patients with pericardial diseases€¦ · Congenital defects of the pericardium Congenital defects...

Hemodynamic instability is the major concern insurgical patients with pericardial diseases, sincegeneral anesthesia and positive pressure ventila-tion may precipitate cardiac tamponade. In ad-vanced constriction diastolic impairment and my-ocardial fibrosis/atrophy may cause low cardiacoutput during and after surgery.

Elective surgery should be postponed in unstable pa-tients with pericardial comorbidities. Pericardial effu-sion should be drained percutaneously (in local anes-thesia) and pericardiectomy performed for constric-tive pericarditis before any major surgical procedure.In emergencies, volume expansion, catecholamines,and anesthetics keeping cardiac output and systemicresistance should be applied. Etiology of pericardial diseases is an important issue isthe preoperative management. Patients with neoplasticpericardial involvement have generally poor prognosisand any elective surgical procedure should be avoided.For patients with acute viral or bacterial infection orexacerbated metabolic, uremic, or autoimmune disea-ses causing significant pericardial effusion, surgeryshould be postponed until the causative disorder is sta-bilized and signs of pericarditis have resolved.

Key words: pericardium, pericardial effusion, cardiactamponade, constrictive pericarditis,preoperative management

INTRODUCTION

Abroad spectrum of pericardial diseases may influencethe preoperative and perioperative management, in-

cluding congenital defects of the pericardium, perica-rditis (dry, effusive, effusive-constrictive, constrictive),neoplasms, chylopericardium, and cysts. The underlyi-

ng background of these disorders may include: infectious,systemic autoimmune, postmyocardial infarction-/post-

pericardiotomy syndrome, uraemic, toxic, metabolic andautoreactive aetiologies1,2.

PERICARDIAL SYNDROMES AFFECTING PREOP-ERATIVE AND PERIOPERATIVE MANAGEMENT

Congenital defects of the pericardium

Congenital defects of the pericardium are detected in1/10 000 autopsies. Pericardial absence can be partial (left∼70%, right ∼17%) or total bilateral (rare)3. An associa-tion with other congenital cardiac, pulmonary or skeletalabnormalities is found in one-third of patients. Most pati-ents with total pericardial absence are asymptomatic. Car-diac displacement and augmented mobility impose an in-creased risk for traumatic aortic dissection. Partial left-side defects can be complicated by herniation of the heart,which can cause haemodynamic alterations during thegeneral anesthesia or even prolonged ischemic episodes,while partial right defects may cause compression of thevena cava. Before the elective surgical procedure, peri-cardioplasty is indicated to prevent imminent strangula-tion4.

Acute pericarditis

In the preoperative management, occurrence of acutepericarditis is a clear indication to postpone an electivesurgical procedure. Acute pericarditis may be a self-re-solving benign disease but it can also be the first mani-festation of neoplastic, purulent or tuberculous diseasesthat require prompt specific therapy. Importantly, carefuldifferential diagnosis between acute pericarditis and acutecoronary syndrome or aortic dissection is essential. Ge-nerally, pericarditis can be dry, fibrinous or effusive. Ma-jor symptoms are retrosternal or left precordial chest pain(which radiates to the trapezius ridge, and varies with pos-ture, being more prominent when sitting than when ly-ing) and sometimes shortness of breath. A prodrome of

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Preoperative and perioperative management ofpatients with pericardial diseases

Arsen D. Risti}1,3, Dejan Simeunovi}1,3, Ivan Milinkovi}1, Jelena Seferovi}-Mitrovi}1, Ru‘ica Maksimovi}2,3, Petar M. Seferovi}1,3, Bernhard Maisch4

1Department of Cardiology and 2Magnetic Resonance Center 3Clinical Centre of Serbia, Belgrade University School of MedicineDepartment of Internal Medicine and Cardiology,4UKGM GmbH Giessen and Marburg, Marburg Heart Center and Faculty ofMedicine, Philipps-University, Marburg, Germany

/STRU^NI RADUDK 616.11-002-089:65.001.2

DOI:10.2298/ACI1102045R

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fever, malaise, and myalgia is common. The pericardialfriction rub can be transient, mono-, bi- or triphasic. Pleu-ral effusion may be present. Heart rate is usually ra-pidand regular. ECG changes can be non-specific (includingnormal ECG) or very suggestive changes in-cluding PRdepression and concave ST-segment elevation (Figure 1).Echocardiography is essential to detect effu-sion and con-comitant heart or paracardial disease.

