Topical Pharyngeal Anesthesia in Sedated Pediatric Patients Undergoing Esophagogastroduodenoscopy.

OBJECTIVES: Pediatric patients undergoing esophagogastroduodenoscopy (EGD) commonly receive procedural sedation for comfort and to facilitate the procedure. EGD with procedural sedation carries the risk of several airway incidents and/or adverse events (AIAE). Topical pharyngeal anesthetics (TPAs) can blunt the airway reflexes and decrease the incidence of laryngospasm but has not been well studied with EGD under procedural sedation. We aimed to study the effect of adding a TPA to propofol-based sedation on the rate of AIAE. METHODS: This is a single-center, retrospective, observational cohort study. We compare AIAE rates (coughing, gagging, apnea, airway obstruction, and laryngospasm) in children who received TPA as part of their propofol-based procedural sedation for EGD with those who did not receive TPA. RESULTS: In 2021, 73 patients received TPA as part of the procedural sedation for EGD and 123 did not. The overall rate of AIAE was high with 75 (38%) patients experiencing 1 or more AIAE. Patients who received benzocaine spray experienced more AIAE than the control group [adjusted odds ratio (aOR) = 1.16; 95% confidence interval (CI): 1.01-1.34; P = 0.037]. Coughing, gagging, apnea with desaturation rates, and laryngospasm were similar in both groups (coughing aOR = 1.01; 95% CI: 0.91-1.13; P = 0.814; gagging aOR = 1.01; 95% CI: 0.91-1.13; P = 0.814; apnea aOR = 0.99; 95% CI: 0.95-1.04; P = 0.688; laryngospasm OR = 1.01; 95% CI: 0.95-1.07; P = 0.71). The rate of airway obstruction requiring jaw thrust was higher in the benzocaine group but did not reach statistical significance (aOR = 1.11; 95% CI: 0.97-1.26; P = 0.133). CONCLUSION: The use of topical pharyngeal benzocaine in children undergoing EGD with propofol-based sedation is associated with a higher overall AIAE rate. Most of the AIAE were mild incidents and only 7 patients experienced true adverse events.

Decreasing the Incidence of Hypoxia and Airway Maneuvers During GI Procedures.

Many outpatient gastrointestinal procedures are completed with propofol anesthesia. A side effect of propofol is airway obstruction and subsequent hypoxia. This study was designed to determine whether the use of a high-flow nasal cannula is associated with a decreased incidence of hypoxia or airway obstruction in patients undergoing propofol sedation in the gastrointestinal laboratory with a STOP-BANG score ≥5. High-flow nasal cannula was administered at 70 L/min on 27 patients with a STOP-BANG score ≥5 receiving monitored anesthesia care sedation for an esophagogastroduodenoscopy, endoscopic ultrasound, or colonoscopy procedure. Patients were compared to a group from a previous project without the use of high-flow nasal cannula assessing whether hypoxia, apnea, or the need for airway maneuvers occurred. The non-high-flow nasal cannula group required an airway maneuver 53.3% (n = 8) whereas the high-flow nasal cannula group required an airway maneuver 18.5% (n = 5) (p = .021). High-flow nasal cannula was associated with a reduced need for airway maneuvers in patients with a high risk of obstructive sleep apnea undergoing propofol-assisted procedures.

Propofol versus dexmedetomidine during drug-induced sleep endoscopy (DISE) for pediatric obstructive sleep apnea.

