Polysomnographic outcomes of revision adenoidectomy in children with obstructive sleep apnea and recurrent/residual adenoidal hypertrophy.

INTRODUCTION: Recurrent/residual adenoidal hypertrophy after adenotonsillectomy in children can result in obstructive sleep apnea (OSA). We aimed to assess the polysomnographic (PSG) outcomes of revision adenoidectomy in children with recurrent/residual adenoidal hypertrophy and OSA. METHODS: This was a single-center retrospective study that included children with sleep studies that confirmed OSA and known history of adenotonsillectomy who were diagnosed with adenoidal hypertrophy and subsequently underwent revision adenoidectomy. Pre- and postoperative PSG variables of revision adenoidectomy were included in the analysis. RESULTS: A total of 20 children were included in the study. The cohort included 13 males and 7 females with a mean age of 7.8 years (± 3.6 years). The mean BMI z score was 1.96 [1.31, 2.43]. The median duration from adenotonsillectomy performance was 2.3 years [1.4, 4.0]. Overall, revision adenoidectomy resulted in significant improvements in multiple respiratory parameters, including AHI 6.6 [1.4, 13. 7] vs 14.8 [7.4, 20.7], p = 0.02; oxygen desaturations nadir 88.0 [84.0, 93.0] vs 80.0 [72.2, 88.9], p = 0.01; supine AHI 8.6 [1.5, 14.3] vs 17.6 [8.3, 30.2], p = 0.02; and arousal index 12.2 [9.6, 15.7] vs 18.9 [13.4, 24.9], p = 0.04. CONCLUSIONS: Children with recurrent/residual adenoidal hypertrophy after adenotonsillectomy who undergo revision adenoidectomy experience improvements in respiratory event, gas exchange, and arousal index.

Role of neck radiography in assessing recurrent/residual adenoid hypertrophy in children with OSA and history of adenotonsillectomy: a sleep physician perspective.

STUDY OBJECTIVES: Recurrent/residual adenoid hypertrophy after adenotonsillectomy in children can result in obstructive sleep apnea (OSA). We aimed to assess the role of soft tissue neck X-ray (STN-XR) in evaluating recurrent/residual adenoid tissue hypertrophy. METHODS: This was a single-center retrospective study that included children with sleep study-confirmed OSA and a known history of adenotonsillectomy who underwent STN-XR to evaluate for recurrent/residual adenoid tissue hypertrophy. STN-XR nasopharyngeal obliteration and baseline polysomnographic data were analyzed. Multiple linear regression was used to assess the independent relationship between the results of STN-XR and the total apnea-hypopnea index, while controlling for relevant characteristics. RESULTS: The study included 160 participants with a median age of 10 years (quartile [Q] 1 = 7, Q3 = 12.25). More than half of the children were male (59.4%) and the median body mass index z-score was 2.11 (Q1 = 1.23, Q3 = 2.54). STN-XR was normal in 39.4%, and it showed mild, moderate, and complete nasopharyngeal obliteration in 20.6%, 32.5%, and 7.5% of the participants, respectively. Multiple regression analysis showed that moderate and complete nasopharyngeal obliteration was associated with an increase in the mean total apnea-hypopnea index by 109% (P = .0002) and 185% (P = .001), respectively, when compared with children without nasopharyngeal obliteration. However, mild nasopharyngeal obliteration, body mass index z-score, age, sex, and race were not significantly associated with an increase in the total apnea-hypopnea index. CONCLUSIONS: STN-XR was useful in assessing recurrent/residual adenoid tissue hypertrophy in children with OSA and a history of adenotonsillectomy. Moderate and complete nasopharyngeal obliteration were associated with significantly increased apnea-hypopnea index. Pediatric sleep physicians may consider STN-XR in the evaluation of children with OSA and previous history of adenotonsillectomy. CITATION: Senthilvel E, Nguyen QL, Gunaratnam B, Feygin YB, Palani R, El-Kersh K. Role of neck radiography in assessing recurrent/residual adenoid hypertrophy in children with OSA and history of adenotonsillectomy: a sleep physician perspective. J Clin Sleep Med. 2023;19(6):1027-1033.

Fat Embolism Syndrome With Cerebral Involvement: An Underrecognized Complication of Long Bone Fractures.

