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Parapneumonic Pleural Effusion and Empyema Thematic Review Series 2008 Respiration 2008;75:241–250 DOI: 10.1159/000117172 Parapneumonic Pleural Effusion and Empyema Coenraad F.N. Koegelenberga Andreas H. Diaconb Chris T. Bolligera a b Division of Pulmonology, Department of Medicine, Division of Medical Physiology, Department of Biomedical Sciences, University of Stellenbosch and Tygerberg Academic Hospital, Cape Town , South Africa Key Words tween tube thoracostomy (with or without fibrinolytics) and -Parapneumonic pleural effusion ؒ Empyema ؒ Fibrinolytics ؒ thoracoscopy. Open surgical intervention is sometimes re -Thoracoscopy ؒ Thoracotomy ؒ Thoracostomy quired to control pleural sepsis or to restore chest mechan ics. This review gives an overview of parapneumonic effu- sion and empyema, focusing on recent developments and Abstract controversies. Copyright © 2008 S. Karger AG, Basel At least 40% of all patients with pneumonia will have an as- sociated pleural effusion, although a minority will require an intervention for a complicated parapneumonic effusion or empyema. All patients require medical management with Introduction and Definitions antibiotics. Empyema and large or loculated effusions need to be formally drained, as well as parapneumonic effusions At least 40% of all patients diagnosed with pneumonia with a pH ! 7.20, glucose ! 3.4 mmol/l (60 mg/dl) or positive will have an associated pleural effusion, although the mi- microbial stain and/or culture. Drainage is most frequently nority of these will require active intervention [1, 2] . A achieved with tube thoracostomy. The use of fibrinolytics parapneumonic pleural effusion refers to any effusion remains controversial, although evidence suggests a role for secondary to pneumonia or lung abscess [1] . It becomes the early use in complicated, loculated parapneumonic effu- ‘complicated’ when an invasive procedure is necessary sions and empyema, particularly in poor surgical candidates for its resolution, or if bacteria can be cultured from the and in centres with inadequate surgical facilities. Early tho- effusion [1] . Empyema is a term derived from the Greek racoscopy is an alternative to thrombolytics, although its verb empyein (‘to suppurate’) and literally refers to frank role is even less well defined than fibrinolytics. Local exper- pus in the pleural space. Parapneumonic effusion and tise and availability are likely to dictate the initial choice be- empyema remain important medical conditions associ- ated with significant morbidity and mortality [2] . It is estimated that in the United States alone, pleural infec- tions have an incidence of 60,000 per year and a mortal- Previous articles in this series: 1. Froudarakis ME: Diagnos- tic work-up of pleural effusions. Respiration 2008;75:4–13. 2. Jantz ity of approximately 15% [3, 4] . Yet, controversy remains MA, Antony VB: Pathophysiology of the pleura. Respiration 2008;75: regarding the management and specifically the role of 121–133. fibrinolytic therapy. © 2008 S. Karger AG, Basel Coenraad F.N. Koegelenberg 0025–7931/08/0753–0241$24.50/0 Division of Pulmonology, Department of Medicine Fax +41 61 306 12 34 University of Stellenbosch and Tygerberg Academic Hospital E-Mail [email protected] Accessible online at: PO Box 19063, Tygerberg, Cape Town 7505 (South Africa) www.karger.com www.karger.com/res Tel. +27 21 938 9423, Fax +27 21 933 3591, E-Mail [email protected] Epidemiology and Risk Factors and cell lysis result in fluid that most frequently has a pH of ! 7.20, a lactate dehydrogenase 1 3 times the upper Complicated parapneumonic effusions and empyema limit and a low glucose [1, 2, 10] . Rarely, fibrinopurulent are more common at both extremes of age [2, 3] . At least effusions can have a pH in the normal or even in the al- two thirds of patients will have an identifiable risk factor kaline range. This phenomenon is limited to a few patho- at presentation [2] , which may include immunosuppres- gens (e.g. Proteus spp.) with enzymatic activity that can sive states (most frequently HIV infection, diabetes mel- elevate fluid pH, for instance by cleaving urea into am- litus and malnutrition), alcohol or intravenous drug monia [11] . During the fibrinopurulent stage the pleural abuse, bronchial aspiration, poor dental hygiene, gastro- space becomes increasingly infected. Loculations may oesophageal reflux, and chronic parenchymal lung dis- develop and closed or open drainage becomes neces- ease [3, 4] . Microbial virulence and idiosyncrasies of the sary – the point in time where an effusion is referred to immune system are often also implicated, principally in as ‘complicated’. A critical characteristic of the fibrino- individuals with no apparent predisposition. purulent stage of pleural sepsis is the disturbance of