PURPOSE: To test for differences in DISE findings in children sedated with propofol versus dexmedetomidine. We hypothesized that the frequency of ≥ 50% obstruction would be higher for the propofol than dexmedetomidine group at the dynamic levels of the airway (velum, lateral walls, tongue base, and supraglottis) but not at the more static adenoid level. METHODS: A single-center retrospective review was performed on children age 1-18 years with a diagnosis of sleep disordered breathing or obstructive sleep apnea (OSA) who underwent DISE from July 2014 to Feb 2019 scored by the Chan-Parikh scale sedated with either propofol or dexmedetomidine (with or without ketamine). Logistic regression was used to test for a difference in the odds of ≥ 50% obstruction (Chan-Parikh score ≥ 2) at each airway level with the use of dexmedetomidine vs. propofol, adjusted for age, sex, previous tonsillectomy, surgeon, positional OSA, and ketamine co-administration. RESULTS: Of 117 subjects, 57% were sedated with propofol and 43% with dexmedetomidine. Subjects were 60% male, 66% Caucasian, 31% obese, 38% syndromic, and on average 6.5 years old. Thirty-three percent had severe OSA and 41% had previous tonsillectomy. There was no statistically significant difference in the odds of ≥ 50% obstruction between the two anesthetic groups at any level of the airway with or without adjustment for potential confounders. CONCLUSION: We did not find a significant difference in the degree of upper airway obstruction on DISE in children sedated with propofol versus dexmedetomidine. Prospective, randomized studies would be an important next step to confirm these findings.

Acid exposure disrupts mucus secretion and impairs mucociliary transport in neonatal piglet airways.

Tenacious mucus produced by tracheal and bronchial submucosal glands is a defining feature of several airway diseases, including cystic fibrosis (CF). Airway acidification as a driving force of CF airway pathology has been controversial. Here we tested the hypothesis that transient airway acidification produces pathologic mucus and impairs mucociliary transport. We studied pigs challenged with intra-airway acid. Acid had a minimal effect on mucus properties under basal conditions. However, cholinergic stimulation in acid-challenged pigs revealed retention of mucin 5B (MUC5B) in the submucosal glands, decreased concentrations of MUC5B in the lung lavage fluid, and airway obstruction. To more closely mimic a CF-like environment, we also examined mucus secretion and transport following cholinergic stimulation under diminished bicarbonate and chloride transport conditions ex vivo. Under these conditions, airways from acid-challenged pigs displayed extensive mucus films and decreased mucociliary transport. Pretreatment with diminazene aceturate, a small molecule with ability to inhibit acid detection through blockade of the acid-sensing ion channel (ASIC) at the doses provided, did not prevent acid-induced pathologic mucus or transport defects but did mitigate airway obstruction. These findings suggest that transient airway acidification early in life has significant impacts on mucus secretion and transport properties. Furthermore, they highlight diminazene aceturate as an agent that might be beneficial in alleviating airway obstruction.

The Airway Epithelium-A Central Player in Asthma Pathogenesis.

Asthma is a chronic inflammatory airway disease characterized by variable airflow obstruction in response to a wide range of exogenous stimuli. The airway epithelium is the first line of defense and plays an important role in initiating host defense and controlling immune responses. Indeed, increasing evidence indicates a range of abnormalities in various aspects of epithelial barrier function in asthma. A central part of this impairment is a disruption of the airway epithelial layer, allowing inhaled substances to pass more easily into the submucosa where they may interact with immune cells. Furthermore, many of the identified susceptibility genes for asthma are expressed in the airway epithelium. This review focuses on the biology of the airway epithelium in health and its pathobiology in asthma. We will specifically discuss external triggers such as allergens, viruses and alarmins and the effect of type 2 inflammatory responses on airway epithelial function in asthma. We will also discuss epigenetic mechanisms responding to external stimuli on the level of transcriptional and posttranscriptional regulation of gene expression, as well the airway epithelium as a potential treatment target in asthma.

Upper Airway Collapsibility during Dexmedetomidine and Propofol Sedation in Healthy Volunteers: A Nonblinded Randomized Crossover Study.