If associated disease is present in acute pericarditis thelikelihood that it is the cause of the pericardial syndromeis very high5. In these patients, and in patients with self-resolving forms, only non-invasive diagnostic tests are in-dicated. Many of them can be managed as out-patients6.However, in tamponade without findings of inflammationa likelihood ratio of 3.0 for neoplasia has been demons-trated7. A sustained clinical course (> 3 weeks) also incre-ases the likelihood of specific disease. Importantly, puru-lent pericarditis should be considered in predisposing di-seases (pleural empyema, mediastinal infection)8.

Symptomatic treatment of acute pericarditis is based onchest pain management and anti-inflammatory therapy.The treatment of choice is aspirin (1-4 g/day). Ibuprofen(200-600 mg three times a day) and indomethacin (25-50mg three times a day) are the preferred alternatives to as-pirin because of its rare side-effects and the large dose ra-nge9. Three months course of Colchicine (0.5 mg twice aday) added to non-steroidal anti-inflammatory drugs(NSAIDs) is effective for the treatment of acute peri-carditis10 and prevention of recurrences11. Systemic corti-costeroids are indicated for connective tissue diseases,and autoreactive or uraemic pericarditis. Intrapericardialapplication may be effective and mainly avoids systemicside-effects in patients with large autoreactive and ura-emic pericardial effusion that is resistant to conventionaltreatment12. Doses of corticosteroids should be low, as ap-plied in contemporary rheumatology13.

Chronic and recurrent (relapsing) pericarditis

Preoperative and perioperative management of patientswith chronic or recurrent pericarditis is determined by thehemodynamic impact and the volume of pericardial effu-sion. Moderately large and large effusions (separation ofpericardial layers of more than 10 mm in diastole sub-xyphoidally or in the apical area) should be drained beforethe elective surgical procedure in general anesthesia4. Hy-potensive patients with small effusions could be safelyoperated after volume expansion.

A distinction should be made between chronic pericar-ditis (which implies inflammatory activity with pericar-dial pain, fever, etc.) and chronic pericardial effusion. Ex-cept for constrictive pericarditis, chronic (> 3 months) in-flammatory pericarditis is rare. Tuberculous pericarditismay show a subacute clinical course of several weeks, butnot a persistent, sustained evolution. In contrast, pericar-dial effusion can exhibit a stable chronic course lasting formonths or years.

The recurrent or relapsing pericarditis could present asintermittent (symptom-free intervals without therapy) orthe incessant disease (discontinuation of anti-inflamma-

tory therapy ensures a relapse). Massive pericardial effu-sion, overt tamponade and progression to constriction arerare2. The management includes symptomatic treatmentof acute episodes as for acute pericarditis and the preven-tion of recurrences. Colchicine is effective in the preven-tion of relapses10. Corticosteroids should be used only inrefractory/highly symptomatic patients. Pericardiectomyis only indicated in patients with frequent and highly sy-mptomatic recurrences that are unresponsive to any othertherapy4.

Pericardial effusion

Pericardial effusion is the manifestation of pericardialdisease that could have the greatest impact on preopera-tive and perioperative management. Effusion may appearas transudate (hydropericardium), exudate, pyopericardi-um or haemopericardium. Large effusions are commonwith neoplastic, tuberculous, cholesterol, and uraemicpericarditis, myxoedema, and parasitoses2,7. Loculated ef-

FIGURE 1.

TYPICAL ELECTROCARDIOGRAM IN ACUTE PERI-CARDITIS. NOTE PR DEPRESSION (WHITE ARROW)AND CONCAVE ST-SEGMENT ELEVATION (BLACKARROW).

FIGURE 2.

ELECTROCARDIOGRAM IN CARDIAC TAMPOANDE.NOTE LOW QRS AND T WAVE VOLTAGES (LESSTHAN 5 MM), AND ELECTRICAL ALTERNANS OFTHE QRS VAWES.

