End-tidal carbon dioxide (ETCO) monitoring is useful in many situations. However, ETCO monitoring is unreliable in patients with acute respiratory distress syndrome (ARDS) due to widespread lung inflammation. In our study, we attempt to establish the gradient between the arterial pressure of carbon dioxide (PaCO) and ETCO in patients with ARDS, which we defined as the PaETCO gradient. The main objective of the study was to establish a PaETCO gradient in each severity of ARDS. We analyzed 35 patients with ARDS and a total of 88 arterial blood gases were included. PaCO, PaO/FiO and ETCO were measured. Patients were stratified into mild, moderate and severe ARDS as classified by the Berlin ARDS criteria. PaCO and ETCO were compared at each severity stratification. The mean PaCO was 50.0, the mean ETCO was 26.6 and the gradient among all samples was 23.24 (±12.02). The mean gradient for each severity is as follows: mild: 19.3 (±9.9), moderate: 27.9 (±13.2) and severe: 23.9 (±7.8). The difference between the PaETCO gradient of the mild to moderate (p=0.001) and mild to severe groups (p=0.01) reached statistical significance. However, the difference between the moderate to severe groups did not reach statistical significance (p=0.48). We found the gradient between PaCO and ETCO in patients with ARDS is vast and tends to worsen with increasing severity of ARDS. This indicates that the gradient between the 2 may be used as an indicator of increasing severity of ARDS.

Libman-Sacks endocarditis is characterized by sterile and verrucous lesions that predominantly affect the aortic and mitral valves. In most cases, patients do not have significant valvular dysfunction. However, patients with significant valvular dysfunction may present with serious complications such as cardiac failure, arrhythmias, and thromboembolic events. Recently, association of Libman-Sacks endocarditis with antiphospholipid antibody syndrome (APS) has been made. APS is most commonly defined by venous and arterial thrombosis, recurrent pregnancy loss, and thrombocytopenia. While the syndrome can be a primary syndrome, it is usually secondary to systemic lupus erythematosus. Catastrophic antiphospholipid syndrome (CAPS) can be a life-threatening presentation of APS and can occur in 1% of patients with antiphospholipid syndrome. We present a very rare case of a young female patient with lupus-negative Libman-Sacks endocarditis complicated by CAPS.

Post-transplant immunosuppression is necessary to prevent organ rejection. Immunosuppression itself can introduce complications arising from opportunistic infections. We present a case of disseminated blastomycosis manifested only as a skin lesion in an asymptomatic patient post-orthotopic heart transplantation. A 64-year-old female who had recently undergone orthotopic heart transplant for end-stage ischemic cardiomyopathy presented for a scheduled routine cardiac biopsy. The patient had no current complaints other than a crusted plaque noticed at her nasal tip. It initially manifested 6 months after surgery as a pimple that she repeatedly tried to manipulate resulting in redness and crust formation. Her immunosuppressive and prophylactic medications included: mycophenolate, tacrolimus, prednisone, bactrim, acyclovir, valganciclovir, pyrimethamine/sulfadiazine, and fluconazole. On physical examination, she was flushed, with a large and exquisitely tender crusted necrotic lesion involving almost the entire half of the nose anteriorly, the left forehead and right side of the neck. She had decreased air entry over the right lung field as well. A computed tomography (CT) image of the chest was ordered to investigate this concerning physical exam finding in the post-transplant state of this patient on immunosuppressive therapy. Chest CT revealed bilateral nodular pulmonary infiltrates with confluence in the posterior right upper lobe. Blood cultures for aerobic and anerobic organisms were negative. Both excisional biopsy of the nasal cutaneous ulcer and bronchial biopsy demonstrated numerous fungal yeast forms morphologically consistent with Blastomyces. Cultures of both specimens grew Blastomyces dermatitidis, with methicillin-resistant Staphylococcus aureus (MRSA) superinfection of the nose. She received 14 days of intravenous (IV) amphotericin B for disseminated blastomycosis and 7 days of IV vancomycin for MRSA. Her symptoms and cutaneous lesions improved and she received maintenance itraconazole treatment for 1 year. This case illustrates a delicate balance that must be struck between suppressing the immune response to prevent graft rejection and avoiding over-immunosuppression that can lead to susceptibility to infection. Thus, in any post-transplant patient, a vigorous history and physical must be performed given that infections may present without symptoms and cause grave consequences.