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Pericardial Disease
 

Pericardial Disease

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    Pericardial Disease Pericardial Disease Presentation Transcript

    • Pericardial Diseases Piti Niyomsirivanich, MD. Reference : Libby: Braunwald's Heart Disease: A Textbook of Cardiovascular Medicine, 8th ed.
    • ANATOMY AND PHYSIOLOGY OF THE PERICARDIUM
      • The pericardium is composed of two layers
        • the visceral pericardium
          • single layer of mesothelial cells adherent to the epicardial surface of the heart
        • the fibrous parietal layer
          • about 2 mm thick in normal humans and surrounds most of the heart.
          • acellular and contains both collagen and elastin fibers.
          • Collagen  low levels of stretch
      • The pericardial space or sac is contained within these two layers and normally contains up to 50 ml of serous fluid .
      • The parietal pericardium has ligamentous attachments to the diaphragm, sternum , and other structures in the anterior mediastinum.
      • The only noncardiovascular macrostructures associated with the pericardium are the phrenic nerves , which are enveloped by the parietal pericardium.
    •  
      • the normal pericardium does have functions
        • it maintains the position of the heart relatively constant.
        • function as a barrier to infection and provides lubrication between visceral and parietal layers.
      • The pericardium is well innervated with mechanoreceptors and chemoreceptors and phrenic afferents.
        • reflexes arising from the pericardium and/or epicardium (e.g., the Bezold-Jarisch reflex), as well as transmission of pericardial pain .
      • its restraining effect on cardiac volume.
        • At low applied stresses  it is elastic
        • As stretch increases  stiff
        • The contact pressure is proportionally more important for the right heart , whose filling pressures are normally lower than the left heart.
    • THE PASSIVE ROLE OF THE NORMAL PERICARDIUM IN HEART DISEASE
      • When the cardiac chambers dilate rapidly,
        • the restraining effect can become markedly augmented
        • resulting in a hemodynamic picture
          • resembling both cardiac tamponade and constrictive pericarditis
        • The most common example is acute RV myocardial infarction (MI),
        • the right heart dilates markedly and rapidly
        • total heart volume > pericardial reserve volume.
        • increased pericardial constraint
        • paradoxical pulse ,Kussmaul sign
      • Chronic cardiac dilation (e.g., caused by dilated cardiomyopathy or regurgitant valvular disease)
        • the pericardium undergoes chronic adaptation to accommodate marked increases in cardiac volume.
    • ACUTE PERICARDITIS
      • defined as symptoms and/or signs resulting from pericardial inflammation of no more than 1 to 2 weeks' duration .
      • can occur in a wide variety of these diseases (denoted by asterisks), but the majority of cases are idiopathic .
    • Categories of Pericardial Disease and Selected Specific Etiologies
      • Idiopathic   
      • Infectious   
        • Viral (echovirus, coxsackievirus, adenovirus, cytomegalovirus, hepatitis B, infectious mononucleosis, HIV/AIDs)    Bacterial ( Pneumococcus, Staphylococcus, Streptococcus, mycoplasma, Lyme disease, Haemophilus influenzae, Neisseria meningitidis, and others)    Mycobacteria (Mycobacterium tuberculosis, Mycobacterium avium-intracellulare)    Fungal (histoplasmosis, coccidiomycosis)    Protozoal   
      • Immune-inflammatory   
        • Connective tissue disease [*] (systemic lupus erythematosus, rheumatoid arthritis, scleroderma, mixed)    Arteritis (polyarteritis nodosa, temporal arteritis)    Inflammatory bowel disease    Early post–myocardial infarction    Late post–myocardial infarction (Dressler syndrome), [*] late postcardiotomy/thoracotomy, [*] late posttrauma [*] Drug induced [*] (e.g., procainamide, hydralazine, isoniazid, cyclosporine)    Neoplastic disease    Primary: mesothelioma, fibrosarcoma, lipoma, and so on    Secondary [*] : breast and lung carcinoma, lymphomas, Kaposi sarcoma
    • Categories of Pericardial Disease and Selected Specific Etiologies
      • Radiation induced [*] Early postcardiac surgery    Hemopericardium    Trauma    Post–myocardial infarction free wall rupture    Device and procedure related: percutaneous coronary procedures, implantable defibrillators, pacemakers, post–arrhythmia ablation, post–atrial septal defect closure, post–valve repair/replacement    Dissecting aortic aneurysm    Trauma    Blunt and penetrating, [*] post–cardiopulmonary resuscitation [*]    Congenital    Cysts, congenital absence    Miscellaneous   
        • Cholesterol (“gold paint” pericarditis)    Chronic renal failure, dialysis related    Chylopericardium    Hypothyroidism and hyperthyroidism    Amyloidosis    Aortic dissection
      • The incidence is difficult to quantify
        • > there are undoubtedly many undiagnosed cases .
