Pleuritis is defined as inflammation of the pleura. The pleural space, a thin fluid-filled space between the lung and the thoracic cavity, enables the smooth frictionless movement of the lung during respiration. It is lined by 2 layers of pleura: the visceral (covering the lung) and the parietal (covering the thoracic cage). Pain receptors are present on the parietal pleura. Irritation and inflammation of the pleura presents with symptoms of sharp lancing, fleeting pain in the chest that is exacerbated by deep breathing, coughing, sneezing, or Valsalva (forced expiration against a closed airway) and Mueller manoeuvres (reverse of Valsalva manoeuvre).
It is important to exclude potentially life-threatening conditions such as pulmonary embolism, acute coronary syndrome, aortic dissection, and pneumothorax during evaluation. Pneumonia must also be considered. Though not causes of pleuritis per se, conditions such as pericarditis, perforated viscus, and costochondritis should be considered in the differential diagnosis when patients present with chest pain that is pleuritic in nature.
The pleural space is a potential space that can be filled with a variety of substances including transudative fluid, exudative fluid, pus, blood, air, or chyle. The pleural lining consists of a single layer of mesothelial cells supported by connective tissue. This layer not only acts as a mechanical envelope but also serves a biological role. It regulates diffusion of substances into the pleural space and plays an integral role in inflammatory responses to stimuli such as infection, traumatic injury, or introduction of foreign substances such as air, blood, or asbestos. Mesothelial cells recognise invasion of the pleural space and initiate recruitment of cells through coordinated expression of cytokines, chemokines, and vascular adhesion molecules. Prompt resolution of the inflammation may allow the pleural surface to return to normal with no sequelae. However, prolonged inflammation will result in distortion of normal structure by fibrosis, adhesions, and scarring. Resolution of inflammation is directed by initiation of neutrophil apoptosis by mesothelial cells.
- Bacterial pneumonia
- Pulmonary embolism
- Non-mesothelioma malignancy
- Acute coronary syndrome
- Viral pleuritis
- Asbestos-related benign pleural disease
- Pulmonary/extrapulmonary tuberculosis (TB)
- Connective tissue disorders
- Drug reactions
- Aortic dissection
- Post-cardiac injury syndrome (PCIS)
- Acute pancreatitis
- Chronic pancreatitis
Steve Walker, MBChB
Pleural Research Fellow
SW declares that he has no competing interests.
Nicholas Maskell, FRCP, DM
Consultant Senior Lecturer
Department of Clinical Sciences
University of Bristol
NM has received an honorarium from BD for sitting on their advisory board. Their products have no relation to the topic of this monograph.
Dr Steve Walker and Dr Nicholas Maskell would like to gratefully acknowledge Dr Kathryn Bateman, Dr Praveen Mannam, and Dr Terence K. Trow, previous contributors to this monograph. The contributors would also like to thank Dr Ami N. Rubinowitz, Assistant Professor of Medicine, Division of Radiology, Yale University School of Medicine, New Haven, CT, for providing the images.
KB and PM declare that they have no competing interests. TKT is on the Advisory Board for Encysive, Actelion, United Therapeutics, and Gilead Pharmaceuticals and the Speaker's Bureau for Encysive, Actelion, and United Therapeutics.
Philip W. Ind, BA (Cantab), MB BChir, MA (Cantab), FRCP
Honorary Senior Lecturer
Imperial College Healthcare Trust
PWI declares that he has no competing interests.
Sangeeta Bhorade, MD
Associate Professor of Medicine and Medical Director
Lung Transplant Program
University of Chicago Hospitals
SB declares that she has no competing interests.
Sanjay Sethi, MD
Professor of Medicine
Pulmonary/Critical Care/Sleep Medicine
University at Buffalo
State University of New York
Pulmonary/Critical Care/Sleep Medicine
VA Western New York Healthcare System
SS declares that he has no competing interests.
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