COP Presenting With Bilateral Pleural Effusions in a 23-Year-Old

A 23-year-old female with no significant past medical history presented to the emergency department with three days of dyspnea, productive cough, and generalized fatigue. She reported fever at home reaching 40°C and reduced oral intake. She denied nausea, vomiting, headache, skin rash, joint pain, dry eyes, or dry mouth. There was no history of recent travel, sick contacts, prior antibiotic use, or family history of rheumatologic disease.

On examination she was alert and not in respiratory distress, with a respiratory rate of 20 breaths per minute, heart rate 102, blood pressure 104/59 mmHg, and SpO2 99% on room air. Chest auscultation revealed bilateral coarse crackles more prominent at the right lower zone. She was admitted with a provisional diagnosis of community-acquired lobar pneumonia and started on IV ceftriaxone 2 g daily plus oral azithromycin 500 mg daily.

Despite two days of broad-spectrum antibiotic therapy, the patient continued to spike fevers and required 2L supplemental oxygen. A follow-up chest radiograph revealed obliteration of the right costophrenic angle consistent with pleural effusion with new opacities in the right lower and middle zones. Ceftriaxone was discontinued and piperacillin/tazobactam was started.

Figure 1

Initial Chest Radiograph — Right Lower Zone Opacity

Heterogeneous opacity in the right lower lung zone (black arrow) representing airspace disease initially attributed to lobar community-acquired pneumonia. This appearance is essentially indistinguishable from bacterial pneumonia — a diagnostic trap that COP routinely exploits. The clinical implication: when this pattern fails to improve with appropriate antibiotics over 48–72 hours, the differential must be actively expanded beyond infection.

Figure 2

Follow-Up Radiograph — Developing Pleural Effusion

Obliteration of the right costophrenic angle by pleural effusion (black arrow) with new opacities now involving the right lower and middle zones — a radiographic evolution that occurred despite two days of broad-spectrum antibiotic coverage. Worsening radiographic findings during active antibiotic therapy is a pivotal warning sign: in infectious pneumonia, imaging often stabilizes or slightly worsens before improving; true progression on adequate treatment should prompt urgent re-evaluation of the diagnosis.

Chest ultrasonography confirmed a right-sided anechoic pleural effusion without septations, and a pigtail catheter was placed, draining approximately 400 mL of turbid exudative fluid (LDH 1464 U/L, meeting Light's criteria). Linezolid was added to cover possible staphylococcal superinfection. The pigtail was removed after five days.

Figure 3

Chest Ultrasound — Anechoic Pleural Effusion

Right-sided anechoic pleural effusion without internal septations or solid components (black arrow) on chest ultrasonography. Anechoic appearance argues against a complex empyema or hemorrhagic effusion. The exudative nature by Light's criteria — pleural LDH of 1464 U/L against serum LDH suggesting active inflammation — in the absence of infection on culture is consistent with COP-associated pleural involvement, which occurs in approximately 10–35% of organizing pneumonia cases.

Figure 4

Post-Drainage Radiograph — Lung Re-Expansion

Full lung expansion following pigtail catheter removal (black arrow indicates residual right-sided opacity). Despite successful drainage and lung re-expansion, the residual parenchymal opacity persisted — an important radiographic clue that the underlying process was not simply a parapneumonic effusion but reflected ongoing COP-related airspace disease that would require specific immunosuppressive therapy, not further antibiotic escalation.

Four days after pigtail removal, follow-up CT revealed bilateral moderate airspace disease with consolidation and ground-glass opacities more pronounced on the right, a mild left-sided pleural effusion, and a mild right-sided pneumothorax with small right effusion. Despite continued antibiotic coverage with documented fever and persistent respiratory symptoms, all cultures from blood, sputum, and two sets of blood draws showed no growth. A new left-sided opacity had also appeared.