46 A.D. Risti} et al. ACI Vol. LVIII

fusions are more common in postsurgical, trauma, and pu-rulent pericarditis. Slowly developing large effusions canbe remarkably asymptomatic, while rapidly accumulatingsmall effusions can create tamponade. ECG may demon-strate low QRS and T wave voltages, PR-segment depre-ssion, ST-T changes, bundle branch block and electricalalternans (Figure 2)3. Microvoltage and electrical alter-nans are reversible after effusion drainage14. In chest radi-ography large effusions are depicted as globular cardio-megaly with sharp margins ("water bottle") (Figure 3a).The size of effusion can be graded by echocardiography:

1) small (echo-free space in diastole < 10 mm), 2) moderate (10-20 mm), 3) large (>20 mm), or 4) very large (>20 mm and compression of the heart)

(Figure 4)4.

In large effusions, the heart may move freely within thepericardium (’swinging heart’) inducing pseudo-prolapseand pseudosystolic anterior motion of the mitral valve, pa-radoxical motion of the interventricular septum, and mid-systolic aortic valve closure.

Cardiac tamponade

Imminent cardiac tamponade is an absolute contraindi-cation for the surgical procedure in general anesthe-sia15,16. Additional hypotension responsible for the hemo-dynamic worsening can be caused by anesthesia-inducedperipheral vasodilatation, direct myocardial depression bysome anesthetics, or by decreased venous return causedby increased intrathoracic pressure associated with posi-tive pressure ventilation.

Cardiac tamponade is a compressive disorder of theheart (continuum ranging from a mild to a life-threateningcondition), caused by effusion accumulation and the in-creased intrapericardial pressure. In spite of the great va-lue of contemporary echocardiography, cardiac tampo-nade remains a clinical diagnosis. The classical clinicalfindings include features of venous hypertension and pul-sus paradoxus (inspiratory reduction >20 mmHg in sy-stolic blood pressure). Orthopnoea, cough, and dysphagia,occasionally with episodes of unconsciousness, can be ob-served3,15.

Up to one-third of patients with asymptomatic large pe-ricardial chronic effusions develop unexpected cardiactamponade15. Triggers for tamponade include hypovolae-mia, paroxysmal tachyarrhythmia, and intercurrent acutepericarditis. Indications for pericardial drainage are dem-onstrated in the Figure 54.

Cardiac tamponade is an absolute indication for urgentpericardial drainage in the local anesthesia4,17-20. Medicaltreatment could be only a temporary measure until peri-cardiocentesis or surgical relief (e.g. in dissection of theaorta) can be performed. The benefit of inotropic supportfor hypotensive patients, with or without vasodilators (e.g.dobutamine), is controversial21,22. Volume infusion, how-ever, is useful for patients with hypovolemia15. Althoughwe have never noticed such an event in our clinical prac-tice, it was reported that intravenous administration of flu-id can even precipitate tamponade in normovolemic orhypervolemic patients23.

Although severely hypoxic patients or those inclining torespiratory arrest must be intubated and ventilated duringthe preparation for pericardiocentesis, prolonged, positivepressure ventilation should be avoided since it decreasesthe cardiac output further24. The initial procedural morta-lity in the large surgical pericardioscopy series from Lille(France) was caused by the precipitation of critical tam-ponade in general anesthesia and mechanical ventila-tion25. In patients with cardiac arrest and a large amountof pericardial fluid, external cardiac compression has novalue, before at least a part of the pericardial effusion isevacuated. If the resuscitation is still performed withoutpericardiocentesis, systolic pressure may even slightly ri-se, but diastolic pressure will fall and further reduce co-ronary perfusion pressure15. Intravenous administration of

FIGURE 3.

A) CHEST RADIOGRAPHY (FRONTAL VIEW) IN A PA-TIENT WITH LARGE PERICARDIAL EFFUSION WITHGLOBULAR CARDIOMEGALY WITH SHARP MAR-GINS ("WATER BOTTLE" APPEARANCE) AND B)MASSIVE PERICARDIAL CALCIFICATIONS IN THELATERAL VIEW IN A PATIENT WITH CHRONIC CON-STRICTIVE PERICARDITIS - "PANZER HERZ" SIGN.

Br. 2 Preoperative and perioperative management of patients 47with pericardial diseases

diuretics is contraindicated and could be fatal in patientson the edge of their compensatory mechanisms in tampo-nade23. If needed due to concomitant heart failure or effu-sive-constrictive pericarditis, diuretics can be applied aftersuccessful drainage of the pericardial effusion.

