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.