Fat embolism syndrome (FES) occurs when fat particles are aberrantly distributed into the microcirculation, and it often manifests as either hypoxemia, neurological deficit, or petechial rash. Although cases have been reported in the literature since the twentieth century, no formal diagnostic criteria have been universally adopted, and FES remains a diagnostic challenge. We present a unique case of FES from a long bone fracture, leading to pulmonary embolism with paradoxical arterial embolization and cerebral infarction, and provide a review of the related literature.

Thiosemicarbazone-Modified Cellulose: Synthesis, Characterization, and Adsorption Studies on Cu(II) Removal.

Thiosemicarbazide-modified cellulose (MTC) has been studied for removing heavy metals in the water source or for extracting some precious metals. The conditions of synthesis of MTC and Cu(II) removal were optimized by single-variable analysis through oxidation-reduction on titration and photometry. The results of Fourier-transform infrared spectroscopy, Brunauer-Emmett-Teller, and thermogravimetric analyses show that MTC exists in the thioketone form with a high surface area and heat durability. The Cu(II) removal was of pseudo-second order and the isotherm equation correlated best with the Langmuir equation. MTC has the maximum capacity of adsorption, which is q m = 106.3829 mg g-1. Furthermore, MTC can be regenerated without the loss of adsorption efficiency after ten cycles of adsorption and desorption.

Complement-coated antibody-transfer (CCAT); serum IgA1 antibodies intercept and transport C4 and C3 fragments and preserve IgG1 deployment (PGD).

In periodontal disease, IgG1 and IgA1 antibodies produced in situ deposit on antigens in the affected tissues. Thus, there is an interest in the effect of co-deposited IgA1 antibodies on complement activation by IgG1-immune complexes. In the present study, we first analyzed the effect of IgA1-immune complexes on complement using human IgA1 antibodies to dansyl (with dansylated human serum albumin serving as the immobilized antigen). It was observed that these IgA1-immune complexes when incubated for prolonged times with 33% human serum as a source of complement received C4b and C3b deposition. As C4b and C3b deposited on the IgA1 antibodies and on the antigenic surface, the complement-coated IgA1 antibodies departed. These fluid-phase complement-coated IgA1 antibodies were transferred to antigen-coated microtiter-ELISA plates, where they became bound to the antigens. Thus, the complement-coated IgA1 antibodies retained their antigen-binding function, especially as a proportion of their covalently bound C3b progressively degraded to iC3b and C3d. Genetically engineered carbohydrate-deficient mutant human IgA1 antibodies were used to assess the role of carbohydrate in accepting the C4b and C3b depositions, and these studies indicated that the carbohydrate on the Fc-region of IgA1 played a positive role. Another interesting finding generated by this study was that when IgA1 was co-deposited with IgG1 antibodies, and serum complement was added, the IgG1 antibodies tended to remain on the antigenic surface. The co-deposited IgA1 antibodies not only controlled (reduced) the rate of the consumption of the first component of complement (C1) and of classical complement pathway activation by IgG1-immune complexes (and therein reduced the rate of complement-mediated dissolution of the IgG1-immune complexes), but also the co-deposited IgA1 antibodies simultaneously intercepted/accepted C4b and C3b, then departed, as complement began to cover the antigenic surfaces. The process in which complement-coated IgA1 antibodies transferred to non-complement-coated antigens is termed complement-coated antibody-transfer/transport (CCAT). In this way, IgA1 antibodies extended the efficiency of the complement system by insuring the specific IgA1 antibody-mediated transport of the captured biologically active complement fragments to those antigens stimulating the IgA1 antibody response but not yet neutralized (completely coated) with complement. Simultaneously by impeding the rate of C1 consumption and by intercepting C4b and C3b, IgA1 antibodies slowed C4b and C3b deposition on the antigenic surface and on the co-deposited IgG1 antibodies. Thus, in the presence of ongoing complement activation, the deposition of serum IgA1 antibodies enabled the co-deposited IgG1 antibodies to better maintain their ability to interact with antigens. We termed this latter phenomenon, preservation of IgG antibody deployment (PGD). In summary, co-deposited IgA1 antibodies maximized the efficiency of the complement system, transported their covalently bound complement fragments to specific antigens and sustained the effective deployment of IgG1 antibodies directed to those same antigens.