      • At autopsy, the frequency is approximately 1 percent .
      • Pericarditis is relatively common in patients presenting to the ER
        • > 5 % of nonischemic chest pain
        • 1% of cases with ST elevation.
    • History and Differential Diagnosis
      • almost always presents with chest pain .
      • A few cases are diagnosed during evaluation of associated symptoms
        • such as dyspnea or fever
        • incidentally in noncardiac manifestations of systemic diseases
          • such as rheumatoid arthritis or systemic lupus erythematosus (SLE).
      • The pain of pericarditis can be severe. It is variable in quality but often sharp and almost always pleuritic .
      • Pericardial pain typically has a relatively rapid onset and sometimes begins remarkably abruptly.
        • It is most commonly substernal, but can also be centered in the left anterior chest or epigastrium.
        • Left arm radiation is not unusual.
      • radiation to trapezius ridge, which is highly specific for pericarditis .
      • Pericardial pain is almost always relieved by sitting forward and worsened by lying down.
      • Associated symptoms
        • dyspnea, cough, and occasionally hiccoughs.
      • A history of cancer or an autoimmune disorder, high fevers with shaking chills, skin rash, or weight loss should alert the physician to specific diseases that can cause pericarditis.
      • Diagnoses most easily confused with pericarditis include
        • pneumonia or pneumonitis with pleurisy (which may coexist with pericarditis), pulmonary embolus/infarction, costochondritis, and gastroesophageal reflux disease.
      • Acute pericarditis is usually relatively easily distinguished from myocardial ischemia/infarction on clinical and other grounds, but coronary angiography is occasionally required to resolve this issue.
      • Other considerations include
        • aortic dissection, intraabdominal processes, pneumothorax, and herpes zoster pain (before skin lesions appear.)
        • Finally, acute pericarditis is occasionally the presenting manifestation of a preceding, clinically silent MI.
    • Physical Examination
      • Patients with uncomplicated acute pericarditis often appear uncomfortable and anxious and may have low-grade fever and s inus tachycardia .
      • Otherwise, the only abnormal physical finding is the friction rub caused by contact between visceral and parietal pericardium.
      • The classic rub is pathognomonic of pericarditis.
      • It consists of three components corresponding to ventricular systole, early diastolic filling, and atrial contraction and is similar to the sound made when walking on crunchy snow.
      • The rub is usually loudest at the lower left sternal border , often extends to the cardiac apex , and is best heard with the patient leaning forward .
      • It is often dynamic , disappearing and returning over short periods of time.
      • Sometimes what is considered a pericardial rub has only two or even one component.
    • Laboratory Testing
      • Electrocardiogram
        • The electrocardiogram (ECG) is the most important laboratory test for diagnosing acute pericarditis.
        • The ST segment vector typically points leftward , anterior and inferior , with ST segment elevation in all leads except AVR and often V1.
        • Thus the term “diffuse” is a slight misnomer.
        • Usually, the ST segment is coved upward and resembles the current of injury of acute, transmural ischemia.
      • In other cases the ST segment more closely resembles early repolarization.
      • PR segment depression is also common
        • PR depression can occur in the absence of ST elevation
        • and be the initial ECG manifestation of acute pericarditis
      • ECG abnormalities other than ST elevation and PR depression are unusual in patients presenting soon after the onset of symptoms of acute pericarditis.
      • Subsequent ECG changes are quite variable.
      • In others, the elevated ST segment passes through the isoelectric point
        • and progresses to ST segment depression and T wave inversions in leads with upright QRS complexes.
        • The latter changes can persist for weeks and months.
      • these ECG changes can be difficult to distinguish from myocardial ischemia.
      • ECG abnormalities other than the above should be considered carefully
        • As examples, AV block  Lyme disease,
        • pathological Q  silent MI with pericardial pain as its first manifestation,
        • low voltage or electrical alternans point toward significant effusion.
      • Modest elevations of the white blood cell count , typically 11,000 to 13,000 ml with a mild lymphocytos is, are common in acute idiopathic pericarditis.