Figure 5

Follow-Up CT — Bilateral Disease with Bilateral Pleural Effusions

Bilateral moderate airspace disease characterized by consolidation and ground-glass opacities, more pronounced on the right (dominant side). Note the mild left-sided pleural effusion (white arrow) and right-sided pneumothorax with small effusion (black arrow). The bilateral and progressive nature of the disease — emerging despite escalating antibiotic coverage — is the pattern-breaking finding that should lock in COP as the leading diagnosis: true bacterial lobar pneumonia rarely evolves bilaterally in this manner during active therapy.

Given the lack of response to broad-spectrum antibiotics and progressive radiographic disease, bronchoscopy with BAL and transbronchial biopsy was performed. BAL cytology was negative for malignancy and all cultures including AFB were negative. A full autoimmune panel was negative. Histopathology of the transbronchial biopsy confirmed lung tissue with fibrosis and chronic inflammation consistent with organizing pneumonia. Secondary causes were comprehensively excluded. Oral prednisolone 40 mg daily was initiated.

Figure 6

HRCT Two Weeks Post-Discharge — Partial Response to Steroids

Interval improvement in bilateral airspace disease on HRCT two weeks into oral prednisolone therapy, with residual moderate bilateral ground-glass opacities, middle lobe consolidation, and right-sided pleural effusion (black arrow). The partial but clear improvement validates the diagnosis: COP responds to corticosteroids with characteristic speed, often showing radiographic improvement within two to four weeks. Residual ground-glass opacities at this stage are expected and continue to improve with ongoing therapy.

Figure 7

Six Weeks Post-Discharge — Complete Radiographic Resolution

Complete resolution of bilateral pulmonary opacities and right-sided pleural effusion (black arrows) on chest radiograph six weeks after discharge. This dramatic response underscores the exquisite steroid-sensitivity of COP — in most cases, bilateral consolidations, ground-glass opacities, and even associated pleural effusions resolve completely with an adequate corticosteroid course. The rapidity and completeness of response here is both therapeutically gratifying and diagnostically confirmatory.

Discussion

Bilateral pleural effusions as a presenting feature of COP represent one of its most diagnostically challenging atypical presentations. Pleural effusion occurs in approximately 10–35% of organizing pneumonia cases but is more commonly expected in secondary organizing pneumonia than in the cryptogenic form — making its presence in a young patient with no identifiable secondary cause particularly instructive. In this case, the exudative nature of the pleural fluid by Light's criteria (LDH 1464 U/L) initially reinforced the presumption of an infectious parapneumonic effusion, leading to escalating antibiotic coverage. The absence of organisms on two pleural fluid cultures and multiple blood cultures — alongside the progressive bilateral spread of opacities despite antibiotics — was the critical inflection point where infectious etiology became untenable and the diagnostic framework had to shift.

The diagnostic pathway in COP follows a predictable logic of exclusion: secondary causes (infection, autoimmune disease, malignancy, medication, radiation) must be systematically ruled out before the "cryptogenic" label is applied. In this patient, a comprehensive exclusion strategy was employed — negative autoimmune serology, negative cultures across every modality, negative BAL cytology for malignancy, negative COVID-19 and influenza PCR — before the diagnosis was secured histologically via transbronchial biopsy. The bilateral pleural effusions in COP are thought to arise from the same inflammatory process affecting the pleural surface; they respond to corticosteroids in parallel with the parenchymal disease and should not be interpreted as indicating a separate diagnosis requiring separate therapy.

The therapeutic response in this case was complete and sustained. Prednisolone 40 mg daily produced clinical improvement within days, with bilateral opacities resolving and pleural effusion clearing over six weeks. The standard approach — initial dose maintained until radiographic response is established, then slow taper over 6–12 months — is designed to prevent the 36% relapse rate documented in systematic reviews. Weight gain is a common and expected early side effect, as it was here. Clinicians should establish a tapering schedule at discharge, schedule follow-up HRCT at 6–8 weeks, and instruct patients to report promptly if dyspnea returns during the taper, as retreatment with the prior effective dose is typically successful.