Pericarditis: Consider pericardiocentesis and lavage

Article

Pericarditis is an inflammatory condition of the pericardial lining of the heart. It is characterized by accumulation of fluid, fibrin or fibrous tissue within the pericardial sac. Pericarditis is seen more commonly in young horses.1,2 There is no breed predilection. Male intact horses may be at increased risk.1

Pericarditis is an inflammatory condition of the pericardial lining of the heart. It is characterized by accumulation of fluid, fibrin or fibrous tissue within the pericardial sac. Pericarditis is seen more commonly in young horses.1,2 There is no breed predilection. Male intact horses may be at increased risk.1

Pathophysiology and clinical signs

Most horses present with a history of fever and depression. The most common clinical sign is tachycardia.1 Typically horses show signs of right heart failure. Three types of pericarditis have been distinguished: effusive, fibrinous and constrictive. Effusive pericarditis results in the accumulation of fluid in the pericardial sac.3 Fibrinous pericarditis is characterized by fibrin in the pericardial sac. Fibrinoeffusive pericarditis, the most-common form in the horse, occurs when both fibrin and fluid accumulate within the pericardial sac.1 The large amount of fluid or fibrin in the pericardial sac interferes with diastolic filling of the low-pressure right heart. Impaired venous return results in decreased diastolic myocardial perfusion and contractility, stroke volume and cardiac output decline. Venous distention, jugular pulses, edema and ascites develop as clinical signs of right-sided heart failure. Cardiac tamponade is the term used to describe the state of hemodynamic compromise caused by the excessive pericardial fluid and subsequent cardiac decompensation.

Two-dimensional echocardiography of an 8-year-old Quarter Horse gelding with pericardial effusion and epicardial fibrin accumulation. PE = pericardial effusion; LV = left ventricle; RV = right ventricle.

If fibrin matures to fibrous tissue, or pericardial or myocardial injury results in fibrosis, then ventricular compliance may be compromised and constrictive pericarditis may result. In these cases, diastolic filling ceases abruptly when a critical diastolic volume is reached. Without adequate diastolic volume, stroke volume and cardiac output decline, resulting in clinical signs of right heart failure. 4

Fluid and/or fibrin in the pericardial sac should be suspected if muffled heart sounds are present on auscultation but should not be ruled out if heart sounds are not muffled. Pericardial friction rubs are believed to be caused by the rubbing of the inflamed pericardial layers and sound like "a creaking leather saddle," "walking on dry snow" or a saw on wood. 5 Their presence or absence appears to be unrelated to the presence or absence of fluid or fibrin in the pericardial sac.

Etiology

Streptococcus and Actinobacillus species are most frequently isolated from the pericardial fluid in horses with bacterial pericarditis.1, 6-10 Other bacteria include: Escherichia coli, Enterococcus faecalis and Corynebacterium pseudobacterium.9,11 In the spring of 2001, an epidemic of equine pericarditis occurred in Kentucky in association with Mare Reproductive Loss Syndrome. Actinobacillus species were isolated from 11 of 34 cases from the pericardial fluid. Exposure to Eastern Tent Caterpillars was the greatest risk factor, and temporal distribution suggested a point source for infection.12 Changes in immune system function may be responsible for facilitating infection with Actinobacillus species in these cases.

The definitive identification of the etiology of pericarditis in horses is rare, making idiopathic pericarditis the most frequent diagnosis.1 Idiopathic pericarditis in humans is believed to be viral in origin because it frequently occurs in patients with a history of viral respiratory illness, or positive serum titers or viral isolation of respiratory viruses. In horses with pericarditis, as with humans, there is often a history of respiratory disease or concurrent respiratory disease. The association of pericarditis with pleuritis or pleuropneumonia has been well documented.1, 8 13, 14 In several cases, equine herpes virus has been implicated.1, 9

Other less commonly reported causes of equine pericarditis are Mycoplasma felis, neoplasia, trauma from an external thoracic injury, penetrating foreign bodies entering through the gastrointestinal tract and iatrogenic penetration during bone marrow aspiration.15-17

