post cardiac reperfusion syndrome

POST–CARDIAC INJURY (DRESSLER’S) SYNDROMEThe post–cardiac injury syndrome (PCIS) is charac-terized by the development of fever, pleuropericarditis,and parenchymal pulmonary infiltrates in the weeksfollowing trauma to the pericardium or myocar-dium.1,2 In a recent article, noncomplicated post–cardiac injury syndrome was defined as the presence oftemperature > 100.5°F, patient irritability, pericardial

friction rub, and a small pericardial effusion with orwithout pleural effusion following cardiac trauma.3These same authors defined a complicated PCIS as anoncomplicated PCIS plus the need for hospital read-mission with or without the need for pericardiocente-sis or thoracentesis.3 PCIS has been reported follow-ing myocardial infarction, cardiac surgery, blunt chesttrauma, percutaneous left ventricular puncture, pace-maker implantation, and angioplasty.

657

Pleural Effusions Following Cardiac Injuryand Coronary Artery Bypass Graft SurgeryRichard W. Light, M.D.1,2

ABSTRACT

This article discusses the pleural effusions that occur with the post–cardiac in-jury (Dressler’s) syndrome (PCIS) and those that occur after coronary artery bypass graft(CABG) surgery. The PCIS can occur after any type of cardiac injury and is thought tobe due to antimyocardial antibodies. The primary symptoms are fever and chest pain, andpericarditis is frequently present. Pleural effusions are common with PCIS. The primarytreatment for PCIS is a nonsteroidal anti-inflammatory agent or corticosteroids. Follow-ing CABG surgery, most patients will have a small unilateral left-sided pleural effusion,and approximately 10% of patients will have a larger effusion. These large effusions can beseparated into early effusions occurring within the first 30 days of surgery that are bloodyexudates with a high percentage of eosinophils, and late effusions occurring more than30 days after surgery that are clear yellow lymphocytic exudates. The primary symptom ofa patient with a pleural effusion post–CABG surgery is dyspnea; chest pain and fever areuncommon. Most patients with large pleural effusions postCABG surgery are managedsuccessfully with one to three therapeutic thoracenteses.

KEYWORDS: Pleural effusion, CABG surgery, postcardiac injury syndrome

Objectives: Upon completion of this article, the reader should understand the etiology, diagnosis, and management of thepost–cardiac injury syndrome and the pleural effusions that occur after coronary artery bypass surgery.Accreditation: The University of Michigan is accredited by the Accreditation Council for Continuing Medical Education to sponsorcontinuing medical education for physicians.Credits: The University of Michigan designates this educational activity for a maximum of 1.0 hour in category one credits towardthe AMA Physicians Recognition Award.

Seminars in Respiratory and Critical Care Medicine, volume 22, number 6, 2001. Address for correspondence and reprint requests: Richard W.Light, M.D., Saint Thomas Hospital, 4220 Harding Rd., Nashville, TN 37205. E-Mail: [email protected]. 1Saint Thomas Hospital,Nashville, Tennessee; 2Vanderbilt University, Nashville, Tennessee. Copyright © 2001 by Thieme Medical Publishers, Inc., 333 Seventh Avenue,New York, NY 10001, USA. Tel: +1(212) 584-4662. 1069-3424,p;2001,22,06,657,664,ftx,en;srm00117x.

Incidence

The incidence of PCIS has varied markedly from seriesto series. The explanation is obvious when the abovementioned definition is used. If one evaluates patientscritically, most patients with cardiac trauma will meetthe criteria for uncomplicated PCIS. Most patientspost–cardiac trauma will have evidence of a systemic in-flammatory response as evidenced by increased serumlevels of interleukin-6 (IL-6).4 Probably there is a con-tinuum of responses post–cardiac trauma ranging frommild fever and chest soreness to the complete Dressler’ssyndrome with fever, pleuritic chest pain, pleural effu-sion, pericardial effusion, and parenchymal infiltrates.