If it is not possible to relieve cardiac tamponade beforeinduction of anesthesia, ketamine can be used for the in-duction and mainenance of anesthesia, because it incre-ases myocardial contractility, systemic vascular resistan-ce, and the heart rate. An alternative approach could be in-duction of anesthesia with a benzodiazepine followed bymaintenance with nitric oxide plus fentanyl combinedwith pancuronium for sceletal mucle relaxation. Conti-nuos monitoring of arterial and central venous pressureshoud be provided before the induction of anesthesia16.

After release of severe tamponade, there is usually a si-gnificant increase of systemic blood pressure frome seve-re hypotension to sometimes also severe hypertension.This change shoud be anticipated and managed with ap-ropriate intravenous antihypertensive medications, especi-ally if the etiology of tamponade is aortic dissection, chesttrauma, coronary perforation during angioplasty proce-dures, or iatrogenic myocardial perforation during pace-meker lead implantation or endomyocardial biopsy1, 18.

Constrictive pericarditis

Constrictive pericarditis is a clinical syndrome definedby impaired expansion of the heart by a rigid, chronicallyinflamed/thickened pericardium. The syndrome may,however, exist in approx. 20% of cases in the absence ofpericardial thickening, with ultrastructural changes only26. The predominant form is chronic constriction withoutpericardial effusion. Effusive-constrictive forms are equ-ally important27. Acute/subacute forms, transient constri-ctive pericarditis, epicardial constriction, and occult/sub-clinical forms are rather rare28,29.

Patients complain of fatigue, peripheral oedema, brea-thlessness and abdominal swelling. In decompensated pa-tients venous congestion, hepatomegaly, pleural effusionsand ascites may occur, aggravated by a protein-losing en-teropathy. In few instances, haemodynamics can be addi-tionally impaired by a systolic dysfunction (myocardial fi-brosis or atrophy)21,22. Restrictive cardiomyopathy is thecondition that may create the most serious differential dia-gnostic problems8. Much less frequently, pulmonary em-bolism, right ventricular infarction, pleural effusion, orchronic obstructive lung diseases can also be confusedwith constrictive pericarditis3. Physical findings, chest ra-diography (Figure 3b), echocardiography, computerizedtomography, magnetic resonance imaging, haemodyna-mics, and endomyocardial biopsy contribute to establi-shing the diagnosis30.

Pericardiectomy is the only treatment for permanentconstriction. Symptomatic management (diuretics, digita-lis, beta-blockers) diminishes congestion and tachyar-rhythmias before surgery. Antituberculous treatment ismandatory in tuberculous constrictions for at least 2 mo-nths before the surgery4.

Management of anesthesia should include drugs and te-chniques that minimize changes in heart rate, systemic va-scular resistance, venous return, and myocardial contrac-tility16. Combinations of opiates, benzodiazepines, and ni-tric-oxide with or without low doses of volatile anesthet-ics are acceptable for maintenance of anesthesia. Musclerelaxants with minimal circulatory effects are the bestchoices, although a modest increase in heart rate as seenwith administration of pancuronium is also acceptable.Preoperative optimization of intravascular volume is esse-ntial. When hemodynamic compromise (hypotension) due

ACUTE PERICARDITISACUTE PERICARDITIS

ECHOCARDIOGRAPHYECHOCARDIOGRAPHY

Symptomatic managementExercise restriction, hospitalisation only in pts with fever >38° C, subacute onset, immunodepression, trauma, oral anticoagulant therapy, and myopericarditis Pain management and prevention of recurrences- Aspirin 800 mg tid or qid + Colchicine, 1.0 to 2.0 mg for the first day and then 0.5 to 1.0 mg/d for 3 months

Symptomatic managementExercise restriction, hospitalisation only in pts with fever >38° C, subacute onset, immunodepression, trauma, oral anticoagulant therapy, and myopericarditis Pain management and prevention of recurrences- Aspirin 800 mg tid or qid +

Colchicine, 1.0 to 2.0 mg for the first day and then 0.5 to 1.0 mg/d for 3 months

PERICARDIOCENTESISPERICARDIAL DRAINAGE

(best with cardiac catheterization)



