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PERICARDITIS

Sophy A. Jesty1

Pericarditis is an uncommon but not rare condition in the horse. Early

recognition of the disease is necessary for optimal outcome. Horses with cardiac
tamponade secondary to pericarditis represent a true medical emergency.
In horses, pericarditis has been associated with viral and bacterial infections
(equine herpesvirus type 1 [EHV – 1], equine herpesvirus type 2 [EHV – 2], influenza
virus, Streptococcus spp., Actinobacillus equuli, Pseudomonas spp., Pasteurella
multocida, Staphylococcus aureus, Actinobacter spp., Escherichia coli, Enterococcus
faecalis, Corynebacterium pyogenes, Mycoplasma felis, Propionibacterium acnes,
Corynebacterium pseudotuberculosis and Clostridium spp.), immune – mediated
disese such as eosinophilic pericarditis, neoplasia, trauma, and contiguous spread of
an inflammatory process from adjacent or nearby tissues. Many cases of pericarditis
in horses, however, are considered idiopathic.
Three outbreaks of pericarditis have been reported. The most thoroughly
investigated occurred in spring of 2001 (and to a lesser extent in 2002) in association
with mare reproductive loss syndrome (MRLS) in Kentucky and surrounding areas
(Sophy A. Jesty, 2009; Colin C. Schwarzwald, 2018). Other manifestations of MRLS
included early and late fetal losses, endophthalmitis, weak late – term foals, and
Actinobacillus spp. – associated encephalitis. Approximately 60 horses were affected
with pericarditis. In all cases, echocardiography revealed fibrin adherent to the
pericardium and a variable volume of fluid in the pericardial space, and many horses
also had concurrent pneumonia. Repeated pericardiocentesis was necessary in
virtually all affected horses; pericardial lavage was performed in fewer cases.
In approximately two thirds of these cases, fluid was characterized as an
aseptic fibrinous effusion, whereas sepsis was the etiology in one third of cases.
Bacteria isolated from the septic effusions by use of standard culture techniques
included A. equuli, Streptococcus spp., P. multocida, S. aureus, Actinobacter and
Pseudomonas spp. A. equuli was the most common isolate and may be
pericardiotropic in horse; Streptococcus spp. were the second most common. The
variety of bacterial isolates obtained makes it likely that bacterial infection of the
pericardial space was opportunistic and developed secondary to a separate
predisposing factor. Horses with both aseptic and septic fibrinous pericarditis all had
negative results of testing for equine viral arteritis (EVA); EHV – 1, - 2 and – 4;
equine influenza virus; Mycoplasma spp., and Histoplasma spp. Bacterial isolates
from horses that died included A. equuli, Streptococcus zooepidermicus and
1
Sophy A. Jesty – Pericarditis. In: N. Edward Robinson, Kim A. Sprayberry. Current Therapy
in Equine Medicine. Sixth Edition. Saunders Elsevier, 2009.
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Enterococcus faecalis. Viruses and mycoplasma were not isolated. Polymerase chain
reaction assay of pericardial fluid yield positive results for EHV-2, which is
ubiquitous among horses.
The clinical manifestation of MRLS were associated with a point-source
exposure to eastern tent caterpillars and it has been hypothesized that gastrointestinal
damage from caterpillar setae lead to embolization of normal gastrointestinal tract
flora that are delivered to the fetal fluids, pericardium and aqueous humor. In support
of the hypothesis, microgranulomatous lesions were observed round the setae
embedded in the submucosal lining of the gastrointestinal tract of affected horses.
Interestingly, the Actinobacillus strains isolated from pericardial fluid are the same as
those found in the gastrointestinal tract of normal healthy horses.