      • Higher counts are an alert for the presence of other etiologies.
      • The erythrocyte sedimentation rate (ESR) should be no more than modestly elevated in acute idiopathic pericarditis.
      • Unusually high values may be a clue to etiologies such as autoimmune diseases or tuberculosis.
    • Cardiac Enzymes and Troponin Measurements
      • Surprisingly large numbers of patients with a diagnosis of
        • acute pericarditis without other evidence of myocarditis or MI have elevated creatine kinase MB fraction and/or troponin I values
      • Pericarditis patients with elevated biomarkers of myocardial injury almost always have ST segment elevation.
      • elevations of troponin I without creatine kinase
        •  adjacent epicardial inflammation rather than a true myocarditis
    • Chest Radiograph
      • CXR is usually normal in uncomplicated acute idiopathic pericarditis.
      • Occasionally, small pulmonary infiltrates or pleural effusions are present,
      • bacterial pericarditis often occurs in conjunction with severe pneumonia .
      • Mass lesions and enlarged lymph nodes suggestive of neoplastic disease also have great significance.
      • Tuberculous pericarditis can occur with or without associated pulmonary infiltrates.
      • Pulmonary vascular congestion may signal coexistent, severe myocarditis.
    • Echocardiography
      • The echocardiogram is normal in most patients with acute idiopathic pericarditis.
      • The main reason for its performance is to exclude an otherwise silent effusion .
      • Moderate or larger effusions are unusual
    • Natural History and Management
      • keep in mind that controlled data are limited .
      • Initial management should be focused on screening for specific etiologies
        • In young women  test for SLE.
      • Acute idiopathic pericarditis is a self-limited disease without significant complications or recurrence In 70 to 90 percent of patients.
      • If laboratory data support the clinical diagnosis, symptomatic treatment with nonsteroidal antiinflammatory drugs (NSAIDs) should be initiated
      • Because of its excellent safety profile, we prefer ibuprofen (600 to 800 mg po three times daily) with discontinuation if pain is no longer present after 2 weeks .
      • Many patients have gratifying responses to the first dose or two of an NSAID , and most respond fully and need no additional treatment.
      • Reliable patients with no more than small effusions who respond well to NSAIDs need not be admitted to a hospital .
      • Patients who do not respond well initially , have larger effusions, or suspicion of an etiology other than idiopathic pericarditis should be hospitalized for additional observation, diagnostic testing, and treatment as needed.
      • Patients who respond slowly or inadequately to NSAIDs may require supplementary narcotic analgesics to allow time for a full response and/or a brief course of colchicine or prednisone .
      • Colchicine is administered as a 2 to 3 mg oral loading dose followed by 1 mg daily for 10 to 14 days .
      • Prednisone 60 mg by mouth is administered daily for 2 days with tapering to zero over a week .
      • Perhaps 15 to 30 percent of patients with acute, apparently idiopathic pericarditis who respond satisfactorily to treatment as outlined earlier suffer a relapse after completion of initial therapy
      • A pericardial biopsy to look for a specific etiology in patients with recurrent pain without effusion is rarely indicated
      • Treatment of recurrent pain is empirical.
      • For an initial relapse, a second 2-week course of a NSAID is often effective.
      • we favor colchicine prophylaxis . Substantial experience has accumulated using chronic colchicine as prophylaxis for recurrent pericardial pain including that caused by idiopathic pericarditis and other etiologies (postthoracotomy, SLE).
      • As earlier, the usual dose is a 2- to 3-mg oral load followed by 1 mg by mouth daily.
      • Nonsteroidal immunosuppressive therapy with drugs such as azathioprine and cyclophosphamide … experience is extremely limited
    • PERICARDIAL EFFUSION AND TAMPONADE
    • Etiology
        • Idiopathic pericarditis and any infection, neoplasm, autoimmune, or inflammatory process (including postradiation and drug induced) that can cause pericarditis can cause an effusion
        • high incidence of progression to tamponade are bacterial (including mycobacteria), fungal , and human immunodeficiency virus (HIV)-associated infections and neoplastic involvement.
    • Pathophysiology and Hemodynamics
      • Formation of an effusion is a component of the response to inflammation when there is an inflammatory and/or infectious process affecting the pericardium.
      • pericardial tumor implants
      • Lymphomas  by obstructing pericardial lymph drainage.