SUBXIPHOID PERICARDIOTOMY

AND DRAINAGE


AND DRAINAGE

Suspected purulent, TBCor neoplastic effusion


TAMPONADE orPE>20 mm in diastole


NO TAMPONADEPE 10-20 mm in diastole


NO TAMPONADEPE <10 mm in diastole


PERICARDIOSCOPY ANDPERICARDIAL/EPICARDIAL BIOPSY

FOLLOW-UPECHOCARDIOGRAPHY

FOLLOW-UPECHOCARDIOGRAPHYINTRAPERICARDIAL THERAPYINTRAPERICARDIAL THERAPY

ACUTE PERICARDITISACUTE PERICARDITIS

ECHOCARDIOGRAPHYECHOCARDIOGRAPHY

Symptomatic managementExercise restriction, hospitalisation only in pts with fever >38° C, subacute onset, immunodepression, trauma, oral anticoagulant therapy, and myopericarditis Pain management and prevention of recurrences- Aspirin 800 mg tid or qid + Colchicine, 1.0 to 2.0 mg for the first day and then 0.5 to 1.0 mg/d for 3 months

Symptomatic managementExercise restriction, hospitalisation only in pts with fever >38° C, subacute onset, immunodepression, trauma, oral anticoagulant therapy, and myopericarditis Pain management and prevention of recurrences- Aspirin 800 mg tid or qid +

Colchicine, 1.0 to 2.0 mg for the first day and then 0.5 to 1.0 mg/d for 3 months






AND DRAINAGE


AND DRAINAGE









PERICARDIOSCOPY ANDPERICARDIAL/EPICARDIAL BIOPSY

FOLLOW-UPECHOCARDIOGRAPHY

FOLLOW-UPECHOCARDIOGRAPHYINTRAPERICARDIAL THERAPYINTRAPERICARDIAL THERAPY

FIGURE 5.

ALGORITHM FOR THE PREOPERATIVE MANAGE-MENT OF ACUTE PERICARDITIS, PERICARDIAL EF-FUSION, AND CARDIAC TAMPONADE. MODIFIEDWITH PERMISSION ACCORDING TO THE EUROPEANSOCIETY OF CARDIOLOGY GUIDELINES ON DIAG-NOSIS AND MANAGEMENT OF PERICARDIAL DIS-EASES

FIGURE 4.

TWO-DIMENSIONAL ECHOCARDIOGRAPHY IN APATIENT WITH LARGE PERICARDIAL EFFUSIONAND RIGHT ATRIAL COLLAPS. FRAME A - SYSTOLE,NO COLLAPS OF THE RIGHT ATRIUM (BLACK AR-ROW). FRAME B - DIASTOLE, PRONOUNCED RIGHTATRIAL COLLAPS (BLACK ARROW).


to increased intrapericardial pressure is present prior tosurgery, management of anesthesia is as described for ca-rdiac tamponade. Invasive monitoring of arterial and cen-tral venous pressure is helpful because removal of adhe-rent pericardium may be a tedious and long operation of-ten associated with significant fluid/blood losses. Cardiacarrhythmias are common, presumably reflecting directmechanical stimulation of the heart. Intravenous fluidsand blood products may be necessary to treat the signifi-cant fluid/blood losses associated with pericardiectomy.

Perioperative mortality is 6-12% in the current series31-33, but can be up to 40% if patients with extensive myo-cardial atrophy/fibrosis are not excluded29,30. Major com-plications include acute cardiac insufficiency and ventri-cular wall rupture28. If surgery is carried out early, long-term survival after pericardiectomy corresponds to that ofthe general population31-33. Postoperative respiratory in-sufficiency may necessitate prolonged mechanical ven-ti-lation. Supraventricular tachyarrhythmias and low car-diac output may complicate the postoperative period.

Predictors of poor survival are prior radiation, worse re-nal function, higher pulmonary artery systolic pressure,abnormal left ventricular systolic function, lower serumsodium level, and older age33. Surprisingly, pericardialcalcification had no impact on survival. In a controlledstudy of 143 patients with constrictive tuberculous perica-rditis, prednisolone therapy as an adjunct to streptomycin,isoniazid, rifampicin, and pyrazinamide reduced the 2-year mortality (4% vs. 11%), decreased the need for re-peated pericardial drainage or surgery (21% vs. 30%), andthe incidence of late constriction (8% vs. 12%)34. The 10-year follow-up revealed adverse outcomes in 27% of pa-tients treated with prednisolone in contrast to 38% on pla-cebo, deaths from pericarditis being 3% vs. 11%, respecti-

vely. In a multivariate analysis prednisolone reduced theoverall death rate, and substantially reduced the risk of de-ath from pericarditis35.