Clinical signs
The rapidity of onset of clinical signs of pericarditis varies considerably,
ranging from acute pericardial fluid accumulation, with or without pericardial fibrosis.
Clinical signs are seen when diastolic cardiac filling is impaired, leading to systemic
venous congestion and decrease cardiac output. This can develop as intrapericardial
pressure increases with pericardial fluid accumulation (cardiac tamponade) or when
fibrosis of the pericardium restricts normal distensibility. Development of increased
pericardial pressure depends on the volume of pericardial fluid, rate of accumulation,
and properties of the pericardium itself. Because the right side of the heart can
withstand less transmural pressure than the left side before collapsing, signs of right-
sided cardiac dysfunction develop first.
Common owner complaints at initial evaluation are often nonspecific and
include fever, poor appetite, lethargy, weight loss, colic and tachypnea. Signs of
cardiac or respiratory tract disease are common reasons for referral of an affected
horse from another veterinarian. Clinical signs appreciated in most horses with cardiac
tamponade include tachycardia, jugular and other systemic venous distension, ventral
edema, weak pulses, pale or cyanotic mucous membranes and quiet heart sounds if the
volume of pericardial fluid is substantial.
Clinical signs detected in many horses with cardiac tamponade include
pericardial friction rubs if the effusion is fibrinous, depression, fever, tachypnea or
dyspnea and quiet lung sound ventrally.
Pericardial friction rubs are classically triphasic in that they are heard during
atrial contraction, ventricular contraction and after early diastolic filling.
Pulsus paradoxus may also be detected in horses with cardiac tamponade and
is appreciated as an exaggeration of the normal decrease in systemic blood pressure
that occurs during inspiration. This decrease is a result of decreased left ventricular
stroke volume during inspiration because of increased venous return and right
ventricular filling at the expense of left ventricular filling, a transient reduction in the
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filling gradient between the pulmonary veins and the left atrium, and a decrease in the
contribution of the interventricular septum to left ventricular contraction. In many
cases, peripheral pulses are sometimes too week for pulsus paradoxus to be
appreciated in horses with cardiac tamponade.

Diagnosis
A hemogram may reveal changes consistent with an infection or a stress
leukogram, including leukocytosis, neutrophilia (with or without a left shift), and
hyperfibrinogenemia. Results of a serum biochemistry panel may be normal or may
indicate dehydration, hypoproteinemia, electrolyte derangements from pericardial
accumulation of fluid (third-space fluid), or changes consistent with end-organ
damage from cardiac tamponade such as azotemia and high liver enzyme activities.
An electrocardiogram will likely reveal tachycardia and low-amplitude QRS
complexes. Electrical alternans, or beat-to-beat alternation of R-wave amplitude, is a
specific but not sensitive indication of cardiac tamponade.
Radiography may reveal an enlargement cardiac silhouette, but cardiac
margins may be difficult to assess if pleural effusion is present.

Echocardiogram from a horse with pericardial effusion (PE), depicting

the right parasternal long-axis two-chambers view of the heart

Electrocardiogram (ECG) from a horse with severe pericardial effusion.

Low – amplitude QRS complexes (red circle); wide breathing movements cause
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the ECG path to deviate = the blue arrow (electrical alternans ws not apparent in this ECG)

Echocardiography is the diagnostic modality of choice for diagnosis of

pericarditis in horses. Ultrasonography enables assessment of the volume and
character of fluid, the presence and amount of fibrin, and the degree of cardiac
tamponade as evidenced by chamber sizes and right atrial and ventricular collapse.
Specific characterization of the nature of the pericardial fluid requires
collection of a sample via pericardiocentesis. Fluid should be analyzed cytologically
and submitted for aerobic and anaerobic bacterial culture with antimicrobial
sensitivity and for viral and mycobacterial isolation. Blood can be collected for
analysis of serum antibody titers against EHV-1, EVA virus, and influenza virus at the
time of diagnosis of pericarditis and 3 to 4 weeks later to assess for increase or
decreases in titer of fourfold or greater.
Cardiac-derived enzymes, such as cardiac troponin I, can be sensitive and
specific markers of cardiac damage and should be assessed as an estimate of the
degree of myocardial involvement.

