Post cardiac injury syndrome (PCIS) is a heterogenic group of disorder occurring in response to a variety of cardiac insults including cardiac surgery, blunt chest wall trauma, coronary, and endovascular interventions. PCIS occurs rarely after cardiac device placement and there are few case reports in the literature regarding PCIS post pacemaker insertion. We present an interesting case of delayed PCIS presenting as bilateral pleural effusion after transvenous pacemaker placement mimicking a cardiac perforation.
PCIS is an inflammatory process involving pleura and pericardium in response to a variety of cardiac insults. It has been reported post endovascular procedures, myocardial infarction, cardiac surgery, and trauma. PCIS occurs in response to endocardial, myocardial, and Epicardial injury. PCIS is rarely reported in response to pacemaker device insertion, radiofrequency ablation with few case reports in literature.2-4 PCIS usually present with concomitant pleural and pericardial effusion in all majority of cases reported and to best of our knowledge, there is no reported case with only pulmonary involvement in form of effusion without pericardial involvement. Pathognomonic features include dyspnea, fever, pleuropericardial pain, pericardial involvement with or without effusion, pulmonary involvement in the form of effusion or parenchymal disease, and laboratory abnormalities including but not limited to raised inflammatory markers. Mechanism of pacemaker induced PCIS is poorly understood but probably involves microtrauma and endocardial injury with resultant immune mediated sterile inflammation in the pleuropericardial region in susceptible individuals.
PCIS presenting with pericardial effusion is common in patient with concomitant steroid use, temporary pacemaker placement, increasing age, low BMI, and helical screw lead use.1 Epicardial pacemaker implantation placement and active fixation atrial leads are also associated with increased risk.6 Increased incidences with atrial leads are related to a thin atrial wall, leading to susceptibility to perforation and irritation.
The spectrum of disease range from pericarditis, pericardial effusion to tamponade and massive pleuropericardial effusions. Dyspnea, fever and raised inflammatory marker should raise the suspicion for PCIS. PCIS may resemble early/delayed cardiac perforation.5 In our case, cardiac perforation was also considered, however no objective evidence of perforation was demonstrated. It is imperative to differentiate PCIS from lead perforation to prevent unnecessary diagnostic and therapeutic interventions. Lead perforation may cause a change in pacing parameters in interrogation, however, PCIS is less likely to cause such changes. Concomitant anticoagulation, female sex, and steroids use increases the risk of lead perforation but don’t affect the risk of developing PCIS. Instead, current steroid use may theoretically prevent or decrease the severity of PCIS. Right heart perforation is likely to mimic PCIS as it can go unrecognized and patient may remain asymptomatic because of low pressure system, causing spontaneous healing and fibrosis.9
Stelzner et. Tal and colleagues reported pleuropulmonary manifestation in PCIS, but only one of the cases reported in their study involved pacemaker implantation. Pleura fluid analysis reports exudative in the majority of cases. It may be difficult to differentiate exudative effusion from PCIS vs infectious cause especially early during the course. A high PH may favor the diagnosis of PCIS as demonstrated in this study.7 Another large registry of pleural fluids analysis in PCIS patient reported that all the effusions were exudative, occupying < 1/3rd of hemithorax and bloody in most cases.8 Investigation for pacemaker induced PCIS should include device interrogation, Chest radiograph with a lateral view, Echocardiogram and Computerized tomography(CT) of the chest, blood test including erythrocyte sedimentation rate and complete blood counts. Some investigators have suggested a role of anti heart antibodies in diagnosis, however, their clinical significance remains unclear.11 CT scan of the chest is the best test to detect cardiac perforations. The pleural fluid analysis may provide valuable diagnostic information. Literature review reports less than 20 cases of PCIS following cardiac devices. ESR was raised in the majority of cases (all). Pericardial effusion with or without tamponade was found in all cases. Pleural effusion in 61% of cases.10 This case is very important because of lack of associated pericardial effusion, and occurrence of hemorrhagic pleural effusion mimicking diagnosis of lead perforation. Clinical and laboratory feature may help in differentiating between PCIS and lead perforation, however, CT scan is invaluable in cases with an unclear diagnosis. We expect the incidence of PCIS to rise due to the increased number of new cardiac devices implantation. Frequent diagnostic and therapeutic delays occur as PCIS remains an exclusive diagnosis. Treatment involved anti-inflammatory agents including nonsteroidal anti inflammatory agents, steroids and colchicine. Late lead rupture is life threatening condition mimicking PCIS and should always be considered. Exudative pleural effusion in the setting of Parapneumonic effusion is also among the differential. Physicians should be aware of this entity and occurrence of concomitant perforation should be evaluated.