BACKGROUND: Dexmedetomidine is a sedative promoted as having minimal impact on ventilatory drive or upper airway muscle activity. However, a trial recently demonstrated impaired ventilatory drive and induction of apneas in sedated volunteers. The present study measured upper airway collapsibility during dexmedetomidine sedation and related it to propofol. METHODS: Twelve volunteers (seven female) entered this nonblinded, randomized crossover study. Upper airway collapsibility (pharyngeal critical pressure) was measured during low and moderate infusion rates of propofol or dexmedetomidine. A bolus dose was followed by low (0.5 µg · kg · h or 42 µg · kg · min) and moderate (1.5 µg · kg · h or 83 µg · kg · min) rates of infusion of dexmedetomidine and propofol, respectively. RESULTS: Complete data sets were obtained from nine volunteers (median age [range], 46 [23 to 66] yr; body mass index, 25.4 [20.3 to 32.4] kg/m). The Bispectral Index score at time of pharyngeal critical pressure measurements was 74 ± 10 and 65 ± 13 (mean difference, 9; 95% CI, 3 to 16; P = 0.011) during low infusion rates versus 57 ± 16 and 39 ± 12 (mean difference, 18; 95% CI, 8 to 28; P = 0.003) during moderate infusion rates of dexmedetomidine and propofol, respectively. A difference in pharyngeal critical pressure during sedation with dexmedetomidine or propofol could not be shown at either the low or moderate infusion rate. Median (interquartile range) pharyngeal critical pressure was -2.0 (less than -15 to 2.3) and 0.9 (less than -15 to 1.5) cm H2O (mean difference, 0.9; 95% CI, -4.7 to 3.1) during low infusion rates (P = 0. 595) versus 0.3 (-9.2 to 1.4) and -0.6 (-7.7 to 1.3) cm H2O (mean difference, 0.0; 95% CI, -2.1 to 2.1; P = 0.980) during moderate infusion of dexmedetomidine and propofol, respectively. A strong linear relationship between pharyngeal critical pressure during dexmedetomidine and propofol sedation was evident at low (r = 0.82; P = 0.007) and moderate (r = 0.90; P < 0.001) infusion rates. CONCLUSIONS: These observations suggest that dexmedetomidine sedation does not inherently protect against upper airway obstruction.

Nasopharyngeal Tube Effects on Breathing during Sedation for Dental Procedures: A Randomized Controlled Trial.

WHAT WE ALREADY KNOW ABOUT THIS TOPIC: Dental procedures under sedation can cause hypoxic events and even death. However, the mechanism of such hypoxic events is not well understood. WHAT THIS ARTICLE TELLS US THAT IS NEW: Apnea and hypopnea occur frequently during dental procedures under sedation. The majority of the events are not detectable with pulse oximetry. Insertion of a nasal tube with small diameter does not reduce the incidence of apnea/hypopnea. BACKGROUND: Intravenous sedation is effective in patients undergoing dental procedures, but fatal hypoxemic events have been documented. It was hypothesized that abnormal breathing events occur frequently and are underdetected by pulse oximetry during sedation for dental procedures (primary hypothesis) and that insertion of a small-diameter nasopharyngeal tube reduces the frequency of the abnormal breathing events (secondary hypothesis). METHODS: In this nonblinded randomized control study, frequency of abnormal breathing episodes per hour (abnormal breathing index) of the patients under sedation for dental procedures was determined and used as a primary outcome to test the hypotheses. Abnormal breathing indexes were measured by a portable sleep monitor. Of the 46 participants, 43 were randomly allocated to the control group (n = 23, no nasopharyngeal tube) and the nasopharyngeal tube group (n = 20). RESULTS: In the control group, nondesaturated abnormal breathing index was higher than the desaturated abnormal breathing index (35.2 [20.6, 48.0] vs. 7.2 [4.1, 18.5] h, difference: 25.1 [95% CI, 13.8 to 36.4], P < 0.001). The obstructive abnormal breathing index was greater than central abnormal breathing index (P < 0.001), and half of abnormal breathing indexes were followed by irregular breathing. Despite the obstructive nature of abnormal breathing, the nasopharyngeal tube did not significantly reduce the abnormal breathing index (48.0 [33.8, 64.4] h vs. 50.5 [36.4, 63.9] h, difference: -2.0 [95% CI, -15.2 to 11.2], P = 0.846), not supporting the secondary hypothesis. CONCLUSIONS: Patients under sedation for dental procedure frequently encounter obstructive apnea/hypopnea events. The majority of the obstructive apnea/hypopnea events were not detectable by pulse oximetry. The effectiveness of a small-diameter nasopharyngeal tube to mitigate the events is limited.

