Jesada Kanjanaumporn

Objectives: Access to the frontal sinus after receiving angled Draf 2a frontal sinusotomy remains challenging, while adequate postoperative irrigation is essential in managing chronic inflammatory sinus disease. This study compared frontal sinus irrigation distribution between the angled Draf 2a and Carolyn's window approaches, a modification of Draf 2a which removes the nasofrontal beak by drilling to permit direct 0° endoscopic access. Methods: Fresh human cadaver heads underwent sequential dissection with angled Draf 2a followed by Carolyn's window approach. Each cavity was irrigated using a 250 mL high‐pressure squeeze bottle filled with 1/1000 10% fluorescein‐labeled water in the Frankfort horizontal position. Fluid irrigation was recorded using an endoscope placed within the frontal sinus. Blinded grading of fluid distribution was performed using a 0–4 scale: 0 (nasal cavity only), 1 (frontal recess), 2 (medial half), 3 (lateral half), and 4 (complete lavage). Scores were compared between two surgical approaches. Results: Eight cadaveric specimens (16 frontal sinuses) were evaluated. Compared with angled Draf 2a frontal sinusotomy, Carolyn's window approach achieved a greater distribution: grade 1 (50.0% vs. 0%), grade 2 (31.3% vs. 0%), grade 3 (6.3% vs. 43.8%), and grade 4 (12.5% vs. 56.3%). The median (IQR) distribution grade following angled Draf 2a frontal sinusotomy was 1.5 (1, 2), and 4 (3, 4) for the Carolyn's window approach ( p < 0.01). Conclusion: Carolyn's window significantly enhances frontal sinus irrigation compared to angled Draf 2a by improving access and distribution. This technique is robust for enhancing postoperative topical therapy in chronic frontal sinus disease. Level of Evidence: N/A.

Key Points: Defining eosinophilic chronic rhinosinusitis is crucial for treatment strategies. There is a lack of data of the cut‐point of tissue eosinophil count from real‐world study. The cut‐point of three eosinophils/high‐powered field indicates high clinical severity.

Introduction The odor identification test is an efficient and rapid way to assess and screen a patient’s sense of smell. The original Sniffin’ Sticks odor identification test (SST) consisted of 16 smells developed for a European population. However, this identification test can be influenced by cultural differences, such as variations in food culture, ethnicity and language. We propose developing a test that uses odors more familiar and specific to the Association of Southeast Asian Nations (ASEAN) population. Methods The study involved four stages: (1) A familiarity questionnaire to select odors, (2) Testing of selected odors on healthy participants from different regions, (3) Application of the developed test on healthy subjects and those with smell disorders, and (4) Test-retest reliability assessment. A total of 466 participants aged 16 to 87 years were involved across all stages. The final ASEAN Sniffin’ Sticks odor identification test (ASST) was conducted on 106 healthy subjects (HS) and 68 subjects with smell disorders, including 29 with Parkinson’s disease (PD) and 39 with sinonasal diseases (Ear, Nose, and Throat [ENT]). Results Mean scores of 15.75 ± 0.62 were found in the HS group, 9.07 ± 3.67 in the PD group, and 10.90 ± 4.87 in the ENT group, out of a total possible score of 16. The 10th percentile value (score of 15) in HS aged 17–35 was used as cutoff between normal olfaction from those with a smell disorder. There were significant differences between the HS group and both the PD and ENT groups (p < 0.001), but no significant difference was found between the PD and ENT groups (p = 0.068). The ASST demonstrated high test-retest reliability, with a correlation (r) = 0.92 (p < 0.001). Conclusion The ASST provides a reliable tool for evaluating olfactory function and detecting olfactory loss associated with various conditions in the ASEAN region.

Background: Acute invasive fungal rhinosinusitis (AIFR) is a life-threatening disease mainly affecting immunocompromised patients. Early detection is therefore key to improving patient survival. To date, there are still no standard clinical criteria for AIFR diagnosis. Objective: This study develops a predictive model that utilizes clinical presentation and computed tomography (CT) findings to diagnose AIFR. Methods: A retrospective cohort study was conducted on patients with high risk for AIFR at King Chulalongkorn Memorial Hospital over the past 15 years (2008-2022). We constructed several multivariate logistic regression models for AIFR diagnosis based on different subsets of variables from 3 categories: signs/symptoms, endoscopy, and CT imaging. Results: There were 67 AIFR-positive patients and 68 AIFR-negative patients. Combining variables from 3 categories, a 6-variable model (fever, visual loss, mucosal discoloration, crusting, mucosal loss of contrast, retroantral fat stranding) achieved the highest area under the receiver operating characteristic curve of 0.8900 (74.63% sensitivity, 89.71% specificity). Conclusions: We proposed predictive models for AIFR diagnosis in high-risk patients using clinical variables. The models can be used to guide the decision for further management such as biopsy or surgical intervention.

