Chest
Volume 100, Issue 4, October 1991, Pages 943-952
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Fibroproliferative Phase of ARDS: Clinical Findings and Effects of Corticosteroids

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Most patients with adult respiratory distress syndrome (ARDS) survive the initial insult which caused respiratory failure only to succumb later to sepsis caused by nosocomial pneumonia or to pulmonary fibrosis. Clinical criteria and analysis of the tracheal aspirate are notoriously inadequate for establishing a diagnosis of ventilator-associated pneumonia. We implemented a comprehensive diagnostic protocol to determine the cause of sepsis in ARDS patients who had been ventilated for more than three days and who had no bronchoscopic evidence of pneumonia. Nine patients with late ARDS who had fever (89 percent), leukocytosis (89 percent), a new localized infiltrate (78 percent), purulent tracheal secretions (89 percent), low systemic vascular resistance (50 percent), and marked uptake of gallium in the lungs (100 percent) had no source of infection identified. Open-lung biopsy specimens from seven patients showed the fibroproliferative phase of diffuse alveolar damage and confirmed absence of pneumonia. Treatment with prolonged high doses of corticosteroids was associated with a marked and rapid improvement in lung injury score (p<0.003 at five days). Our findings indicate that the fibroproliferative process occurring in the lungs of patients with late ARDS gives rise to clinical manifestations identical to those of pneumonia and is potentially responsive to steroid treatment.

Section snippets

CASE REPORT

A 42-year-old woman (No. 1) with a history of lupus pernio in remission and dysfunctional uterine bleeding developed acute watery diarrhea, abdominal pain, and vaginal spotting. She presented to the emergency room with a systolic BP of 60 mm Hg, metabolic acidosis (lactate 10 mmol/L), and disseminated intravascular coagulation with a platelet count of 11,000/cu mm and prothrombin time and partial thromboplastin time that were twice control values. Her cardiac output was 9.8 L/min and pulmonary

Patient Population

During the course of 16 months, 14 patients were identified with late ARDS and fever. Of these, seven patients were excluded from further diagnostic evaluation upon identification of an infectious source for their fever (four pneumonia, one peritonitis, one wound infection and drug fever, one pancreatitis and deep venous thrombosis). The remaining seven patients with no identifiable source of infection and the two index cases constitute our study population and are subsequently characterized.

Clinical Presentation

The type of illness or injury precipitating ARDS, the APACHE II score, and organ system failure involvement on presentation to the intensive care unit are shown in Table 3. The clinical presentation that prompted an investigation to identify the etiology of sepsis is shown in Table 4. All patients developed clinical manifestations consistent with pneumonia an average of 11 days into mechanical ventilation. Their mean temperature was 38.8°C. All but one had leukocytosis (mean count, 18,740/cu

DISCUSSION

Adult respiratory distress syndrome is the pulmonary manifestation of a diffuse microcirculatory injury that causes exudation of a protein-rich fluid into the pulmonary interstitium and alveolar spaces, thus producing difluse infiltrates on chest roentgenogram, altered oxygen exchange with severe hypoxemia, and a reduction in total thoracic compliance. Most patients (85 percent)1 with ARDS survive the initial illness that resulted in respiratory failure, only to succumb later either to sepsis

CONCLUSION

Our findings, and those of others, have shown that the fibroproliferative phase of late ARDS gives rise to an inflammatory syndrome manifesting with fever, leukocytosis, low systemic vascular resistance, diffuse alveolar infiltrates, diffuse and intense bilateral pulmonary uptake of gallium, and BAL neutrophilia. Bronchoscopy with collection and analysis of distal airway secretions excluded bacterial pneumonia in patients who had clinical findings suggestive of a lower respiratory tract

ACKNOWLEDGMENTS:

The authors wish to acknowledge the expert contribution of Vicky Franke for secretarial support, Dr. David Armbruster for helpful suggestions, and Dr. Elizabeth Tolley for statistical analysis. This study could not have been done without the dedicated service provided by the Thoracic Surgery faculty and fellows.

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    Presented at the annual meeting of the American College of Chest Physicians, Toronto, October 1990.

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