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Pericardial effusion

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Abdelrahman Ibrahim Abushouk, MD[2], Cafer Zorkun, M.D., Ph.D. [3], Varun Kumar, M.B.B.S

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Overview

Overview

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Abdelrahman Ibrahim Abushouk, MD[2], Mugilan Poongkunran M.B.B.S [3]

Overview

There is limited information about the historical perspective of pericardial effusion. However, percutaneous pericardiocentesis was first described in 1840 by Frank Schuh. By the 20th century, pericardiocentesis became the established technique for diagnosing and treating pericardial effusion. Before echocardiography, surgeons used a blind-subxiphoid approach; however, this was associated with serious organ injuries. However, the introduction of echo-guided pericardiocentesis improved the accuracy and safety of the procedure. The technique has been further refined over the past four decades.Pericardial effusion can be classified according to the nature of pericardial fluid into transudative, exudative, hemorrhagic, and malignant. Further, it can be classified according to the underlying cause into idiopathic, infectious, neoplastic, and post-operative. In addition, Horowitz et al. developed a classification for pericardial effusions based on echocardiographic findings (the degree of separation between the pericardium and epicardium). Pericardial effusion usually results from a disturbed equilibrium between the production and reabsorption of pericardial fluid. This can occur in infections and inflammations where there is increased production of pericardial fluid, increased microvascular pressure as in cardiac failure and renal failure cause, decreased plasma oncotic pressure as in cirrhosis and nephrotic syndrome, or in malignancy and hypothyroidism where there is inadequate drainage of the fluid. Pericardial effusion can be classified into serous, bloody and chylous effusions based on the composition of the effusion fluid. Infections and inflammation usually cause serous effusion while bloody effusions are as a result of trauma to the heart. Though iatrogenic causes and infections are the common etiologies, pericardial disease may also be a feature of other disorders such as inflammatory bowel disease. Aortic dissection or free wall rupture should also be considered in patients with unstable hemodynamics and pericardial tamponade.Most pericardial effusions are caused by inflammation of the pericardium, a condition called pericarditis. As the pericardium becomes inflamed, extra fluid is produced, leading to a pericardial effusion. Viral infections are one of the main causes of pericarditis and pericardial effusions. Infections causing pericardial effusions include cytomegalovirus, coxsackie virus, echovirus, and HIV. However, other conditions like injury to the pericardium or heart from a medical procedure, myocardial infarction, uremia, autoimmune disease and cancer should be considered in differential diagnosis of pericardial effusion.The underlying cause of pericardial effusion depend on the region where the patient is living. While malignancy is the most common cause of pericardial effusion in developed countries, infections such as tuberculosis and HIV seems to be the main etiologies of pericardial effusion in developing countries. Few studies have highlighted the following as possible risk factors for pericardial effusion (in the presence of a cause): older age, hypertension, diabetes mellitus, coronary artery disease, and atrial fibrillation. Patients with uncomplicated pericarditis usually have a self-resolving course within 2 weeks and can be managed on an outpatient basis. However Cardiac tamponade, purulent pericardial effusion, immunocompromised state, history of cancer, dialysis, use of oral anti-coagulation require urgent intervention. The prognosis of pericardial effusion depends on the underlying etiology being especially poor in patients with neoplastic pericardial effusion and very good in idiopathic/viral pericarditis. Pericardial effusion is a relatively common finding and sometimes the clinical picture of the patient leads directly to the cause for pericardial effusion. Mild pericardial effusion is a relatively a common finding, especially in elderly women and they are usually asymptomatic. Common symptoms may include fever, fatigue, muscle aches, shortness of breath, nausea, vomiting, and diarrhea. Large, serious pericardial effusions, or smaller ones that develop quickly, may cause other symptoms that include shortness of breath, palpitations (sensation that the heart is pounding or beating fast), light-headedness , and cool, clammy skin. The vital signs of a patient with small pericardial effusion are often normal. Fever suggests an underlying infectious or inflammatory cause, and the presence of a purulent effusion must be ruled out. The common signs include tachycardia, pulsus paradoxus, hypotension in cardiac tamponade, jugular venous distension, prominent Y descent, Kussmaul’s sign, pleural dullness, decreased breath sounds, distant heart sounds, hepatomegaly, ascites in chronic cases, and ankle edema in chronic cases. Laboratory investigations for pericardial effusion include the leukocyte count, C-reactive protein, and ESR for ruling out inflammatory causes. The cardiac troponin is elevated if there is an injury to the underlying myocardium, a condition termed as myopericarditis. Diagnostic pericardiocentesis and biopsy help in identifying an underlying infectious or malignant process. The EKG in patients with pericardial effusion may demonstrate low voltages (micro-voltages or short QRS complexes) and electrical alternans.Chest X ray is normal in cases of mild-moderate pericardial effusion. Cardiomegaly is seen when pericardial effusion > 250 ml. However it can be used to rule out other causes of chest pain. The American College of Cardiology (ACC), the American Heart Association (AHA), and the American Society of Echocardiography in their recommendations on echocardiography gave strong recommendations for echocardiography in pericardial disease. The finding usually include presence of moderate and large pericardial effusion, swinging of the heart within the effusion and reversal of right atrial and right ventricular diastolic transmural pressures. Echocardiography should be performed if there is a suspicion of tamponade (e.g. distended neck veins, pulsus paradoxus). Computed tomography is an effective diagnostic tool in cases of pericardial effusion as it helps us to narrow down on the etiology by determining the amount and nature of the pericardial fluid. CT is useful especially in identifying hemorrhagic effusions or clots within the pericardium. A pericardial effusion is often incidentally noted on CT scans obtained for other indications. The mainstay of treatment for pericardial effusion is pericardial fluid drainage. Indications for pericardiocentesis or a pericardial window include cardiac tamponade, for diagnostic purposes if there is suspected purulent, tuberculosis, or neoplastic pericarditis, and the presence of a large, persistent, symptomatic pericardial effusion.



