End-tidal capnographic monitoring to detect apnea episodes during flexible bronchoscopy under sedation.

BACKGROUND: Apnea developing as a result of oversedation is a potential clinical problem in patients undergoing flexible bronchoscopy (FB) under sedation. However, there are no reports of evaluation using a standardized method of the frequency of occurrence of apnea episodes during FB under sedation. The aim of this study was to investigate the frequency of apnea episodes during FB under sedation in the clinical setting by end-tidal capnography. METHODS: This study was a single-institution retrospective review of a prospectively maintained database and medical records, including capnographic data, from April 2015 to March 2016. We enrolled patients who were sedated with midazolam and underwent diagnostic FB under end-tidal capnographic monitoring. Apnea was defined as cessation of airflow for more than 10 s. RESULTS: Data from a total of 121 eligible patients were analyzed. A total of 131 apnea episodes (median duration 33 s) were recorded in 59 patients (48.8%). Prolonged apnea episodes lasting for more than 30 s occurred in 24 patients (19.8%). Furthermore, 55 apnea episodes (42.0%) were followed by a decline of the SpO2 by ≥4% from the baseline. CONCLUSIONS: In this study, end-tidal capnography revealed the occurrence of apnea episodes at a high frequency in patients undergoing FB under sedation in the clinical setting.

A case presenting with rapid renal damage caused by immunoglobulin D lambda-type multiple myeloma accompanied by granular lymphocyte proliferative disorder.

A 69-year-old man was referred to our hospital for severe anemia. The atypical lymphocyte count, including granular lymphocytes, was 2,750/µL. Lymphocyte surface marker analysis showed CD3+, CD5+, CD16+, and CD56+ cells. Mixed T cell- and natural killer cell-type granular lymphocyte proliferative disorder (GLPD) was diagnosed. Because his serum creatinine levels deteriorated rapidly over the next 3 months, from 0.96 to 3.27 mg/dL, he was admitted to our hospital. The serum levels of immunoglobulins (Ig) other than IgD had decreased, and monoclonal protein was detected in the gamma-globulin region. Immunoelectrophoresis revealed IgD and lambda (λ) proteins in the serum and λ-type Bence-Jones protein in the urine. Renal biopsy examination revealed widespread tubular atrophy and interstitial fibrosis, and cast formation with λ protein deposits in tubular lumens, indicating cast nephropathy. These results indicated that the rapid renal damage was caused by IgD λ-type multiple myeloma accompanied by GLPD. The clinical course of GLPD is not usually aggressive and the findings of physical examinations are not significant. GLPD is usually associated with cytopenia (neutropenia or anemia), viral infections, collagen diseases, neoplasms such as malignant lymphoma, or chronic infections. To date, there are only 2 case reports of GLPD accompanied by multiple myeloma but without renal function or renal histological findings. When the clinical course of GLPD is aggressive and is accompanied with rapid renal damage, multiple myeloma should be considered as a complication.