perikard izliv uvod

7/27/2019 perikard izliv uvod

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Assessment of pericardial effusionOverview

Summary

Aetiology

Emergencies

Urgent considerations

DiagnosisStep-by-step

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SummaryPericardial effusion is a frequent finding that occurs due to primary pericardial disease or in relation to a myriad

of systemic disease processes. The significance of effusions lies in their relationship to an underlying disease

state and in their potential to affect a patient's haemodynamics.

Epidemiology

Data from the Framingham cohort suggest that pericardial effusion may be present in up to 6.5% of the adult

population. In the Framingham cohort, the incidence increased with age, with only 1.2% of patients


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although once the pericardial pressure-volume relationship reaches its non-compliant stage, expansion is limited

and small increases in volume produce a dramatic increase in pericardial pressure, severely impairing

ventricular filling.

Diagram

showing the anatomy of the pericardium; the stippled area represents the subfascial connective tissue planeFrom: Marchand

P. Thorax. 1951;6:359-368

Types of pericardial effusion

The mechanism of abnormal fluid collection depends on the underlying aetiology, but is typically due to injury of

the pericardium and may be classified as acute or chronic, and small or large. Chronic effusion has been defined

as an effusion that persists for >3 months; and acute, as


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The fluid may be serous, purulent, haemorrhagic, chylous, or serosanguineous, but the nature of the effusion

adds little to the characterisation of the aetiology. Effusions are categorised as transudates or exudates.

Exudative effusions may be idiopathic, iatrogenic, or due to infection, malignancy, trauma, cardiorespiratory, and

autoimmune processes. Exudative effusions result from acute or chronic pericardial inflammation, with high

levels of protein.

Cardiac tamponade occurs when pericardial pressure increases and limits cardiac filling. The severity of

tamponade is determined by its effect on cardiac output and haemodynamics, but even when hypotension is not

present, tamponade is a serious condition that may rapidly progress and requires urgent evaluation. Effusions

that are small and thought to be transudative are unlikely to be clinically significant.

Pericardial constriction

Chronic pericardial effusion may share similar clinical symptoms and signs with pericardial constriction. The 2

conditions may co-exist, or constriction may develop as a later consequence of the underlying aetiology of the

pericardial effusion, particularly following tuberculous pericarditis or after cardiac surgery. Differentiating these 2

conditions may be difficult and requires advanced imaging techniques.

AetiologyThere are many causes of pericardial effusion, with varyingprevalence.[4] [5] The most common causes are typically idiopathic andviral.[2] Other causes include bacterial, collagen vascular disorders,vasculitis, Dressler's syndrome, certain medicines, malignancy, CHF, MI,trauma, surgery, uraemia, hypothyroidism, and amyloidosis.

The likelihood that an effusion will lead to tamponade depends on the size,rapidity of formation, and nature of the effusion. For instance, when bloodrapidly fills the pericardium as a result of aortic dissection, much less fluid isneeded to produce tamponade than in a gradually increasing effusion, inwhich the pericardium has time to grow.

Idiopathic effusions are the most common single cause of effusion, and thusthey seem to be a frequent cause of tamponade. However, the likelihood thatan idiopathic or viral effusion will produce tamponade is low. In contrast,

malignant effusions and tuberculous effusions are likely to producetamponade. In a study of moderate-to-large effusions, 60% of malignant and7% of tuberculous effusion eventually led to tamponade.[4]

Aside from effusions producing tamponade, effusions that are the result ofbacterial infection deserve special note because of the high mortalityattributed to this disease. Purulent pericarditis was uniformly fatal in the pre-antibiotic era, and even modern reports cite mortality rates of 40%.[6]
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IdiopathicIdiopathic effusions are those in which a definitive diagnosis cannot beobtained. It is generally assumed that most cases are due to viral infection,either acute or chronic. As in viral pericarditis, patients generally present withfeatures typical of acute pericarditis and experience a self-limiting, benigncourse. However, idiopathic effusions may persist, recur, and, when large,progress to tamponade.[3]Evaluation of fluid tends to demonstrate bloody fluid, a low WBC count with amonocyte predominance, normal glucose, and low specific gravity.[7]

InfectiousViral

Viral pericarditis rarely produces effusions large enough to cause tamponade.