      • effusions in situations with no obvious inflammation (e.g., uremia) is poorly understood.
      • Cardiac tamponade is characterized by a continuum from an effusion causing minimally detectable effects to full-blown circulatory collapse.
      • Determinants of the hemodynamic consequences of pericardial effusion are the level of pressure in the pericardial sac and the ability of the heart to compensate for elevated pressure.
      • Large, slowly accumulating effusions are often well tolerated , presumably because of chronic changes in the pericardial pressure-volume relation.
      • The compensatory response to a significant pericardial effusion includes
        • increased adrenergic stimulation and parasympathetic withdrawal , which cause tachycardia and increased contractility.
      • those receiving beta-adrenergic blocking drugs are more susceptible to the effects of a pericardial effusion.
      • As fluid accumulates in the pericardial sac,
        • Lt-Rt A and V diastolic pressures rise
        • severe tamponade pressure in the pericardial sac, typically 15 to 20 mm Hg
      • cardiac volumes progressively decline.
      • The decreased preload mainly accounts for the small stroke volume.
      • two other hemodynamic abnormalities are characteristic of tamponade.
        • One is loss of the y descent of the right atrial or systemic venous pressure
        • The second characteristic hemodynamic finding is the paradoxical pulse
          • large decline in systemic arterial pressure during inspiration (usually defined as a >10 mm Hg drop in systolic pressure)
        • Also seen in
          • constrictive pericarditis, pulmonary embolus, and pulmonary disease with large variation in intrathoracic pressure.
    •  
    • Low Pressure Temponade
      • Low pressure tamponade occurs when there is a decrease in blood volume in the setting of a preexisting effusion that would not otherwise be significant.
      • diuretics are administered to patients with effusions
      • Low pressure tamponade is observed during hemodialysis
    • Regional tamponade
      • sometimes encountered after cardiac surgery
        • should be suspected whenever hemodynamic abnormalities exist in a setting in which a regional or loculated effusion is present.
        • Large pleural effusions can also compress the heart
    • Clinical Presentation
      • Asymptomatic unless tamponade is present.
      • Patients with tamponade may complain of true dyspnea , the mechanism of which is uncertain because no pulmonary congestion occurs.
      • In pericardial effusion without tamponade
        • the cardiovascular examination is normal except that if the effusion is large , the cardiac impulse may be difficult or impossible to palpate and the heart sounds muffled .
        • Tubular breath sounds may be heard in the left axilla or left base because of bronchial compression.
        • Beck's triad of hypotension, muffled heart sounds, and elevated jugular venous pressure remains a useful clue to the presence of severe tamponade
      • Patients with tamponade are almost always uncomfortable, with signs reflecting varying degrees of reduced cardiac output and shock including tachypnea; diaphoresis; cool extremities; peripheral cyanosis; depressed sensorium; and, rarely, yawning.
      • hypotension is usually present , although in early stages compensatory mechanisms maintain the blood pressure.
    • reduced voltage and electrical alternans Low voltage : emphysema, infiltrative myocardial disease, and pneumothorax
    • Chest Radiograph
      • The cardiac silhouette remains normal until pericardial effusions are at least moderate in size.
      • With moderate and larger effusions , the anteroposterior cardiac silhouette assumes a rounded, flasklike appearance .
      • Lateral views may reveal the pericardial fat pad sign , a linear lucency between the chest wall and the anterior surface of the heart representing separation of parietal pericardial fat from epicardium.
    • Echocardiography
      • A pericardial effusion appears as a lucent separation between parietal and visceral pericardium.
      • With a true effusion, separation is present for the entire cardiac cycle .
      • Small effusions are first evident over the posterobasal left ventricle.
      • Early diastolic collapse of the right ventricle and collapse of the right atrium (which occurs during ventricular diastole) are sensitive and specific signs
      • Right atrial collapse is considered more sensitive .
      • RV collapse more specific for tamponade
      • Distention of the caval vessels that does not diminish with inspiration is also a useful sign
      • Doppler velocity recordings demonstrate exaggerated respiratory variation in right- and left-sided venous and valvular flow,
    •  
    • Other Imaging Modalities
      • Computed tomography (CT) and magnetic resonance imaging (MRI) are useful adjuncts to echocardiography in the characterization of effusion and tamponade
      • Neither is ordinarily required and/or advisable in sick patients
      • Attenuation similar to water suggests transudative, greater than water malignant, bloody or purulent, and less than water chylous effusion.