Historical Perspective

There is limited information about the historical perspective of pericardial effusion. However, percutaneous pericardiocentesis was first described in 1840 by Frank Schuh. By the 20th century, pericardiocentesis became the established technique for diagnosing and treating pericardial effusion. Before echocardiography, surgeons used a blind-subxiphoid approach; however, this was associated with serious organ injuries. However, the introduction of echo-guided pericardiocentesis improved the accuracy and safety of the procedure. The technique has been further refined over the past four decades.

Classification

Pericardial effusion can be classified according to the nature of pericardial fluid into transudative, exudative, hemorrhagic, and malignant. Further, it can be classified according to the underlying cause into idiopathic, infectious, neoplastic, and post-operative. In addition, Horowitz et al. developed a classification for pericardial effusions based on echocardiographic findings (the degree of separation between the pericardium and epicardium).

Pathophysiology

Pericardial effusion usually results from a disturbed equilibrium between the production and reabsorption of pericardial fluid. This can occur in infections and inflammations where there is increased production of pericardial fluid, increased microvascular pressure as in cardiac failure and renal failure cause, decreased plasma oncotic pressure as in cirrhosis and nephrotic syndrome, or in malignancy and hypothyroidism where there is inadequate drainage of the fluid.

Causes

Pericardial effusion can be classified into serous, bloody and chylous effusions based on the composition of the effusion fluid. Infections and inflammation usually cause serous effusion while bloody effusions are as a result of trauma to the heart. Though iatrogenic causes and infections are the common etiologies, pericardial disease may also be a feature of other disorders such as inflammatory bowel disease. Aortic dissection or free wall rupture should also be considered in patients with unstable hemodynamics and pericardial tamponade.

Differentiating Pericardial Effusion from Other Diseases

Most pericardial effusions are caused by inflammation of the pericardium, a condition called pericarditis. As the pericardium becomes inflamed, extra fluid is produced, leading to a pericardial effusion. Viral infections are one of the main causes of pericarditis and pericardial effusions. Infections causing pericardial effusions include cytomegalovirus, coxsackie virus, echovirus, and HIV. However, other conditions like injury to the pericardium or heart from a medical procedure, myocardial infarction, uremia, autoimmune disease and cancer should be considered in differential diagnosis of pericardial effusion.

Epidemiology and Demographics

The underlying cause of pericardial effusion depend on the region where the patient is living. While malignancy is the most common cause of pericardial effusion in developed countries, infections such as tuberculosis and HIV seems to be the main etiologies of pericardial effusion in developing countries.

Risk Factors

Few studies have highlighted the following as possible risk factors for pericardial effusion (in the presence of a cause): older age, hypertension, diabetes mellitus, coronary artery disease, and atrial fibrillation.

Screening

There is insufficient evidence to recommend routine screening for pericardial effusion.

Natural History, Complications, and Prognosis

Patients with uncomplicated pericarditis usually have a self-resolving course within 2 weeks and can be managed on an outpatient basis. However Cardiac tamponade, purulent pericardial effusion, immunocompromised state, history of cancer, dialysis, use of oral anti-coagulation require urgent intervention. The prognosis of pericardial effusion depends on the underlying etiology being especially poor in patients with neoplastic pericardial effusion and very good in idiopathic/viral pericarditis.;

Diagnosis

Diagnostic Study of Choice

Pericardial effusion is primarily diagnosed based on the clinical evaluation along with electrocardiographic and chest radiograph findings, which may suggest the presence of a pericardial effusion. Echocardiography must be performed in all patients with possible pericardial effusion. Echocardiography is an excellent method for detection and estimation of the size of pericardial effusions.

History and Symptoms

Pericardial effusion is a relatively common finding and sometimes the clinical picture of the patient leads directly to the cause for pericardial effusion. Mild pericardial effusion is a relatively a common finding, especially in elderly women and they are usually asymptomatic. Common symptoms may include fever, fatigue, muscle aches, shortness of breath, nausea, vomiting, and diarrhea. Large, serious pericardial effusions, or smaller ones that develop quickly, may cause other symptoms that include shortness of breath, palpitations (sensation that the heart is pounding or beating fast), light-headedness , and cool, clammy skin.

Physical Examination

The vital signs of a patient with small pericardial effusion are often normal. Fever suggests an underlying infectious or inflammatory cause, and the presence of a purulent effusion must be ruled out. The common signs include tachycardia, pulsus paradoxus, hypotension in cardiac tamponade, jugular venous distension, prominent Y descent, Kussmaul’s sign, pleural dullness, decreased breath sounds, distant heart sounds, hepatomegaly, ascites in chronic cases, and ankle edema in chronic cases

Laboratory Findings

Laboratory investigations for pericardial effusion include the leukocyte count, C-reactive protein, and ESR for ruling out inflammatory causes. The cardiac troponin is elevated if there is an injury to the underlying myocardium, a condition termed as myopericarditis. Diagnostic pericardiocentesis and biopsy help in identifying an underlying infectious or malignant process.

Electrocardiogram

The EKG in patients with pericardial effusion may demonstrate low voltages (micro-voltages or short QRS complexes) and electrical alternans.

X-ray

Chest X ray is normal in cases of mild-moderate pericardial effusion. Cardiomegaly is seen when pericardial effusion > 250 ml. However it can be used to rule out other causes of chest pain.

Echocardiography and Ultrasound

The American College of Cardiology (ACC), the American Heart Association (AHA), and the American Society of Echocardiography in their recommendations on echocardiography gave strong recommendations for echocardiography in pericardial disease. The finding usually include presence of moderate and large pericardial effusion, swinging of the heart within the effusion and reversal of right atrial and right ventricular diastolic transmural pressures. Echocardiography should be performed if there is a suspicion of tamponade (e.g. distended neck veins, pulsus paradoxus).