Viral infection is the most common cause of acute pericarditis and is specifically identified in up to 50%

of cases. Coxsackie, echovirus, adenovirus, cytomegalovirus, Epstein-Barr, mumps, rubella, parvovirus B19,

and HIV are among the many viral causes of acute pericarditis.

Associated clinical history, such as time of year, exposures, and acute onset, help distinguish viral

aetiologies from other causes. Evaluation of fluid reveals characteristics similar to idiopathic effusion.[7]

Bacterial

Uniformly fatal if untreated. The mortality is 40% in appropriately treated patients.[8] Bacterial pericarditis is a fulminant condition with an acute onset, but up to 50% of patients do not report

chest pain, and thus the condition needs to be considered in all ill patients who present with pericardial effusion

and fever.[6]

Patients at higher risk for bacterial pericarditis include those on dialysis, immunosuppressed patients,

alcoholic people, and patients who have recently had cardiac surgery.

The most likely causes include Staphylococcus aureus, Streptococcus pneumoniae,

andNeisseria species, although more modern reports note an increase in anaerobic infections particularly in the

setting of head and neck infections.

Fluid analysis often is purulent, and has a very elevated WBC with a neutrophil predominance.[7]

Tuberculous

Rare (4%) in developed countries, but is responsible for up to 70% of pericarditis in certain countries.

Tuberculous pericarditis remains the most common cause of pericarditis in Africa.
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The diagnosis should be suspected in patients with acute pericarditis that does not have the expected

rapid resolution of symptoms with supportive care.

Mortality is 85% in untreated cases and as high as 40% in treated cases. Between 30% and 50% of

patients develop constrictive pericarditis.[8] [9]

Fungal

Reports of histoplasmosis and Candida-related pericarditis with subsequent effusions have been

reported, but they are rare. In nearly all reported cases, patients had a known predisposing condition for fungal

infection.[10]

Parasitic

Trypanosoma cruziinfection (Chagas' disease) may rarely be associated with acute Chagas myocarditis

or chronic Chagas cardiomyopathy.

Although acute Chagas myocarditis is rare, pericardial effusion is seen commonly (42%) when it

occurs.[11]

Immune-mediatedCollagen vascular disorders

SLE: pericardial disease is common in lupus and is part of the diagnostic criteria. While autopsy studies

show that the pericardium is affected in 62% of patients, clinically evident pericarditis occurs in 25% of patients

over the course of their disease. Typically, pericarditis occurs in the setting of generalised serositis and, in

patients with pericardial effusion, a pleural effusion is present in 76% of cases. In patients with clinically

recognised pericarditis, tamponade develops in 13% of cases.[12]

Wegener's granulomatosis: pericarditis is the most common cardiac manifestation in this systemic

inflammatory vasculitic disease. Mild subclinical pericardial effusions occur in 55% of patients, and tamponade

may occur, although rarely. It is often difficult to determine whether effusion is primarily related to Wegener's or

is a consequence of pathology in other organs, such as the kidneys.[13]

Dressler's phenomenon

This syndrome was first described in the 1950s as a syndrome of pericardial chest pain and fever in the

weeks to months following an acute myocardial infarct. It is now known that this condition and others similar to it,

including post-pericardiotomy and post-commissurotomy syndrome, are caused by antibodies to heart antigens.

The course is characteristically benign and the effusion has exudative characteristics. Once a common disease,

in the era of reperfusion therapy the incidence of Dressler's phenomenon has dramatically decreased.[14]

Drug-induced

Hydralazine, procainamide, and isoniazid are the most common drugs identified as a cause of drug-

induced lupus erythematosus.
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Pericarditis occurs in a similar proportion to idiopathic lupus, but reports of tamponade are rare.

Typically, the disease and its manifestations resolve following cessation of the offending agent.[15]

Amyloid

Cardiac involvement is common in systemic amyloidosis and pericardial effusion occurs in as many as

58% of patients with cardiac amyloid. In all but a few cases, the size of the effusion is small or moderate andtamponade is rare.[16]

EndocrineHypothyroidism

Myxoedematous effusions accumulate very slowly as a result of capillary leak. As a result, effusions

rarely lead to tamponade and have high protein content.