    • Management of Pericardial Effusion and Tamponade
      • suspected bacterial or tuberculous pericarditis, bleeding into the pericardial space
    • Effusions Without Actual or Threatened Tamponade
      • In many cases of effusion when tamponade is neither present nor threatened, a cause will be evident or suggested on the basis of the history (e.g., known neoplastic or autoimmune disease, radiation therapy) and/or previously obtained diagnostic tests.
      • When a diagnosis is not clear , an assessment of specific etiologies of pericardial disease should be undertaken.
      • TB ,autoimmune diseases and infections (e.g., Lyme disease) and hypothyroidism should be considered
      • Serial titers of antibodies to viruses are usually not helpful
      • In obvious cases
      • In occasional situations where pericardiocentesis is necessary for diagnostic purposes, consideration should be given to open drainage with biopsy .
      • Occasional patients with large, asymptomatic effusions and no evidence of tamponade.
        • The effusions are by definition chronic .
      • They are in general stable, and specific etiologies usually do not emerge over time .
      • there is a rationale for closed pericardiocentesis following routine evaluation for specific etiologies
      • Before undertaking pericardiocentesis , a course of a NSAID or colchicine should be considered .
    • Effusions with Actual or Threatened Tamponade
      • These patients should be considered as having a true or potential medical emergency.
      • Most patients require pericardiocentesis to treat or prevent tamponade.
      • idiopathic pericarditis , mild tamponade can be treated with a course of a NSAID and/or colchicine and monitored in the hope that their effusions will shrink rapidly.
      • Patients with autoimmune diseases can be treated in the same way and/or with a course of corticosteroids
      • in whom a decision is made to defer pericardiocentesis
        • Hemodynamic monitoring with a pulmonary artery balloon catheter is often useful
      • Once actual or threatened tamponade is diagnosed, intravenous hydration should be instituted
      • intravenous positive inotropes (dobutamine, dopamine) can be employed but are of limited efficacy
      • Hydration and positive inotropes are temporizing measures and should not be allowed to substitute for or delay pericardiocentesis
      • closed pericardiocentesis is the initial treatment of choice
      • subxiphoid needle insertion performed under echocardiographic guidance
      • Once the needle has entered the pericardial space, a modest amount of fluid should be removed (perhaps 50 to 150 ml) in an effort to produce some degree of hemodynamic improvement.
      • Then a guidewire should be inserted
      • the needle replaced with a pigtail catheter .
      • The catheter can be manipulated with continuing echocardiographic guidance to maximize the amount of fluid removed
      • If echocardiographic guidance is unavailable, the needle should be directed toward the right shoulder and then replaced with a catheter for subsequent fluid removal
      • If a pulmonary artery catheter has been inserted into the right heart,
        • pulmonary capillary wedge and systemic arterial pressures and cardiac output should be monitored before, during, and after the procedure.
      • Following pericardiocentesis, repeat echocardiography and in many cases continued hemodynamic monitoring are useful to assess fluid reaccumulation .
    • Analysis of Pericardial Fluid
      • The fluid has the features of a plasma ultrafiltrate.
      • analysis of pericardial fluid does not usually have a high yield in identifying the etiology
      • routine pericardial fluid measurements should include specific gravity, white blood cell count and differential, hematocrit, and protein content
      • Blood in pericardial fluid is nonspecific
      • Chylous effusions can occur after traumatic or surgical injury to the thoracic duct or obstruction by a neoplastic process.
      • Cholesterol rich (“ gold paint ”) effusions occur in severe hypothyroidism .
      • Pericardial fluid should be routinely stained and cultured for detection of bacteria, including tuberculosis, and fungi.
      • As much fluid as possible should be submitted for detection of malignant cells
      • adenosine deaminase (ADA), interferon-gamma, and polymerase chain reaction (PCR
        • we believe that a relatively rapid test for tuberculosis (ADA, PCR) should be routine because of the general difficulty of diagnosing tuberculous pericarditis
    • Pericardioscopy and Percutaneous Biopsy
      • Some experts advocate the routine use of pericardioscopic-guided biopsy in patients with pericardial effusion who do not have an etiologic diagnosis.
        • fluoroscopy-guided parietal pericardial biopsy
        • extended sampling (18 to 20 samples).