Clinical pathology

No specific clinical laboratory findings are characteristically associated with pericarditis. Depending on the etiology, one may see a leukocytosis or a hyperfibrinogenemia. Anemia of chronic disease may be present if the pericarditis is longstanding or associated with chronic respiratory disease. Prerenal or renal azotemia, hyponatremia and hyperkalemia are associated with heart failure.1

Normal pericardial fluid contains <1,500 x 106 nucleated cells/L and has a protein content of <25 mg/dL.18 Septic pericarditis is characterized by increased numbers of degenerative neutrophils in the pericardial fluid with or without the presence of bacteria. Cultures of pericardial fluid rarely yield positive results and if possible should be performed before antimicrobial therapy is instituted.1, 3, 8, 9 Typically, idiopathic or immune-mediated pericarditis results in increased protein and non-degenerate neutrophils in the pericardial fluid.3, 19 Other diagnostic tests that can be performed include viral titers for equine herpes virus, equine viral arteritis and equine influenza. If respiratory disease is present, then culture and sensitivity, and cytology of pleural and transtracheal wash fluids are recommended.

Echocardiography

Echocardiography is undoubtedly the most useful diagnostic tool in the diagnosis and treatment of pericarditis. Pericardial fluid can be seen as an anechoic space separating the parietal pericardium from the epicardial surface of the heart. Fibrin is hypoechoic to hyperechoic, usually shaggy and variably distributed throughout the pericardial sac. Echocardiography is also invaluable for assessing the impact of the pericarditis on cardiac function. Echocardiographic findings consistent with cardiac tamponade include: decreases in cardiac chamber sizes, right-atrial collapse, right-ventricular early diastolic collapse, and left atrial collapse. Pericardial thickening is often not appreciable. In addition, it is useful for guidance of pericardiocentesis and monitoring for fluid reaccumulation and resolution of fibrin.

Electrocardiography

Decreased amplitude of the QRS complex and electrical alternans are electrocardiographic findings traditionally associated with pericardial effusions.20 Decreased QRS amplitude is due to fluid dampening and short circuiting the electrical signal. Electrical alternans is due to the swinging of the heart in the pericardial fluid and is a pathognomonic finding.

Radiography

Use of thoracic radiographs in the diagnostic workup of pericarditis is questionable, unless respiratory disease is suspected.

Treatment and prognosis

Treatment should include rest for all animals. Broad-spectrum antibiotics are recommended if bacterial involvement is suspected. When viral or immune-mediated etiologies are suspected, and signs of active bacterial infections are absent, cortico-steroids can be administered. The use of steroids in suspected virally mediated pericarditis is controversial in both human and equine medicine. The bulk of the evidence suggests that the benefit of decreasing the immune-mediated sequelae of viral infections outweighs the risk of viral recrudescence.3, 19, 21

When effusions are compromising cardiac function, pericardiocentesis and lavage are treatments of choice.3, 8,19, 22 Drainage of the pericardial effusion usually results in immediate attenuation of the signs of cardiac compromise. An electrocardiogram should be performed during the procedure to monitor for arrhythmias. Lavage of the pericardial sac with 1-2 liters of 0.9% saline is recommended. One liter of 0.9% saline spiked with antibiotics such as sodium penicillin, gentomicin or ceftiofur has been found to be successful.1, 8 Twice-daily lavage is recommended until the amount of fluid drained is less than the amount of fluid infused. Fortunately, in horses, constrictive pericarditis is rarely a sequela to other more common forms of pericarditis. There is only one report of an attempted pericardiectomy in a horse and the surgery proved unsuccessful.4

The prognosis for horses with idiopathic pericarditis is favorable.1, 3 Septic pericarditis carries a guarded prognosis, but with drainage and lavage, a positive outcome can be achieved.1, 23 Thus, current data demonstrate that when properly diagnosed and aggressively treated, pericarditis need not be a fatal or even a future performance-limiting disease.