When Dressler first described the syndrome fol-lowing myocardial infarction, he stated that the inci-dence was 3 to 4%.1 Subsequent articles have indicatedthat the incidence is less than 1% following myocardialinfarction.5 However, if the patient has pericarditis inthe few days following the myocardial infarction, thenthe incidence of PCIS is approximately 15%.6 In recentyears the incidence of PCIS after myocardial infarctionhas decreased to less than 0.5%. This has been attrib-uted to the increased use of thrombolytics resulting inearly reperfusion and less tissue damage.7

The reported incidence of PCIS following car-diac surgery has varied from 153 to 30%.2 In a recent se-ries of 266 children undergoing cardiac surgery, the in-cidence of uncomplicated PCIS was 11.2%, whereas theincidence of complicated PCIS was only 3.4%.3 In anolder series of 966 adults undergoing cardiac surgery atJohns Hopkins Hospital, the incidence of PCIS was17.8%.8 To be classified as having the PCIS in this se-ries, patients were required to have two or three of thefollowing signs and symptoms during their hospitaliza-tion or follow-up visit: (1) fever greater than 37.8°C,(2) significant anterior chest pain suggestive of pericar-dial inflammation, and (3) a two- or three-componentpericardial friction rub on auscultation.8 The incidenceof PCIS was comparable after all types of cardiac sur-gery. However, there was a higher incidence of PCIS ifthe patient had a history of pericarditis or if the patienthad taken corticosteroids previously.8

Etiology

The etiology of the PCIS is not completely known, butit appears to have an immunologic basis. When themyocardium is injured, cellular components, includingautoantigens, are released. These autoantigens can pro-voke an autoimmune antibody reaction by antimyocar-dial antibodies. Subsequently, complement is activated,C3 and C4 levels fall, and leukocytes are mobilized.

There is a close relationship between the occur-rence of PCIS and the development of antimyocardialantibodies in patients undergoing surgical procedures

involving the pericardium. In one prospective study of257 patients, 67 patients (26%) developed high titers ofantimyocardial antibodies, and all 67 developed PCIS.2In contrast, none of 102 patients without a rise in anti-body titers and only 4 of 93 patients with intermediatetiters developed the syndrome.2 There is not a clear-cutrelationship between the development of antimyocar-dial antibodies and PCIS in patients with myocardialinfarction. In one study of 136 patients with myocardialinfarction, there was no association between the devel-opment of the syndrome and the presence of antimy-ocardial antibodies.5

Epidemiological studies have indicated thatthere are other factors that appear to be associated withthe development of the post–cardiac injury syndrome.There is a seasonal variation in the post-cardiac injurysyndrome, with the highest incidence corresponding tothe time of the highest prevalence of viral infection inthe community.9 De Scheerder and coworkers have hy-pothesized that a concurrent viral infection may triggerthe immune response.10

Clinical Manifestations

The clinical manifestations of PCIS include fever, chestpain, pericarditis, pleuritis, and/or pneumonitis. As com-mented upon previously in this article, however, manypatients are given the diagnosis of PCIS with only two ofthe five manifestations. Following myocardial infarction,the symptoms usually develop in the second or thirdweek; an occasional patient develops symptoms withinthe first week, whereas a larger percentage develop symp-toms only after the third week.11 Following cardiac sur-gery, the syndrome is seen at an average of 3 weeks butcan occur any time between 3 days and 1 year.12

The two cardinal symptoms of PCIS are chestpain and fever. The chest pain often precedes the onsetof fever and varies from crushing and agonizing, mimick-ing myocardial ischemia, to a dull ache to pleuritic chestpain. A pericardial friction rub is present in almost allpatients and a pericardial effusion is present in the ma-jority. Laboratory evaluation reveals a peripheral leuko-cytosis and an elevated erythrocyte sedimentation rate(> 100 mm/hr) in most patients.2,13 The chest radio-graph reveals pulmonary infiltrates in the majority ofpatients.13 Approximately 80% of the patients will havea pleural effusion, and the effusions are bilateral in ap-proximately 50%.13 When the effusions are unilateral,they are more commonly on the left than on the right.The pleural fluid is an exudate with a normal pH and anormal glucose level.13 The pleural fluid is franklybloody in about 30% of patients, and the differential cellcount may reveal predominantly polymorphonuclearleukocytes or mononuclear cells depending upon theacuteness of the process.13