    • CONSTRICTIVE PERICARDITIS
    • Etiology
      • The pathophysiological consequence of pericardial scarring is markedly restricted filling of the heart
      • results in elevation and equilibration of filling pressures in all chambers and the systemic and pulmonary veins.
      • almost all ventricular filling occurs early in diastole
      • Systemic venous congestion results in hepatic congestion, peripheral edema, ascites, and sometimes anasarca and cardiac cirrhosis.
      • Failure of transmission of intrathoracic pressure changes during respiration to the cardiac chambers
      Septal bounce
    • Clinical Presentation
      • usual presentation consists of signs and symptoms of predominantly right heart failure .
        • include lower extremity edema, vague abdominal complaints, and some degree of passive hepatic congestion
        • As the disease becomes more severe, hepatic congestion worsens and can progress to ascites and/or anasarca, as well as jaundice caused by cardiac cirrhosis.
    • Physical Examination
      • markedly elevated jugular venous pressure with a prominent, rapidly collapsing y descent combined with a normally prominent x descent
      • W , M
      • AF
        • the x descent is lost, prominent y descent
        • The latter is difficult to distinguish from tricuspid regurgitation
      • Kussmaul sign, an inspiratory increase in systemic venous pressure, is usually present
      • A paradoxical pulse occurs in perhaps one third of patients with constrictive pericarditis
      • pericardial knock, an early diastolic sound best heard at the left sternal border and/or the cardiac apex.
        • corresponds to the early, abrupt cessation of ventricular filling
      • Widening of second heart sound splitting may also be present
      • Other signs of chronic hepatic congestion include jaundice, spider angiomata, and palmar erythema. Lower extremity edema is usually present, and anasarca
    • Electrocardiogram
      • Nonspecific T wave abnormalities are often observed, as well as reduced voltage . Left atrial abnormality may also be present.
    • Chest Radiograph
      • Pericardial calcification is seen in a minority of patients and should raise the suspicion of tuberculous pericarditis
    • Echocardiogram
      • pericardial thickening , abrupt displacement of the interventricular septum during early diastole
      • signs of systemic venous congestion
      • Doppler flow velocity measurements reveal exaggerated respiratory variation
        • help distinguish restrictive cardiomyopathy from constrictive pericarditis
    • Cardiac Catheterization and Angiography
      • assists in discriminating between constrictive pericarditis and restrictive cardiomyopathy
      • Right and left heart pressures should be recorded simultaneously
    • Computed Tomography and Magnetic Resonance Imaging
      • detecting even minute amounts of pericardial calcification & Thickness
      • normal pericardium measured by CT is less than 2 mm.
      • MRI sensitivity > CT
    • Differentiating Constrictive Pericarditis from Restrictive Cardiomyopathy
    • Management
      • Constrictive pericarditis is a progressive disease.
      • surgical pericardiectomy is the only definitive treatment & should not be delayed once the diagnosis is made.
      • may respond to a course of corticosteroids
      • diuretics and salt restriction
      • beta-adrenergic blockers and calcium antagonists that slow the heart rate should be avoided
        • sinus tachycardia is a compensatory mechanism,
    • Pericardiectomy
      • performed through either a median sternotomy or a left fifth interspace thoracotomy
      • radical excision of as much of the parietal pericardium as possible
      • The visceral pericardium is then inspect
      • Resection should be considered if it is involved in the disease process.
      • Pericardiectomy has a 5 to 15 percent perioperative mortality in patients with constrictive pericarditis
    • Prognosis
      • From 70 to 80 percent of patients remain free from adverse cardiovascular outcomes at 5 years,
      • and 40 to 50 percent at 10 years after pericardiectomy .
      • Long-term results are worst in patients with
        • radiation-induced disease, impaired renal function, relatively high pulmonary artery systolic pressure, reduced LV ejection fraction, low serum sodium, and advanced age
    • SPECIFIC CAUSES OF PERICARDIAL DISEASE
    • Viral Pericarditis
      • Etiology and Pathophysiology
        • most common form of pericardial infection
        • caused by either direct damage resulting from viral replication or immune responses .
        • Echo and Coxsackie viruses are the most common
        • Cytomegalovirus has a predilection for immunocompromised patients
        • most definitive way to diagnose viral pericarditis is detection of DNA by PCR or in situ hybridization in pericardial fluid
    • Viral Pericarditis
      • Clinical Features and Management
        • In patients with chronic, confirmed viral pericarditis, several immune-mediated treatments are under investigation
        • none have been shown to be effective to date .