Dr. Abby Maxson Sage is head of the Large Animal Internal Medicine Division at the University of Minnesota (UM) College of Veterinary Medicine, where she has been an associate professor since 2003. She has held several other faculty positions at UM and the University of Pennsylvania New Bolton Center, where she also completed her residency. She earned her VMD in 1987 and became a diplomate of the American College of Veterinary Internal Medicine in 1995.

REFERENCES

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2. Seahorn JL, Slovis NM, Reimer JM, et al. Case-control study of factors associated with fibrinous pericarditis among horses in central Kentucky during spring 2001. J Am Vet Med Assoc 2003; 223(6): 832-838.

3. Freestone JF, Thomas, WP, Carlson GP, et al. Idiopathic effusive pericarditis with tamponade in the horse. Equine Vet J 1987; 19: 38-42.

4. Hardy J, Robertson JT, Reed, SM. Constrictive pericarditis in a mare: attempted treatment by partial pericardiectomy. Equine Vet J 1992; 24: 151-154.

5. Lorell BH. Pericardial Diseases. In: Braunwald E, ed. Heart Disease. A textbook of cardiovascular medicine. Philadelphia: WB Saunders 1997: 1478-1534.

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9. Bolin DC, Donahue JM, Vickers ML, et al. Microbiologic and pathologic findings in an epidemic of equine pericarditis. J Vet Diagn Invest 2005; 17(1): 38-44.

10. Davis JL, Gardner SY, Schwabenton B, et al. Congestive heart failure in horses: 14 cases (1984-2001). J Am Vet Med Assoc 2002; 220(10): 1512-1515.

11. Perkins SL, Magdesian KG, Thomas WP, et al. Pericarditis and pleuritis caused by Corynebacterium pseudotuberculosis in a horse. J Am Vet Med Assoc 2004; 224(7): 1133-1138.

12. Seahorn JL, Slovis NM, Reimer JM, et al. Case-control study of factors associated with fibrinous pericarditis among horses in central Kentucky during spring 2001. J Am Vet Med Assoc 2003; 223(6): 832-838.

13. Dill SG, Simoncini DC, Bolton GR, et al. Fibrinous pericarditis in the horse. J Am Vet Med Assoc 1982; 180: 266-271.

14. Wagner PC, Miller RA, Merritt F, et al. Contrictive pericarditis in the horse. J Equine Med Surg 1977; 1: 242-247.

15. Morley PS, Chirino-Trejo M, Petrie L, et al. Pericarditis and pleuritis caused by Myocplasma felis in a horse. Equine Vet J 1996; 28(3): 237-240.

16. Voros K, Felkai C, Szilagyi Z, et al. Two-dimensional echocardiographically guided pericardiocentesis in a horse with traumatic pericarditis. J Am Vet Med Assoc 1991; 198(11): 1953-1956.

17. Bertone JJ, Dill SG. Traumatic gastropericarditis in a horse. J Am Vet Med Assoc 1985; 187(7): 742-743.

18. Bernard W, Lamb J. Pericardial disease, in Robinson NE, ed. Current Therapy in Equine Medicine 3. Philadelphia, WB Saunders Co., 1992; pp 402-405.

19. Robinson JA, Marr CM, Reef VB, et al. Idiopathic, aseptic, effusive, fibrinous, nonconstrictive pericarditis with tamponade in a Standardbred filly. J Am Vet Med Assoc 1992; 201: 1593-1598.

20. Fowler NO. Pericardial disease. Heart Disease Stroke 1992; 1: 85-94.

21. Spodick DH. The normal and diseased pericardium: current concepts of pericardial physiology.

22. Reef VB, Gentile DG, Freeman DE. Successful treatment of pericarditis in a horse. J Am Vet Med Assoc 1984; 185: 94-98.

23. May KA, Cheramie HS, Howard RD, et al. Purulent pericarditis as a sequela to clostridial myositis in a horse. Equine Vet J 2002; 34(6): 636-640.

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