Explosive pleuritis: a rare case of fever and chest pain

Pleurisy is characterized by pleural inflammation resulting from various factors, including primary diseases or systemic conditions. Pleurisy can manifest suddenly (hyperacute) in emergencies like a pneumothorax or pulmonary embolism, leading to signs and symptoms such as tachypnea and dyspnea.[1] Viral and bacterial pneumonia can also trigger pleuritic pain acutely within hours to days, potentially causing parapneumonic effusions.[1] In fact, parapneumonic effusions occur in up to 20% to 40% of hospitalized patients with pneumonia.[2] Subacute or chronic pleurisy (lasting days to weeks) is linked to diseases like rheumatoid arthritis, malignancy, or tuberculosis.[1]

On rare occasions, pleural inflammation can be intense leading to explosive pleuritis. Explosive pleuritis is an extremely uncommon and critical medical condition characterized by the rapid development of pleural effusion within 24 h, leading to significant lung compression and mediastinal shift.[3] The exact definition of explosive pleuritis remains a subject of debate among experts.[4]Approximately 11 cases of explosive pleuritis were reported between 1986 and 2020.[4] This condition is commonly associated with bacterial infections that can access the pleural space through various means, including direct spread from bronchopulmonary infections like pneumonia, lung abscesses, and bronchiectasis.[5] Here, we report a specific case of explosive pleuritis, highlighting its rapid progression through multiple imaging tests within 24 h of presentation.

A 42-year-old male with no significant medical history presented to the emergency department (ED) with a two-day history of fever, pleuritic chest pain, and shortness of breath. His fever at home was measured with a maximum temperature of 38.9 °C, and he had accompanying symptoms of chills, muscle aches, and night sweats. He described his chest pain as localized to the right lower lateral aspect of the chest, exacerbated by deep inspiration, while coughing and chest movement. The patient also reported recent sick contact at home: his son had been experiencing fever for the past two weeks. Over the 24 h preceding his presentation to the ED, the patient’s shortness of breath worsened, prompting him to seek medical attention. On initial evaluation, vital signs were notable for mild tachycardia of 110 beats/min, a temperature of 38.5 °C, respiratory rate of 20 breaths/min, and oxygen saturation of 100% on room air. Physical examination revealed that his lungs were clear to auscultation with no increased work of breathing, and the patient did not require supplemental oxygen.

Initial laboratory investigations showed leukocytosis (15,400 cells/mL), elevated inflammatory markers, and mildly elevated liver function indicators. The initial chest X-ray appeared normal (Supplementary Figure 1). Notably, the patient had an elevated D-dimer levels, prompting a computed tomography angiography (CTA) scan to rule out pulmonary embolism. CTA did not reveal a pulmonary embolism but did show a small right-sided pleural effusion, which was likely the source of the patient’s pleuritic chest pain. Given the known sick contact and viral symptoms, the provisional diagnosis was an acute viral infection and potential discharge from the ED.

Despite receiving nonsteroidal anti-inflammatory drugs and acetaminophen, the patient’s fever and tachycardia persisted. He also continued to experience chest pain and began to develop increased breathing, so the admission decision for further evaluation and treatment.

Subsequent imaging the next day with a chest X-ray (Figure 1A) and CT scan of the abdomen and pelvis demonstrated an expanding and moderate right pleural effusion with adjacent compressive atelectasis. The interventional pulmonology team was consulted, and a chest tube was placed (Figure 1B), which drained approximately 1,400 mL of yellow-orange fluid on day 3 of hospitalization. Analysis of the pleural fluid showed a pH of 6.9 with low glucose and significantly elevated white blood cell counts, indicating an exudative effusion and possible empyema. The patient remained febrile (39.4 °C) with worsening leukocytosis and bandemia (Supplementary Table 1), necessitating treatment with multiple broad-spectrum antibiotics.

Figure 1.

The results of the chest X-ray of our patient after admission and after the placement of a chest tube. A: the right-sided pleural effusion on day 2; B: the clearance of pleural fluid following chest tube placement on day 3.

Despite adequate chest tube placement that was confirmed in subsequent imaging studies, a large pleural effusion had re-accumulated. This caused additional concern for pneumonia patients with lung abscess (Figure 2A) and prompted consultation with the thoracic surgery team. The thoracic surgery team elected to perform a right thoracoscopy with drainage of the pleural effusion and pleurodesis. A very large right pleural effusion, predominantly serous in nature, was completely drained, amounting to roughly 2.4 L. A large bore chest tube was inserted following the procedure (Figure 2B).

Figure 2.

The results of the chest X-ray of our patient before and after the thoracotomy procedure. A: reaccumulation of large pleural effusion; B: clearance of effusion post-thoracotomy procedure.

