Artificial respiratory instrument can be applied in
Case 260
【Discussion】
BAL (bronchoalveolar lavage) indicates normal range macrophages 85-90%, lymphocytes 9-11% and neutrophils 1% (1). That indicates the percentage of neutrophils in BAL is least in normal person. The marked elevation of neutrophils occurs in bacterial pneumonia, acute interstitial pneumonia (AIP) and acute respiratory distress syndrome (ARDS)(2, 3). Pathologic findings of AIP and ARDS are usually common: diffuse alveolar damage (DAD)(4). However, radiologic findings differ between ARDS and AIP. ARDS is shown bilateral lesions with consolidation on chest CT while AIP is shown the lesion with ground glass opacity associated with melon skin pattern or crazy paving appearance in bilateral lower lobes on chest CT (5-7).
The differences between AIP and ARDS are known that AIP occurs from unknown origin, namely idiopathic, while ARDS occurs from dedicated causes such as sepsis from bacterial or viral infection, aspiration pneumonia, contusion (4-7). AIP is sometimes called ARDS from unknown origin. However, the radiologic image of AIP is a little different from ARDS described above (7).
Pathologic findings revealed AIP stages: exudative, proliferative organizing and fibrotic (7). In the exudative stage, it showed necrosis of alveolar cell type Ⅰ, hyperplasia of alveolar cell type Ⅱ, infiltration of lymphocyte and neutrophils in the septum and hyaline membrane covering surface of alveolar cell line. This is corresponded to ground glass opacity with crazy paving pattern on chest CT. In the proliferative organizing stage, it showed proliferation of fibroblastic & myo-fibroblastic cells that are differentiated from alveolar cell type Ⅱ in the alveolar septum and often protrusion of them into alveolar space. In the fibrotic stage, remnant fibrosis with bronchus and/or bronchioles traction inducing tortuous bronchioles and cystic formation like honeycomb appearance (7).
When respiratory failure that indicate PaO2 less than 60mmHg or SpO2 less than 90% occurs in AIP, artificial respirator is used (4, 5). In our case, the worst respiratory failure was SpO2 lowered 86% (PaO2 approximately 56mmHg) with FiO2 0.8, indicative of PF ratio was 70 mmHg that implied severe respiratory failure (ARDS) state (After artificial respirator under PEEP 8 mm H2O, the respiratory state improved to SpO2 94% (PaO2 approximately 64%) with FiO2 0.5 indicative of PF ratio 128 mmHg.
The prognosis of AIP was poor, 6-month fatal rate is approximately 50% (4, 5). It depends on the regenerative potency of pulmonary cell type II that play roles of stem cell, inducing to differentiate into alveolar cell type1, fibroblast and myo-fibroblast. Unfortunately, the value of KL-6 was 2219 U/mL, quite high, implying poor prognosis.
【Summary】
We presented a sixty-six-year-old male for respiratory failure after PTGBD. Gas analysis revealed that SpO2 lowered 86% (PaO2 approximately 56mmHg) with FiO2 0.8, indicative of PF ratio was 70 mmHg, indicative of severe respiratory failure state (PF ratio < 100 mm Hg). Chest CT depicted bilateral diffuse ground glass opacity with crazy paving pattern including patchy consolidation. Laboratory test revealed KL-6 2219 U/mL. It is borne in mind that conspicuous elevation of neutrophils in BAL occurs in bacterial pneumonia, AIP and ARDS. ARDS is termed when the causes of respiratory failure are identical, while AIP is termed in case of unknown causes. Although histologic findings of AIP and ARDS are diffuse alveolar damages, CT findings are little different in a point that the main CT finding of AIP was melon skin appearance while that of ARDS vary, consolidation surpasses ground glass opacity. It is probably because alveolar cell type I damages more than alveolar cell type II and granulation protrusion is almost limited in alveolar line. When the damages of type II alveolar cell grow greater, poor prognosis is anticipated such as our case.
【References】
1.Kahn, F.W. et al. "Diagnosing bacterial respiratory infection by bronchoalveolar lavage". Journal of Infectious Diseases. 1987; 155 (5):826–9.
2.Nieto, JMS, et al . "The role of bronchoalveolar lavage in the diagnosis of bacterial pneumonia". European Journal of Clinical Microbiology and Infectious Diseases. 1995; 14 : 839–50.
3.Meyer, KC, et al. "An official American Thoracic Society clinical practice guideline: The clinical utility of bronchoalveolar lavage cellular analysis in interstitial lung disease" (PDF). American Journal of Respiratory and Critical Care Medicine. 2012; 185 (9): 1004–14.
4.Artigas A, et-al. The American-European Consensus Conference on ARDS, part 2. Ventilatory, pharmacologic, supportive therapy, study design strategies and issues related to recovery and remodeling. Intensive Care Med. 1998;24 (4): 378-98.
5.Bernard GR, Artigas A, Brigham KL et-al. Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination. Consensus Committee. J Crit Care. 1994;9 (1): 72-81. Pubmed citation
6.Desai SR, Wells AU, Rubens MB et-al. Acute respiratory distress syndrome: CT abnormalities at long-term follow-up. Radiology. 1999;210 (1): 29-35.
7.Ichikado K, et al. Acute Interstitial Pneumonia Comparison of High-Resolution Computed Tomography Findings between Survivors and Nonsurvivors. Am J Respir Crit Care Med. 2002 Jun 1;165(11):1551-6
2022.3.11