Patient-centered structured interdisciplinary bedside rounds provide a venue for increased rounding efficiency, provider satisfaction, and consistent teaching, without impacting patient/family perception.

BackgroundTo date there are limited data in the literature to guide the initial evaluation for etiologies of apnea in full‐term infants born at greater than or equal to 37 weeks conceptional age (apnea of infancy [AOI]). Pediatricians and pediatric pulmonologists are left to pursue a broad, rather than targeted and a stepwise approach to begin diagnostic evaluation.MethodsWe performed a retrospective chart review of 101 symptomatic full‐term infants (age under 12 months) diagnosed with apnea with an inpatient multichannel pneumogram (six channels) or a fully attended overnight pediatric polysomnogram in our outpatient sleep center accredited by American Academy of Sleep Medicine (AASM), scored using the standards set forth by the AASM. The infant was diagnosed as having AOI if the apnea hypopnea index (AHI) was greater than 1 (AHI is defined as the number of apnea and hypopnea events per hour of sleep). The final diagnosis/etiology was determined based on physician clinical assessment and work up. We then determined the frequency for each diagnosis.ResultsWe found that the three most common etiologies were gastroesophageal reflux disease (GERD) (48/101), upper airway abnormalities/obstruction (37/101), and neurological diseases (19/101). There were significant numbers of infants with multiple etiologies for AOI.ConclusionBased on the frequencies obtained, pediatric practitioners caring for full‐term infants with apnea of unknown etiology are advised to begin with evaluation of more likely causes such as GERD and upper airway abnormalities/obstruction before evaluating for less common causes.

Coexistence of systemic sclerosis and sarcoidosis is rare. Both have predominant lung manifestations, each with distinctive features on computed tomography (CT) of the chest. We present herein a 52-year-old male with limited systemic sclerosis manifested primarily by sclerodactyly and subsequently by shortness of breath. A series of CT scans of the chest were reviewed. Initial CT chest one year prior to sclerodactyly onset revealed bilateral hilar and right paratracheal, prevascular, and subcarinal adenopathy. Five-year follow-up demonstrated thin-walled cysts, mediastinal lymphadenopathy, and nonspecific nodules. Due to progression of dyspnea, follow-up CT chest after one year again demonstrated multiple cysts with peripheral nodularity and subpleural nodules, but no longer with hilar or mediastinal adenopathy. Diagnostic open lung biopsy was significant for noncaseating granulomas suggestive of sarcoidosis. This is the first known case of a patient with systemic sclerosis diagnosed with sarcoidosis through lung biopsy without radiographic evidence of hilar or mediastinal lymphadenopathy at the time of biopsy. A review of cases of concomitant sarcoidosis and systemic sclerosis is discussed, including the pathophysiology of each disease with shared pathways leading to the development of both conditions in one patient.

INTRODUCTION:Mucormycosis is an opportunistic fungal infection caused by the ubiquitous filamentous fungi, Rhizomucor spp, a species of fungus associated with high mortality rates. Although it has been documented to affect every organ system, the most common sites are rhinocerberal, lungs, and skin, with dissemination in 23% of cases. Here we present a rare yet fatal case of an immunocompromised individual with confirmed pulmonary mucormycosis associated with diaphragmatic rupture.CASE PRESENTATION: 54-year-old male with history of CAD, CHF, Afib, antiphospholipid syndrome, IPF, and ESRD who initially presented with worsening shortness of breath while receiving hemodialysis. Patient was previously hospitalized two weeks prior to arrival for possible IPF flare and was discharged on short course of PO steroids. On arrival, the patient was found to have leukocytosis and airspace disease in the left lower lobe. He was admitted for suspected HCAP. His sputum culture grew normal flora and leukocytosis improved on broad spectrum antibiotics. Prednisone was also started for suspected IPF flare. On day 3, bronchoscopy with BAL was performed to r/o other opportunistic infections. On day 5, patient's respiratory status and blood pressure abruptly declined requiring intubation. CXR revealed left pneumothorax and pneumoperitoneum. Chest tube was placed and he was transferred to the ICU. CT abdomen/pelvis revealed a left pneumothorax, diaphragmatic rupture, hematoma in the left upper abdomen, moderate free intraperitoneal air, and extensive subcutaneous emphysema. At this time, BAL cultures came back positive for Rhizomucor. CT surgery was consulted for possible intervention, however, prior to initiating treatment, the patient went into PEA arrest and later expired.DISCUSSION: Upon review of the imaging and lab findings, it was determined that the patient likely swallowed a mucor spore that later proliferated in the acidic environment of the gut leading to gastric perforation, and eventually, diaphragmatic rupture; a rare complication discussed in a 2018 case report. A presumed mechanism of action proposed by prior studies has shown mucor's ability to traverse across tissue planes. CONCLUSIONS:The rapid decline in this case made it difficult for healthcare providers to respond in a timely manner. Therefore, it is important for physicians to have a high index of suspicion for mucormycosis in patients on steroids as these infections can progress rapidly if not identified and treated early in the hospital course. Case reports have shown that even on a short steroid taper mucor infections may occur.

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