Typically, effusions resolve within weeks to months following institution of hormone replacement

therapy.[17]

NeoplasticMalignant effusions

Are among the most likely to cause tamponade, in which lung cancer, breast cancer, lymphomas, and

leukaemias are the most prevalent underlying malignancies. Malignant effusion due to metastatic cancer is

rarely the presenting finding, although it may be the first sign of metastases; thus, a history of known malignancy

increases clinical suspicion.

Primary malignancies (rare)

Angiosarcoma is the most common form of malignant cardiac tumour.[18] It typically originates in the

right atrium, but may also exist separately or extend into the pericardium.

Others include mesothelioma and malignant teratoma.[19] [18]

Accumulation of pericardial fluid may be gradual or rapid when erosion intothe pericardial blood vessels occurs. Effusions are exudative in quality, andcytological analysis of pericardial fluid will be positive in 65% to 85% of

patients.[20]

CardiacAortic dissection
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Pericardial haemorrhage occurs in the setting of proximal type A dissection and can rapidly produce

tamponade with small volumes of pericardial blood. The mortality is 60% and accounts for most deaths of

patients with type A dissection.[21]

CHF

Pericardial fluid has been noted to accumulate in patients with CHF as part of generalised volumeoverload. The volume of fluid is generally small and tamponade is not a recognised complication. Pleural

effusions are present in 92% of heart failure patients with pericardial effusion.[22] The fluid is characteristically

transudative, but they may be misclassified as exudates in the setting of diuresis.[23]

Post cardiac surgery

Post-cardiac surgery effusion occurs in up to 85% of patients.[24] In a study of 803 post-cardiac surgery

patients who had echocardiography performed on post-operative day 8, effusion was common, but only 1.6% of

patients had large effusions. Valve surgery was significantly associated with the presence of large effusion and

tamponade. Most patients were receiving anticoagulation that was thought to contribute to the effusion.[25]

The clinical characteristics of post-operative effusions differ from medical effusion. In a retrospective

review of 208 post-operative patients with symptomatic effusion requiring intervention, malaise (90%) was the

most common symptom, followed by dyspnoea (65%) and chest pain (33%). Hypotension and pulsus paradoxus

were present in only 27% and 17% of patients, although hypotension was more common in early effusions,

which were predominantly due to bleeding complications, also associated with anticoagulation.[26]While typical

circumferential effusions occur post-operatively, up to 58% are loculated. Fever is a common finding (40%) and

is usually part of a post-cardiotomy syndrome, but post-operative infection must always be considered.

Pericardial constriction post-surgery is a rare but important occurrence, which usually presents many

months to years after cardiac surgery, often in patients where signs of post-cardiotomy syndrome were noted

peri-operatively. Echocardiography, CT imaging, and cardiac catheterisation may all be necessary to confirm the

diagnosis.

Post cardiac intervention

The incidence of percutaneous cardiac intervention-related effusions has increased significantly in

recent decades, consistent with the increase in the frequency of coronary intervention and introduction of new

interventional procedures such as ablation and valvuloplasty. In a review of 1127 patients requiring

pericardiocentesis over 21 years, intervention-related effusions accounted for 14% of all patients requiring

pericardiocentesis in the last 7 years of the study, making it the third most common aetiology.[27]

Non-cardiac physicians are unlikely to encounter these patients, as symptoms develop

rapidly.[28] While the incidence of cardiac perforation is exceedingly low overall (0.08%), there is variability with

regard to particular interventions. The incidence of cardiac perforation following diagnostic catheterisation is

0.006%, whereas in valvuloplasty it is 1.9%.

Traumatic
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Direct penetrating injuries of the heart are usually the result of stab wounds orgunshots and have a high pre-hospital mortality. For patients who reach ahospital, emergency department echocardiography is 96% accurate in thediagnosis of traumatic effusion.[29]

Radiation-relatedIn the course of radiotherapy for thoracic malignancies such as Hodgkin'slymphoma and breast cancer, the heart and pericardium may be exposed tohigh doses of radiation. Pericarditis related to radiation may be acute ordelayed.

The acute variety presents just following therapy, and typically manifests similar to acute pericarditis of

other forms.

Delayed pericarditis may present as acute pericarditis or as an asymptomatic effusion. Reports on theincidence of pericarditis vary depending on the total dose of radiation given, but as many as 20% of patients

receiving radiation to the entire pericardium and as few as 2% of patients with subcarinal blocks develop

disease.