658 SEMINARS IN RESPIRATORY AND CRITICAL CARE MEDICINE/VOLUME 22, NUMBER 6 2001

Diagnosis

The diagnosis of PCIS should be considered in any pa-tient who develops a pleural effusion following traumato the heart and who is febrile and has chest pain. Sincethere are no specific tests with which to establish thediagnosis, the diagnosis is made by excluding otherdiseases that can produce identical symptoms in thepatient post–cardiac injury. The main diagnoses to ex-clude are pleural effusions post–coronary artery bypass(CABG) surgery, congestive heart failure, pulmonaryembolism, and pneumonia with a parapneumonic effu-sion or empyema.14 Pleural effusions due to PCIS andthose due to CABG surgery are distinguished primarilyby the patient’s symptoms; patients with pleural effu-sions due to PCIS invariably have chest pain and fever,whereas those with pleural effusions post–CABG sur-gery have dyspnea, but no chest pain or fever. Conges-tive heart failure is excluded if the pleural fluid is an ex-udate. The possibility of pulmonary embolism can beevaluated with a spiral computed tomography (CT)scan or with a perfusion lung scan. It is important not tomistakenly diagnose the PCIS as a pulmonary em-bolism. Anticoagulation is contraindicated with thePCIS syndrome because patients with the syndrome areat risk for developing hemopericardium and tampon-ade.15 The possibility of pneumonia is high if the pa-tient has purulent sputum, and the diagnosis of pleuralspace infection is established if the pleural fluid culturesare positive or the pleural fluid is purulent. One reportsuggested that the diagnosis of the syndrome could beestablished by demonstrating a high titer of antimyo-cardial antibody and a low complement level in thepleural fluid.16

Prevention and Treatment

There is no known means by which to prevent the devel-opment of PCIS. Mott and coworkers3 randomized 246children who were undergoing cardiac surgery with car-diopulmonary bypass to receive intravenous methylpred-nisolone (1 mg/kg) or saline prior to cardiopulmonarybypass and q 6 hours for four doses post-surgery. Theyfound that the incidence of PCIS was identical in thetwo groups. Possibly a different result would have beenobtained if the corticosteroids had been given for alonger duration.

Once the syndrome has developed, it usually re-sponds to treatment with anti-inflammatory agentssuch as aspirin or indomethacin. My choice is indo-methacin 25 to 50 mg every 8 hours. Although a singleepisode of the PCIS is usually self-limited, recurrencesare frequent. Recurrent episodes become progressivelymore resistant to treatment with nonsteroidal anti-inflammatory agents, but usually respond to corticoster-oid therapy.17 Prednisone is administered orally in doses

of 40 to 60 mg daily with rapid tapering over 8 to10 days.17 If symptoms recur when the prednisone is ta-pered, additional courses are indicated.

One report suggested that the development ofthe PCIS postoperatively in patients who had under-gone CABG surgery was a very serious event becausethe grafts were likely to be occluded by the inflamma-tory process.12 When 31 subsequent patients weretreated with prednisone, 30 mg per day for a week andtapering doses for 5 weeks thereafter, in addition to as-pirin 600 mg qid, only 16% of the grafts became oc-cluded.12 However, it should be noted that this reporthas not been validated since it was originally publishedin 1976.

PLEURAL EFFUSIONS POST–CORONARYARTERY BYPASS SURGERYMore than 600,000 patients undergo CABG surgery inthe United States each year.18 Given that approximately10% of the patients who undergo CABG surgery willdevelop a pleural effusion occupying more than 25% ofthe hemithorax in the subsequent month,19 CABG sur-gery is one of the more common causes of pleural effu-sions in the United States.

Incidence

Many patients who undergo CABG surgery will de-velop a small, left-sided pleural effusion in the first fewdays postoperatively. In one study of 122 patients, theincidence of pleural effusion on the routine chest radio-graph 6 days postoperatively was 42%.20 In this study,the incidence of pleural effusion was nearly identical inpatients who received internal mammary artery (IMA)graphs (43%) and in those that received only saphenousvein grafts (SVG) (41%).20 Approximately 80% of theeffusions in this series were small (occupying less thanone intercostal space) and were unilateral left-sided.20

In a second study the same investigators performedchest ultrasound at 7, 14, and 30 days postoperatively on47 patients and reported that the prevalence of pleuraleffusion was 89% at 7 days, 77% at 14 days, and 57% at30 days.21 The higher incidence of effusion in this latterseries was attributed to the increased sensitivity of ultra-sound as compared with the chest radiograph at detect-ing pleural fluid. The majority of the pleural effusionswere unilateral and left sided in this series. In contrastto the previous study, the prevalence of pleural effusionswas higher in this series if the patients received an IMAgraft.21 In a third study, Landymore and Howell re-ported that at the time of discharge from the hospital,the incidence of pleural effusion was 91% in 34 patientswho had received an IMA graft and had the pleuraopened, whereas the incidence of pleural effusion was

