid glucose (p=0.022, r = 0.474), and pleural fluid pH (p<0.001, r = 0.811). HI was correlated with ADA levels (p=0.005, r = -0.552). We observed a statistically significant correlation of HI with pleural fluid total cell number (p<0.001, r = -0.657) and polymorphonuclears percentage (p=0.02, r = -0.590), as well as days to afebrile (p=0.046, r = -0.411), duration of chest tube placement (p<0.001, r = -0.806), and days of hospitalization (p=0.013, r = -0.501). Discussion. HI presents a fast, easily applicable, objective, and quantitative marker of pleural inflammation that reliably reflects the intensity of pleural inflammation and could potentially guide therapeutic management of PPE. © 2020 Charalampos Varsamas et al.
URI
http://hdl.handle.net/11615/80414
Collections
  • Δημοσιεύσεις σε περιοδικά, συνέδρια, κεφάλαια βιβλίων κλπ. [19735]

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