Pleural effusion is a common occurrence in emergency rooms (ER) around the world and a constant reason for a pulmonology consultation. In the United States, nearly 1.5 million cases of pleural effusion are diagnosed each year. Congestive heart failure (CHF) is the most common cause followed by pneumonia. Traditionally, pleural effusions are divided into transudate and exudate. Transudate implies an intact capillary membrane but increases hydrostatic pressure due to fluid overload. Exudative effusion is a result of capillary damage secondary to an inflammatory process.
Pleural effusions can be treated with thoracentesis, and they do not recur if the underlying cause is corrected. However, a significant number of effusions do not resolve or if treated, come back very quickly. These types of effusion cause a significant healthcare burden, and they are very uncomfortable for the patient and difficult for caregivers.
Malignant pleural effusions (MPE) are the most common among these refractory pleural effusions. Lymphoma, breast, and lung cancers are the leading cause of MPEs. Among non-malignant pleural effusions, CHF and hepatic-hydrothorax are most common.
Visceral pleura covers the lung surfaces and inter-lobar fissures, while the parietal pleura covers the mediastinum, chest wall, and diaphragm. Both the lungs have three separate visceral and parietal pleurae. Therefore, pneumothorax of one lung does not result in bilateral pneumothoraxes. There is a "real" space between the visceral and parietal pleura. This pleural space surrounds the lung and is approximately 10 to 15 micrometers wide.
It consists of a mesothelial cell layer and a sub-pleural layer. It overlies the costal fascia and ribs. The mesothelial layer of parietal pleura consists of stomata for lymphatic drainage.
The visceral pleural also consists of a layer of mesothelial cells and a sub-pleural layer. Visceral pleura is thin cranially and thick caudally due change in the density of the sub-pleural layer.
Malignant Pleural Effusions
An intrapleural catheter (IPC) is the treatment of choice for MPEs associated with respiratory failure. Lung cancer is the most common cause of MPEs followed by breast cancer and lymphoma.
Non Malignant Pleural Effusions
There is growing literature supporting IPC for chronic non-malignant effusions associated with respiratory failure or dyspnea affecting the quality of life. The most common reason is CHF followed by hepatic-hydrothorax. There have been few reported cases of chylothorax, of unknown or uncorrectable etiology, successfully treated with IPC.
Post-Lung Transplantation and Chronic Pleural Infection
There is some success reported with IPCs in treating post lung transplant chronic effusions and pleural infections. However, there is no current recommendation to use IPC for these patients. It should include the therapy of last resort.
There are no absolute contraindications for IPC insertion. The common contraindications for any minor surgical procedures will hold for IPC placement as well.
IPC catheter is a 66 cm catheter made of soft silicone. It has fenestration on either side on the insertion end up to 24 cm and a one-way valve on the drainage end. There is a soft polyester foamy cuff at the junction of proximal two-thirds and distal one-third. This cuff promotes tissue ingrowth to provide stability to the catheter against accidental pull-out or entanglement. It usually comes in a packet containing the catheter, a metal catheter introducer, a regular dilator, and a peel-off dilator with the inner regular dilator, local anesthetic, sutures, scalpel, scissors, and artery forceps.
Have the patient rest on his or her back and then raise the head of the bed to 45 degrees. Expose the lateral chest wall by raising and folding the arm at the elbow over the head. If the patient can not hold his arm for the duration of the procedure, then use tape or a sling to secure it against the bed.
Use bedside ultrasound to assess the size of pleural effusion and a suitable site should be selected. The site is selected, preferably, in the safety triangle around the four intercostal space in the mid-axillary line.
Clean the area with antiseptic, and use surgical drape to ensure aseptic technique. Use surgical gowns, gloves and mask just as placing the central venous catheter.
Give local anesthesia at the pre-selected site (site-1). Start by injecting into the skin and the subcutaneous tissue, and finally, puncture the pleura and confirm easy flow of fluid. Ensure that there is no resistance from puncturing the skin to the pleura. In other words, the path of the needle should be completely unrestricted to allow easy dilatation of the tissue later on. Remove the syringe and insert guidewire. Then remove the needle. Give 1 to 1.5 cm incision at site-1; the guide wire should be in the middle of the incision (incision-1).
Next, select another site (site-2), 5 cm below and inferior to site-1. Give local anesthesia. Make 1 cm vertical incision (incision-2). Now give generous local anesthesia in the area between the 2 incisions. This is to anesthetize the "tunnel" for the IPC. Take the metal introducer and attach the proximal end of the catheter to its distal end which has grooves to hold the catheter and avoid slipping during insertion.
Insert the metal introducer from incision-2 toward incision-1. Apply gentle pressure and rotating motion to create a percutaneous tunnel. Once the introducer is out from incision-1, pull the catheter out and adjust in a way that the polyester cuff is in the subcutaneous tissue approximately 1cm from the incision-2. Remove the introducer from the catheter.
Dilate the catheter tract like central line insertion using Seldinger technique. Now use the dilator with the detachable outer core and a regular inner dilator. Insert this dilator till the edges touch the skin. Remove the inner dilator and the guide wire. There will be a gush of pleural fluid. Insert the proximal end of the IPC through the dilator into the pleural cavity. Once all the fenestrations are inside the pleural cavity, then start peeling off the outer dilator and simultaneously pushing the remaining catheter. Once the catheter is fully inserted, make sure that there is no kinking of the catheter. Lastly, suture both the incisions and apply a dry dressing. Sutures can be removed in 1 week.