CT scan

Computed tomography is an effective diagnostic tool in cases of pericardial effusion as it helps us to narrow down on the etiology by determining the amount and nature of the pericardial fluid. CT is useful especially in identifying hemorrhagic effusions or clots within the pericardium. A pericardial effusion is often incidentally noted on CT scans obtained for other indications.

MRI

MRI allow assessment of the entire chest and detection of associated abnormalities in the mediastinum, lungs and adjacent structures. MRI also delineate more precisely the spacial distribution of pericardial effusion in complex pericardial collections. It may be very useful in the investigation of the presence and extension of neoplastic disease.

Treatment

Medical Therapy

Treatment of pericardial effusion depends on the underlying cause and the severity of the problem. Some pericardial effusions remain small and never require treatment. Patients with acute inflammatory signs may get symptomatic relief with anti-inflammatory drugs. If the effusion is compromising heart function and causing cardiac tamponade, it will need to be drained, most commonly by a needle inserted through the chest wall and into the pericardial space.

Interventions

The mainstay of treatment for pericardial effusion is pericardial fluid drainage. Indications for pericardiocentesis or a pericardial window include cardiac tamponade, for diagnostic purposes if there is suspected purulent, tuberculosis, or neoplastic pericarditis, and the presence of a large, persistent, symptomatic pericardial effusion.

Primary Prevention

Secondary Prevention

References

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Classification

Classification

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Abdelrahman Ibrahim Abushouk, MD[2], Cafer Zorkun, M.D., Ph.D. [3], Varun Kumar, M.B.B.S

Overview

Pericardial effusion can be classified according to the nature of pericardial fluid into transudative, exudative, hemorrhagic, and malignant. Further, it can be classified according to the underlying cause into idiopathic, infectious, neoplastic, and post-operative. In addition, Horowitz et al. developed a classification for pericardial effusions based on echocardiographic findings (the degree of separation between the pericardium and epicardium).

Classification

Pericardial effusion can be classified according to the pericardial fluid nature into[1][2]:

  • Malignant
    • Metastasis (direct or seeding through pericardiocentesis)

Further, it can be categorized according to the underlying cause into[3][4]:

Horowitz et al. developed a classification for pericardial effusions based on echocardiographic findings.[5] This classification has been endorsed by the European Society of Cardiology[6].

References

  1. ↑ Refaat MM, Katz WE (2011). “Neoplastic pericardial effusion”. Clin Cardiol. 34 (10): 593–8. doi:10.1002/clc.20936. PMC 6652358 Check |pmc= value (help). PMID 21928406.
  2. ↑ Levy PY, Habib G, Collart F, Lepidi H, Raoult D (2006). “Etiological diagnosis of pericardial effusion”. Future Microbiol. 1 (2): 229–39. doi:10.2217/17460913.1.2.229. PMID 17661668.
  3. ↑ Santas E, Núñez J (2016). “Prognostic implications of pericardial effusion: The importance of underlying etiology”. Int J Cardiol. 202: 407. doi:10.1016/j.ijcard.2015.09.051. PMID 26432490.
  4. ↑ Levy PY, Habib G, Collart F, Lepidi H, Raoult D (2006). “Etiological diagnosis of pericardial effusion”. Future Microbiol. 1 (2): 229–39. doi:10.2217/17460913.1.2.229. PMID 17661668.
  5. ↑ Horowitz MS, Schultz CS, Stinson EB, Harrison DC, Popp RL (1974). “Sensitivity and specificity of echocardiographic diagnosis of pericardial effusion”. Circulation. 50 (2): 239–47. doi:10.1161/01.cir.50.2.239. PMID 4846631.
  6. ↑ Maisch B, Seferović PM, Ristić AD, Erbel R, Rienmüller R, Adler Y; et al. (2004). “[Guidelines on the diagnosis and management of pericardial diseases. Executive summary]”. Rev Esp Cardiol. 57 (11): 1090–114. doi:10.1016/s0300-8932(04)77245-0. PMID 15544758.


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Pathophysiology

Pathophysiology

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Abdelrahman Ibrahim Abushouk, MD[2], Varun Kumar, M.B.B.S.

Overview

Pericardial effusion usually results from a disturbed equilibrium between the production and reabsorption of pericardial fluid. This can occur in infections and inflammations where there is increased production of pericardial fluid, increased microvascular pressure as in cardiac failure and renal failure cause, decreased plasma oncotic pressure as in cirrhosis and nephrotic syndrome, or in malignancy and hypothyroidism where there is inadequate drainage of the fluid.

Pathophysiology

Physiology

  • Pericardium surrounds the heart and it consists of two layers, parietal and visceral layers [1].
  • The space between the layers is known as the pericardial cavity.
  • It usually contains small amount of fluid, approximately 15-50ml, which acts as a lubricating agent between the layers.
  • This fluid enters the pericardial space from the capillaries into the visceral pericardium.
  • This fluid is drained by lymphatics [2].
  • When this fluid production-drainage mechanism is altered, excess fluid accumulates in the pericardial cavity and this is referred to as pericardial effusion.
Normal gross anatomy of the pericardium space and fluid. Credit: Anatomist90 [3]


Pathogenesis

Therefore, pericardial effusion occurs when there is:

  • Increased capillary membrane permeability: Infection or inflammation may lead to exudative fluid or hemorrhagic effusion which have high protein levels. The pericardial effusion observed in the following conditions results from increased permeability of the capillary membrane [4].

Genetics

There are no known genetic causes of pericardial effusion.

Associated Conditions

Conditions associated with pericardial effusion include:

Gross Pathology

On gross pathology, enlarged cardiac cavity, compressed cardiac chambers (with large effusions), heart swinging within the effusion fluid are characteristic findings of pericardial effusion. Further, the color of the effusion fluid may give an insight into the possible effusion cause.

Microscopic Pathology

On microscopic histopathological analysis, there are no characteristic features of pericardial effusion. However, analysis of the pericardial fluid itself may give insights into the underlying cause e.g. numerous pus cells would indicate a pyogenic/inflammatory cause, lymphocytes indicate viral infection, and malignant cells indicate malignant seeding into the pericardium.

