Patterns of reply and Predictors of Outcome Pulmonary fibroproliferation (PFP) is directly or indirectly the leading cause of death in patients with late ARDS.

Patterns of reply and Predictors of Outcome

Pulmonary fibroproliferation (PFP) is directly or indirectly the leading cause of death in patients with late ARDS. We previously reported our experience using intravenous corticosteroids (IVC) in 8 patients with late ARDS and now have expanded our observation to a total of 25 patients with austere fibroproliferation (mean lung injury score [LIS] 3) and progressive respiratory failure (RF) Thirteen patients had open-lung biopsy before treatment. Patients were started upon IVC treatment (IVCT) an average of 15 [+ or -] 75 days into mechanical ventilation (MV) Significant physiologic improvement (SPI) to IVCT was defined as a reduction in LIS of greater than 1 point or an increase in [PaO.sub.2]:[FIO.sub.2] ratio of greater than 100 We observ three patterns of response: rapid responder (RR) had an SPI by dint of day 7 (n=15); delayed responder (DR) had an SPI on day 14 (n=6); nonresponders (NR) were without SPI from day 14 (n=4). Overall, the following significant mean changes were seen within 7 days of IVCT: LIS from 3 to 2 (p=0001) [PaO.sub.2]:[FIO.sub.2] from 162 to 234 (p=00004) begin to appear from 11 to 6.8 cm [Hsub2]O (p=0001) chest radiograph score from 38 to 30 (p=0009) and VE from 16 to 136 L/min (p=001) progress to maturity of pneumonia was related to the pattern of reply Surveillance bronchoscopy was effective in identifying pneumonia in eight afebrile patients. Nineteen of 25 (76 percent) patients survived the ICU admission. Comparisons were made between survivors (S) and nonsurvivors (NS) and among the three clusters of responders. At the time ARDS unraveled no physiologic or demographic variable could discriminate between s and NS. At the time of IVCT, simply liver failure was more every-day in nonsurvivors (p=0.035). Histologic findings at open-lung biopsy and pattern of physiologic rejoinder clearly predicted outcome. The port of preserved alveolar architecture (p=0045) myxoid symbol fibrosis (p=0.045), coexistent intraluminal bronchiolar fibrosis (p=00045) and lack of arteriolar subintimal fibroproliferation (p=0045) separated s from NS. ICU survival rate was 86 percent in responder and 25 percent in nonresponders (p=003) merely one death resulted from refractory respiratory failure.

Fibroproliferation is a stereotypical reaction of the lung to injury characterized by dint of intra-alveolar proliferation of myofibroblasts and collagen deposition, transforming the initial protein-rich exudate into granulation tissue. Unfortunately, this reparative proces is as a common thing [i]or[/i] matter ineffective. Progressive fibro-proliferation is directly or indirectly the leading cause of death in patients with late adult respiratory distress syndrome (ARDS). Directly it causes respiratory death in 15 to 40 percent of patients. Indirectly, it causes ventilator subject territory that predisposes the host to the unravelling of nosocomial infections, particularly pneumonia. We have previously reported our experience using intravenous corticosteroid treatment (IVCT) in eight febrile patients with late ARDS who had histologic evidence of pulmonary fibroproliferation in lung tissue obtained by way of open-lung biopsy and no identifiable source of infection by way of an extensive diagnostic evaluation.[1] Within 7 days of IVCT, we observ a marked improvement in the lung injury score (LIS). Seven of the eight patients survived ICU admission. Our findings were similar to those previously reported by dint of Ashbaugh and Maier[2] and wild swan and Kearl.[3,4] However, IVCT was not universally happy We, therefore, prospectively evaluated 25 patients with late ARDS (including the 8 in our original report) who received intravenous corticosteroids (IVC) for extricate treatment of progressive respiratory failure (mean LIS 3) The sense of this study was to identify [1] patterns of physiologic replication to IVCT and [2] variables predicting the physiologic replication and outcome. The findings of this self-controll clinical, interventional inquiry provide the scientific basis to design a blinded randomized application of mind to assess the effect of IVC in succession the proliferative phase of late ARDS.

METHODS

Patient Population

Twenty-five patients, 8 male and 17 female, received IVCT for late ARDS between July 1989 and September 1992 All patients met diagnostic criteria for ARDS as described by way of Fowler et al.[5] Patients were considered candidates for IVCT if they had [1] evidence of progressive respiratory failure with worsening LIS, and [2] no evidence of active infection. ARDS was caused by the agency of a direct injury to the lung in 10 patients and indirect injury in 15 patients. Direct injuries leading to ARDS included pneumonia in seven chemical aspiration in couple and near drowning in common Indirect injuries leading to ARDS included sepsis in seven (urosepsis, three; candidemia-line sepsis, two; intra-abdominal infection, one; toxic onset one), pancreatitis in three, sickle confined apartment crisis in one, hemorrhagic stroke in one, sudden cardiac death in single and intracranial hemorrhage in two

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