Infection Similar to a long-term urinary catheter, bacteria can colonize an IPC. The pleural fluid culture will be positive, but there will no signs or symptoms or characteristic biochemical profile pathognomonic for empyema. In some patients, diagnosis of pleural infection might be challenging since most MPEs have low pH, high lactate dehydrogenase, and may be low glucose as well. So far, the incidence of IPC-related pleural infection is not known. Also, the diagnostic criteria for a diagnosis of pleural infection are same for patients with IPCs.
Skin flora most commonly Staphylococcus aureus is reported in case reports followed by Pseudomonas aeruginosa. Fsych et al. reported, in a large multicenter trial involving 1021 patients, the incidence of infection to be only 4.8% and mortality of 0.29%.
Infection usually happens 6 to 8 weeks post-insertion and is more likely related to post-insertion care rather than bacterial colonization during the procedure. Interestingly, IPC-related pleural infection often leads to pleurodesis, particularly with a Staphylococcus infection.
There is no documented increased risk of pleural infection with IPCs in immunocompromised patients. This is well documented in patients with hematological malignancies on chemotherapy.
Catheter Tract Metastasis (CTM)
It is not uncommon for patients treated with IPC for MPEs to develop painful nodules near the insertion site or the point of entry into the parietal pleura. Treatment is analgesia and radiotherapy. Mesothelioma is notorious for causing CTM. The cause of this complication remains unknown.
Residual Loculated Effusions
It is postulated that presence of an IPC promotes fibrin deposition and this fibrin can form loculations and, thus, renders IPC non-functional. This complication usually happens at least 8 weeks post insertion. Treatment is fibrinolytic therapy tPA, through the IPC. This is usually very successful but carries a small risk of significant pleural hemorrhage.
Cachexia is very common in cancer patients. Since the pleural fluid is rich in proteins, the risk of malnutrition is thought to be substantial. A prospective trial followed patients with IPC for 1 year but found no significant risk of malnutrition.
Fibrous tissue grows around and inside the IPC blocking of few holes. It seldom affects drainage. A complete blockage is rare and happens in less than 5% of cases. Mild blockage usually responds to saline flushes.
This usually happens when an IPC is removed. Because the polyester cuff promotes inflammation and fibrosis, leading tight anchoring of the catheter. The risk is reported to be about 10%. This is usually managed by surgical exploration or just leaving the catheter fragments inside the body. No complications have been reported from retained fragments of IPC.
Traditionally, refractory or recurrent pleural effusions were treated with repeated thoracentesis. This was associated with more pain and discomfort and poor quality of life along with the high risk of complications. Then, pleurodesis was introduced, a method of obliterating pleural space. It is achieved via chemical or surgical pathways. Chemical pleurodesis involves instilling of a sclerosing agent (talc, bleomycin, doxycycline) into the pleural space via a chest tube. The sclerosing agent promotes inflammation and later on fibrosis of the visceral and parietal pleural surfaces. Thoracoscopy or VATS can be used for mechanical abrasion of the pleural surfaces.
Pleurodesis was successful only in 60% to 70% of patients because it requires a completely expandable lung to ensure total apposition of the pleural surfaces. Unfortunately, the lung is not fully expandable in the majority of patients with MPEs. Patients with endobronchial lesions and interstitial fibrosis also have un-expandable or "trapped" lung that will render pleurodesis unsuccessful in most cases.
Indwelling pleural catheters (IPC)have revolutionized the management of MPEs. FDA approved IPC in 1997. They are now the treatment of choice in patients with MPEs and the evidence for their efficacy is growing for non-malignant pleural effusions as well.
Advantages of IPC
Length of Stay
The typical length of stay for pleurodesis is from 2 to 5 days; whereas, IPC is done as an out-patient procedure.
Surgical pleurodesis is done under general anesthesia. Chemical pleurodesis is done via chest tube placed under local anesthesia, but it is associated with significant pain due to a bigger incision. IPC is placed under local anesthesia and is very well tolerated. Most patients do not require anything stronger than over the counter NSAIDs.
The prolonged (more than 6 months) survival in cancer patients has been associated with reduced efficacy of chemical pleurodesis of only 50%. Approximately, 32% patients require a repeat pleural procedure due to the failure of pleurodesis. In comparison, IPCs are successful more than 90% of the time.
There is no difference in improvement of dyspnea with both procedures within 6 months, but after 6 months post procedure, IPC is superior to pleurodesis in relieving dyspnea and improving quality of life.
Chemical pleurodesis work by inducing pleural and systemic inflammation. Sometimes this inflammation can be severe and leads to hypoxemia and respiratory failure. This complication is most commonly seen with talc which is also the most effective chemical sclerosing agent. IPC insertion avoids this complication altogether.
Pleurodesis It is achieved in a median time of 11 weeks. Favorable factors include breast and gynecologic malignancies, completely re-expansion of the lung post IPC placement, positive pleural fluid cytology, and no history of chest wall irradiation.
One study showed that IPCs are more cost-effective as compared to talc pleurodesis if expected survival is less than 3 months; however, not if survival is more than 3 months.