References

  1. ↑ Hoit BD (2017). “Anatomy and Physiology of the Pericardium”. Cardiol Clin. 35 (4): 481–490. doi:10.1016/j.ccl.2017.07.002. PMID 29025540.
  2. ↑ Rodriguez ER, Tan CD (2017). “Structure and Anatomy of the Human Pericardium”. Prog Cardiovasc Dis. 59 (4): 327–340. doi:10.1016/j.pcad.2016.12.010. PMID 28062264.
  3. ↑ https://commons.wikimedia.org/wiki/File:Slide14gggg.JPG/
  4. ↑ Vakamudi S, Ho N, Cremer PC (2017). “Pericardial Effusions: Causes, Diagnosis, and Management”. Prog Cardiovasc Dis. 59 (4): 380–388. doi:10.1016/j.pcad.2016.12.009. PMID 28062268.
  5. ↑ Patel Y, Agarwal V, Argulian E (2018). “Relation of Blood Pressure to Severity of Pericardial Effusion”. Am J Cardiol. 121 (11): 1409–1412. doi:10.1016/j.amjcard.2018.02.023. PMID 29580632.
  6. ↑ Scardulla F, Rinaudo A, Pasta S, Scardulla C (2015). “Mechanics of pericardial effusion: a simulation study”. Proc Inst Mech Eng H. 229 (3): 205–14. doi:10.1177/0954411915574012. PMID 25833996.
  7. ↑ Refaat MM, Katz WE (2011). “Neoplastic pericardial effusion”. Clin Cardiol. 34 (10): 593–8. doi:10.1002/clc.20936. PMC 6652358 Check |pmc= value (help). PMID 21928406.


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Causes

Causes

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mugilan Poongkunran M.B.B.S [2]; Cafer Zorkun, M.D., Ph.D. [3]; Varun Kumar, M.B.B.S., Abdelrahman Ibrahim Abushouk, MD[4]

Overview

Pericardial effusion can be classified into serous, bloody and chylous effusions based on the composition of the effusion fluid. Infections and inflammation usually cause serous effusion while bloody effusions are as a result of trauma to the heart. Though iatrogenic causes and infections are the common etiologies, pericardial disease may also be a feature of other disorders such as inflammatory bowel disease. Aortic dissection or free wall rupture should also be considered in patients with unstable hemodynamics and pericardial tamponade.

Causes

Life Threatening Causes

Life-threatening causes include conditions which may result in death or permanent disability within 24 hours if left untreated.

Common Causes

Causes by Organ System

Cardiovascular Acute myocardial infarction, aortic dissection, aortic rupture, bacterial pericarditis, benign obstruction of thoracic duct, Cantu syndrome, capillary leak syndrome, cardiomyopathy, congestive heart failure, constrictive pericarditis, dilated cardiomyopathy, dissecting aortic aneurysm, Dressler’s syndrome, hypersensitivity pericarditis with eosinophilia, hypertrichotic osteochondrodysplasia, Kawasaki disease, myocardial rupture, heart surgery, fungal pericarditis, pyogenic pericarditis, rheumatic pericarditis, tuberculous pericarditis, uremic pericarditis, ventricular aneurysm, viral pericarditis
Chemical / poisoning Asbestosis, silicosis
Dermatologic Behcet syndrome[1], Cantu syndrome, hypertrichotic osteochondrodysplasia
Drug Side Effect Anticoagulants, bleomycin,Bosutinib, certolizumab pegol, chemotherapy, cyclophosphamide, cytarabine, dantrolene, daunorubicin, doxorubicin, hydralazine, isoniazid, minoxidil, Oprelvekin, penicillin, phenylbutazone, phenytoin, procainamide, Sargramostim, sirolimus
Ear Nose Throat Temporal arteritis[2]
Endocrine Addisonian crisis, hypothyroidism, myxedema
Environmental No underlying causes
Gastroenterologic Acute pancreatitis, cirrhosis, inflammatory bowel disease, Whipple’s
Genetic Cantu syndrome, congenital disorders of glycosylation, Gaucher disease, hypertrichotic osteochondrodysplasia, Jacobs arthropathy-camptodactyly syndrome, Mulibrey nanism syndrome, recurrent hereditary polyserositis
Hematologic Coagulopathy, leukemia, lymphoma
Iatrogenic Cardiac catheterization, cardiopulmonary resuscitation, cathether ablation for arrhythmias, coronary artery bypass grafting, dialysis, heart surgery, percutaneous coronary intervention, postpericardiotomy syndrome, radiation, TAVI, thoracic surgery, valvuloplasty
Infectious Disease Actinomycosis, adenovirus, alveolar hydatid disease, amebiasis, aspergillus, blastomycosis, borrelia, brucellosis, candida, coccidiomycosis, coxsackie B Virus, cytomegalovirus, Ebstein-Barr virus, echinococcus, echovirus, entamoeba histolytica, escherichia coli, francisella, fungal pericarditis, haemophilus influenza, hepatitis B, histoplasmosis, influenza, klebsiella, legionella, Lyme disease, meningococci, mumps, mycobacterium tuberculosis, mycoplasma pnuemonia, neisseria, nocardia, pneumococci, pneumonia, proteus, pseudomonas, pyogenic pericarditis, rheumatic fever, rickettsia, salmonella, scrub typhus, staphylococcus, streptococci, syphilis, toxoplasmosis, tuberculous pericarditis, tularemia, varicella, viral pericarditis
Musculoskeletal / Ortho Cantu syndrome, hypertrichotic osteochondrodysplasia
Neurologic No underlying causes
Nutritional / Metabolic Malnutrition, congenital disorders of glycosylation
Obstetric/Gynecologic Ovarian hyperstimulation syndrome
Oncologic Breast cancer, carcinoid, fibroma, Kaposi’s sarcoma, leukemia, lung cancer, lymphoma, melanoma, mesothelioma, neoplasia that has spread to the pericardium, ovarian cancer, sarcoma, Sipple syndrome
Opthalmologic No underlying causes
Overdose / Toxicity No underlying causes
Psychiatric No underlying causes
Pulmonary Bronchogenic cyst, lung cancer, pneumonia, sarcoidosis
Renal / Electrolyte Nephrotic syndrome, renal failure, uremic pericarditis
Rheum / Immune / Allergy Acute rheumatic fever, amyloidosis, ankylosing spondylitis, Behcet syndrome, collagen vascular disease, Dressler’s syndrome, inflammatory bowel disease, Kawasaki disease, mixed connective tissue disease, polyarteritis nodosa, polymyositis, Reiter’s syndrome, rheumatic pericarditis, rheumatoid arthritis, sarcoidosis, scleroderma, Still’s disease, systemic lupus erythematosus, systemic sclerosis, temporal arteritis, Wegener’s
Sexual Neisseria gonorrhoeae[3], treponema pallidum
Trauma Blunt or penetrating chest trauma, esophageal rupture, esophogeal perforation, gastric perforation, pancreatic-pericardial fistula
Urologic No underlying causes
Dental No underlying causes
Miscellaneous Hypoalbuminemia, idiopathic, radiation