The effects of low-dose macrolide (LDM) therapy on pediatric chronic rhinosinusitis (CRS) patients are unknown. This study aimed to assess the effectiveness of LDM for treating pediatric refractory CRS. A retrospective study was conducted by a medical chart review. Pediatric CRS patients (age <15 years) who received LDM after standard medical treatments failure between 2013 and 2019 were identified. The LDM treatments with any macrolide agents, doses, and regimens were included. Any co-interventions were allowed. Duration of the LDM therapy was ≥6 weeks. Outcomes were the total nasal symptoms by the visual analogue scale (TNS), presence of individual symptoms, physician-assessment nasal discharge and adverse events. Six patients (67% male, mean age 7±3.4 years) were assessed. All patients had failed to intranasal steroids and nasal saline irrigation but continued. The addition of LDM significantly improved TNS (mean difference ± standard deviation 5.83 ± 1.33; 95% confidence interval 4.44–7.23, p< 0.001). At the end of treatment, the numbers of patients with individual symptoms were decreased: nasal obstruction (100%–67%), rhinorrhea (83%–50%), hyposmia (50%–0%), cough (100%–33%), and physician-assessment thick mucoid discharge (33%–0%). No patients had facial pain. One patient reported mild tolerable nausea. Preliminary findings of this study showed some beneficial effects of LDM added to intranasal steroids and nasal saline irrigation in pediatric CRS after standard treatments failure. The beneficial effects included the improvements of the TNS and individual nasal symptoms and decrease in thick mucoid discharge.

Background Non‐allergic rhinitis is defined as dysfunction and non‐infectious inflammation of the nasal mucosa that is caused by provoking agents other than allergens or microbes. It is common, with an estimated prevalence of around 10% to 20%. Patients experience symptoms of nasal obstruction, anterior rhinorrhoea/post‐nasal drip and sneezing. Several subgroups of non‐allergic rhinitis can be distinguished, depending on the trigger responsible for symptoms; these include occupation, cigarette smoke, hormones, medication, food and age. On a cellular molecular level different disease mechanisms can also be identified. People with non‐allergic rhinitis often lack an effective treatment as a result of poor understanding and lack of recognition of the underlying disease mechanism. Intranasal corticosteroids are one of the most common types of medication prescribed in patients with rhinitis or rhinosinusitis symptoms, including those with non‐allergic rhinitis. However, it is unclear whether intranasal corticosteroids are truly effective in these patients. Objectives To assess the effects of intranasal corticosteroids in the management of non‐allergic rhinitis. Search methods The Cochrane ENT Information Specialist searched the Cochrane ENT Register; Cochrane Central Register of Controlled Trials (CENTRAL 2019, Issue 7); PubMed; Ovid Embase; CINAHL; Web of Science; ClinicalTrials.gov; ICTRP and additional sources for published and unpublished trials. The date of the search was 1 July 2019. Selection criteria Randomised controlled trials (RCTs) comparing intranasal corticosteroids, delivered by any means and in any volume, with (a) placebo/no intervention or (b) other active treatments in adults and children (aged ≥ 12 years). Data collection and analysis We used the standard methodological procedures expected by Cochrane. The primary outcomes were patient‐reported disease severity and a significant adverse effect ‐ epistaxis. Secondary outcomes were (disease‐specific) health‐related quality of life, objective measurements of airflow and other adverse events. We used GRADE to assess the certainty of the evidence for each outcome. Main results We included 34 studies (4452 participants); however, only 13 studies provided data for our main comparison, intranasal corticosteroids versus placebo. The participants were mainly defined as patients with perennial rhinitis symptoms and negative allergy tests. No distinction between different pheno‐ and endotypes could be made, although a few studies only included a specific phenotype such as pregnancy rhinitis, vasomotor rhinitis, rhinitis medicamentosa or senile rhinitis. Most studies were conducted in a secondary or tertiary healthcare setting. No studies reported outcomes beyond three months follow‐up. Intranasal corticosteroid dosage in the review ranged from 50 µg to 2000 µg daily. Intranasal corticosteroids versus placebo Thirteen studies (2045 participants) provided data for this comparison. These studies used different scoring systems for patient‐reported disease severity, so we pooled the data in each analysis using the standardised mean difference (SMD). Intranasal corticosteroid treatment may improve patient‐reported disease severity as measured by total nasal symptom score compared with placebo at up to four weeks (SMD ‐0.74, 95% confidence interval (CI) ‐1.15 to ‐0.33; 4 studies; 131 participants; I² = 22%) (low‐certainty evidence). However, between four weeks and three months the evidence is very uncertain (SMD ‐0.24, 95% CI ‐0.67 to 0.20; 3 studies; 85 participants; I² = 0%) (very low‐certainty evidence). Intranasal corticosteroid treatment may slightly improve patient‐reported disease severity as measured by total nasal symptom score change from baseline when compared with placebo at up to four weeks (SMD ‐0.15, 95% CI ‐0.25 to ‐0.05; 4 studies; 1465 participants; I² = 35%) (low‐certainty evidence). All four studies evaluating the risk of epistaxis showed that there is probably a higher risk in the intranasal corticosteroids group (65 per 1000) compared to placebo (31 per 1000) (risk ratio (RR) 2.10, 95% CI 1.24 to 3.57; 4 studies; 1174 participants; I² = 0%) (moderate‐certainty evidence). The absolute risk difference (RD) was 0.04 with a number needed to treat for an additional harmful outcome (NNTH) of 25 (95% CI 16.7 to 100). Only one study reported numerical data for quality of life. It did report a higher quality of life score in the intranasal corticosteroids group (152.3 versus 145.6; SF‐12v2 range 0 to 800); however, this disappeared at longer‐term follow‐up (148.4 versus 145.6) (low‐certainty evidence). Only two studies provided data for the outcome objective measurements of airflow. These data could not be pooled because they used different methods of outcome measurement. Neither found a significant difference between the intranasal corticosteroids and placebo group (rhinomanometry SMD ‐0.46, 95% CI ‐1.06 to 0.14; 44 participants; peak expiratory flow rate SMD 0.78, 95% CI ‐0.47 to 2.03; 11 participants) (very low‐certainty evidence). Intranasal corticosteroids probably resulted in little or no difference in the risk of other adverse events compared to placebo (RR 0.99, 95% CI 0.87 to 1.12; 3 studies; 1130 participants; I² = 0%) (moderate‐certainty evidence). Intranasal corticosteroids versus other treatments Only one or a few studies assessed each of the other comparisons (intranasal corticosteroids versus saline irrigation, intranasal antihistamine, capsaicin, cromoglycate sodium, ipratropium bromide, intranasal corticosteroids combined with intranasal antihistamine, intranasal corticosteroids combined with intranasal antihistamine and intranasal corticosteroids with saline compared to saline alone). It is therefore uncertain whether there are differences between intranasal corticosteroids and other active treatments for any of the outcomes reported. Authors' conclusions Overall, the certainty of the evidence for most outcomes in this review was low or very low. It is unclear whether intranasal corticosteroids reduce patient‐reported disease severity in non‐allergic rhinitis patients compared with placebo when measured at up to three months. However, intranasal corticosteroids probably have a higher risk of the adverse effect epistaxis. There are very few studies comparing intranasal corticosteroids to other treatment modalities making it difficult to draw conclusions.