Those receiving >40 Gy of radiation without subcarinal blocks are at thegreatest risk of significant pericardial pathology.

Tamponade is not infrequent and some evidence of tamponade has beenreported to occur in up to one half of all cases. Pericardial constriction may

also be seen as a longer-term consequence of mediastinal irradiation.

RenalUraemia

Pericardial effusion in renal disease has been described in uraemia related to acute renal failure and as

a consequence of inadequate dialysis in patients with chronic renal failure. Features of acute pericarditis are

common in uraemic pericarditis and can occur in dialysis-related effusions. A pericardial friction rub in a patient

with acute renal failure warrants an echocardiogram to evaluate for pericardial effusion. These effusions are

characteristically transudative with low protein content.[30]

Urgent considerationsSee Differential Diagnosis for more details

Cardiac tamponade

Tamponade is present when pericardial effusion increases the intrapericardial pressure, compressing the

cardiac chambers so that cardiac filling is impaired, leading to hypotension and cardiovascular collapse.
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Tamponade exists as a haemodynamic spectrum ranging from trivial compression with minimal effects on

cardiac output to fatal cardiovascular collapse.

Normally the pericardial pressure is lower than the heart chamber pressures so that the transmyocardial

pressure gradient (pressure inside the heart minus pressure in the pericardium) favours cardiac filling. As

pericardial pressure increases with a growing effusion, the pericardial pressure equalises initially with the rightatrium, producing diastolic collapse of the right atrium. The body attempts to compensate by increasing central

venous pressures in order to prevent further collapse, and by increasing sympathetic nervous system output to

maintain stroke volume and cardiac output. The effect is tachycardia and jugular venous distension. As effusion

progresses, pericardial pressures increase to >10 mmHg and surpass right ventricular diastolic pressure, which

is demonstrated on echocardiography as collapse of the right ventricular free wall. When pericardial pressures

approach 25 mmHg, catheter-based pressure measurements reveal equalisation of diastolic pressure in each

cardiac chamber and a transmyocardial pressure that is essentially zero. All 4 chambers in the heart are

collapsed and tamponade is severe, with signs of reduced cardiac output and hypotension. At this stage, the

pericardial volume is fixed and the heart can only be filled if blood is leaving the heart. Thus, atrial filling occurs

in systole when the ventricles are evacuating. Furthermore, increases in the volume of one chamber must

produce a corresponding decrease in the other chamber's volume by a phenomenon known as ventricular

interdependence. During inspiration, when the stroke volume of the right ventricle is increased, the left ventricle

stroke volume is decreased, producing a fall in blood pressure. The opposite occurs during expiration. This

phenomenon of increased ventricular interdependence produces the examination finding of pulsus

paradoxus.[31] [32]

The presence or absence of pulsus paradoxus is very important in assessing pericardial effusion. A value >12

mmHg has a sensitivity of 98% and specificity of 83% for the detection of tamponade.[33]

Pulsus paradoxus is an increase (>10 mmHg) of the normal inspiratory decrease in systemic blood pressure. To

measure pulsus paradoxus, the blood pressure cuff is inflated above systolic blood pressure. The cuff is deflated

slowly, listening for the first Korotkoff sound, which will be intermittent and heard during quiet expiration. The

difference (in mmHg) between this first Korotkoff sound and the pressure at which a Korotkoff sound is heard

with each beat is the pulsus paradoxus. Normal value is


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Pulsus paradoxus >10 mmHg

Increased jugular venous pressure.

Hypotension and increased jugular venous pressure are relative.

DiagnosisWhen tamponade is suspected, the presence or absence of pulsus paradoxus is very important. A value >12

mmHg has a sensitivity of 98% and specificity of 83% for the detection of tamponade (although 10 mmHg is

often given as evidence of pulsus paradoxus).[33]However, pulsus paradoxus is often absent in the early stages

of tamponade and may not be present in the presence of other common conditions including hypovolaemia,

post-operative effusion, haemorrhage, pulmonary hypertension, pulmonary embolus, right ventricular infarct, and

asthma. Pulsus paradoxus may also be difficult to measure in an acutely unwell patient, and simply noting

disappearance of the pulse on palpation during inspiration suggests significant tamponade.

