Malignant Pleural Effusions: Management Options

David J. McCracken, MRCP; Jose M. Porcel, MD; Najib M. Rahman, DPhil

Disclosures

Semin Respir Crit Care Med. 2018;39(6):704-712. 

In This Article

Symptom Control

At present, conventional interventions for MPE all have demonstrated statistically and clinically significant improvements in dyspnea scores and quality of life measurements irrespective of the method chosen. The AMPLE study, published in late 2017, confirmed the original findings from the TIME2 trial in 2012, both of which randomized patients to either talc slurry pleurodesis or IPC. AMPLE measured mean improvements in dyspnea using a visual analog scale between 0 and 100 mm. Improvements of 14.5 mm in the IPC group and 17.4 mm in the talc pleurodesis group were demonstrated, respectively, after only 1 day, and these were maintained throughout the full 12-month follow-up period. This served to further consolidate the findings from TIME2 which had originally demonstrated that 74% of patients undergoing drainage and talc pleurodesis experienced clinically significant improvement in their breathlessness compared with 86% of patients with IPCs, although the difference between the two groups was not statistically significant. Mean improvements of 30.2 and 37 mm were recorded, respectively, at day 42 on a visual analog scale and were far in excess of an established clinically significant difference of 19 mm. Outcomes from both studies also resulted in similar improvements in quality of life measurements between the treatment arms. However, AMPLE used the EQ-5D score in contrast to the cancer-specific EORTC QLQ-30 measurement recorded in TIME2.[8,9]

The mechanism by which these interventions achieve improvements in dyspnea has yet to be fully defined. The resolution of simple compressive atelectasis by drainage of fluid, leading to improvements in oxygenation is evident in the literature, but appears unlikely to fully explain the underlying pathophysiology, as these results are independent of the degree of lung re-expansion.[10,11] The actual pathophysiology of dyspnea may therefore be better explained by the increase in pleural pressure from a large effusion. This may in turn lead to diaphragmatic inversion, abnormal or paradoxical movement, or diaphragm dysfunction (potentially related to muscle stretch). The subsequent return of normal diaphragmatic shape, position, and function following drainage may therefore be likely to best account for improvements in dyspnea (Figure 2).[12,13]

Figure 2.

Ultrasound images demonstrating diaphragmatic inversion preprocedure with resolution following aspiration.

The optimum volume of fluid to be removed during an intervention in order to achieve symptom control also remains unclear. When undertaking therapeutic aspiration, the British Thoracic Society (BTS) guidelines suggest that less than 1,500 mL be drained in one attempt.[14] The literature review suggests that this limit is conservative as significantly larger volumes are documented as having been safely aspirated, including one case of 6.5 L in one sitting.[15] The perceived increased risks of re-expansion pulmonary edema and pneumothorax have led to retention of these conservative recommendations. The first symptoms of one of these complications may be the development of cough or chest pain, and therefore, these features are often used as an indication for discontinuation of the procedure.[14–16] It should also be noted that complete removal of fluid leaving a dry pleural space is not required if symptomatic benefit is the goal. Large volume aspiration of approximately 1 L of pleural fluid, allowing residual effusion to remain, has been shown to be effective in the improvement of dyspnea in more than 80% of patients.[17] This would appear to confirm that the proposed mechanism of dyspnea in these cases is likely primarily related to diaphragmatic pressure and the subsequently altered breathing mechanics in contrast to lung function compromise, passive atelectasis, or lung compression.

Comments

3090D553-9492-4563-8681-AD288FA52ACE

processing....