Severe acute interstitial lung disease after nivolumab in three non-small cell lung cancer patients with imaging findings of airway obstruction adjacent to lung tumors.

Nivolumab has been associated with unique adverse events known as immune-related adverse events. Although interstitial lung disease (ILD) is a life-threatening immune-related adverse event, the risk of ILD during nivolumab treatment is unclear. In this report, we encountered three patients with stage IV non-small cell lung cancer with signs of lung obstruction caused by tumor-mediated compression on imaging who developed acute ILD within 10 days of commencing nivolumab treatment. The first case involved a 74-year-old Japanese female never-smoker, the second a 67-year-old Japanese female never-smoker, and the third a 75-year-old Japanese female current-smoker. The first patient was administered nivolumab as third-line chemotherapy, the second was administered nivolumab as fifth-line chemotherapy, and the third was administered nivolumab as second-line chemotherapy. Regardless of aggressive treatments for ILD, 2 of 3 patients died. The findings of these cases suggest that obstructive findings in the lungs, which easily cause infections, may be an important risk factor for nivolumab-induced ILD.

Orolingual Angioedema During or After Thrombolysis for Cerebral Ischemia.

BACKGROUND AND PURPOSE: Orolingual angioedema (OLAE) is a life-threatening complication of intravenous thrombolysis. Our objective was to compare outcomes of patients with and without OLAE. METHODS: We prospectively included consecutive patients who received intravenous thrombolysis for cerebral ischemia at Lille University Hospital. We examined tongue and lips every 15 minutes during thrombolysis and ≤30 minutes after. We evaluated the 3-month outcome with the modified Rankin scale (mRS) and compared outcomes of patients with and without OLAE. RESULTS: Of 923 consecutive patients, 20 (2.2%) developed OLAE. None of them needed oro-tracheal intubation. They were more likely to be under angiotensin-converting enzyme inhibitors (adjusted odds ratio [adjOR], 3.9; 95% confidence interval [CI], 1.6-9.7; P=0.005) to have total insular infarcts (OR, 5.0; 95% CI, 1.5-16.5; P=0.004) and tended to develop more symptomatic intracerebral hemorrhages. Results concerning angiotensin-converting enzyme inhibitors were not modified after adjustment for propensity scores (OR, 4.4; 95% CI, 1.6-11.9; P=0.004) or matched analysis based on propensity scores (OR, 3.4; 95% CI, 1.3-8.1; P=0.010). Patients with OLAE did not significantly differ at 3 months for the proportion of patients with mRS score of 0 to 1 (adjOR, 0.9; 95% CI, 0.3-2.1), mRS score of 0 to 2 (adjOR, 0.8; 95% CI, 0.1-1.8), and death (adjOR, 1.1; 95% CI, 0.3-3.8). CONCLUSIONS: OLAE occurs in 1 of 50 patients who receive intravenous thrombolysis, 1 of 10 in case of total insular infarct, and 1 of 6 if they are under angiotensin-converting enzyme inhibitors. Their long-term outcome does not differ from that of other patients.

Continuous negative external pressure (cNEP) reduces respiratory impairment during screening colonoscopy: a pilot study.