Causes in Alphabetical Order


References

  1. ↑ Scarlett JA, Kistner ML, Yang LC (1979). “Behçet’s syndrome. Report of a case associated with pericardial effusion and cryoglobulinemia treated with indomethacin”. Am J Med. 66 (1): 146–8. PMID 420242.
  2. ↑ Garewal HS, Uhlmann RF, Bennett RM (1981). “Pericardial effusion in association with giant cell arteritis”. West J Med. 134 (1): 71–2. PMC 1272467. PMID 7210667.
  3. ↑ Wilson J, Zaman AG, Simmons AV (1990). “Gonococcal arthritis complicated by acute pericarditis and pericardial effusion”. Br Heart J. 63 (2): 134–5. PMC 1024342. PMID 2317408.


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Differential Diagnosis

Differential Diagnosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Abdelrahman Ibrahim Abushouk, MD[2]

Overview

Most pericardial effusions are caused by inflammation of the pericardium, a condition called pericarditis. As the pericardium becomes inflamed, extra fluid is produced, leading to a pericardial effusion. Viral infections are one of the main causes of pericarditis and pericardial effusions. Infections causing pericardial effusions include cytomegalovirus, coxsackie virus, echovirus, and HIV. However, other conditions like injury to the pericardium or heart from a medical procedure, myocardial infarction, uremia, autoimmune disease and cancer should be considered in differential diagnosis of pericardial effusion.

Differentiating Pericardial Effusion from other Diseases

Chest pain or pressure are common symptoms. A small effusion may be asymptomatic. Larger effusions may cause cardiac tamponade, a life-threatening complication and the signs of impending tamponade include dyspnea, low blood pressure, and distant heart sounds. There are several other cardiac insults with similar symptoms that should be considered in differential diagnosis of pericardial effusion[1][2][3][4][5][6][7][8][9][10][11][12][13][14][15][16][17][18][19][20]:

Diseases Diagnostic tests Physical Examination Symptoms Past medical history Other Findings
CT scan and MRI EKG Chest X-ray Tachypnea Tachycardia Fever Chest Pain Hemoptysis Dyspnea on Exertion Wheezing Chest Tenderness Nasalopharyngeal Ulceration Carotid Bruit
Pulmonary embolism
  • On CT angiography:
    • Intra-luminal filling defect
  • On MRI:
    • Narrowing of involved vessel
    • No contrast seen distal to obstruction
    • Polo-mint sign (partial filling defect surrounded by contrast)
 ✔ ✔ ✔ (Low grade) ✔ ✔ (In case of massive PE) ✔ – – – –
Congestive heart failure
  • Goldberg’s criteria may aid in diagnosis of left ventricular dysfunction: (High specificity)
    • SV1 or SV2 + RV5 or RV6 ≥3.5 mV
    • Total QRS amplitude in each of the limb leads ≤0.8 mV
    • R/S ratio <1 in lead V4
 ✔ ✔ ✔ – – ✔ – – – –
Percarditis
  • ST elevation
  • PR depression
  • Large collection of fluid inside the pericardial sac (pericardial effusion)
  • Calcification of pericardial sac
 ✔ ✔ ✔ (Low grade) ✔ (Relieved by sitting up and leaning forward) – ✔ – – – –
  • May be clinically classified into:
    • Acute (< 6 weeks)
    • Sub-acute (6 weeks – 6 months)
    • Chronic (> 6 months)
Pneumonia ✔ ✔ ✔ ✔ – ✔ ✔ – – –
Vasculitis

Homogeneous, circumferential vessel wall swelling

✔ ✔ ✔ ✔ ✔ ✔ – ✔ ✔ ✔
Chronic obstructive pulmonary disease (COPD)
  • On CT scan:
  • On MRI:
    • Increased diameter of pulmonary arteries
    • Peripheral pulmonary vasculature attentuation
    • Loss of retrosternal airspace due to right ventricular enlargement
    • Hyperpolarized Helium MRI may show progressively poor ventilation and destruction of lung
 ✔ ✔ – – – ✔ ✔ – – –