    • Bacterial Pericarditis
      • Etiology and Pathophysiology
        • characterized by a purulent effusion
        • Direct extension from pneumonia or empyema
        • most common agents are staphylococci , pneumococci, and streptococci .
        • Hematogenous spread during bacteremia and contiguous spread after thoracic surgery
    • Bacterial Pericarditis
      • Etiology and Pathophysiology
        • Anaerobic organisms
        • can also result from rupture of perivalvular abscesses into the pericardial space
        • Rarely , pericardial invasion spreads along facial planes from the oral cavity
        • Neisseria can evoke a sterile effusion accompanied by systemic reactions such as arthritis, pleuritis, and ophthalmitis.
        • This does not require antibiotic therapy and responds to antiinflammatory drugs.
      • Clinical Features
        • usually high-grade fever with shaking chills and tachycardia
        • A pericardial friction rub is present in the majority.
        • can take a fulminant course with rapid development of tamponade
        • Laboratory findings include
          • leukocytosis with marked left shift.
          • Pericardial fluid shows polymorphonuclear leukocytosis, low glucose, high protein, and elevated lactate dehydrogenase levels .
        • chest radiograph shows widening of the cardiac silhouette if the effusion is large
      • With gas-producing organisms a lucent air fluid interface may be observed.
      • The ECG shows typical ST segment and T wave changes of acute pericarditis , , along with low voltage
      • Echocardiography almost always demonstrates a significant pericardial effusion with or without adhesions
      • Cardiac tamponade is common and can be confused with septic shock.
      • Management
        • proven bacterial pericarditis should be considered a medical emergency
        • prompt closed pericardiocentesis or surgical drainage performed.
        • Gram stained and cultured for aerobic and anaerobic bacteria
        • Fungal and tuberculosis staining and cultures should also be performed.
      • Purulent pericardial effusions are likely to recur. Thus surgical drainage with construction of a window is often necessary
      • Intrapericardial streptokinase has been administered to selected patients with purulent and/or loculated effusions and may obviate the need for a window
      • The prognosis of bacterial pericarditis is generally poor , with survival in the range of 30 percent even in modern series.
    • Pericardial Disease and Human Immunodeficiency Virus
      • Pericardial disease is the most common cardiac manifestation of HIV
        • the most common abnormality is an effusion
        • Most are small; asymptomatic
        • related to enhanced cytokine
        • Congestive heart failure, Kaposi sarcoma, tuberculosis, and other pulmonary infections are independently associated with moderate to large effusions,
      • In some cases the HIV virus itself appears to be the etiology.
      • Tuberculosis is the most common etiology of pericardial effusion in African HIV patients .
      • Constrictive pericarditis is rare . When present it is usually secondary to Mycobacterium tuberculosis
      • Clinical Features
        • Symptomatic patients with pericardial disease usually present with dyspnea or chest pain
        • The most common infectious agents identified in symptomatic effusions are M. tuberculosis and Mycobacterium avium-intracellulare .
          • Cryptococcus neoformans, cytomegalovirus, and Mycobacterium kansasii
        • Lymphomas and Kaposi sarcoma are the most common neoplasms associated with effusion
      • Management
        • Asymptomatic patients with small to moderate pericardial effusions do not require treatment .
        • Most are idiopathic and usually remain asymptomatic or resolve spontaneously .
        • Symptomatic, large effusions should be drained
    • Tuberculous Pericarditis
      • Etiology and Pathophysiology
        • patients with pulmonary tuberculosis, 1 to 8 percent develop pericardial involvement.
        • 7 percent of patients who developed cardiac tamponade .
      • Clinical Features
        • subacute to chronic, with fever, malaise, and dyspnea in association with a pericardial effusion
        • Cough, night sweats, orthopnea, weight loss, and ankle edema are also common
        • The most frequent findings are radiographic cardiomegaly, pericardial rub, fever, and tachycardia
        • Findings related to large effusions, paradoxical pulse , hepatomegaly, increased venous pressure , pleural effusion, and distant heart sounds are common
      • A definitive diagnosis is made by isolating the organism from pericardial fluid or biopsy.
      • the yield for isolation from pericardial fluid is low .
      • probability of making a diagnosis is increased if both pericardial fluid and biopsy specimens are examined
      • a definite role for pericardial biopsy . Pericardial tissue reveals either granulomas or organisms in 80 to 90 percent of cases
      • Granulomas can be found in rheumatoid and sarcoid pericardial disease.