BACKGROUND AND STUDY AIMS: Drugs administered during gastrointestinal procedures cause increased collapsibility of the upper airway, which may lead to respiratory impairment. We evaluated the ability of continuous negative external pressure (cNEP) to lessen respiratory impairment during screening colonoscopy. PATIENTS AND METHODS: The initial 24 patients served as controls, while the next 30 received cNEP. cNEP was delivered by a soft silicone collar placed over the anterior neck. The primary endpoint was the frequency of respiratory impairment, defined as either: (i) a decline from baseline of > 4 % in oxygen saturation, or (ii) apnea lasting ≥ 20 seconds. RESULTS: Mean respiratory impairment episodes were 3.50 in the no-cNEP group vs. 1.92 in the cNEP group, a reduction of 45 % (P = 0.022). Apneas ≥ 20 seconds occurred in 74 % of the no-cNEP group and 28 % of the cNEP group (P = 0.002). While 42 % of the no-cNEP group required increased supplemental oxygen, this was true for only 10 % of the cNEP group (P = 0.01). cNEP adverse events were minimal. CONCLUSIONS: During screening colonoscopy, sedation-related respiratory impairment is significantly reduced by cNEP.ClinicalTrials.gov NCT01895062.

R-134a (1,1,1,2-Tetrafluoroethane) Inhalation Induced Reactive Airways Dysfunction Syndrome.

R-134a (1,1,1,2-tetrafluoroethane) is widely used as a refrigerant and as an aerosol propellant. Inhalation of R-134a can lead to asphyxia, transient confusion, and cardiac arrhythmias. We report a case of reactive airways dysfunction syndrome secondary to R-134a inhalation. A 60-year-old nonsmoking man without a history of lung disease was exposed to an air conditioner refrigerant spill while performing repairs beneath a school bus. Afterward, he experienced worsening shortness of breath with minimal exertion, a productive cough, and wheezing. He was also hypoxic. He was admitted to the hospital for further evaluation. Spirometry showed airflow obstruction with an FEV1 1.97 L (45% predicted). His respiratory status improved with bronchodilators and oral steroids. A repeat spirometry 2 weeks later showed improvement with an FEV1 2.5 L (60% predicted). Six months after the incident, his symptoms had improved, but he was still having shortness of breath on exertion and occasional cough.

[A Case of Life-Threatening Angioedema Occurred During Prolonged Angiotensin-Converting Enzyme Inhibitor Treatment].

Although angiotensin-converting enzyme (ACE) inhibitors are widely used as the first choice drug for treating hypertension, we have only a superficial understanding of their relationship to angioedema. We report a case of life-threatening angioedema. The case was a 60-year-old man who had been taking an ACE inhibitor for hypertension for 11 years. He visited his home doctor for dyspnea, and tongue and neck swelling. He was transported to our hospital because of the possibility of airway obstruction. On admission, his tongue and neck swelling became more severe. We performed an intubation using an endoscope and started airway management. We also stopped his ACE inhibitor. The severe tongue and neck swelling improved gradually and he was extubated on day 3. On the fifth day he was discharged. We diagnosed angioedema caused by an ACE inhibitor. Although the risk of airway obstruction with ACE inhibitors is acknowledged, we have only a superficial understanding of how prolonged ACE inhibitor treatment induces angioedema. So we should consider angioedema in cases of taking ACE inhibitors, especially in cases of prolonged treatment.

Bradykinin and capsaicin induced airways obstruction in the guinea pig are platelet dependent.

INTRODUCTION: Airways obstruction induced by intravenously administered bradykinin is abolished in guinea pigs treated with indomethacin, which has been shown to be, at least in part thromboxane dependent. As thromboxane is primarily generated from circulating platelets, we investigated whether airways obstruction induced by bradykinin, and other spasmogens, is platelet dependent and the role platelet aggregation played in this response. METHODS: Guinea pigs were chronically treated with busulfan to induce thrombocytopenia. Total lung resistance was measured in anaesthetised and mechanically ventilated control and thrombocytopaenic animals to various stimuli that induce airways obstruction. In other experiments, platelet aggregation was assessed in vitro in response to the same stimuli: guinea pigs were anaesthetized, blood was collected and centrifuged to generate firstly platelet-rich plasma and then platelet-poor plasma. Platelets were resuspended in HEPES buffer and platelet aggregation was assessed. RESULTS: Busulfan treatment significantly reduced the number of circulating platelets in guinea-pigs by 85.5%, but had no significant effect on the number of circulating leukocytes. Treatment with busulfan had no significant effect on bronchoconstriction induced by the direct acting spasmogens histamine or methacholine. However, platelet depletion significantly increased airways obstruction induced by Substance P, but caused a significant reduction in airways obstruction induced by bradykinin, bombesin or capsaicin (P < 0.05). None of these stimuli however were able to exhibit a direct effect on platelet aggregation in vitro. Moreover, busulfan did not significantly alter the contractility of guinea-pig isolated trachea in response to capsaicin. CONCLUSION: Airways obstruction induced by bombesin, capsaicin and bradykinin is platelet dependent, but not secondary to platelet aggregation.