PLEURAL EFFUSIONS FOLLOWING CARDIAC INJURY AND CABG SURGERY/LIGHT 659

58% in 33 patients who had received an IMA graft butin whom the pleura was not opened.22

The natural history for the small, unilateral, left-sided effusions is gradual resolution.21,22 However, incertain patients, the effusion enlarges and producessymptoms. Hurlbut and associates23 obtained chest ra-diographs 8 weeks postoperatively on 76 patients whohad received IMA grafts and reported that 5 of 55 pa-tients (9.1%) who underwent pleurotomy and 3 of21 patients (14.5%) who had an IMA without pleu-rotomy had a pleural effusion at the 8-week follow-upvisit. Four of these 76 patients underwent thoracentesis.In a recent prospective study from our institution,19 theprevalence of pleural effusions at approximately 30 dayspost-operatively on chest radiographs in 349 patientswho had undergone CABG surgery was 63%. Althoughmost of the effusions were small, 34 of the 349 patients(9.7%) had a pleural effusion that occupied more than25% of the hemithorax. The incidence of large effusionswas higher in the 282 patients who received an IMAgraph (10.9%) than in the 67 patients that received onlySVG graphs (4.5%).

Etiology

The pathogenesis of the pleural effusions followingCABG surgery is not definitely known. The early,small, left-sided effusions are probably related to thetrauma of surgery including phrenic nerve injury andatelectasis. Large effusions (those occupying more than25% of the hemithorax) can be divided into two cate-gories: those occurring within the first 30 days andthose occurring after the first 30 days.24,25 The early ef-fusions are usually bloody with a median hematocritabove 5%. The likely etiology of these effusions istrauma from the surgery and postoperative bleedinginto the pleural space.25

The etiology of the effusions occurring later isunclear. These effusions tend to be clear with a predom-inance of lymphocytes in the pleural fluid.24,25 It hasbeen suggested that these effusions are manifestationsof the PCIS.26 However, it is unlikely that these effu-sions represent the PCIS because the two main clinicalmanifestations of the PCIS are chest pain and fever3;both symptoms are very uncommon in patients withpleural effusions more than 30 days after surgery.19

The observation that the pleural fluid associatedwith the late effusions post–CABG is lymphocytic sug-gests an immunological etiology. To my knowledgethere have been no studies of the serum levels of an-timyocardial or antimesothelial cell antibodies in theseindividuals. Antimyocardial antibody was detected inthe pleural fluid and in the serum of one patient with apleural effusion secondary to PCIS post–CABG sur-gery. However, we could detect no antimyocardial anti-body in the pleural fluid of 25 patients with pleural ef-

fusions post-CABG (unpublished observations) whodid not have fever and chest pain.

When pleural specimens from patients undergo-ing thoracoscopy for persistent post-CABG pleural ef-fusions are examined, there is an intense lymphocyticpleuritis with little fibrosis within the first few monthsof surgery (Fig. 1).27 Immunohistochemical analysisdemonstrates that there is a mixed population of lym-phocytes with a predominance of B cells.27 As time goeson, there is a gradual decrease in the cellular infiltrateand a gradual increase in the degree of fibrosis.27 After1 year or more, the pleura is markedly thickened withincreased amounts of dense fibrous tissue (Fig. 2). Thefibrous component is typically paucicellular, but it doescontain collections of entrapped cells that are cytoker-atin immunoreactive, compatible with mesothelialcells.27

The occurrence of pleural effusions post–CABGsurgery is increased if the patient receives topical hypo-thermia at the time of surgery with iced slush. Nikasand coworkers studied 505 nonrandomized consecutivepatients undergoing CABG surgery and reported that60% of the 191 patients who received topical hypother-mia had a pleural effusion, whereas only 25% of the314 patients who did not receive topical hypothermiadeveloped a pleural effusion.28 Moreover, 25% of thosein the hypothermia group required a thoracentesis,whereas only 8% of those in the control group requireda thoracentesis.28 In a second study, Allen and associatesreported that the incidence of pleural effusion was 50%in 50 patients who received topical hypothermia butonly 18% in 50 patients who did not receive topical hy-pothermia.29 These data suggest that cold injury to thephrenic nerve resulting in atelectasis may cause thepleural effusion.

