A relationship between lung scarring and cancer has been recognized for many decades but more evidence is needed to strengthen this association. A 34-year-old nonsmoker male with a history of left lower lobe lung scar secondary to a pulmonary contusion from a motor vehicle accident in 2012 was admitted with shortness of breath and cough. A computed tomography (CT) angiography of the chest demonstrated bilateral pulmonary emboli, left lower lobe mass, left lung septal thickening, and mediastinal lymphadenopathy. A CT-guided biopsy of the mass was performed, and pathology was consistent with lung adenocarcinoma. Staging work-up revealed a widely metastatic disease. The patient developed severe complications requiring hospitalization after the first cycle of chemotherapy and subsequently passed away. Lung scar carcinoma originates around peripheral scars resulting from a variety of infections, injuries, and lung diseases. It has poor prognosis because it metastasizes from relatively small lesions. Our case further endorses that lung scarring can potentially lead to the development of cancer. Furthermore, we want to highlight the need to conduct studies to determine if monitoring this patient population with periodic imaging can have a survival benefit.

A 40-year-old female presented to a rural hospital with crushing substernal chest pain. An initial electrocardiogram showed ST elevation in lead II and aVF with elevated troponin I. She was immediately transferred to a tertiary care hospital. An emergent coronary angiogram did not show any significant coronary artery disease. On the second day, the patient experienced recurrence of severe chest pain with ST elevations in leads I, aVL, V5-V6, ST depressions in V1-V3, T-wave inversion over V2-V5. The troponin I level increased to > 40 ng/ml (normal 0.0 to 0.04 ng/ml). An emergent angiogram was performed revealing local dissection of the mid to distal left main coronary artery and a totally occluded diagonal artery. It was deemed unsafe to perform percutaneous coronary intervention because it was a non-flow limiting left main coronary artery dissection and was difficult to cannulate with the guide catheter. Subsequently, an elective angiogram was performed after a 48-hour interval to evaluate the progression of dissection and to make a definitive decision for revascularization versus medical management. On the third angiogram, stenosis seen in the diagonal branch on the previous angiogram progressed to dissection, and local dissection of the left main coronary artery seen on the previous angiogram spontaneously resolved. The patient was symptom-free and hemodynamically stable. It was decided to manage the patient conservatively due to the spontaneous resolution of occlusion in the diagonal artery and dissection of the left main coronary artery. The patient was started on conservative medical treatment. A magnetic resonance angiography of the right internal carotid artery revealed a “string of beads” appearance, which confirmed the diagnosis of fibromuscular dysplasia. She was followed closely in the clinic and has remained asymptomatic for the past one year.

Prekallikrein (PK) deficiency is extremely rare, and manifestations are not well characterized due to a small number of cases reported and the lack of scientific clarity about its role in clot formation in vivo. Here, we report a case of a 64-year-old male, with no known history of abnormal bleeding, who scheduled to undergo deep brain stimulator placement for control of his Parkinson's disease. During pre-procedure testing, activated partial thromboplastin time (PTT) was found to be prolonged at 146 seconds. Mixing studies were suggestive of a coagulation factor deficiency. His PTT characteristically became shorter with prolonged incubation, providing a clue at testing for PK levels, which were found to be severely low. He, subsequently, underwent surgery without any complications. Our case further highlights the clinical pearls for diagnosis and further endorses that these patients can safely undergo surgical procedures without the need for plasma transfusions or factor concentrate usage.

A 34-year-old female with a past medical history of systemic lupus erythematosus (SLE) and a deep venous thrombosis experienced substernal chest pain for 24 hours. Her physical exam was remarkable for brown macular rash over the face. Her initial electrocardiogram showed ST depression in lead V3–V6 along with an elevated troponin I level of 1.23 ng/dl (normal 0.0–0.4) that increased to 2.33 ng/dl in a four-hour duration. Cardiac catheterization revealed mild 10–20% focal plaque in the mid left anterior descending artery and otherwise normal coronary arteries. Laboratory data revealed an erythrocyte sedimentation rate of 98 mm/hour (normal 1–20), C-reactive protein of 25 mg/L (normal 0.0–2.9), and positive antinuclear antibody. In the absence of a significant coronary atherosclerosis along with elevated inflammatory markers, inflammation of coronary microcirculation was considered as an underlying pathophysiology of myocardial infarction. The patient was started on immunosuppression therapy with hydroxychloroquine and prednisone. Her chest pain improved and she was discharged in a stable condition. The patient remained stable and symptom-free over a follow-up period of nine months.