Prognosis
Traditionally, the prognosis for horses with pericarditis was considered to be
uniformly poor, but more recent reports have proven this notion incorrect. If
pericarditis is recognized early and treated appropriately, the prognosis improves
dramatically. Horses with idiopathic or presumptive viral or immune-mediated
pericarditis have a good prognosis for full recovery. Horses with septic pericarditis
have a fair prognosis, assuming adequate antimicrobial treatment is provided. Horses
with neoplastic or traumatic pericarditis have a poorer prognosis for recovery. With
fibrinous pericarditis, constrictive pericarditis may develop months to years later, but
this complication is rare in horses.

Treatment
Pericardiocentesis should be performed as long as it is safe to do so; this
procedure can be both diagnostic and therapeutic. It is safest when performed with
ultrasonographic guidance. Traditionally pericardiocentesis in large animals has been
performed in the left fifth intercostal space near the level of costochondral junction.
Use of this site protects the thinner right wall of the heart. Alternatively, some
clinicians prefer to approach from the right fifth intercostal space to avoid the
coronary vessels, which are larger on the left side. The most optimal location for
pericardiocentesis should be determined with the aid of ultrasonography, and the site
may differ from horse to horse.
Pericardiocentesis without removal of fluid should be performed only when
the volume of pericardial fluid is small enough that insertion of a large –bore catheter
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for drainage is dangerous. In this scenario, a 10 – to 14-gauche over-the-needle

