Discussion
Pericardial effusions are usually associated with non-specific symptoms,
yet a significant proportion of patients are asymptomatic, and its
diagnosis constitutes an incidental finding3 unless
accompanied by acute pericarditis presenting with pericardial chest
pain, pericardial rubs, and new widespread ST-elevations or PR
depressions on ECG1. Cardiac tamponade physiology
develops when the ability of the pericardium to stretch is surpassed by
the speed of pericardial fluid accumulation.
When a large or rapidly evolving pericardial effusion is detected, it is
pivotal to assess, hemodynamic significance, and associated diseases. In
small, incidental, and asymptomatic effusions, conservative management
is an appropriate initial approach, with drainage needed in cases of
diagnostic dilemma or secondary to other causes (i.e., Malignancy,
chronic infections such as tuberculosis). Drainage has also been
suggested for cases non-responsive to medical treatment, or patients
with large chronic and recurrent effusions, to prevent potential
complications such as infection or constriction4.
Given the life-threatening consequences of cardiac tamponade, its
treatment involves immediate drainage of the pericardial fluid,
preferably by needle pericardiocentesis except in the case of purulent
pericarditis where the surgical approach is indicated5. In cases associated with acute pericarditis, the
drug choice is nonsteroidal anti-inflammatories (NSAIDs).
Glucocorticoids should be used in low doses as a second line if NSAIDS
fail, in patients with contraindications to NSAIDs, or in patients with
associated comorbidities such as renal failure, pregnancy, or systemic
inflammatory disease. 6,8. Adjunctive low-dose
colchicine helps reduce recurrence 7. Unless
pericardial tuberculosis.
Among its causes, chylopericardium is a rare entity of pericardial
effusion that can be primary (idiopathic), accounting for 3% of
non-traumatic chylothorax; and more commonly secondary to trauma,
malignancy, thoracic surgery, infection such as tuberculosis, congenital
lymphangioleiomyomatosis or lymphangiectasia, and less commonly due to
thrombosis of the vena cava or subclavian vein. Pericardial fluid
analysis usually shows a milky appearance with high triglyceride levels,
cholesterol to triglyceride ratio of less than one, lymphocytic
predominance, and negative cytology for malignancy. Clinically
chylopericardium can variate from an asymptomatic patient to signs of
cardiac tamponade. It has a documented prevalence of 0.22% and 0.5% in
post-operated pediatric patients, it is not well documented in the adult
population
Purulent effusion is usually manifested as a febrile disease that should
be managed aggressively, if untreated carries a high rate of mortality,
intravenous empiric antibiotics, and urgent drainage is
crucial5. Purulent effusions are often heavily
loculated and as such, subxiphoid pericardiotomy should be considered.
It is differentiated from chylopericardium by the neutrophilic
predominance on cellular content, significantly lower triglyceride
levels, and causative agent identified on culture. In our case, we
hypothesize that the patient had primary chylopericardium which has been
stable on multiple echocardiograms, and given her recent history of
facial trauma, oropharyngeal bacteria translocation led to hematogenous
dissemination into the pericardial sac, as no other sources of infection
were identified. Non-hematological spread, such as Ludwig Angina
(spreading to the mediastinum) was considered in the differential but
ruled out with the CT scan and physical exam.
Although lymphangiography-lymphangioscintigraphy was not performed, the
pericardial fluid analysis met all the criteria for chylopericardium.
She was initially diagnosed with pericardial effusion at age of 6,
therefore, we believe that the most probable etiology is a primary
chylopericardium. Chylopericardium is taught to be bacteriostatic in
nature and rarely is heard of being infected in non-immunocompromised
patients. To our knowledge, this would be the first time a case of
infected spontaneous chylopericardium is described. Superinfection of
this fluid, confirmed by cultures growing SDSE, caused her acute
illness.
SDSE is an emerging human pathogen closely related to Streptococcus
pyogenes. Although SDSE is regarded as less virulent, an upsurge
incidence of cases with severe clinical manifestations has been
documented 9. Given its rarity, there is no
evidence-based data to guide the management of this entity, however in
our experience, it seems to adequately respond to similar management to
purulent effusion, respondent to IV antibiotics and anti-inflammatory
agents, nevertheless, its associated outcomes and complications are yet
to be elucidated.