References

  1. ↑ Brenes-Salazar JA (2014). “Westermark’s and Palla’s signs in acute and chronic pulmonary embolism: Still valid in the current computed tomography era”. J Emerg Trauma Shock. 7 (1): 57–8. doi:10.4103/0974-2700.125645. PMC 3912657. PMID 24550636.
  2. ↑ “CT Angiography of Pulmonary Embolism: Diagnostic Criteria and Causes of Misdiagnosis | RadioGraphics”.
  3. ↑ Bĕlohlávek J, Dytrych V, Linhart A (2013). “Pulmonary embolism, part I: Epidemiology, risk factors and risk stratification, pathophysiology, clinical presentation, diagnosis and nonthrombotic pulmonary embolism”. Exp Clin Cardiol. 18 (2): 129–38. PMC 3718593. PMID 23940438.
  4. ↑ “Pulmonary Embolism: Symptoms – National Library of Medicine – PubMed Health”.
  5. ↑ Ramani GV, Uber PA, Mehra MR (2010). “Chronic heart failure: contemporary diagnosis and management”. Mayo Clin. Proc. 85 (2): 180–95. doi:10.4065/mcp.2009.0494. PMC 2813829. PMID 20118395.
  6. ↑ Blinderman CD, Homel P, Billings JA, Portenoy RK, Tennstedt SL (2008). “Symptom distress and quality of life in patients with advanced congestive heart failure”. J Pain Symptom Manage. 35 (6): 594–603. doi:10.1016/j.jpainsymman.2007.06.007. PMC 2662445. PMID 18215495.
  7. ↑ Hawkins NM, Petrie MC, Jhund PS, Chalmers GW, Dunn FG, McMurray JJ (2009). “Heart failure and chronic obstructive pulmonary disease: diagnostic pitfalls and epidemiology”. Eur. J. Heart Fail. 11 (2): 130–9. doi:10.1093/eurjhf/hfn013. PMC 2639415. PMID 19168510.
  8. ↑ Takasugi JE, Godwin JD (1998). “Radiology of chronic obstructive pulmonary disease”. Radiol. Clin. North Am. 36 (1): 29–55. PMID 9465867.
  9. ↑ Wedzicha JA, Donaldson GC (2003). “Exacerbations of chronic obstructive pulmonary disease”. Respir Care. 48 (12): 1204–13, discussion 1213–5. PMID 14651761.
  10. ↑ Nakawah MO, Hawkins C, Barbandi F (2013). “Asthma, chronic obstructive pulmonary disease (COPD), and the overlap syndrome”. J Am Board Fam Med. 26 (4): 470–7. doi:10.3122/jabfm.2013.04.120256. PMID 23833163.
  11. ↑ Khandaker MH, Espinosa RE, Nishimura RA, Sinak LJ, Hayes SN, Melduni RM, Oh JK (2010). “Pericardial disease: diagnosis and management”. Mayo Clin. Proc. 85 (6): 572–93. doi:10.4065/mcp.2010.0046. PMC 2878263. PMID 20511488.
  12. ↑ Bogaert J, Francone M (2013). “Pericardial disease: value of CT and MR imaging”. Radiology. 267 (2): 340–56. doi:10.1148/radiol.13121059. PMID 23610095.
  13. ↑ Gharib AM, Stern EJ (2001). “Radiology of pneumonia”. Med. Clin. North Am. 85 (6): 1461–91, x. PMID 11680112.
  14. ↑ Schmidt WA (2013). “Imaging in vasculitis”. Best Pract Res Clin Rheumatol. 27 (1): 107–18. doi:10.1016/j.berh.2013.01.001. PMID 23507061.
  15. ↑ Suresh E (2006). “Diagnostic approach to patients with suspected vasculitis”. Postgrad Med J. 82 (970): 483–8. doi:10.1136/pgmj.2005.042648. PMC 2585712. PMID 16891436.
  16. ↑ Stein PD, Dalen JE, McIntyre KM, Sasahara AA, Wenger NK, Willis PW (1975). “The electrocardiogram in acute pulmonary embolism”. Prog Cardiovasc Dis. 17 (4): 247–57. PMID 123074.
  17. ↑ Warnier MJ, Rutten FH, Numans ME, Kors JA, Tan HL, de Boer A, Hoes AW, De Bruin ML (2013). “Electrocardiographic characteristics of patients with chronic obstructive pulmonary disease”. COPD. 10 (1): 62–71. doi:10.3109/15412555.2012.727918. PMID 23413894.
  18. ↑ Stein PD, Matta F, Ekkah M, Saleh T, Janjua M, Patel YR, Khadra H (2012). “Electrocardiogram in pneumonia”. Am. J. Cardiol. 110 (12): 1836–40. doi:10.1016/j.amjcard.2012.08.019. PMID 23000104.
  19. ↑ Hazebroek MR, Kemna MJ, Schalla S, Sanders-van Wijk S, Gerretsen SC, Dennert R, Merken J, Kuznetsova T, Staessen JA, Brunner-La Rocca HP, van Paassen P, Cohen Tervaert JW, Heymans S (2015). “Prevalence and prognostic relevance of cardiac involvement in ANCA-associated vasculitis: eosinophilic granulomatosis with polyangiitis and granulomatosis with polyangiitis”. Int. J. Cardiol. 199: 170–9. doi:10.1016/j.ijcard.2015.06.087. PMID 26209947.
  20. ↑ Dennert RM, van Paassen P, Schalla S, Kuznetsova T, Alzand BS, Staessen JA, Velthuis S, Crijns HJ, Tervaert JW, Heymans S (2010). “Cardiac involvement in Churg-Strauss syndrome”. Arthritis Rheum. 62 (2): 627–34. doi:10.1002/art.27263. PMID 20112390.

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Epidemiology and Demographics

Epidemiology and Demographics

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Varun Kumar, M.B.B.S., Abdelrahman Ibrahim Abushouk, MD[2]

Overview

The underlying cause of pericardial effusion depend on the region where the patient is living. While malignancy is the most common cause of pericardial effusion in developed countries, infections such as tuberculosis and HIV seems to be the main etiologies of pericardial effusion in developing countries.[1][2]

Epidemiology and Demographics

Age

Pericardial effusion occurs commonly in fourth or fifth decade of life. However, it can occur in all age groups. Patients with AIDS are at higher risk of developing effusion earlier when compared to general population.[3]

Gender

There is no sexual predilection observed in occurrence of pericardial effusion.

