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INTRODUCTION: Systemic lupus erythematosus (SLE) is a multisystemic, autoimmune connective tissue disorder, with a prevalence of 20 to 150 cases per 100,000 in the US. and estimated incidence of 1 to 25 per 100,00 in North America. Cardiac complications are common for patients with SLE, but an initial presentation with pericardial effusion is rare. CASE PRESENTATION:Our patient is a 57-year-old Hispanic female with type 2 diabetes mellitus, chronic kidney disease stage 3 and obesity, who presented with a syncopal episode at home. She was found slumped over in her chair and had difficulty speaking. Blood sugar was 35, for which she was resuscitated and transported to the nearest hospital where a full workup for syncope was done The only remarkable finding was a large pericardial effusion on transthoracic echocardiogram (TTE). She was transferred to our facility for possible pericardiocentesis. No tamponade physiology was noted at the time of transfer. During her hospitalization, she remained asymptomatic, denying chest pain, dyspnea, orthopnea, pleuritic pain, dizziness, or fatigue. She had no further syncope or hypoglycemia. TTE repeated on day 4 of hospitalization showed the same large pericardial effusion (figure 1). Bedside examination demonstrated no pulsus paradoxus or electrical alternans. She remained hemodynamically stable and pericardiocentesis was not recommended by cardiology.The etiology of the pericardial effusion was initially unclear. She had no uremia, history of viral illness, heart failure, drug abuse, or prior autoimmune disorders. An autoimmune panel revealed the following: positive ANA and doublestranded DNA antibodies. She was diagnosed with SLE and started on a combination of prednisone, mycophenolate mofetil, and hydroxychloroquine per rheumatology recommendations. She was lost to follow up after discharge. DISCUSSION:The prevalence of SLE is 10-fold higher in females versus males, and there is evidence of an overall decreasing prevalence among middle age in the last decade. Our patient's age at presentation makes her a relative oddity. No additional systemic symptoms were identified at the time and she was said to have followed up with a rheumatologist out of state. She was discharged in stable condition with follow up for further outpatient management.CONCLUSIONS: With pericardial effusions, further investigation and treatment is prudent, as this condition can result in cardiac tamponade and obstructive shock. In this case, it led to this patient's diagnosis of SLE prior to other systemic manifestations. Though transthoracic echocardiogram may indicate early tamponade physiology, bedside examination for pulsus paradoxus and electrical alternans are a clinician's best tools for evaluating for and diagnosing cardiac tamponade.

INTRODUCTION:Roughly 42 million Americans have reported trying cocaine via myriad methods in their lifetime. Since the early 2000s, spontaneous pneumomediastinum as a result of intranasal cocaine use has been demonstrated though it remains a relatively rare occurrence. Though complications such as coronary vasospasm and thrombosis may prove a greater threat to life, it should remain a part of the clinician's differential when treating a patient with a history of cocaine abuse and chest pain. CASE PRESENTATION:A healthy 20-year-old male presented with chest pain, cough, and neck pain for 3 days. He was drinking with a friend and "snorted" cocaine a few times on the same night. A few hours into the evening, he experienced a sudden, sharp retrosternal chest pain, without radiation, and exacerbated by deep breathing. He denied trauma and denied vomiting, dry heaving, gagging, or other symptoms to cause concern for GI perforation as cause, despite drinking heavily that night.On evaluation, his oxygen saturation measured 98% on room air with normal pulse, blood pressure and temperature. Physical examination revealed extensive neck and chest wall subcutaneous emphysema. Electrocardiogram demonstrated normal sinus rhythm without arrhythmias or segmental changes. CT of the chest demonstrated large amounts of air in the superior mediastinum. Based on his history, severity of presentation, and laboratory investigations, there was no concern for mediastinitis or esophageal rupture. He did not require oxygen supplementation and his pain was well controlled, so he was discharged to his home. DISCUSSION: In 1939, Louis Virgil Hamman (1877-1946 described the co-occurrence of subcutaneous emphysema with spontaneous pneumomediastinum, thus coining the term Hamman's Syndrome for this particular malady. Subcutaneous emphysema occurs primarily within the head and neck due to anatomical proximity to the airway and pneumomediastinum as a result of cocaine insufflation is thought to be due to barotrauma, with rapid changes in intrathoracic and intra-alveolar pressures as the individual snorts and performs Valsalva maneuver. Though typically self-limited, complications of spontaneous pneumomediastinum to be aware of include airway compression, pneumopericardium, and mediastinitis.CONCLUSIONS: In a case of Hamman's Syndrome without a history of illicit drug use or trauma, it is prudent to investigate other secondary causes of spontaneous pneumomediastinum, such as esophageal or tracheobronchial rupture, that can prove fatal. Particularly in young males who abuse cocaine, the astute clinician must search for underlying causes of chest pain with recent drug use: coronary artery spasm or thrombosis, arrhythmia, pneumothorax, or pneumomediastinum.