Respiratory morbidity in a coffee processing workplace with sentinel obliterative bronchiolitis cases.

RATIONALE: Obliterative bronchiolitis in former coffee workers prompted a cross-sectional study of current workers. Diacetyl and 2,3-pentanedione levels were highest in areas for flavoring and grinding/packaging unflavored coffee. METHODS: We interviewed 75 (88%) workers, measured lung function, and created exposure groups based on work history. We calculated standardized morbidity ratios (SMRs) for symptoms and spirometric abnormalities. We examined health outcomes by exposure groups. RESULTS: SMRs were elevated 1.6-fold for dyspnea and 2.7-fold for obstruction. The exposure group working in both coffee flavoring and grinding/packaging of unflavored coffee areas had significantly lower mean ratio of forced expiratory volume in 1 s to forced vital capacity and percent predicted mid-expiratory flow than workers without such exposure. CONCLUSION: Current workers have occupational lung morbidity associated with high diacetyl and 2,3-pentanedione exposures, which were not limited to flavoring areas.

Effect of a neck collar on upper airway size in children sedated with propofol-midazolam combination during magnetic resonance imaging.

INTRODUCTION: Propofol and midazolam are widely used for pediatric magnetic resonance imaging (MRI) sedation. Increasing depth of sedation may be associated with airway obstruction. A neck collar supporting the mandible and maintaining the head in slight extension may be beneficial in maintaining airway patency. AIM OF THE STUDY: Primary aim: To assess upper airway size with and without a neck collar during pediatric MRI sedation with propofol-midazolam. Secondary aim: To evaluate complications encountered during the procedure. MATERIALS AND METHODS: Sixty patients aged 2-4 years scheduled for MRI of the brain were selected. They were sedated with intramuscular midazolam 0.1 mg·kg(-1) 30 min before the procedure. Patients were sedated with i.v. propofol 1 mg·kg(-1) and continued with 50-100 µg·kg(-1) ·min(-1) . T1 3D fast-field echo axial sequence from the nasopharyngeal roof to subglottic region was taken with and without application of a neck collar. Airway dimensions were measured and analyzed at the base of the tongue, soft palate, and at the epiglottis. RESULTS: At the base of the tongue and soft palate, the cross-sectional area (CSA) and the anteroposterior diameter of the airway were respectively statistically significantly higher when the neck collar was applied. The CSA at the epiglottis was significantly less with application of the neck collar. Complications were not significantly different between the two sequences. CONCLUSION: Application of a soft neck collar in children aged 2-4 years may enhance the retropalatal and retroglossal airway dimensions during pediatric sedation in the supine position.

Antifibrinolytic mechanisms in acute airway injury after sulfur mustard analog inhalation.