Thus, a transthoracic echocardiogram is obtained in all patients with suspected effusion based on history or

examination. A study of 110 patients with moderate or large pericardial effusion attempted to determine the utility

of common echocardiography findings in patients with clinical findings of tamponade.[34] Right atrial collapse

was the most sensitive finding for tamponade (90%), whereas abnormal systolic venous flow was the most

specific finding in tamponade (92%). The combination of collapse of the right atrium and ventricle plus abnormal

systolic venous flow was 98% specific for tamponade. Marked variation in atrioventricular inflow velocities is also

an important echocardiographic finding in patients with pericardial effusion that may either confirm clinical

tamponade or suggest an intermediate stage before overt tamponade.[35] Of note, 10% of patients with clinical

tamponade did not have any echocardiographic findings of collapse. Furthermore, collapse of any cardiac

structure was present in 34% of patients without clinical tamponade, representing echocardiographic

tamponade.[34] Thus, the physical examination is especially important in the evaluation of tamponade.

Management

The cornerstone of treatment of tamponade is emergency drainage of the pericardial fluid. Pericardiocentesis is

traditionally performed in the catheterisation laboratory, but bedside echocardiography-assisted

pericardiocentesis is widely employed in some centres.[27]Surgical drainage with creation of a pericardial

window is indicated for recurrent effusions or in cases of traumatic haemopericardium.[8]

Red flags

Metastatic malignancy

Bacterial pericarditis

Tuberculous pericarditis

Fungal pericarditis

Angiosarcoma

Mesothelioma

Malignant teratoma
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Cough

Fever: high fever and toxic appearance suggest bacterial aetiology and should prompt urgent pericardial

drainage

Dyspnoea

Lethargy

Medical history (e.g., collagen vascular disease, amyloidosis, cancer)

Medicine history (drug immune-mediated effusion)

Examination findings suggestive of pericardial effusion:

A pericardial friction rub, which is a high-pitched scratching sound best heard over the left sternal border

with the patient leaning forwards at end-expiration. Rubs may be 1, 2, or 3 parts, corresponding to the periods of

greatest heart movement in the cardiac cycle. The pericardial friction rub may also be transient, and thus it is

useful to examine patients suspected of pericarditis on multiple occasions.

Distant heart sounds with a quiet precordium is a common finding in pericardial effusion, although in

patients with pulmonary hypertension or dilated cardiomyopathy, an anterior impulse is often present.

The presence or absence of pulsus paradoxus is very important. A value >12 mmHg has a sensitivity of

98% and specificity of 83% for the detection of tamponade.[33]

Pericardial constriction may produce similar examination findings totamponade with pulsus paradoxus and elevated jugular venous pressure. Apericardial knock may be evident during palpation and/or auscultation, andconstriction is also often associated with gross liver enlargement and ascites.

ImagingPatients with suspected pericardial effusion and symptoms of acutepericarditis should receive an ECG and CXR. In most circumstances, patientsshould have an echocardiogram for detection of pericardial effusion, but

when examination findings suggest tamponade, a transthoracicechocardiogram is essential.

When inflammation involves the epicardium, the ECG may show diffuse ST-segment elevation and PR depression signalling generalised epicardialinjury. View image If the pericardial effusion is large enough, the heart mayswing in the pericardial fluid, producing beat-to-beat variation of theventricular, and occasionally the atrial, axis on the ECG known as electrical
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alternans. CXR may show a water bottle-shaped cardiac silhouette with adistinct, fat pericardial fat stripe suggesting a large pericardial effusion. ViewimageWhen effusion is suspected on examination, the preferred test to confirm thediagnosis is transthoracic echocardiogram. It is a non-invasive and effective

diagnostic modality that detects effusion when >50 mL of fluid is present.Circumferential effusions are easily visualised as an echo-dense space. ViewimageView imageView image Observed diastolic collapse of the rightventricle or right atrium, predominantly systolic inferior vena caval flow, andmarked variation in mitral and tricuspid inflow velocities with respiration are allsigns of tamponade.

Pericardial constriction should be suspected when clinical features of aneffusion are present but imaging demonstrates no or minimal effusion.Pericardial thickening may be noted on echocardiography or CT imaging.

Marked respiratory variation in mitral and tricuspid inflow velocities is also afeature of pericardial constriction.