Background: Local allergic rhinitis (LAR) is characterized by chronic rhinitis with localized nasal allergic response to allergens in the absence of systemic immunoglobulin (IgE)-mediated disease assessed by skin prick test (SPT) or specific serum IgE level. Nasal provocation test (NPT) is the gold standard for the diagnosis of LAR. Nasal eosinophilia is a known inflammatory marker in allergic rhinitis. We hypothesized that nasal eosinophilia can be used as a screening tool for LAR. Objective: To determine the applicability of nasal eosinophilia as a diagnostic tool for LAR. Methods: Forty-eight perennial nonallergic rhinitis (NAR) patients with SPT negative were recruited. Nasal cytology analysis was performed. NPTs with 3 allergens (mixed mites, mixed cockroaches, and Bermuda grass) were performed to diagnose LAR. Nasal symptoms combined with nasal patency were used to determine the results of NPT. The sensitivity, specificity, positive predictive value, and negative predictive value of nasal eosinophilia as a diagnostic tool of LAR were calculated. Results: LAR was diagnosed in 41.6% of the NAR patients. Nasal eosinophilia was found in 58% of the NAR patients. The sensitivity of nasal eosinophilia for diagnosing LAR was 80%, the specificity was 57.14%, the positive predictive value was 57.14%, and the negative predictive value was 80%. The most common allergen of LAR was mixed mites. Conclusion: Nasal eosinophilia on nasal cytology was a good screening tool for diagnosing LAR because of its high sensitivity and simplicity of the procedure. Unfortunately, the low specificity of nasal eosinophilia makes the NPT necessary for confirmation of LAR.

Background: This study aims to compare histopathology of nasal polyp and ethmoid mucosa for diagnosing eosinophilic mucin rhinosinusitis (EMRS). Methodology: Patients with chronic rhinosinusitis with polyps (CRSwNP) were enrolled. Using eosinophilic mucin as a reference, histopathology of polyp apex, polyp pedicle and ethmoid mucosa was compared for density of tissue eosinophil and sensitivity for diagnosing EMRS. Associations with asthma were assessed for each site. Results: Thirty patients with CRSwNP were enrolled. When polyp apex, polyp pedicle and ethmoid mucosa were assessed for tissue eosinophilia, consistent results were reported in 16 patients (53%). Median tissue eosinophil was greater in polyp apex (58, IQR: 7-100) than ethmoid mucosa (10, IQR: 2-21), but not different from polyp pedicle (22, IQR: 1-96). Sensitivity for diagnosing EMRS were 100% (95% CI: 47.8-100) for polyp apex, 60% (95% CI: 14.7-94.7) for polyp pedicle, 80% (95% CI: 28.4-99.5) for ethmoid mucosa. Associations with asthma were significant for polyp pedicle, and ethmoid mucosa but not polyp apex. Conclusion: Density of tissue eosinophil was greater in nasal polyp than in ethmoid mucosa. Histopathology of polyp apex had good sensitivity for diagnosing EMRS. Polyp pedicle and ethmoid mucosal eosinophilia associated with asthma.