It appears that pleural fluid leukocyte metabolism is primarily responsible for the low pH effusion associated with esophageal rupture.
Only elimination of polymorphonuclear leukocytes from the pleural space by rendering animals leukopenic with nitrogen mustard, prevented a low pH effusion after esophageal rupture.
To determine the possible mechanisms responsible for the low pH pleural effusion associated with esophageal rupture we evaluated the following possibilities: (1) gastric acid reflux, (2) bacterial metabolism, and (3) leukocyte metabolism.
Inter-observer reliability for synovitis and PD was moderate (kappa 0.46, and 0.56, respectively) and for joint effusion low (kappa 0.23).
There were more signs of purpura/ecchymosis, gastrointestinal bleeding, ascites/pleural effusion, low platelet count and narrow pulse pressure in recurrent shock patients compared with patients who had a single shock, similarly to the severity signs of dengue infection [ 2].
The results showed that shorter admission day (fewer days prior to admission), purpura/ecchymosis, ascites/pleural effusion, low platelet count and narrow pulse pressure were independently associated with recurrent shock.
Lefèvre et al identified additional poor prognostic factors in patients with SSc with pulmonary hypertension in a meta-analysis including patients with WHO groups II and III pulmonary hypertension: pericardial effusion, low 6MWD, high mean pulmonary arterial pressure, poor cardiac index, and elevated mRAP were poor prognostic factors.
Eleven variables – male gender, older age, comorbid conditions, tachypnoea, tachycardia, multilobar infiltrate or pleural effusion, low or high white blood cell count, hypoxaemia, high blood urea nitrogen, acidosis, hyponatraemia – were independently associated with admission to ICU on days 1 to 3, and were used to derivate the REA-ICU index.
Probable pulmonary embolism: one typical lesion with a corresponding low-grade pleural effusion.
