Airway Occlusion Research Articles

Occlusion of the upper airway does not augment the cardiovascular response to arousal from sleep in humans

The cardiovascular response to an arousal from sleep at the termination of an obstructive apnea is more than double that to a spontaneous arousal. We investigated the hypothesis that stimulation of respiratory mechanoreceptors, by inspiring against an occluded airway during an arousal from sleep, augments the accompanying cardiovascular response. Arousals (>10 s) from stage 2 sleep were induced by a 1-s auditory tone (85 dB) during a concomitant 1-s inspiratory occlusion (O) and without an occlusion [i.e., control arousal (C)] in 15 healthy men (mean +/- SE: age, 25 +/- 1 yr). Arousals were associated with a significant increase in mean arterial blood pressure (MAP) at 4 s (P < 0.001) and a significant decrease in R-R interval at 3 s (P < 0.001). However, the magnitude of the cardiovascular response was not different during C compared with O (MAP: C, 86 +/- 3 to 104 +/- 3 mmHg; O, 86 +/- 3 to 105 +/- 3 mmHg; P = 0.99. R-R interval: C, 1.12 +/- 0.03 to 0.89 +/- 0.04 s; O, 1.11 +/- 0.02 to 0.87 +/- 0.02 s, P = 0.99). Ventilation significantly increased during arousals under both conditions at the second breath (P < 0.001); this increase was not different between the two conditions (C: 4.40 +/- 0.29 to 6.76 +/- 0.61 l/min, O: 4.35 +/- 0.34 to 7.65 +/- 0.73 l/min; P = 0.31). We conclude that stimulation of the respiratory mechanoreceptors by transient upper airway occlusion is unlikely to interact with the arousal-related autonomic outflow to augment the cardiovascular response in healthy young men.

“Back to Sleep” and Unexplained Death in Infants

Investigation of body position in infants with sudden and apparently unexplained death. Determination of the upper airway space of the infants in different positions by computed tomography (CT) scan. Comparison of the CT scan, the body position at death scene, and the autopsy results. Prospective investigation on all infants referred to a specialized center investigating abrupt and apparently unexplained death of infants. Full-term infants with sudden and clinically unexplained death. Four extra infants studied at different postmortem times to verify absence of change in measurement in postmortem CT scan over time. Position of infant when found dead. CT scan of upper airway in 3 positions (prone face down, prone head rotated, supine nose up), presence or absence of upper airway obstruction, level and length of the obstruction, presence or absence of cause of death, and presence or absence of small maxillomandibular complex at autopsy. Twenty-seven children had unexpected crib deaths (17 of them determined to be sudden infant death syndrome at autopsy). Fourteen children were found dead in the prone position; for 8 of them, this was their normal sleeping position. Airway occlusion behind the base of tongue was seen on CT scan in 24 of the 27 infants (89%) when placed prone head down; in 13 (48%) when placed prone with the head rotated to the side, and in 5 (18%) infants in the supine position. Four infants had mild facial dysplasia and had been found dead in the supine position; in 3 of them, sudden infant death syndrome was found to be the cause of death. The stability of CT scan findings over time was demonstrated after death in 3 different body positions. Supine sleeping position may not be necessarily protective when small jaws are present, and sleeping position may also be a factor in abrupt deaths in infants even if "explained by autopsy."

The treatment of Sleep Apnea Syndrome: looking for new answers for old problems

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Laser endotracheal tube failure: Kinking of the Rüsch Lasertubus resulting in near-total airway occlusion

We report a case in which kinking of the Lasertubus resulted in near-total occlusion of the endotracheal tube, which in turn precluded adequate ventilation. Although the reporting of kinked endotracheal tubes is not uncommon in the anesthesia literature, our case is unique with respect to the physical mechanism responsible for tube deformation.

