Hypothyroidism is a well-known cause of pericardial effusion with an incidence of about 3-27%. If not diagnosed in time it can lead to potentially serious complications, such as cardiac tamponade leading to hemodynamic instability. It should be considered as a causative or exacerbating agent in any patient presenting with pericardial effusion and known, suspected or laboratory evidence of hypothyroidism, e. g., elevated TSH or reduced serum free T4. We present a case of a 50-year-old woman with a Past Medical Hx of hypertension, intermittently insulin-treated type 2 diabetes for 20 years, coronary artery disease, and hypothyroidism with medical non-compliance, and s/p right BKA. She initially presented to an outside hospital for altered mental status (specifically, inability to follow simple commands and orientation only to self). She was transferred to this facility for evaluation of limb ischemia. She was agoitrous with no reported palpable thyroid abnormalities. Her admission chest x-ray exhibitedan enlarged cardiac silhouette. Her initial serology was significant for a serum TSH of 178 uIU/mL (NL: 0.45-5.33 uIU/mL), FreeT4 <0.25 ng/dl (NL: 0.58-1.64 ng/dl),Free T3 1.65 pg/mL (NL: 2.5-3.9 pg/mL), andhighly elevated anti-thyroglobulin and anti-peroxidase antibodies. She was diagnosed as having primary hypothyroidism secondary to Hashimoto's thyroiditis. She was re-started on levothyroxine (L-T4) at a dose of 150 mcg on day 1, which was reduced to 100 mcg daily on days 2-4 but readjusted to 125 mcg daily on days 5-8 and 150 mcg daily thereafter. During the 25 th day of admission in the Rehabilitation unither serum TSH showed a gradual decline from 178 to 22 prior to discharge. Her Free T4 increased to 1.18 and her Free T3 increased to 2.24 by discharge. Her pericardial effusion was managed by placement of a pericardial window. Pericardiocentesis yielded over 600 ml of clear serous fluid (protein content 5.1 gm/dl) without evidence of malignancy, infection or inflammation. This case highlights the importance of not only recognizing the diagnosis of hypothyroidism but of assessing the duration and adequacy of its management. Likewise, an enlarged cardiac silhouette in this setting should be considered as possibly representing a pericardial effusion and impending source of a cardiac tamponade. Presentation: No date and time listed
Introduction: Spontaneous coronary artery dissection (SCAD) is a rare condition; an intimal tear or bleeding of vasa vasorum leads to the creation of a false lumen filled with intramural hematoma. The hematoma causes coronary stenosis, leading to subsequent myocardial ischemia. SCAD is the cause of Acute Coronary Syndrome (ACS) in 0.1 to 4% of cases. Men account for less than 10% of cases, with a mean age of 48.6. Case Study: A 19-year-old male with prior medical history of morbid obesity and marijuana use was transferred from another hospital to our service after presenting with non-ST elevation MI. He was admitted following 30 minutes of a throbbing/pressure-like sensation in his throat, one episode of vomiting, and paresthesia in his left arm that spontaneously resolved. Initial EKG showed sinus rhythm with early repolarization changes. His troponin rose from 0.2 to 18 ng/mL. Upon admission, his high sensitivity troponin peaked at 15,000 pg/mL. Repeat EKG showed dynamic changes with T wave inversions in the inferolateral leads. The patient underwent an angiogram showing a diffuse, mid-LAD 40% de novo spontaneous dissection and a diffuse, distal-LAD 20% de novo spontaneous dissection with TIMI grade 3 and 2 flow, respectively. A repeat angiogram two days later showed improved coronary artery flow and deemed a low-risk lesion with stable patient hemodynamics; no intervention followed. The patient was treated conservatively with DAPT and discharged home with an outpatient Cardiology follow-up. A plan to have further imaging in 4 weeks to assess hematoma resolution was made. Conclusions: This case demonstrates an atypical presentation of SCAD in a very low-risk patient, given his sex, age, and clinical presentation of nonspecific chest pain. This case highlights the importance of high clinical suspicion for SCAD regardless of ACS risk profile in a patient presenting with chest pain.
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