A rare pulmonary manifestation of Crohn's disease: Acute fibrinous and organizing pneumonia presenting as multifocal nodules.

Acute Fibrinous and Organizing Pneumonia (AFOP) is a rare pulmonary disease, and it has not been recorded in literature as a pulmonary manifestation of Crohn's disease. A 22-year-old individual with an extensive history of Crohn's disease presented to the hospital initially for hematochezia and diarrhea. Computed tomography of her abdomen and pelvis showed multiple pulmonary nodules bilaterally. The patient did not report cough, sputum production, or dyspnea. Autoimmune and infectious workup were overall unremarkable. A CT-guided percutaneous biopsy of a peripheral lung nodule was performed showing features consistent with AFOP. The patient was ultimately treated with a long taper of prednisone and Ustekinumab for Crohn's disease. Follow-up CT-chest showed interval reduction and improvement in lung nodules, which correlated with better control of the patient's Crohn's disease. Pulmonary manifestations of IBD are varied, including pleural disease, bronchiectasis, and organizing pneumonia. Bronchiolitis obliterans organizing pneumonia has been described more frequently in patients with ulcerative colitis compared to Crohn's. Pulmonary nodules are a rare manifestation of IBD and often tend to be granulomatous or necrobiotic. AFOP is a rare entity with no previously reported association with IBD. Secondary AFOP can be caused by autoimmune diseases, drug reactions, infections, or radiation. Treatment of AFOP is usually immunosuppression by glucocorticoids.

Autopsy study of fatal invasive pulmonary aspergillosis: Often undiagnosed premortem.

Invasive aspergillosis (IA) is a serious complication in immunocompromised and critically ill patients but is difficult to diagnose. We sought to examine how often cases go undiagnosed and to understand the presenting clinical and radiologic features associated with fatal IA. We reviewed cases of fatal IA confirmed at autopsy (N = 67) between 1999 and 2019 at a tertiary academic hospital. At autopsy, pulmonary involvement was present in 97% of cases--46% were limited to the lungs and 51% had concomitant extrapulmonary involvement. Immunosuppression with either glucocorticoids and/or other immunosuppressive agents was present in 85%. Among those not immunocompromised (15%), chronic lung disease was present in 70%, and a respiratory coinfection was found in 50%. Chest imaging abnormalities including consolidation, ground glass opacities, halo sign, cavitation, and air crescent sign were present in 49%, 49%, 37%, 22%, and 7% of cases, respectively. Diagnostic bronchoscopy was performed in 61% of cases and yielded aspergillus in 63% of those cases by either bronchoalveolar lavage (galactomannan and/or culture), bronchial washings, or transbronchial biopsy cultures. Either a respiratory coinfection or other systemic coinfection was diagnosed in 64%. The performance of diagnostic bronchoscopy was associated with accurate pre-mortem identification of IA (p = 0.001). Clinicians correctly identified IA as the cause of death in only 27% of fatal IA cases identified at autopsy. Complex presenting features, high rates of co-infections, and low rates of invasive diagnostic procedures may have led to missed diagnoses of IA.

Myocardial Infarction and Cardiac Arrest in a Patient With Severe Undiagnosed Hypothyroidism During Bronchoscopy.

Thyroid hormones have an integral role in cardiac homeostasis, and hypothyroidism may be associated with impaired myocardial contractility, altered endothelial function, and blunted response to catecholamines. Herein, the case of a patient with undiagnosed severe hypothyroidism, who developed an acute myocardial infarction and cardiac arrest during sedation for bronchoscopy, is described. He required prolonged resuscitation, which included coronary catheterization and placement of an intra-aortic balloon pump. The resuscitation was noteworthy for blunted physiologic responses to large doses of epinephrine; in particular, persistent bradycardia without evidence of conduction abnormalities. On admission to the intensive care unit, he was hypothermic (31.4°C), bradycardic, and hypotensive. Laboratory investigations revealed profound hypothyroidism, and thyroid hormone replacement was initiated. Within hours of initiation of thyroid hormone replacement, the need for vasopressor support was reduced. He had a complete recovery and was discharged home neurologically intact. The authors of the present report believe that this favorable neurologic outcome could be attributed to efficient resuscitation, prompt coronary revascularization, and profound hypothermia likely related to a hypothyroidism-associated hypometabolic state.