Laboratory evaluationThe aetiology of pericardial effusion is found in up to 60% of patients on initialevaluation.[4]Thus, all patients require a thorough history and physicalexamination. The utility of routine laboratory evaluation, including FBCs,chemistry, rheumatoid factors, antinuclear antibodies, and serum C-reactiveprotein, is not well established, as they lead to a specific diagnosis in only

10% to 15% of cases.[37] It is more useful to order laboratory tests asdetermined by the clinical picture.

FBC: a very elevated leukocyte count may suggest bacterial pericarditis.

Chemistry: findings such as an elevated creatinine are sensitive for renal failure and may suggest a

uraemic aetiology.

Thyroid-stimulating hormone: when elevated, it suggests that hypothyroidism may be contributing to

pericardial effusion.

Serum C-reactive protein: is elevated in most cases of acute pericarditis and so may not be helpful in

determining the underlying aetiology.

Erythrocyte sedimentation rate: is often elevated in acute pericarditis and so may also be unhelpful in

determining the underlying aetiology.

Rheumatoid factor: when rheumatoid arthritis is suspected, this is a useful test.
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Antinuclear antibody: when SLE is suspected, this is a useful test.

Troponin: troponin levels are often elevated in pericarditis and do not portend a worse prognosis.

Blood cultures: when bacterial pericarditis is suspected, this is an essential test.

Viral cultures: although positive cultures may aid in the diagnosis of viral pericarditis, there is little clinical

utility in ordering them, as most cases of viral pericarditis are benign and self-limiting, and a positive test would

not change management.

HIV: when evidence of immunosuppression is present on examination, or the patient has risk factors for

infection, this test may alter the differential diagnosis.

PericardiocentesisWhen initial tests do not reach a diagnosis, invasive pericardiocentesis may

be necessary for further diagnostic evaluation. The diagnostic yield of fluid ortissue analysis obtained by either percutaneous or surgical methods is verylow when performed for strictly diagnostic purposes in patients without anobvious cause on initial evaluation.[38] The balance of current opinionrecommends drainage in the following circumstances:

Tamponade

Large effusion (>2.0 cm) with evidence of tamponade on echocardiogram

Large effusion (>2.0 cm) without evidence of tamponade that persists for >3 months

Suspected tuberculous or bacterial pericarditis.[2] [3] [34] [39]

In the analysis of pericardial fluid, the first step should be to separateeffusions into transudates and exudates by determining the following:

LDH >200 U/decilitre (sensitivity 98%)

Total protein >30 g/L (3.0 g/dL) (sensitivity 97%)

Fluid to serum LDH >0.6 (sensitivity 94%, diagnostic accuracy 87%)

Fluid to serum protein >0.5 (sensitivity 96%).

If any one of these criteria is met, the patient has an exudate. The mostaccurate test to distinguish transudative from exudative effusion is a fluid toserum LDH >0.6 with an accuracy of 87%.[7] [23]
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The ability to separate pericardial effusions into exudates and transudateshas been disputed. In a study of 120 patients undergoing pericardiocentesisfor effusion of various aetiologies, there were no differences in the absoluteor relative LDH and protein contents among any of the various causes ofeffusion.[40] In the study, 118 of 120 patients would have been classified as

having exudates according to Light's criteria. Thus, while the biochemicalcharacteristics of pericardial effusion may suggest a particular entity, theyremain only one aspect in the overall diagnosis.Other tests are used to provide a definitive diagnosis of an underlyinginfectious or neoplastic cause:[22]

Viral cultures of pericardial fluid: culture and virus-specific staining techniques may identify a specific

pathogen. These methods can be used to confirm the presence of viral pericarditis and have a yield of

approximately 14%.[41]

Viral PCR is used to identify specific viral elements, and has a diagnostic yield of 40%.[41]

Gram stain and culture: culture is more sensitive than Gram stain for bacterial infections, but when either

reveals a specific pathogen it is very helpful. In fungal infections, a positive fungal pericardial fluid culture

confirms the diagnosis and provides guidance when selecting antifungal medication.

Pericardial adenosine deaminase activity (ADA) >667 nkat/L (40 U/L) suggests tuberculous pericarditis.

The sensitivity is 88% and specificity 83%. As cultures are less sensitive, this indirect test has become the

standard test in the diagnosis of pericardial tuberculosis.

