Intrapericardial urokinase irrigation and systemic corticosteroids: an alternative to pericardectomy for persistent fibrino-purulent pericarditis.

A 39-year-old man was admitted for upper abdominal pain and shortness of breath. The chest roentgenogram demonstrated cardiomegaly and left lower lobe atelectasis. Echocardiography showed circumferential pericardial effusion with signs of cardiac tamponade. Pericardial biopsy and fluid analysis were consistent with fibrino-purulent pericarditis. Despite broad-spectrum antibiotics, percutaneous and subsequently surgical drainage, pericardial effusion and tamponade recurred. We report successful treatment of a non-resolving fibrino-purulent pericardial effusion by combined intrapericardial irrigation of fibrinolytics and systemic corticosteroids administration as an alternative to pericardectomy.

Protective effects of hypercapnic acidosis on ventilator-induced lung injury.

To investigate whether respiratory acidosis modulates ventilator-induced lung injury (VILI), we perfused (constant flow) 21 isolated sets of normal rabbit lungs, ventilated them for 20 min (pressure controlled ventilation [PCV] = 15 cm H(2)O) (Baseline) with an inspired CO(2) fraction adjusted for the partial pressure of CO(2) in the perfusate (PCO(2) approximately equal to 40 mm Hg), and then randomized them into three groups. Group A (control: n = 7) was ventilated with PCV = 15 cm H(2)O for three consecutive 20-min periods (T1, T2, T3). In Group B (high PCV/normocapnia; n = 7), PCV was given at 20 (T1), 25 (T2), and 30 (T3) cm H(2)O. The targeted PCO(2) was 40 mm Hg in Groups A and B. Group C (high PCV/hypercapnia; n = 7) was ventilated in the same way as Group B, but the targeted PCO(2) was approximately equal to 70 to 100 mm Hg. The changes (from Baseline to T3) in weight gain (Delta WG: g) and in the ultrafiltration coefficient (Delta K(f) = gr/min/ cm H(2)O/100g) and the protein and hemoglobin concentrations in bronchoalveolar lavage fluid (BALF) were used to assess injury. Group B experienced a significantly greater Delta WG (14.85 +/- 5.49 [mean +/- SEM] g) and Delta K(f) (1.40 +/- 0.49 g/min/cm H(2)O/100 g) than did either Group A (Delta WG = 0.70 +/- 0.43; Delta K(f) = 0.01 +/- 0.03) or Group C (Delta WG = 5.27 +/- 2.03 g; Delta K(f) = 0.25 +/- 0.12 g/min/cm H(2)O/ 100 g). BALF protein and hemoglobin concentrations (g/L) were higher in Group B (11.98 +/- 3.78 g/L and 1.82 +/- 0.40 g/L, respectively) than in Group A (2.92 +/- 0.75 g/L and 0.38 +/- 0.15 g/L) or Group C (5.71 +/- 1.88 g/L and 1.19 +/- 0.32 g/L). We conclude that respiratory acidosis decreases the severity of VILI in this model.

Effects of mean airway pressure and tidal excursion on lung injury induced by mechanical ventilation in an isolated perfused rabbit lung model.

OBJECTIVE: To study the relative contributions of mean airway pressure (mPaw) and tidal excursion (V(T)) to ventilator-induced lung injury under constant perfusion conditions. DESIGN: Prospective, randomized study. SETTING: Experimental animal laboratory. SUBJECTS: Fifteen sets of isolated rabbit lungs. INTERVENTIONS: Rabbit lungs were perfused (constant flow, 500 mL/min; capillary pressure, 10 mm Hg) and randomized to be ventilated at identical peak transpulmonary pressure (pressure control ventilation [30 cm H2O and frequency of 20/min]) with three different ventilatory patterns that differed from each other by either mPaw or V(T): group A (low mPaw [13.4+/-0.2 cm H2O]/large V(T) [55+/-8 mL], n = 5); group B (high mPaw [21.2+/-0.2 cm H2O]/small V(T) [18+/-1 mL], n = 5); and group C (high mPaw [21.8+/-0.5 cm H2O]/large V(T) [53+/-5 mL], n = 5). MEASUREMENTS AND MAIN RESULTS: Continuous weight gain (edema formation), change in ultrafiltration coefficient (deltaKf, vascular permeability index), and histology (lung hemorrhage) were examined. In group A, deltaKf (0.08+/-0.08 g/min/cm H2O/100 g) was less than in group B (0.28+/-0.19 g/min/cm H2O/100 g) or group C (0.41+/-0.29 g/min/cm H2O/100 g) (p = .05). Group A experienced significantly less hemorrhage (histologic score, 5.4+/-2.2) than groups B (10.3+/-2.1) and C (11.1+/-3.0) (p < .05). A similar trend was observed for weight gain. In contrast to tidal excursion, mPaw was found to be a significant factor for lung hemorrhage and increased Kf (two-way analysis of variance; p < .05). Weight gain (r2 = .54, p = .04) and lung hemorrhage (r2 = .65, p = .01) correlated with the mean pulmonary artery pressure changes that resulted from the implementation of the ventilatory strategies. The difference between the changes in mPaw and mean pulmonary artery pressure linearly predicted deltaKf (p = .005 and .05, respectively, r2 = 0.73). CONCLUSIONS: Under these experimental conditions, mPaw contributes more than tidal excursion to lung hemorrhage and permeability alterations induced by mechanical ventilation.

