Affiliations: Oklahoma City, OK
Dr. Tawk is Assistant Professor of Medicine, and Dr. Kinasewitz is Professor of Medicine and Chief Pulmonary and Critical Care Medicine, University of Oklahoma Health Sciences Center.
Correspondence to: Gary T. Kinasewitz, MD, FCCP, University of Oklahoma Health Sciences Center, 920 Stanton L. Young Boulevard, WP, Oklahoma City, OK 73104; e-mail: email@example.com
Postthoracotomy pain is relatively easy to understand given the trauma to the chest wall and ribcage that occurs during surgery.1Approximately one half of the patients who undergo thoracotomy will continue to have chronic pain unrelated to recurrent disease 1 year after surgery.2–3 Video-assisted thoracic surgery is less invasive but is still associated with significant long-term morbidity.4Even simple pleural sclerosis by abrasion or talc poudrage for benign disease such as spontaneous pneumothorax results in chronic pain in 10 to 30% of patients 1 year after video-assisted thoracic surgery.5–7 While it is tempting to blame injury to the intercostal nerve or adjacent rib for the chronic pain, the answer may lie within the thoracic cavity.
The goal of any procedure designed to obliterate the pleural space is to create fibrous adhesions firmly joining the visceral and parietal pleura. Previous experimental studies of pleurodesis have focused on the inflammatory response to various sclerosing agents and the subsequent development of fibrous bands that connect the opposing pleural surfaces. In this issue of CHEST (see page 702), Montes and colleagues8 closely examine the adhesions that develop in a rabbit model of talc pleurodesis, and note they are actually complex structures containing newly formed blood vessels, lymphatics, and nerve fibers within the collagenous bands. The nerve fibers within these adhesions are thin myelinated axons suggestive of Aδ, nerve fibers that are pain-conducting fibers. The clinical significance of these observations is unclear.
We can glean a clue as to their importance, however, if we look below the diaphragm. Our colleagues in gynecology and general surgery have been dealing with the problem of pelvic and intra-abdominal adhesions for years. Careful examination of these adhesions has revealed the presence of thin myelinated and unmyelinated nerve fibers in 60 to 100% of these adhesions.9–12 These nerve fibers have the morphologic characteristics of pain fibers and react with antibodies to the neuropeptides calcitonin gene-related peptide, expressed by sensory neurons, and substance P, present in pain-conducting fibers.12Adhesions were the most common pathology observed in a group of women undergoing laparoscopy for chronic pelvic pain.13While adhesions were also noted in some asymptomatic control subjects undergoing tubal ligation, adhesions were three times more common and tended to be tighter and more restrictive of organ movement in patients with chronic pain. Many but not all women with adhesions have chronic pain; and even in the absence of symptoms, manipulation of the adhesions evokes a feeling of discomfort.14
Are adhesions between the parietal and visceral pleura responsible for the chest wall pain that develops in some patients following pleurodesis? The study by Montes et al8 suggests a plausible mechanism, but careful examination of pleural tissue from patients and correlation with clinical symptoms is required before the question can be answered. Until then, we must be aware of this possibility when considering pleurodesis for a benign disease and advise our patients accordingly.
The authors have no conflicts of interest to disclose.
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