A preoperative sleep study with nasal airway occlusion in pharyngeal flap surgery

Purpose Obstructive sleep apnea is a major complication of pharyngeal flap surgery. The purpose of the present study is to predict preoperatively the risk of upper airway obstruction after surgery. Material and methods We performed an overnight sleep study preoperatively and postoperatively in 16 pediatric patients considered for pharyngeal flap surgery. Preoperative sleep study was done for two nights, once in normal breathing condition and once with complete nasal occlusion by packing of nostril with tampon gauze. Results In preoperative sleep recordings in normal breathing condition, all subjects had a normal apnea hypopnea index (AHI) less than 5/h. In preoperative recording with complete nasal occlusion, five patients exceeded 5/h in AHI. In particular, for two patients who had AHI higher than 15/h, we gave up a surgery in one case and performed pharyngeal flap operation for the other following a tracheotomy for severe disturbance of oral breathing. The remaining 14 subjects underwent surgery without airway obstructive complications. There was strong correlation between preoperative AHI with nasal tampon gauze and AHI at two weeks postoperatively (r = 0.88 P < .0001). There was no significant correlation between preoperative AHI in normal breathing condition and postoperative AHI (P > .05). Conclusions These results exhibit preoperative sleep study with complete nasal airway occlusion represent postoperative breathing condition well during early postoperative period. Preoperative sleep study with complete nasal airway occlusion with nasal tampons could be useful for predicting the risk of upper airway obstruction secondary to pharyngeal flap surgery.

Oral appliances and hypomandibular surgery in the treatment of snoring and obstructive sleep apnea

This course is designed for oral and maxillofacial surgeons to expand understanding of sleep disorders. An overview of sleep disorders, including techniques of evaluation and multiple modalities of treatment will be reviewed. Patients with primary snoring and/or obstructive sleep apnea frequently fail to respond to or are not appropriate candidates for behavior measures such as weight loss or change in sleep position. Frequently, those individuals also cannot tolerate or refuse treatment with nasal CPAP. Therefore, many types of oral appliances have been used successfully to move the base of the tongue forward in order to enlarge the upper airway. Despite considerable variation of the design of these appliances, the positive clinical effects have been remarkably consistent. The American Sleep Disorders Association review in 1995 concluded that, in patients studied, the mean apnea/hypopnea index (AHI) was reduced from 47 to 19, with approximately half of the patients treated, achieving an AHI of less than 10. Overall compliance seemed significantly higher than nasal CPAP. As a result, they produced practice parameters for the treatment of snoring and obstructive sleep apnea with oral appliances. For those treating obstructive sleep apnea and upper airway resistance syndrome, oral appliances offer a reasonable non-surgical approach and/or presurgical evaluation tool for a variety of patients. Oral and maxillofacial surgeons working in conjunction with other sleep specialists are uniquely trained to offer this service. Since all conservative medical measures used to manage snoring and sleep disordered breathing, including CPAP, BiPAP, oral appliances, and weight loss, etc, have limitations such as patient tolerance and patient compliance, combined surgical procedures offer encouraging results in the treatment of patients with moderate to severe obstructive sleep apnea. Although maxillomandibular osteotomy appears to offer impressive success rates, consent for such surgery is mediated by patient acceptance, the severity of symptoms, and the level of upper airway collapse. Since no single surgical procedure, except tracheostomy, consistently and completely opens the upper airway, we have developed a philosophy directed toward surgery, which not only would achieve high acceptance rates but offers significant success in a wide variety of patients. Multiple potential sites of airway occlusion include the soft palate, lateral pharyngeal walls, and base of the tongue; thus uvulopharyngopalatoplasty (UPPP) in conjunction with skeletal mobilization techniques to advance the anterior mandibular attachments of the tongue and suprahyoid musculature can improve both oral and hypopharyngeal cross-sectional anatomy. Genioglossus advancement via mortised genioplasty allows a large soft tissue pedicle to be significantly advanced and rigidly fixated. Several genioglossus advancement techniques will be discussed in detail. The outcome data of several hundred patients treated at the University of Pennsylvania Center for Sleep Disorders will be reviewed in detail.

Surfactant for RDS: When and how?