the physiological equilibrium between clotting and fibrino- lysis within the pleural space [2, 12] . Several mediators for Pathogenesis the activation of the coagulation cascade and inhibition of fibrinolysis have been suggested: TNF- ␣ , for example, Although pleural infection may occur as a primary has been shown to stimulate the release of plasminogen event, most cases of pleural sepsis are secondary to pneu- activator inhibitors from pleural mesothelial cells. Ale- monias, lung abscesses or infective exacerbations of bron- man et al. [13] were able to show increased levels of plas- chiectasis. It should be noted that the associated pulmo- minogen activator inhibitor-2 and depressed levels of nary consolidation may be minimal [2] . Other identifi- tissue plasminogen activator (tPA) during complicated able causes include thoracic surgery, diagnostic proce- pleural sepsis. Although the exact mechanisms behind dures involving the pleural space, trauma, oesophageal the procoagulate state still need to be elucidated, its ef- rupture, transdiaphragmatic spread and rarely bronchial fects are well-known: pleural surfaces coated with fibrin obstruction [5] . Primary pleural infections are presum- and fibrin strands with secondary adhesions and locula- ably most often due to the haematogenous spread of or- tions, all complicating pleural fluid drainage. ganisms from gingival and upper respiratory tract infec- The third and final stage of pleural infection is the or- tions (with cultures yielding oropharyngeal flora and an- ganizing phase [1, 2] . Fibroblasts grow into the pleural aerobes) [2, 6] or due to Mycobacterium tuberculosis [7] . space from both the visceral and parietal pleura. This The development of a parapneumonic effusion occurs eventually results in a thick pleural peel, which restricts in three clinically relevant stages that represent a con- chest mechanics and often necessitates a surgical decor- tinuous spectrum [1, 8] . A rapid influx of exudative fluid tication to address restrictive impairment. Recent re- into the pleural space is observed in up to 40% of patients search on animal models has suggested a cardinal role for with pneumonia and heralds the first or exudative stage transforming growth factor- ␤1 as a fibrogenic cytokine [1, 2] . The accumulation of fluid is thought to be a direct in the development of pleural fibrosis [14] . result of increased pulmonary interstitial fluid traversing the pleura to enter the pleural space [1] and an increase in vascular permeability secondary to pro-inflammatory Bacteriology cytokines [2, 9] , e.g. interleukin-8 and tumour necrosis factor- ␣ . During this stage pleural fluid culture is nega- The reported bacteriology of pleural sepsis varies sig- tive for bacteria, fluid pH is 1 7.20, the glucose level is nificantly between community-acquired and nosocomi- within the normal range and lactate dehydrogenase re- al infections [2] . Maskell et al. [15] reported the large pro- mains ! 3 times the upper limit of normal [1, 2] . Most spective MIST 1 trial (Multicenter Intrapleural Sepsis patents with uncomplicated parapneumonic effusions Trial 1) in 2005. Their study included 430 subjects across will respond to antibiotics alone and drainage is gener- 52 centres in the United Kingdom. Of these, 232 (54%) ally not required [1, 2, 10] . had positive pleural cultures. The Streptococcus milleri Untreated exudative effusions may develop into fibri- group was the most common pathogen (29%), followed nopurulent effusions. This second stage is characterized by staphylococci (21%) and Streptococcus pneumoniae by positive microbial cultures. Ongoing phagocytosis (16%). Anaerobes were isolated in 15%. Other isolates in- 242 Respiration 2008;75:241–250 Koegelenberg/Diacon/Bolliger Fig. 1. A series of images obtained from the same patient who pre- sented with a complicated parapneumonic effusion. a The chest radiograph: note the inhomogeneous nature of the left-sided opacity, the absence of the associated costophrenic angle, and the apparent air lucencies within the opacity. b A thoracic US re- vealed a classic septated complicated parapneumonic effusion. Note the strands of echogenic material within the loculations. L = Loculations; S = septae. c A chest CT scan did not show any loculations within the pleural fluid collection. Note the underly- ing pulmonary consolidation that was not apparent on the chest radiograph. C = Consolidation; E = effusion. cluded other streptococci, Haemophilus influenzae , en- monia’ picture with pleuritic chest pain, fever spikes and terobacteria, M. tuberculosis , and Nocardia . The same in- a failure to improve on apparently adequate antibiotic vestigators previously reported that nosocomial pleural therapy. Elderly individuals, immunocompromised pa- infections
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