Developed Countries

  • Malignant pericardial effusion is seen in approximately 50-60% of patients presenting with pericardial effusion who have history of malignancy.[4][5]
  • Among patients presenting with pericarditis or pericardial effusion with no history of malignancy, undiagnosed underlying malignancy was detected in 4-7%.[6][7][8]
  • Viral infection of the pericardium is another leading cause of pericardial effusion.[9][10][11] Pericarditis most often affects men aged 20 – 50. It usually follows respiratory infections, most commonly echovirus or coxsackie virus. In children, it is most commonly caused by adenovirus or coxsackie virus. The incidence and prevalence of viral pericardial effusion varies with season and region.

Developing Countries

  • Pericardial effusion secondary to HIV and tuberculosis is one of the major cause of acute pericarditis in developing countries.[12]
  • Tuberculous pericarditis, caused by mycobacterium tuberculosis, is found in approximately 1% of all autopsied cases of TB and in 1% to 2% of instances of pulmonary TB.[13] It accounted for 69.5% (162 of 233) of cases referred for diagnostic pericardiocentesis in a study in Western Cape Province of South Africa[14] while the same accounts for 4% of cases in developed countries.[15]
  • The incidence of pericardial effusion in patients with asymptomatic AIDS was 11% per year before the introduction of effective highly active antiretroviral therapy (HAART). The 6 month survival rate of AIDS patients with effusion was significantly shorter (36%) than the survival rate without effusions (93%). This shortened survival rate remained statistically significant after adjustment for lead-time bias and was independent of CD4 count and albumin level.[16]

References

  1. ↑ Maisch B, Ristic A, Pankuweit S (2010). “Evaluation and management of pericardial effusion in patients with neoplastic disease”. Prog Cardiovasc Dis. 53 (2): 157–63. doi:10.1016/j.pcad.2010.06.003. PMID 20728703.
  2. ↑ Atar S, Chiu J, Forrester JS, Siegel RJ (1999). “Bloody pericardial effusion in patients with cardiac tamponade: is the cause cancerous, tuberculous, or iatrogenic in the 1990s?”. Chest. 116 (6): 1564–9. PMID 10593777.
  3. ↑ Meenakshisundaram R, Sweni S, Thirumalaikolundusubramanian P (2010). “Cardiac isoform of alpha 2 macroglobulin: a marker of cardiac involvement in pediatric HIV and AIDS”. Pediatr Cardiol. 31 (2): 203–7. doi:10.1007/s00246-009-9584-1. PMID 19915889.
  4. ↑ Gornik HL, Gerhard-Herman M, Beckman JA (2005). “Abnormal cytology predicts poor prognosis in cancer patients with pericardial effusion”. J Clin Oncol. 23 (22): 5211–6. doi:10.1200/JCO.2005.00.745. PMID 16051963.
  5. ↑ Porte HL, Janecki-Delebecq TJ, Finzi L, Métois DG, Millaire A, Wurtz AJ (1999). “Pericardoscopy for primary management of pericardial effusion in cancer patients”. Eur J Cardiothorac Surg. 16 (3): 287–91. PMID 10554845.
  6. ↑ Permanyer-Miralda G, Sagristá-Sauleda J, Soler-Soler J (1985). “Primary acute pericardial disease: a prospective series of 231 consecutive patients”. Am J Cardiol. 56 (10): 623–30. PMID 4050698.
  7. ↑ Imazio M, Cecchi E, Demichelis B, Ierna S, Demarie D, Ghisio A; et al. (2007). “Indicators of poor prognosis of acute pericarditis”. Circulation. 115 (21): 2739–44. doi:10.1161/CIRCULATIONAHA.106.662114. PMID 17502574.
  8. ↑ Imazio M, Demichelis B, Parrini I, Favro E, Beqaraj F, Cecchi E; et al. (2005). “Relation of acute pericardial disease to malignancy”. Am J Cardiol. 95 (11): 1393–4. doi:10.1016/j.amjcard.2005.01.094. PMID 15904655.
  9. ↑ Troughton RW, Asher CR, Klein AL (2004). “Pericarditis”. Lancet. 363 (9410): 717–27. doi:10.1016/S0140-6736(04)15648-1. PMID 15001332.
  10. ↑ Little WC, Freeman GL (2006). “Pericardial disease”. Circulation. 113 (12): 1622–32. doi:10.1161/CIRCULATIONAHA.105.561514. PMID 16567581.
  11. ↑ Imazio M, Brucato A, Adler Y, Brambilla G, Artom G, Cecchi E; et al. (2007). “Prognosis of idiopathic recurrent pericarditis as determined from previously published reports”. Am J Cardiol. 100 (6): 1026–8. doi:10.1016/j.amjcard.2007.04.047. PMID 17826391.
  12. ↑ Chen Y, Brennessel D, Walters J, Johnson M, Rosner F, Raza M (1999). “Human immunodeficiency virus-associated pericardial effusion: report of 40 cases and review of the literature”. Am Heart J. 137 (3): 516–21. PMID 10047635.
  13. ↑ Fowler NO (1991). “Tuberculous pericarditis”. JAMA. 266 (1): 99–103. PMID 2046135.
  14. ↑ Reuter H, Burgess LJ, Doubell AF (2005). “Epidemiology of pericardial effusions at a large academic hospital in South Africa”. Epidemiol Infect. 133 (3): 393–9. PMC 2870262. PMID 15962545.
  15. ↑ Sagristà-Sauleda J, Permanyer-Miralda G, Soler-Soler J (1988). “Tuberculous pericarditis: ten year experience with a prospective protocol for diagnosis and treatment”. J Am Coll Cardiol. 11 (4): 724–8. PMID 3351140.
  16. ↑ Heidenreich PA, Eisenberg MJ, Kee LL, Somelofski CA, Hollander H, Schiller NB; et al. (1995). “Pericardial effusion in AIDS. Incidence and survival”. Circulation. 92 (11): 3229–34. PMID 7586308.