SPECIFIC FORMS OF PERICARDITIS AFFECTINGPREOPERATIVE AND PERIOPERATIVE MANAGE-MENT

Several etiological forms of pericardial disease may re-quire specific management before the elective surgery canbe safely performed. In acute viral or bacterial infectioninvolving the pericardium or exacerbated metabolic, ure-mic, or autoimmune disease causing significant pericar-dial effusion, surgical procedure should be postponed un-til the underlying disease is stabilized and signs of peri-carditis resolved. Treatment of acute idiopathic and viralpericarditis is directed to resolving the symptoms and pre-venting recurrences including 10 days course of aspirin 4-6x600 mg or ibuprofen 800+800+400 mg concomitantlywith colchicine 2x0.5 mg for 3 months4,10.

Purulent pericarditis is a rare, acute, fulminant illnessthat is always fatal if untreated. The mortality rate in tre-ated patients is 40%, mostly because of cardiac tampona-de, toxicity and constriction8. Percutaneous pericardiocen-tesis must be promptly performed. The pericardial fluidobtained should undergo Gram, acid-fast, and fungal stai-ning, followed by cultures of the pericardial and body flu-ids. Rinsing of the pericardial cavity, combined with effe-ctive systemic antibiotic therapy, is mandatory (antista-phylococcal antibiotic plus aminoglycoside, tailored acc-ording to pericardial fluid and blood cultures)4,18. Intra-pericardial instillation of antibiotics (e.g. gentamycin) isuseful but not sufficient. Open surgical drainage and pe-ricardiectomy are required in patients with dense adhesi-ons, loculated and thick purulent effusion, recurrence oftamponade, persistent infection and progression to con-striction4,8,36. Surgical mortality is up to 8%. Instead ofsurgery, pericardiocentesis and frequent irrigation of thepericardial cavity with urokinase or streptokinase hasbeen applied in a few patients37,38. However, the safetyand efficacy of this approach in comparison to surgery re-mains to be investigated.

Pericarditis in a patient with proven extracardiac tuber-culosis is strongly suggestive of a tuberculous aetiology(several sputum cultures should be taken)39. Tuberculouspericarditis can present as acute pericarditis with or wi-thout effusion; cardiac tamponade, acute constrictive pe-ricarditis, subacute constriction, effusive-constrictive, orchronic constrictive pericarditis, and pericardial calcifica-tions2,40,41. The mortality rate in untreated effusive tuber-culous pericarditis approaches 85%. Pericardial constric-tion in these cases is 30-50%39,40,42. The diagnosis ismade by the identification of M. tuberculosis in the peri-cardial fluid/tissue, and/or the presence of caseous granu-lomas in the pericardium. Polymerase chain reaction me-thods can identify M. tuberculosis rapidly from 1 µl of pe-ricardial fluid43. Increased adenosine deaminase activityand interferon-gama concentration in pericardial effusionare also suggestive. The tuberculin skin test may producea false-negative in 25-33% and a false-positive in 30-40%

FIGURE 6.

COMPUTED TOMOGRAPHY DEMONSTRATING ALARGE LOCULATED POST-INFARCTION PERICAR-DIAL EFFUSION AFTER SPONTANEOUSLY HEALEDANTERIOR WALL RUPTURE.


of patients40. The more accurate enzyme-linked immuno-spot (ELISPOT) test detects T cells that are specific forthe M. tuberculosis antigen44. Pericardioscopy and peri-cardial biopsy may improve the diagnostic accuracy25,45.Various antituberculous drug combination regimens of di-fferent durations (6,9,12 months) have been applied-39,40,42,46-48. However, only patients with proven or verylikely tuberculous pericarditis should be treated. Preven-tion of constriction in chronic pericardial effusion of un-determined aetiology by ex iuvantibus antitubercular tre-atment was not successful48. A meta-analysis of tre-at-ment results in effusive and constrictive tuberculous pe-ri-carditis suggested that tuberculostatic treatment com-bined with steroids might be associated with fewer deathsand less frequent need for pericardiocentesis or pericar-diectomy46,47. If given, prednisone should be administe-red in high doses (1-2 mg/kg/day) because rifampicin in-duces its metabolism by the liver4. This is maintained for5-7 days and progressively reduced in 6-8 weeks.