As mentioned previously, patients who receive anIMA graft are more likely to develop a large pleural ef-fusion than are those who receive only SVG. In addi-


Figure 1 Pleural specimen from a patient 3 months post–coronary artery bypass graft (CABG) surgery with a persistentpleural effusion. Note the intense lymphocytic pleuritis.

tion, the type of chest drain used postoperativelymay influence the development of pleural effusions.Robinowitz-Elins and associates reported that a thora-centesis was required in only 2 of 295 patients (1%) whoreceived a Blake Drain (19F) postoperatively comparedwith 48 of 1547 (3.1%) who received a conventionalchest tube (32F).30 We recently reported that patientswho underwent CABG surgery off pump (without car-diopulmonary bypass) had a lower incidence of largepleural effusion 4 weeks postoperatively than did thosewho underwent CABG surgery with cardiopulmonarybypass.31

Clinical Manifestations

The primary symptom of patients with pleural effusionpost–CABG is dyspnea. In a recent study from our in-stitution, 22 of 29 patients (75.9%) with an effusion oc-cupying more than 25% of the hemithorax complainedof dyspnea, but only 3 (10.3%) complained of chest pain

and only 1 (3.4%) complained of fever.19 It should benoted that almost every patient with the PCIS syn-drome has both chest pain and fever.

The pleural effusions that occur after CABGsurgery tend to be unilateral on the left side. In thestudy from our institution in which chest radiographswere obtained approximately 4 weeks post-surgery,196 of 349 patients (62%) had pleural effusions.19 Theeffusions were unilateral or larger on the left in155 (73.4%), whereas they were unilateral on the rightor larger on the right in only 14 (7.2%).19

As mentioned previously, the larger pleural effu-sions that occur after CABG can be divided into thosethat occur within the first 30 days of surgery and thosethat occur more than 30 days after surgery.25,26 Thepleural fluid from the early effusions is bloody with amedian red blood cell count of > 700,000 cells mm3

(Table 1).25 The pleural fluid is frequently eosinophilicwith median eosinophil percentage of nearly 40.25 Themedian pleural fluid lactate acid dehydrogenase (LDH)level is approximately twice the upper limit of normalfor serum.25 Because the pleural fluid is bloody, it islikely that the LDH in the pleural fluid is LDH-1,which is the LDH from the red blood cells. The pleuralfluid protein is in the exudative range, and the pleuralfluid glucose is not reduced.25

The pleural fluid from the late-appearing pleuraleffusions is quite different from the bloody fluid withthe high eosinophil count and the high LDH level seenin the early effusions. The fluid from the late effusionsis usually a clear yellow exudate that contains predomi-nantly lymphocytes. In one series the median lympho-cyte percentage in 26 pleural fluids from late effusionswas 68%, whereas the median eosinophil percentagewas 0.25 The median level of LDH is approximately theupper normal limit for serum. The pleural fluid proteinis in the exudative range, and the pleural fluid glucose isnot reduced.25 The pleural fluid adenosine deaminase isbelow 40 IU/L.32


Figure 2 Pleural specimen from a patient 12 months post–coronary artery bypass graft (CABG) surgery with a persistentpleural effusion. Note the dense fibrous tissue.

Table 1 Comparison of the Characteristics of the Pleural Fluid in Patients with the PCIS

Syndrome, Early Effusions Post–CABG Surgery and Late Effusions Post–CABG Surgery

PCIS Early Post–CABG Late Post–CABG

Appearance Bloody or Bloody Clear Yellowserosanguineous

Differential WBC PMNs or Neutrophils and SmallMononuclear cells Eosinophils lymphocytes