This issue of The Journal contains two articles about surfactant therapy for respiratory distress syndrome (RDS). The big picture is that surfactant treatments for RDS are safe and very effective and are the standard of care. However, considerable controversy remains about when to treat infants at risk for or with RDS, how to give those treatments, and what sort of ventilatory support is best and for how long. Variables generating uncertainty are timing of treatment (at delivery/after initial stabilization), ventilatory support before and after treatment (continuous positive airway pressure [CPAP]/mechanical ventilation and type of mechanical ventilation), techniques for treatment (pharyngeal at delivery, number and volumes of boluses for each treatment, management after treatment). Each variable is further complicated by the gestational age/birth weight of each infant and the clinical status of the infant at birth. The Texas Neonatal Research Group performed a multicenter randomized trial to ask if larger infants (≥1250 g) with RDS and an oxygen requirement of ≥40% would benefit from immediate intubation and surfactant treatment compared with expectant management with surfactant treatment if the respiratory disease progressed. For this group of infants, an early intervention with surfactant treatment was of no benefit. This result supports the current clinical trend to use CPAP therapy for larger infants with RDS. Kaiser, Gauss, and Williams evaluated the effect of surfactant treatment on cerebral blood flow in very-low-birth-weight (VLBW) infants using continuous monitoring. They demonstrate that routine surfactant treatments result in a peak increase in Pco2 of about 20 mm Hg 15 minutes after the surfactant treatment. The increase in Pco2 is associated with an increase in cerebral blood flow velocity, demonstrating intact autoregulation of cerebral blood flow in these VLBW infants. The peak increase in Pco2 at 15 minutes probably results from airway occlusion with the surfactant suspension. The importance of the study is that it points out that surfactant therapy does cause transient physiologic changes that need to be balanced against benefit. For example, the decision to treat an infant on CPAP with surfactant requires intubation followed by surfactant instillation. Both procedures cause physiologic abnormalities that need to be recognized. Strategies for when to treat which patient and how remain hot topics in neonatology.

Surfactant for RDS: When and how?

This issue of The Journal contains two articles about surfactant therapy for respiratory distress syndrome (RDS). The big picture is that surfactant treatments for RDS are safe and very effective and are the standard of care. However, considerable controversy remains about when to treat infants at risk for or with RDS, how to give those treatments, and what sort of ventilatory support is best and for how long. Variables generating uncertainty are timing of treatment (at delivery/after initial stabilization), ventilatory support before and after treatment (continuous positive airway pressure [CPAP]/mechanical ventilation and type of mechanical ventilation), techniques for treatment (pharyngeal at delivery, number and volumes of boluses for each treatment, management after treatment). Each variable is further complicated by the gestational age/birth weight of each infant and the clinical status of the infant at birth. The Texas Neonatal Research Group performed a multicenter randomized trial to ask if larger infants (≥1250 g) with RDS and an oxygen requirement of ≥40% would benefit from immediate intubation and surfactant treatment compared with expectant management with surfactant treatment if the respiratory disease progressed. For this group of infants, an early intervention with surfactant treatment was of no benefit. This result supports the current clinical trend to use CPAP therapy for larger infants with RDS. Kaiser, Gauss, and Williams evaluated the effect of surfactant treatment on cerebral blood flow in very-low-birth-weight (VLBW) infants using continuous monitoring. They demonstrate that routine surfactant treatments result in a peak increase in Pco2 of about 20 mm Hg 15 minutes after the surfactant treatment. The increase in Pco2 is associated with an increase in cerebral blood flow velocity, demonstrating intact autoregulation of cerebral blood flow in these VLBW infants. The peak increase in Pco2 at 15 minutes probably results from airway occlusion with the surfactant suspension. The importance of the study is that it points out that surfactant therapy does cause transient physiologic changes that need to be balanced against benefit. For example, the decision to treat an infant on CPAP with surfactant requires intubation followed by surfactant instillation. Both procedures cause physiologic abnormalities that need to be recognized. Strategies for when to treat which patient and how remain hot topics in neonatology.

Optimum pressure support (Ps) during the weaning of COPD patients: changes in airway occlusion pressure (P0,1), breathing patterns, hemodynamics and blood gases

Department of Anaesthesiology and Reanimation, Haydarpapa Numune Teaching and Research Hospital, Istanbul, Turkey

Effects of withdrawal of phasic lung inflation during normocapnia and hypercapnia on the swallowing reflex in humans.