catheter can be inserted into the pericardial space and fluid aspirated for diagnostic
purposes. If the depth of the fluid in the pericardial space is greater than 5 cm,
insertion of a catheter large enough to enable drainage should be attempted with a
trocar catheter; the diameter of the catheter should be as large as can safely be
accommodated by the horse (typically 16 to 28 French).
The skin, subcutaneous tissue, and intercostal muscles should be blocked with
a local anesthetic, and a stab incision should be made in the skin for placement of the
trocar catheter. Advancement of the trocar through the body wall can be difficult, and
the horse may object; sedation may be required. Sometimes a popping sensation is felt
as the trocar catheter penetrates the parietal pericardium. When fluids starts to fill the
tube, the catheter should be advanced over the trocar into the pericardial space so it
will not be dislodged as fluid drains and the pericardial space diminishes. The catheter
can be advanced until only 5 to 10 cm remain external to the horse or until the heart is
felt beating at the tip of the catheter, at which point the catheter should be retracted
slightly. Drainage from the pericardial space (as opposed to the pleural space) is likely
when the catheter is inserted from the left fifth intercostal space at the costochondral
junction, but the position can be confirmed echocardiographically. The speed of
drainage is dictated by the size of the tube. Some clinicians prefer to remove
pericardial slowly to ameliorate the effects of fluid shifts and hemodynamic
decompensation.
Improvement in heart rate and pulse quality are seen promptly, after relatively
small volumes of fluid have been drained; this is because the effects of cardiac
tamponade operate on the steep phase of the pressure-volume curve, and even a small
decrease in fluid volume can decrease pressure substantially. Intravenous (IV) access
should be established before pericardiocentesis to facilitate quick administration of
medication during the procedure. Continual ECG monitoring throughout the
procedure is important because arrhythmias (usually ventricular in origin) can
develop. Development of an arrhythmia is not a contraindication for continuing, but
the depth of the catheter’s penetrance into the pericardial space should be decreased.
IV fluids should be administered during the procedure or just afterward because
cardiac output will surge once tamponade is relieved, and fluid administration
promotes adequate perfusion of organs that may have been affected by ischemia.
Use of diuretics before pericardiocentesis is performed is contraindicated;
these drugs will not decrease the volume of pericardial fluid quickly enough to be of
any use, and by decreasing preload, diuretics decrease cardiac filling and exacerbate
cardiac tamponade. Furosemide could potentially be administrated after pericardial
drainage to increase renal blood flow.
Once pericardial drainage has been accomplished, the catheter can be left
indwelling by securing it in place with a Chinese finger tie. The tube should be
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clamped shut or left open with a one –way Heimlich valve or a condom taped in place
to decrease the risk of ascending infection or development of pneumopericardium.
Leaving an indwelling tube is advisable until the character of the pericardial
fluid has been evaluated, an assessment can be made concerning the rate of fluid
reaccumulation, and any intrapericardial (IP) medications have been administered.
Often this means that a pericardial tube will remain indwelling for 1 to 3 days. Some
clinicians prefer to perform serial pericardiocentesis instead of leaving an indwelling
tube in place to decrease the risks of ascending infection or pneumopericardium.
Regardless of whether the fluid is septic or nonseptic pericardial lavage can be
beneficial, especially if there is fibrin in the pericardial space. Twice-daily lavage with
5 L of balanced polyionic fluids will allow for flushing out of fibrin, inflammatory
cells, infectious organisms, and immune complexes. Leaving approximately 1 L of
fluid in the pericardial space at the end of each lavage helps prevent adhesions from
between the epicardial and pericardial surfaces. The pericardial tube can be left in
place until it dislodges, until the volume of fluid that reaccumulates in 24 hours is less
than 1 L, or until local instillation of medication is no longer warranted.
Specific treatments depend on the nature of the pericardial fluid. Until this has
been determined, treatment with broad-spectrum, bactericidal, IV antimicrobials is
advised. Combinations such as penicillin and an aminoglycoside or fluoroquinolone
should be considered. If the pericardial fluid is septic (indicated by a high number of
degenerate neutrophils or bacteria, especially within macrophages), continuation of IV
antimicrobials for at least 7 to 14 days is beneficial, after which antimicrobials should
be administered orally for another 2 to 4 weeks. The choice of antimicrobial should be
made on the basis of culture and susceptibility results. Until then, broadspectrum
antimicrobial coverage should be continues. Intrapericardial infusion of antimicrobials
should also be performed while the pericardium tube remains in place. Choices
include sodium penicillin, gentamicin, ceftiofur, ampicillin or ticarcillin, all of which
are considered safe to instill in the pericardial space. Sodium penicillin is preferable to
potassium penicillin for intrapericardial instillation in case the high concentration of
potassium in the pericardial space triggers arrhythmias. The antimicrobials (10 x 10 6
international units of sodium penicillin or 1 g gentamicin) can be mixed in 1 L of
balanced polyionic fluids and left in the pericardial space after drainage, twice daily.
If, as is often the case, the pericardial fluid is nonseptic, antimicrobials can
be discontinued. Systemic or intrapericardial instillation of corticosteroids (20 to 50
mg dexamethasone, IV or intrapericardial (IP), every 24 hours; 100 mg prednisolone
sodium succinate, IP; 30 mg triamcinolone acetonide IP) should be considered in
horses with presumed immune-mediated pericarditis, which often has a viral etiology.
Systemic nonsteroidal anti-inflammatory agents can be used to control discomfort
regardless of the nature of the pericarditis.
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Other medications that have been used in management of horses with

pericarditis include anticoagulants (heparin at 5000 international units, IP), drugs that
prevent fibrosis (colchicine at 0.01 to 0.03 mg/kg, PO every 24 hours), an anti-
inflammatory agent with rheological properties (pentoxifyline at 7.5 mg/kg, PO every
8 to 12 hours), and antioxidant (vitamin E at 6000 to 8000 international units/horse,
PO, every 24 hours). The efficacy of these medications is unproven, but
administration could be helpful in some horses.
Treatment for constrictive pericarditis requires surgical pericardectomy or
pericardiotomy. If constriction arises in the parietal pericardium, the procedure can be
curative. If, however, constriction arises in the visceral pericardium, the surgery is
difficult; in addition, there is a risk of epicardial hemorrhage, and the prognosis is
poor because of the likelihood of continued constriction.

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