Pleurisy

Etiology: from infections to systemic pathologies

Since pleurisy is a complication, the spectrum of its causes is extremely broad. They are usually divided into two large groups.

Infectious causes:

• Bacteria: most commonly pneumococci, staphylococci, and streptococci (causing parapneumonic effusions), as well as Mycobacterium tuberculosis (tuberculous pleurisy). In lung abscesses or empyema, anaerobes actively participate. Less commonly, the pathogens are gonococci and enterobacteria.
• Viruses: Coxsackie, ECHO, influenza virus.
• Fungi and parasites: rare, occurring in candidiasis, actinomycosis, amebiasis, or echinococcosis.

The source of infection can be neighboring foci of purulent inflammation: mediastinitis, peritonitis, liver abscess, as well as erysipelas, osteomyelitis, and phlegmon. Pleurisy often occurs as a postoperative complication after intrathoracic interventions.

Aseptic (non-infectious) causes:

• Neoplasms: lung cancer, pleural mesothelioma, lymphomas, and metastatic lesions.
• Autoimmune processes: rheumatoid arthritis, systemic lupus erythematosus, systemic sclerosis.
• Vascular catastrophes: pulmonary infarction associated with pulmonary embolism, as well as Dressler's syndrome (combination of post-infarction pericarditis and pleurisy).
• Other factors: chest trauma, enzymatic aggression in pancreatitis, uremia in chronic renal failure, subdiaphragmatic abscesses.

Pathogenesis and clinical variants

In response to the action of an infectious or aseptic agent, a massive release of inflammatory mediators (specifically, cytokines and prostaglandins) occurs. This leads to a sharp increase in the permeability of the pleural capillaries. The further course of events follows one of two paths:

1. Dry (fibrinous) pleurisy. Fluid exudation is minimal. Due to increased vascular permeability, fibrin is actively deposited on the surface of the pleural layers. The pleura loses its smoothness and becomes rough. During respiratory movements, the layers rub against each other, which irritates pain receptors. Over time, the fibrinous deposit may resolve.

1. Exudative pleurisy. The exudation process continues, and fluid begins to rapidly accumulate in the pleural cavity. Large volumes of effusion cause compression of lung tissue, leading to atelectasis and progressive dyspnea. With massive accumulation (up to several liters), the mediastinal organs shift to the healthy side.

Nature of the exudate

Analysis of the pleural fluid allows establishing the primary cause of the pathology:

• Serous effusion is characteristic of tuberculosis, pulmonary embolism, and neoplasms.
• Serofibrinous effusion most often accompanies classic pneumonia.
• Purulent effusion (pleural empyema) indicates an aggressive bacterial infection or a ruptured lung abscess.
• Hemorrhagic exudate is typical for tumor invasion, trauma, and pulmonary embolism.
• Chylous effusion (accumulation of lymph) occurs exclusively with mechanical damage to the thoracic lymphatic duct.

Clinical presentation of dry pleurisy

The leading syndrome in fibrinous involvement is intense chest pain. The pain is acute and stabbing in nature. It is localized predominantly in the lower lateral regions and sharply intensifies with deep breathing, coughing, any movements, or tilting the torso toward the healthy side (due to tension on the affected pleura).

The patient reflexively assumes a forced position: lying on the affected side. This limits the respiratory excursion of the affected half of the chest, and the pain subsides. Additionally, shallow breathing, low-grade fever, and a dry, "sparing" cough are observed, which the patient tries to suppress due to the pain syndrome.

Rules for formulating the diagnosis

Since pleurisy acts as a secondary process, in the diagnosis structure it is recorded as a complication of the underlying disease with mandatory indication of the nature of the effusion, the side of involvement, and the estimated volume of fluid.

Practical examples:

• Primary: Community-acquired right-sided lower lobe pneumonia, severe course. Complication: right-sided exudative parapneumonic pleurisy (500 ml).
• Primary: Central cancer of the right lung (squamous cell, T3N2M1). Complication: right-sided massive exudative tumor pleurisy (2000 ml), hemorrhagic.
• Primary: Systemic lupus erythematosus, activity grade III. Complication: bilateral exudative pleurisy (400 ml on the right, 300 ml on the left).

Class and exam questions

What else to study on this topic

• Clinical presentation and diagnostics of exudative pleurisy
• Purulent pleurisy (pleural empyema): clinical course and surgical tactics
• Specifics of tumor and hemorrhagic effusions
• Dressler's syndrome: mechanisms of immune involvement of serous membranes
• Enzymatic pleurisy in acute pancreatitis

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.