Fungal pericarditis may be endemic (Histoplasma, Coc-cidioides) or opportunistic (Candida, Aspergillus, Bla-stomyces, Nocardia, Actinomyces). Diagnosis is obtainedby staining and culturing pericardial fluid or tissue or bydetermination of antifungal antibodies in serum2. NSAIDscan support the treatment with antifungal drugs (flucona-zole, ketoconazole, itraconazole, amphotericin B)4.

Most patients with uraemic pericarditis respond to fre-quent haemodialysis (heparin-free to avoid haemopericar-dium) with resolution of chest pain and pericardial effu-sion within 1-2 weeks49. Peritoneal dialysis may be the-rapeutic in pericarditis that is resistant to haemodialysis,or if heparin-free haemodialysis cannot be performed.NSAIDs and systemic corticosteroids have limited succe-ss when intensive dialysis is ineffective. Cardiac tampo-nade and large effusions resistant to dialysis must be tre-ated with pericardiocentesis. Large, non-resolving symp-tomatic effusions can be treated with intrapericardial insti-llation of corticosteroids (triamcinolone hexacetonide 50mg every 6 hours for 2 to 3 days)4. Pericardiectomy is in-dicated only in refractory, severely symptomatic patients.Colchicine may worsen the impaired renal function, butbenefit was also noted in a resistant case of uraemic peri-carditis50.

Pericarditis may also occur in several systemic autoim-mune diseases2. Intensified preoperative treatment of theunderlying disease and symptomatic management are in-dicated4.

Post-cardiac injury (postpericardiotomy) syndrome de-velops within days to months after cardiac/pericardial in-jury2. Cardiac tamponade is more common following val-ve surgery than coronary artery bypass grafting and maybe related to the postoperative use of anticoagulants15. Sy-mptomatic treatment is the same as for acute pericarditisand repeat surgery is rarely needed. Benefit of primaryprevention using perioperative treatment with colchicinewas recently proven in a randomized COPPS trial51.

Postinfarction pericarditis occurs as an "early" (pericar-ditis epistenocardica) or a "delayed" form (Dressler’s syn-drome)2,9. Epistenocardiac pericarditis, caused by direct

exudation, occurs in 5-20% of transmural myocardial in-farctions within the first 7 days but is rarely discoveredclinically. Dressler’s syndrome arises from one week toseveral months after myocardial infarction, with manifes-tations similar to the post-cardiac injury syndrome. It doesnot require transmural infarction and can also appear as anextension of epistenocardiac pericarditis. Its incidencewas 0.5-5% in the past, particularly in the prethrombolyticera, but the syndrome has become a rarity most probablybecause of advances in treatment of acute myocardial in-farction by cardiac interventions2. High doses of ibupro-fen or aspirin should be given for 2-5 days. Steroids canbe used for refractory symptoms but may delay the heal-ing of infarction4. Surgical revascularization of the myo-cardium should be postponed until the signs of Dressler’ssyndrome have resolved, except in unstable patients withleft-main disease or left-main equivalent16.

Of note, a postinfarction pericardial effusion larger than10 mm is a predictor of ventricular wall rupture (Figure6)52. Urgent surgical treatment is life saving. If this is notfeasible pericardiocentesis and intrapericardial fibrin-glueinstillation could be an alternative53.

Patients with neoplastic pericardial disease have gene-rally very poor prognosis if the pericardial involvement iscaused by metastatic malignant disease. Any elective sur-gical procedure should be avoided, unless its purpose wo-uld be to improve the symptoms or prognosis of the un-derlying neoplastic illness54. The diagnosis is based onthe confirmation of the malignant infiltration within thepericardium by cytology or biopsy4,17,25,45. Notably, in al-most two-thirds of the patients with documented malig-nancy pericardial effusion is caused by non-malignant dis-eases, e.g. radiation pericarditis, or opportunistic infec-tions55. In neoplastic pericardial effusion without tampo-nade systemic antineoplastic treatment as baseline therapycan prevent up to 67% of recurrences2. Pericardial drain-age is recommended in all patients with large effusio-ns/tamponade, but also in patients with moderate effusio-ns 10-20 mm in order to confirm the neoplastic etiologyof pericardial involvement4. Prevention of recurrencesmay be achieved by intrapericardial instillation of sclero-sing, cytotoxic agents, or immunomodulators. Radiationtherapy is effective in patients with radiosensitive tumours(lymphoma and leukaemia)4. Intrapericardial instillationof cisplatin is most effective in secondary lung cancer andthiotepa is valuable in breast cancer pericardial metasta-ses56-59.

