ABSTRACT
Twelve years ago we reported that lymphocytic alveolitis [or bronchoalveolar lavage (BAL) lymphocytosis] correlates with clinical pulmonary involvement in primary Sjogren's syndrome (pSS). Our thesis was based on subtle clinical and functional evidence of interstitial lung disease (ILD) in pSS patients with "high lymphocytic alveolitis" (>15% lymphocytes in BAL). This report is a follow-up study of these patients. Basic clinical and functional re-evaluation of the 22 patients with pSS, studied in 1991, emphasized the differences between those with alveolitis and those without alveolitis. There was no significant functional decline. There were, however, two statistically significant differences between the two groups: (1) only patients with BAL lymphocytosis had to be treated with steroids (5/12 vs. 0/10, P < 0.05) and (2) only patients with BAL lymphocytosis had died in the mean time (6/12 vs. 0/10, P < 0.01). The causes of death were various. On only two occasions were they related to respiratory infections while there were no deaths from respiratory failure secondary to ILD. BAL lymphocytosis appears to be a surprisingly serious index of dismal prognosis in patients with pSS. We offer no unifying pathophysiologic mechanism for it and, therefore, all we propose is that BAL is performed early, in as many patients with pSS as possible. These patients should then be followed up systematically, in order to evaluate if BAL lymphocytosis has any pathophysiologic importance in the development of clinically serious pSS, which is serious enough to lead to death.
Subject(s)
Lung Diseases, Interstitial/pathology , Pulmonary Alveoli/pathology , Sjogren's Syndrome/complications , Sjogren's Syndrome/pathology , Bronchoalveolar Lavage Fluid/cytology , Complement C3/analysis , Complement C4/analysis , Humans , Lung Diseases, Interstitial/etiology , Lung Diseases, Interstitial/mortality , Middle Aged , Prognosis , Pulmonary Fibrosis/diagnosis , Pulmonary Fibrosis/etiology , Pulmonary Fibrosis/pathology , Sjogren's Syndrome/mortality , Sjogren's Syndrome/therapyABSTRACT
BACKGROUND/AIMS: Laparoscopic cholecystectomy is accompanied by significant increase of the respiratory system elastic and resistive properties. These changes are completely abolished after peritoneal deflation. In the present study we examine the volume and flow dependence of respiratory mechanics during four operation phases. METHODOLOGY: Airway pressure and flow were recorded from 17 patients undergoing laparoscopic cholecystectomy. Measurements were done at 4 distinct phases: 1) Before the induction of pneumoperitoneum. 2) Five minutes after pneumoperitoneum induction at Trendelenburg position. 3) Five minutes after positioning the patient at reverse. Trendelenburg. 4) Five minutes after the peritoneal deflation. Data of airway pressure, flow and volume were treated according to the non-linear regression model: Paw = E1.V + E2.V2 + k1.V' + k2.V'. |V'| + k3.V.V' + EEP. RESULTS: The induction of pneumoperitoneum results in: Significant increase of linear elastance and resistance and significant decrease of flow and volume dependence of resistance. No significant changes are noted in volume dependence of elastance and end-expiratory pressure. CONCLUSIONS: The pneumoperitoneum and not the body position causes the changes in respiratory mechanics and their dependencies during laparoscopic cholecystectomy, which, although important, do not predispose to major risks (lung overdistension, alveolar collapse) and they are reversed after peritoneal deflation.