Following the thoracoscopy and pleurodesis, the patient’s condition significantly improved. Vital signs returned to normal, and inflammatory markers as well as leukocytosis improved (Supplementary Table 1). The patient was discharged on day 10 after hospitalization, and his symptoms had resolved entirely.

‘Explosive pleuritis’ was a term coined by Braman and Donat in 1986.[6] They used it to describe rapid ipsilateral pleural effusion development in two patients with invasive group A beta-hemolytic streptococcal infection without initial bronchopneumonia.

The pathogenesis of explosive pleuritis involves intense pleural inflammation triggered by invasive pathogens, most frequently group A beta-hemolytic streptococci.[4] These pathogens exhibit a unique propensity to block peribronchial and subpleural lymphatics with cellular and necrotic debris.[6] Explosive pleuritis can also be triggered by various other etiologies, including malignancy, parapneumonic effusions, hydrothorax related to liver cirrhosis, and idiopathic causes.[3]Additionally, open chest trauma, which can be iatrogenic from thoracotomy complications, and intra-abdominal infections such as subphrenic abscesses may lead to empyema, further emphasizing the multifactorial etiologies of this condition.[3]

The management of explosive pleuritis necessitates prompt intervention to alleviate symptoms and prevent complications. Early consideration of the disease is important when initial symptoms are mild but rapidly progressive. When suspected, early drainage with a chest tube is considered essential, but it is important to acknowledge that minimal fluid drainage is common in explosive pleuritis cases. To enhance drainage and potentially avoid surgical intervention, intrapleural administration of tissue plasminogen activator (tPA) and DNase can be employed to break down loculations. However, in cases where these measures are unsuccessful, surgical decortication may be necessary.[4] Thoracoscopy is less invasive and is the procedure of choice compared to thoracotomy, which is associated with significant morbidity and mortality.[4] Thoracoscopy plays a crucial role for diagnostic and treatment purposes.[7-9] An alternative to open biopsy is suggested when bronchoscopic transbronchial biopsy specimens are inconclusive. It provides reliable tissue samples for diagnosing mesothelioma and allows accurate staging, reducing the need for unnecessary thoracotomy.[9,10] As a treatment, thoracoscopy with pleurodesis can prevent recurrence of pleural effusions. It is particularly important in treatment of recurrent malignant pleural effusions, where the main goal is to relieve symptoms and stop fluid reaccumulation.[11]

By examining the literature on explosive pleuritis, we find that reported cases have similarities to our patient, including the rapid clinical deterioration and characteristic radiological changes observed (Supplementary Table 2). Streptococcus species, particularly group A beta-hemolytic streptococci, emerge as frequently implicated pathogens in explosive pleuritis, and this was also the case for our patient whose culture returned positive for S. pyogenes. However, explosive pleuritis can also result from various other bacterial agents, and in some instances a definitive microbiological diagnosis may prove elusive (Supplementary Table 2).

Fever and chest pain is the predominant symptoms of explosive pleuritis, highlighting the diagnostic challenges due to the presence of these symptoms in numerous conditions. It can affect a wide age range and has noticeable male gender predominance. Despite a diverse prevalence of comorbidities in patients who develop explosive pleuritis, 53% of cases had no identified additional health conditions (Supplementary Table 3). Early evidence of pleural fluid loculation seems to be a hallmark of explosive pleuritis cases. In most cases, the aspiration of pleural fluid was limited, likely due to these widespread loculations. Similar to our patient, some of the patients also required decortication, highlighting the severity of the condition and its occasional need for invasive, potentially high risk interventions. In the reported cases, the onset and duration of explosive pleuritis varied significantly with examples of both acute and insidious presentations. Previous cases also had varied clinical courses, where some patients experienced rapid decompensation and others showed full resolution with early interventions (Supplementary Table 2).

Despite these similarities, our case also demonstrates some distinctive characteristics. One is that we were able to drain a substantial fluid volume of approximately 2.4 L, a significantly higher volume than had been reported in most previous cases. Our case also experienced thoracoscopy with pleurodesis as an effective intervention for rapidly deteriorating and unresolved pleural effusion following chest tube placement. This approach has not been documented in any previously reported cases of explosive pleuritis.

In conclusion, we present a rare case of explosive pleuritis secondary to S. pyogenes infection, characterized by a hyperacute onset of pleuritic chest pain and dyspnea with associated rapid progression of effusion on radiologic studies. With the early placement of a chest tube and subsequent thoracoscopic surgery, the patient had resolution of symptoms and was discharged in good condition. This case highlights the importance of broadening the differential and considering uncommon sequelae of an otherwise straightforward presentation, continually re-assessing the effect of medical management and considering surgical management strategies.

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