Chylopericardium is caused by a communication bet-ween the pericardium and the thoracic duct, predominan-tly as a complication of trauma, congenital anomalies, orsurgery3. The pericardial fluid is sterile, odourless andopalescent with a milky white appearance and the micros-copic finding of fat droplets. The chylous nature of thefluid is confirmed by Sudan III stain for fat and by highconcentrations of triglycerides (5-50g/l), and proteins (22-60g/l)2. Enhanced computerized tomography, alone orcombined with lymphography, can identify not only thelocation of the thoracic duct but also its lymphatic conne-ction to the pericardium. Chylopericardium after thoracic


or cardiac operation is preferably treated by pericardio-centesis and diet (medium-chain triglycerides). If produc-tion of chylous effusion continues, surgical treatment ismandatory. When the course of the thoracic duct can beprecisely identified, its ligation and resection just abovethe diaphragm is effective4.

Pericardial effusion in hypothyroidism occurs in 5-30%of patients with pericardial disease2. Fluid accumulatesslowly and tamponade occurs rarely. In some cases cho-lesterol pericarditis may be observed. The diagnosis is ba-sed on serum levels of thyroxin and thyroid-stimulatinghormone. Therapy with thyroid hormone leads to the re-solution of the pericardial effusion60.

CONCLUSION

Pericardial diseases are infrequent, but potentially life-threatening co-morbidity in patients undergoing surgicalprocedures in general anesthesia. Preoperative and perio-perative care for these patients may be challenging espe-cially regarding the management of hemodynamic insta-bility, as well as the underlying infectious, autoimmune ormetabolic diseases. Proper and timely diagnostic asse-ssment and etiological diagnosis is essential to avoid se-rious perioperative and postoperative complications.

SUMMARY

PREOPERATIVNA PRIPREMA I PERIOPERATIVNITRETMAN BOLESNIKA SA OBOLJENJIMA PERI-KARDA

Hemodinamska nestabilnost je najva‘niji problem upreoperativnoj pripremi bolesnika sa bolestima perikardapošto opšta anestezija i ventilacija pod pozitivnim pritis-kom mo‘e da izazove tamponadu srca. U odmakloj kons-trikciji dijastolna disfunkcija, kao i fibroza i atrofija mio-karda mogu uzrokovati nizak minutni volumen tokom iposle hirurške intervencije.

Elektivne hirurške procedure treba odlo‘iti kod nestabil-nih bolesnika sa perikardnim komorbiditetima. Perikardniizliv treba perkutano drenirati (u lokalnoj anesteziji), akod bolesnika sa hroni~nom konstrikcijom uraditi peri-kardiektomiju pre svake velike hirurške intervencije u op-štoj anesteziji. U urgentnim stanjima treba primeniti ek-spandere intravaskularnog volumena, kateholamine i an-estetike koji ne obaraju minutni volumen niti sistemskuvaskularnu rezistenciju.

Etiologija bolesti perikarda je takodje jedan od va‘nihelemenata u preoperativnoj pripremi bolesnika. Bolesnicisa neoplasti~nim bolestima perikarda imaju generalnološu prognozu i sve velike, elektivne hirurške proceduretreba izbegavati. Kod bolesnika sa akutnom virusnom ilibakterijskom infekcijom kao i kod metaboli~kih, bubre-‘nih ili autoimunih bolesti koje uzrokuju perikarditis, hi-ruršku proceduru treba odlo¤iti dok se osnovna bolest nestabilizije i znaci perikarditisa ne povuku.

Klju~ne re~i: perikard, perikardni izliv, tamponadasrca, konstriktivni perikarditis,preoperativna priprema

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