Pericardial interferon-gamma (IFN-gamma) >200 picograms/L suggests tuberculous pericarditis. Early

reports suggest that this test is 100% sensitive and specific. However, its utility has not yet been demonstrated in

a large trial and it is not widely employed.

Cytology: required to confirm the diagnosis and subtype of tumour. Metastatic malignancy is the most

common cause. Cytology is positive in up to 85% of cases of pericardial metastases.[20] Cytology is also

required to identify the rare primary tumours (angiosarcoma, mesothelioma, and malignant teratoma). Patients

with SLE have lupus erythematous cells, polymorphonuclear white blood cells that have ingested another cell's

nuclear material, which may be seen in the pericardial fluid.

Pericardial biopsyWhen fluid evaluation is non-diagnostic and obtaining a diagnosis isnecessary, pericardial biopsy increases the likelihood of obtaining a diagnosisunder select circumstances. Pericardial biopsy is most useful whenneoplastic or tuberculous effusions are suspected.[5][38]Although thediagnostic yield is historically low and complicated by a high degree of false-negative results, recent advances in pericardioscopy, which allows directvisualisation of the pericardium, has improved the yield (40% diagnostic yield)
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and improved on the rate of false-negative samples (6.7% false-negatives).[42] Biopsy is generally indicated in the course of surgicaldrainage, when large effusions recur without a previous diagnosis, and whentuberculous or malignant aetiologies are suspected.[8]

Differential diagnosisSort by: common/uncommonorcategoryCommonhide allIdiopathic

History Exam 1st test

chest pain, low-grade fever, cough,

dyspnoea

distant heart sounds, cardiac dullness CXR: pericardial effusion

ECG: variable

Viral pericarditis

see our comprehensive coverage of Pericarditis

History Exam 1st test O

chest pain, low-grade fever,

cough, and other non-

specific symptoms - for

example, sore throat and

malaise

pericardial rub, a low-grade temperature


17/20

with low ejection fraction; diastolic heart fa

ventricular ejection fraction normal but LV

abnormal diastolic filling patternsMore

Post-cardiac surgery


post-cardiac surgery, malaise, dyspnoea; any change in

post-operative clinical status should prompt consideration

of an echocardiogram

hypotension mainly in early post-

operative tamponade, pulsus

paradoxus, fever

transthoracic

echocardiogr

effusionMore

Post cardiac intervention


rapid progress to overt tamponade or haemodynamic

collapse in the interventional laboratory; may also present

as a delayed complication

hypotension rapidly progressing to

cardiovascular collapse or overt

tamponade is the rule

transthoraci

echocardiog

effusionMore

Uraemia


hx of kidney disease, non-compliance with dialysis, and

pleuritic thoracic pain consistent with acute pericarditis;

associated symptoms of uraemia such as nausea, vomiting,

mental status changes, and uraemic frost may be present

a pericardial friction rub

indicates pericardial

inflammation

CXR: pleural effusion; m

signs of pulmonary oede

cardiomegalyMore

ECG: peaked T waves, i

PR interval, widened QR

chemistry-renal: elevate

creatinine levelsMore

Uncommonhide allBacterial pericarditis



hx of concomitant infection, for example, pleural

empyema/adjacent pneumonia/bacteraemia; hx of direct

cardiac trauma, immunosuppression, chronic disease, and

alcoholism; high-grade fever; absence of chest pain

toxic appearance with

high fever,

tachypnoea, and

tachycardia

blood

cultures: positiveMore

CXR: pleural effusionMore

ECG: diffuse ST-segment

elevation and PR

depressionMore

Tuberculous pericarditis


History Exam 1st test Other

hx of tuberculosis, pericarditis that does not

resolve as expected; subacute onset in

conjunction with constitutional complaints

distant heart sounds, cardiac

dullness, elevated neck veins,

hepatomegaly, pericardial

CXR: upper lobe

infiltrationMore
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including fever, night sweats, weight loss, and

fatigue; signs of heart failure predominate in

black patients

knock ECG: normalMore

Fungal pericarditis



hx of chronic disease or

suppressed immune system,

fever

may be normal or reveal pericardial friction rub, distant

heart sounds; there are no specific signs suggestive of a

fungal aetiology

blood culture: positiveMore


ECG: diffuse ST-segment ele

and PR depressionMore

Chagas disease

see our comprehensive coverage of Chagas disease


hx exposure to Triatoma species, blood

transfusion, organ transplantation,

immunosuppression, health care or laboratory

occupations, travel to or residence in endemic

areas, ingestion of contaminated food or drink;