This study was done to test the hypothesis that hypercapnia has a direct, inhibitory effect on swallowing. We investigated changes in the frequency and timing of repeated swallows induced by continuous infusion of water into the pharynx before, during, and after transient airway occlusion at normocapnia and hypercapnia in 12 healthy volunteers. Hypercapnia was induced by adding a dead space. Ventilation was monitored using a pneumotachograph, and swallowing was identified by submental electromyogram. We found that hypercapnia decreased the frequency of swallows (8.2 +/- 3.7 vs 11.4 +/- 5.3 swallows.min-1 [mean +/- SD]: hypercapnia vs normocapnia; P < 0.05), together with a loss of the preponderant coupling of swallows with expiratory phase observed at normocapnia. We also found that the withdrawal of phasic lung inflation produced by airway occlusion at end-expiration suddenly increased the swallowing frequency, both at normocapnia (from 11.4 +/- 5.3 to 16.7 +/- 3.7 swallows.min-1; P < 0.01) and at hypercapnia (from 8.2 +/- 3.7 to 22.0 +/- 6.7 swallows.min-1; P < 0.01). Although the degree of increased swallowing frequency during airway occlusion was more prominent at hypercapnia than at normocapnia ( P < 0.05), the distribution of the timing of swallows in relation to the phase of the respiratory cycle during airway occlusion at hypercapnia was similar to that during airway occlusion at normocapnia. The results of our study strongly suggest that the attenuation of the swallowing reflex during hypercapnia is not due to the direct, inhibitory effect of CO2 on the swallowing center, but, rather, is due to the increased inhibitory influence of a lung-volume-related reflex.

Tests of Respiratory Muscle Strength In Neonates

After completing this article, readers should be able to: 1. Describe the underlying cause of respiratory failure in about 50% of preterm infants who require intubation and mechanical ventilation. 2. Compare compliance characteristics of the chest wall in infants, older children, and adults. 3. List some of the conditions seen in neonates that can adversely affect respiratory muscle function. 4. List noninvasive tests for assessing respiratory muscle strength in neonates. Chest wall mechanics of neonates and infants play an essential role in ventilation that frequently is underappreciated. Dysfunction of the respiratory muscles can cause both a disease process and an inability of the patient to compensate for it. As an example, respiratory muscle failure may be the underlying cause in about 50% of preterm infants who have ventilatory failure. (1) In this article, we detail the current understanding of the physiology of the respiratory muscles in neonates and discuss a number of tests designed to assess their function. Mechanically, the respiratory system can be thought of as being composed of two components. The first includes the respiratory muscles, the rib cage, and the anterior abdominal wall, which together make up the “pump,” whose function is to move air in and out of the lungs. The second includes the airways and lung parenchyma through which gas exchange occurs and can be referred to as the “load” on which the pump must act. For ventilation to occur, the respiratory pump must overcome both the frictional (eg, airway resistance) and tissue elastic forces (eg, lung and chest wall compliance) that create the load. The balance between the capabilities of the pump and the magnitude of the load can influence whether respiratory “success” or “failure” occurs. The chest wall, which contains muscles and skeletal structures, undergoes dramatic maturational changes over the first several years of life. In addition …

A prospective, blinded evaluation of indexes proposed to predict weaning from mechanical ventilation.

To conduct a blinded evaluation of the predictors of weaning from mechanical ventilation. A prospective clinical study. A 23-bed general intensive care unit. Ninety-three non-selected patients, ventilated for more than 48 h. The study had two steps: at first, patients' data were used to select the cut-off value for weaning predictors (the minimal false classification). The cut-off value for each index was prospectively assessed in a group of 52 patients. The predictive performance of these indexes was evaluated by calculating the area under the receiver operating characteristic curve. In the prospective-validation set we used Bayes' theorem to assess the probability of each test in predicting weaning. The physicians making decisions about the weaning process were always unaware of the predictive values. Weaning was considered successful if spontaneous breathing was sustained for more than 48 h after extubation. During the first 2 min after discontinuation of mechanical ventilation the following tests were performed: vital capacity, tidal volume, airway occlusion pressure (P(0.1)), minute ventilation, respiratory rate, maximal inspiratory pressure (MIP), respiratory frequency to tidal volume (f/V(T)), P(0.1)/MIP and P(0.1) x f/V(T). The areas under the curve showed that the tests had not the ability to distinguish between successful and unsuccessful weaning. Our results show that all the evaluated indexes are poor predictors of weaning outcome in a general intensive care unit population.