Protein Exudative range Exudative range Exudative rangeLDH Exudative range �2� upper limit �1� upper limit

normal normalGlucose Normal Normal NormalpH Normal Normal NormalAntimyocardial High titer Absent Absent

antibody

Diagnosis

When a patient is seen with a pleural effusion post–CABG surgery, there are several other diagnoses toconsider in addition to the pleural effusion secondary toCABG surgery. The main diagnoses to exclude are con-gestive heart failure, pulmonary embolus, parapneu-monic effusions, the PCIS, and chylothorax.14 Thework-up of the patient is influenced by the patient’ssymptoms. If the patient is asymptomatic and the effu-sion is predominantly left-sided and occupies less than25% of the hemithorax, it can be attributed to the coro-nary artery surgery without performing a thoracentesis.If the patient is febrile or has chest pain, a thoracentesisshould be performed to rule out a pleural infection. Inthis situation, consideration should also be given to thepossibility of a pulmonary embolism. If dyspnea is outof proportion to the size of the effusion, the possibilityof a pulmonary embolism should also be considered. Ifthe effusion is large, the patient should undergo a thera-peutic thoracentesis to verify that a chylothorax is notpresent and to alleviate dyspnea if the patient is dys-pneic. If the effusion is a late effusion with lymphocytespredominating in the pleural fluid, the diagnosis of tu-berculosis should be excluded. This is most easily doneby measuring the level of ADA (adenosine deaminase)in the pleural fluid since the pleural fluid ADA level isalmost always above 40 with tuberculous pleuritis but isalmost always less than 40 with the pleural effusionpost–CABG surgery.32

Treatment

There are no controlled studies that address the treat-ment of the pleural effusion due to CABG surgery. Ifthe effusion is small and the patient is asymptomatic,

no treatment is necessary because such effusions virtu-ally always resolve. If the effusion is larger and thepatient is symptomatic, a therapeutic thoracentesisshould be performed. If a symptomatic effusion recursafter the initial therapeutic thoracentesis, a secondtherapeutic thoracentesis should be considered. If theeffusion recurs, many patients are also given non-steroidal anti-inflammatory agents or prednisone, butthere are no controlled studies documenting the effi-cacy of this approach. In like manner, chemical pleu-rodesis has been successful in some patients. It is im-portant to realize that the great majority of patientswith large pleural effusions will do well with only ther-apeutic thoracentesis. In our prospective study, we fol-lowed 30 patients who had a pleural effusion occupyingmore than 25% of their hemithorax for 12 months.Eight of the patients (27%) received no invasive treat-ment for their pleural effusion, 16 (53%) were treatedwith a single therapeutic thoracentesis, 2 (7%) requiredtwo thoracenteses, and 4 (13%) required three or morethoracenteses.19 One patient was still receiving periodicthoracentesis 12 months post-CABG.

In rare instances, the patient continues to besymptomatic despite several thoracenteses. Over thepast few years we have subjected eight such patients tothoracoscopy. At thoracoscopy, several patients had thinsheets of fibrous tissued that coated the lung and pre-vented it from expanding.27 We hypothesize that thissheet of fibrous tissue “trapped” the lung and preventedit from reexpanding (Fig. 3). The incidence of trappedlung after CABG surgery is not known, but is probablyvery low. At our hospital, where �2500 CABG sur-geries are performed annually, only four case of trappedlung were seen during a recent 2-year period.27 The di-agnosis of trapped lung can be established by measuring


Figure 3 (A) Posterioanterior chest radiograph demonstrating a moderate-sized left pleural effusion in a patient who was 4 monthspost–coronary artery bypass graft (CABG) surgery. (B) Chest computed tomographic scan with contrast of the patient in Figure 3Ademonstrating a loculated left pleural effusion with thickening of the visceral pleural. At thoracoscopy this patient was found to havea thin sheet of fibrous tissue covering the visceral pleural. Decortication resulted in resolution of the pleural effusion.

A B

the pleural pressure as fluid is withdrawn. If the pleuralpressure is initially below �10 cm H2O or if the pleuralpressure falls more than 20 cm H2O per 1000 mL fluidremoved, the diagnosis is strongly supported.33 Afterthe fibrous tissue coating the visceral pleural was re-moved, the lung expanded, and the effusion did notrecur. However, given that most of the patients had amechanical or a chemical pleurodesis at the time of tho-racoscopy, it is not clear that the decortication itself wasresponsible for the resolution of the pleural effusion.27

Thoracoscopy is recommended for an effusionafter CABG that continues to recur for several monthsdespite several therapeutic thoracenteses. At thora-coscopy, any fibrous tissue coating the visceral pleurashould be removed and the parietal pleura should beabraded to create a pleurodesis.

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