      • Measurement of adenosine deaminase (ADA) was the first modern test to markedly improve the accuracy and speed of diagnosis of tuberculous pericarditis
      • ADA greater than 40 units/liter in pericardial fluid has a sensitivity and specificity greater than 90 percent.
      • Increased interferon-gamma in pericardial fluid is an additional marker
      • Management
        • The goals of therapy are to treat symptoms , as well as tamponade
        • Multidrug antimycobacterial treatment is mandatory
        • Corticosteroids did not influence the risk of death or progression to constriction but did speed the resolution of symptoms and decrease reaccumulation of fluid.
        • The outcomes suggested that patients who undergo open drainage are less likely to require repeat pericardiocentesis , and there was a trend in the open drainage group toward reduced development of constriction.
      • If corticosteroids are administered, high doses (1 to 2 mg/kg/day with tapering over 6 to 8 weeks)
    • Uremic Pericarditis and Dialysis-Associated Pericardial Disease
      • Etiology and Pathophysiology
        • Its pathophysiology has never been fully elucidated ,
        • but it is correlated with blood levels of blood urea nitrogen (BUN) and creatinine.
        • The acute or subacute phase is characterized by shaggy, hemorrhagic, fibrinous exudates on both parietal and visceral surfaces with minimal inflammatory cellular reaction.
        • Dialysis-associated pericardial disease is now much more common than classic uremic pericarditis.
        • It is characterized by de novo appearance of pericardial disease in patients undergoing chronic dialysis ,
      • Clinical Features
        • acute pericarditis with chest pain, fever, leukocytosis, and pericardial friction rub .
        • Small, asymptomatic effusions are common
        • Alternatively, patients can present with a pericardial effusion causing hypotension during or after ultrafiltration ( low-pressure tamponade ).
      • Management
        • intensive hemodialysis and drainage in patients with effusions .
        • Pericardial effusions without hemodynamic compromise usually resolve after several weeks of intensive hemodialysis .
        • Treatment of pericardial disease appearing de novo in patients on chronic dialysis is empirical
        • Use of NSAIDs for pericardial pain is reasonable , but corticosteroids are probably ineffective .
        • A pericardial window may be required and is usually the most effective approach in patients with recurring effusions .
    • Early Post–Myocardial Infarction Pericarditis and Dressler Syndrome
      • Etiology and Pathophysiology
        • occurs during the first 1 to 3 days
        • caused by transmural necrosis with inflammation
        • 40 percent of patients with large, Q-wave MIs have pericardial inflammation
        • Thrombolysis and mechanical revascularization appear to have reduced the incidence of this form of pericarditis by at least 50 percent.
        • Late pericarditis
          • described by Dressler and had an estimated incidence of 3 to 4 percent of MI patients
          • Dressler syndrome is believed to have an autoimmune etiology caused by sensitization to myocardial cells
      • Clinical Features
        • early post-MI pericarditis is asymptomatic and identified by auscultation of a rub
        • usually within 1 to 3 days after presentation.
        • Many are monophasic (usually systolic) and can be confused with murmurs of mitral regurgitation or ventricular septal defect .
        • Acute post-MI pericarditis virtually never causes tamponade (except LV free wall rupture)
        • An atypical T-wave evolution consisting of persistent upright T waves or early normalization of inverted T waves has also been described and appears to be highly sensitive for early post-MI pericarditis .
      • Dressler syndrome occurs as early as 1 week to a few months after acute MI .
      • Symptoms include fever and pleuritic chest pain . The physical examination may reveal pleural and/or pericardial friction rubs.
      • The chest radiograph may show a pleural effusion and/or enlargement of the cardiac silhouette , and the
      • ECG often demonstrates ST elevation and T wave changes typical of acute pericarditis .
      • Management
        • Treatment is entirely symptomatic. Augmentation of the usual low-dose aspirin administered to MI patients ( 650 mg three to four times per day for 2 to 5 days )
        • Corticosteroids and perhaps some non-aspirin NSAIDs interfere with conversion of an MI into a scar
        • Dressler syndrome is a self-limited disorder , admission to hospital for observation and monitoring should be considered if there is a substantial pericardial effusion
        • Aspirin or other NSAIDs are effective for symptomatic relief.
        • Colchicine is also likely effective.
        • A short course of prednisone , 40 to 60 mg per day with a 7- to 10-day taper, can be used in patients