Consequences of vascular flow on lung injury induced by mechanical ventilation.

To investigate whether the magnitude of blood flow contributes to ventilator-induced lung injury, 14 sets of isolated rabbit lungs were randomized for perfusion at either 300 (Group A: n = 7) or 900 ml/ min (Group B: n = 7) while ventilated with 30 cm H2O peak static pressure. Control lungs (Group C: n = 7) were ventilated with lower peak static pressure (15 cm H2O) and perfused at 500 ml/min. Weight gain, changes in the ultrafiltration coefficient (DeltaKf) and lung static compliance (CL), and extent of hemorrhage (scored by histology) were compared. Group B had a larger decrease in CL (-13 +/- 11%) than Groups A (2 +/- 6%) and C (5 +/- 5%) (p < 0.05). Group B had more hemorrhage and gained more weight (16.2 +/- 9.5 g) than Groups A (8.7 +/- 3.4 g) and C (1.6 +/- 1.0 g) (p < 0.05 for each pairwise comparison between groups). Finally, Kf (g . min-1 . cm H2O-1 . 100 g-1) increased the most in Group B (DeltaKf = 0.26 +/- 0. 20 versus 0.17 +/- 0.10 in Group A and 0.05 +/- 0.04 in Group C; p < 0.05 for B versus C). We conclude that the intensity of lung perfusion contributes to ventilator- induced lung injury in this model.

Influence of prone position on the extent and distribution of lung injury in a high tidal volume oleic acid model of acute respiratory distress syndrome.

OBJECTIVE: To evaluate the influence of body position on the extent and distribution of experimental lung damage in an oleic acid canine model of acute respiratory distress syndrome, using mechanical ventilation with high tidal volumes and positive end-expiratory pressure (PEEP). DESIGN: Prospective, randomized study. SETTING: Experimental animal laboratory. SUBJECTS: Twelve anesthetized and paralyzed dogs. INTERVENTIONS: Ninety minutes after lung injury was induced by injection of oleic acid, 12 animals were randomized to be ventilated for 4 hrs, in either the supine (supine group, n = 6) or prone (prone group, n = 6) positions, using the same ventilatory pattern (F10(2) 0.6, PEEP > or = 10 cm H2O, and a tidal volume that generated a peak transpulmonary pressure of 35 cm H2O when implemented in the supine position). Regardless of randomization to position, the tidal volumes, F10(2), and PEEP were kept constant and the pulmonary artery occlusion pressure was maintained between 4 and 6 mm Hg for the duration of the study. MEASUREMENTS AND MAIN RESULTS: At the end of the protocol, the lungs were excised for gravimetric determination (wet/dry weight ratio) and histologic examination (histologic score). Changes over time in the static pressure-volume curve of the lungs (obtained in the supine position) were also used as end-point variables. At baseline, hemodynamic and respiratory variables did not differ between groups. Just before randomization to position (90 mins after oleic acid injection), both groups presented similar lung static pressure-volume curves. Pulmonary artery occlusion pressure (4.3 +/- 1.9 vs. 4.8 +/- 1.3 mm Hg [supine vs. prone group]), cardiac output (4.1 +/- 0.4 vs. 5.2 +/- 1.3 L/min [supine vs. prone group]), and venous admixture (36.7 +/- 20.7% vs. 28.3 +/- 19.4% [supine vs. prone group]) were also not significantly (p > .05) different when measured in the supine position. At the end of the experiment, lung gravimetric data in the two experimental groups were not statistically different, suggesting a similar extent of edema. Histologic abnormalities, however, were less in the prone group than in the supine group (p < .01), due primarily to marked differences in extent and severity in the dependent regions of the lungs. Static lung compliance improved over time in the prone group (34 +/- 9 to 46 +/- 19 mL/cm H2O)(p = .02), but not in the supine group (34 +/- 6 to 36 +/- 6 mL/cm H2O). CONCLUSIONS: After oleic acid-induced lung injury, animals ventilated with high tidal volume and PEEP undergo less extensive histologic change in the prone position than in the supine position. The prone position alters the distribution of histologic abnormalities.