symptoms of myocarditis: palpitations,

syncope or pre-syncope

prolonged fever (7 to 30 days)

with nocturnal elevation,

hepatosplenomegaly,

lymphadenopathy, tachycardia

FBC: leukopenia or leukocytosis

with a left shift and

lymphocytosis; hypochromic

anaemia; low platelets

ECG: T wave alteration,

prolonged PR interval, sinus

tachycardia, low QRS voltage

CXR: enlargement of cardiac

area, pleural effusion

microscopy of fresh blood or

thick blood smear: visualisation

of trypomastigotes

Angiosarcoma


chest pain, symptoms of

heart failure

cardiac murmur, signs of

heart failure

transthoracic echocardiogram:intracardiac or

pericardial tumourMore

Mesothelioma

see our comprehensive coverage of Mesothelioma

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19/20

male predominance, third to fifth

decades, hx of asbestos exposure,

symptoms of heart failure

possible vena caval obstruction with

swelling and plethora of the upper

extremities, neck, and head

transthoracic

echocardiogram:pericardial stu

massMore

Malignant teratoma


typically occurs in children with a

mean age of presentation of 16 weeks,

may present as heart failure

signs of heart failure predominate

due to compression of cardiac

structures

transthoracic

echocardiogram:intracardiac or

pericardial tumourMore

SLE

see our comprehensive coverage of Systemic lupus erythematosus

History Exam 1st test Other tests

fatigue, arthralgia,

malar rash, oral ulcers,

and synovitis

malar rash, oral ulcers, arthritis,

photosensitivity rash, discoid rash and

seizures may be present



elevation and PRdepressionMore

pe

an

ant pe

ce

Wegener's granulomatosis

see our comprehensive coverage of Wegener's granulomatosis

History Exam 1st test Other te

nose bleeds, recurrent sinusitis, haemoptysis,

and dyspnoea; constitutional complaints such

as fever, fatigue, and weakness

mucosal inflammation CXR: pleural effusion, pulmonary

infiltratesMore


elevation and PR

depressionMore

Dressler's phenomenon

History Exam 1st test Oth

hx of transmural infarct, hx of

cardiac pericardiotomy

typical pericardial chest pain

with low-grade fever


ECG: diffuse ST-segment elevation and

PR depressionMore

Drug-induced

History Exam 1st test Ot

hx of hydralazine, procainamide,

isoniazid 1 month duration; fatigue,

arthralgia

may be normal or reveal

pericardial friction rub, distant

heart sounds


ECG: diffuse ST-segment elevation

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20/20

Amyloidosis

see our comprehensive coverage of Amyloidosis


Hx of known amyloid, multiple myeloma,

monoclonal gammopathy, or chronic

illness such as rheumatoid arthritis; easy

bruising, fatigue, and weight loss

hepatomegaly ECG: low-voltage ECG with a pseudo-infarct

patternMore

transthoracic echocardiogram:left

ventricular hypertrophy, granular appearance

of myocardium, restrictive transmitral filling

patternMore

Hypothyroidism

see our comprehensive coverage of Primary hypothyroidism


hx of hypothyroidism, thyroid surgery,

lethargy, constipation, cold intolerance

evidence of thyroid surgery, myxoedematous skin

changes, bradycardia, diminished tendon reflexes

TSH: elevatedMore

Aortic dissection

see our comprehensive coverage of Aortic dissection

History Exam 1st test Other test

tearing chest pain radiating to the back with

sudden onset, stroke symptoms due to

accompanying carotid artery dissection

blowing diastolic murmur,

pulse differential between

right and left arms

CXR: widened

mediastinumMore

th

ha

tra

di

ef

Direct penetrating injury


gunshot and stab wounds

to the thorax

gunshot entrance wounds, stab wounds, hypotension often

without elevated neck veins, or pulsus paradoxus

transthoracic echocar

fluidMore

Radiation exposure


hx of chest radiation,

especially without

subcarinal blocks

signs of volume overload with clear lung fields suggests

tamponade; a pericardial rub may be present, which

suggests acute pericarditis


ECG: diffuse ST-segment e


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