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Natural History, Complications and Prognosis

Natural History, Complications and Prognosis

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-In-Chief: Varun Kumar, M.B.B.S., Abdelrahman Ibrahim Abushouk, MD[2]

Overview

Patients with uncomplicated pericarditis usually have a self-resolving course within 2 weeks and can be managed on an outpatient basis. However Cardiac tamponade, purulent pericardial effusion, immunocompromised state, history of cancer, dialysis, use of oral anti-coagulation require urgent intervention. The prognosis of pericardial effusion depends on the underlying etiology being especially poor in patients with neoplastic pericardial effusion and very good in idiopathic/viral pericarditis.

Natural history, Complications and Prognosis

Natural History

  • Pericardial effusion if untreated or if refractory to treatment can lead to accumulation of large amount of fluid around the heart, severe hemodynamic compromise and even death.

Complications

  • Many times, there are no complications of pericardial effusion.
  • The most serious possible complication is cardiac tamponade.
  • If untreated, it can lead to shock which can cause serious complications.
  • If the fluid accumulates too rapidly or is too large, then cardiac tamponade, a condition in which the heart is compressed by the fluid and cannot pump enough blood forward may occur. Cardiac tamponade require urgent intervention including pericardiocentesis. This complication is more common in patients with specific underlying etiologies such as malignancy, tuberculosis[1], or purulent effusion and rarely occurs in idiopathic pericardial effusion.
  • Various complications depend on the etiology of the disease:
    • Idiopathic Cause
      • Idiopathic pericardidial effusion is often self-limited and most patients recover in 2 weeks to 3 months. Idiopathic or viral pericardial disease is associated with a favorable long-term prognosis[2]with few developing recurrences[3].
    • Tuberculous Cause
      • The mortality rate associated with tuberculous pericardial disease in the preantibiotic era was 80-90%.[4] The mortality rate is currently 8-17%.[5][6] The mortality is 17-34% if the tuberculous pericardial effusion is associated with HIV[7].
    • Traumatic Pericardial Injury
      • In penetrating injuries, pericardial effusion and tamponade may develop rapidly. Early detection and early treatment of cardiac tamponade is associated with a good prognosis. Minor perforations, isolated right ventricular wounds, and a systolic blood pressure more than 50 mm Hg are all associated with better outcomes.
    • Malignancy
      • Pericardial effusion secondary to malignancy is associated with poorer outcomes and a more complicated course.
    • Autoimmune Disease
    • Renal Failure
      • Pericardial disease secondary to renal failure is associated with significant morbidity and may result in hemorrhagic pericardial effusion.[8]

Prognosis

  • If pericardial effusion lasts beyond 6 months, then it is termed as chronic pericardial effusion and is usually well tolerated.
  • The prognosis of pericardial effusion depends on the underlying etiology.

References

  1. ↑ Mayosi BM, Burgess LJ, Doubell AF (2005). “Tuberculous pericarditis”. Circulation. 112 (23): 3608–16. doi:10.1161/CIRCULATIONAHA.105.543066. PMID 16330703.
  2. ↑ Ilan Y, Oren R, Ben-Chetrit E (1991). “Acute pericarditis: etiology, treatment and prognosis. A study of 115 patients”. Jpn Heart J. 32 (3): 315–21. PMID 1920818.
  3. ↑ Shabetai R (1990). “Acute pericarditis”. Cardiol Clin. 8 (4): 639–44. PMID 2249218.
  4. ↑ Harvey AM, Whitehill MR. Tuberculous pericarditis. Medicine. 1937; 16: 45–94
  5. ↑ Desai HN (1979). “Tuberculous pericarditis. A review of 100 cases”. S Afr Med J. 55 (22): 877–80. PMID 472922.
  6. ↑ Bhan GL (1980). “Tuberculous pericarditis”. J Infect. 2 (4): 360–4. PMID 7185934.
  7. ↑ Hakim JG, Ternouth I, Mushangi E, Siziya S, Robertson V, Malin A (2000). “Double blind randomised placebo controlled trial of adjunctive prednisolone in the treatment of effusive tuberculous pericarditis in HIV seropositive patients”. Heart. 84 (2): 183–8. PMC 1760932. PMID 10908256.
  8. ↑ Nicholls, AJ. Heart and Circulation. In: Handbook of Dialysis, Daugirdas, JT, Ing, TS (Eds), Little, Brown and Co., New York 1994. p.149.

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Diagnosis

Diagnosis

History and Symptoms | Physical Examination | Laboratory Findings | Electrocardiogram | Chest X-Ray | CT | MRI | Echocardiography | Cardiac Catheterization

Treatment

Treatment

Pericardiocentesis | Pericardial Window

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]; Varun Kumar, M.B.B.S

Overview

Treatment of pericardial effusion depends on the underlying cause and the severity of the problem. Some pericardial effusions remain small and never require treatment. Patients with acute inflammatory signs may get symptomatic relief with anti-inflammatory drugs. If the effusion is compromising heart function and causing cardiac tamponade, it will need to be drained, most commonly by a needle inserted through the chest wall and into the pericardial space.

Treatment

  • Pericardial effusion due to a viral infection usually resolves within a few weeks without treatment.
  • Some pericardial effusions remain small and never require treatment.
  • If the pericardial effusion is due to a condition such as lupus, treatment with aspirin or non-steroid anti-inflammatory drugs may provide benefit.
  • If the effusion is compromising heart function and causing cardiac tamponade, it will need to be drained, most commonly by a needle inserted through the chest wall and into the pericardial space.
  • A drainage tube is often left in place for several days. In some cases, surgical drainage may be required by pericardiocentesis, in which a needle, and sometimes a catheter are used to drain excess fluid. Pericardial window is made surgically in patients with recurrent pericardial effusion which drains the fluid into peritonial cavity[1]

References

  1. ↑ Stuart J. Hutchison (10 December 2008). Pericardial diseases: clinical diagnostic imaging atlas. Elsevier Health Sciences. pp. 93–. ISBN 9781416052746. Retrieved 10 November 2010.


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