Acute lung injury in response to mustard gas (sulfur mustard [SM]) inhalation results in formation of fibrin casts, which obstruct the airway. The objective of this study was to identify fibrinolytic pathways that could be contributing to the persistence of airway casts after SM exposure. Rats were exposed to the SM analog, 2-chloroethyl ethyl sulfide, via nose-only aerosol inhalation. At 4 and 18 hours after exposure, animals were killed and airway-capillary leak estimated by measuring bronchoalveolar lavage fluid (BALF) protein and IgM content. The fibrin clot-degrading and plasminogen-activating capabilities of BALF were also assessed by activity assays, whereas Western blotting was used to determine the presence and activities of plasminogen activator inhibitor-1, thrombin activatable fibrinolytic inhibitor and α2-antiplasmin. Measurement of tissue-specific steady-state mRNA levels was also conducted for each fibrinolytic inhibitor to assess whether its synthesis occurs in lung or at extrapulmonary sites. The results of this study demonstrate that fibrin-degrading and plasminogen-activating capabilities of the airways become impaired during the onset of 2-chloroethyl ethyl sulfide-induced vascular leak. Findings of functionally active reservoirs of plasminogen activator inhibitor-1, thrombin activatable fibrinolysis inhibitor, and α2-antiplasmin in BALF indicate that airway fibrinolysis is inhibited at multiple levels in response to SM.

Inception cohort study of workers exposed to toluene diisocyanate at a polyurethane foam factory: initial one-year follow-up.

BACKGROUND: Isocyanates are one of the most commonly reported causes of occupational asthma; however, the risks of developing isocyanate asthma in modern production facilities remain poorly defined. We evaluated TDI exposure and respiratory health among an inception cohort of workers during their first year of employment at a new polyurethane foam production factory. METHODS: Forty-nine newly hired workers were evaluated pre-employment, 6-months, and 12-months post-employment through questionnaire, spirometry, and TDI-specific serology. Airborne TDI levels were monitored by fixed-point air sampling and limited personal sampling. Qualitative surface SWYPE™ tests were performed to evaluate potential sources of skin exposure. RESULTS: Airborne TDI levels overall were low; over 90% of fixed-point air measurements were below the limit of detection (0.1 ppb). Over the first year of employment, 12 of the 49 original workers (24.5%) were lost to follow-up, no additional workers were enrolled, and seven of the 49 original workers (14.2%) developed either new asthma symptoms (N = 3), TDI-specific IgG (N = 1), new airflow obstruction (N = 1) and/or a decline in FEV1 ≥ 15% (N = 3), findings that could indicate TDI-related health effects. The prevalence of current asthma symptoms was significantly higher in the workers lost to follow-up compared to those who completed the 12-month follow-up (25% vs. 2.7%; P = 0.04). CONCLUSIONS: The findings suggest possible early TDI-related health effects in a modern polyurethane production plant. These findings also highlight the need for further longitudinal evaluation of these workers and the challenges of studying workers at risk for isocyanate asthma.

Retrospective analysis of the clinical course for intubation vs. unspecified laryngeal granulomas.

Intubation laryngeal granulomas (ILGs) are a well-known complication of endotracheal intubation. Cases other than ILGs can be categorized as unspecified laryngeal granulomas (ULGs) since their etiologies are often difficult to confirm. We intended to clarify clinical features of both ILGs and ULGs and that anticoagulant medication could cause the formation and delayed healing of ILGs in terms of wound-healing delay. We compared the results of our treatment of ILGs (n = 16) and ULGs (n = 47) treated between 1998 and 2009 to characterize these patients. The clinical course, treatment (medical vs. surgical), indications for surgical resection, treatment outcome, and use of anticoagulants for preexisting disease were reviewed and compared between these two groups. The resolution rate was significantly better in ILGs (p < .05). Five ILGs and seven ULGs were surgically resected. The main reason for resection was airway obstruction and the need for histological assessment, respectively. The use of anticoagulants was significantly higher in ILGs than ULGs (8/16 vs. 4/47, p < .01). The resolution period was significantly longer in the ILGs patients with anticoagulant medication compared to that in the ILGs patients without anticoagulant medication (152 ± 101 days vs. 76 ± 44 days, p < .05). ILGs may have different clinical course from ULGs, especially in terms of the resolution period. Moreover, administration of anticoagulants may deter healing of small injury due to intubation. Patients taking anticoagulants should be managed carefully during the perioperative period to prevent the occurrence of ILGs.