Pressure gradient, not exposure duration, determines the extent of epithelial cell damage in a model of pulmonary airway reopening.

The reduction of tidal volume during mechanical ventilation has been shown to reduce mortality of patients with acute respiratory distress syndrome, but epithelial cell injury can still result from mechanical stresses imposed by the opening of occluded airways. To study these stresses, a fluid-filled parallel-plate flow chamber lined with epithelial cells was used as an idealized model of an occluded airway. Airway reopening was modeled by the progression of a semi-infinite bubble of air through the length of the channel, which cleared the fluid. In our laboratory's prior study, the magnitude of the pressure gradient near the bubble tip was directly correlated to the epithelial cell layer damage (Bilek AM, Dee KC, and Gaver DP III. J Appl Physiol 94: 770-783, 2003). However, in that study, it was not possible to discriminate the stress magnitude from the stimulus duration because the bubble propagation velocity varied between experiments. In the present study, the stress magnitude is modified by varying the viscosity of the occlusion fluid while fixing the reopening velocity across experiments. This approach causes the stimulus duration to be inversely related to the magnitude of the pressure gradient. Nevertheless, cell damage remains directly correlated with the pressure gradient, not the duration of stress exposure. The present study thus provides additional evidence that the magnitude of the pressure gradient induces cellular damage in this model of airway reopening. We explore the mechanism for acute damage and also demonstrate that repeated reopening and closure is shown to damage the epithelial cell layer, even under conditions that would not lead to extensive damage from a single reopening event.

Sphincter Pharyngoplasty as a Treatment of Velopharyngeal Incompetence in Young People: A Prospective Evaluation of Effects on Sleep Structure and Sleep Respiratory Disturbances

Sphincter pharyngoplasty (SP) appears to be the more "physiologic" surgical technique to treat velopharyngeal incompetence (VPI). This procedure creates a dynamic sphincter of variable diameter and keeps the flexibility of the soft palate. SP also induces velopharyngeal size reduction, mainly in the transverse diameter, which may cause upper airway (UA) occlusions during sleep. To prospectively evaluate the effects of SP by a modified Orticochea procedure on sleep structure and sleep respiratory disturbances. Polysomnographic studies before and after surgery in 17 consecutive patients treated by a modified Orticochea procedure SP for VPI. For the whole group, SP did not induce significant impairment of apnea-hypopnea index or nocturnal oxygen saturation. Slow-wave sleep (SWS) was significantly reduced after surgery (25 +/- 9% of total sleep time [TST] vs 28 +/- 9% of TST before SP [p = 0.04]). Following surgery, there was a trend for an increase in the microarousal index) (p = 0.09) and more specifically in respiratory-related microarousals. SP, although creating a clinically obvious reduction of velopharyngeal diameter, generally did not lead to the occurrence of an obstructive sleep apnea syndrome. However, we found a significant reduction of SWS quantity and a trend toward an increase in the number of cortical microarousals. These findings suggest that the reduction of UA diameter associated with the surgical technique leads to increases in respiratory effort sufficient to induce sleep fragmentation and SWS reduction, even in the absence of apneas or hypopneas.

Cardiovascular consequences of sleep-disordered breathing: past, present and future: report of a workshop from the National Center on Sleep Disorders Research and the National Heart, Lung, and Blood Institute.

Sleep-disordered breathing (SDB), which includes obstructive sleep apnea (OSA) as its most extreme variant, is characterized by intermittent episodes of partial or complete obstruction of the upper airway during sleep that disrupts normal ventilation and sleep architecture and is typically associated with snoring and daytime sleepiness. SDB is common, with an incidence in middle-aged men and women of 4% and 2%, respectively.1 Major risk factors for SDB include obesity, male gender, increasing age, and abnormalities of craniofacial morphology.2 There is an increasing perception that SDB/OSA via various mechanisms increases cardiovascular morbidity and mortality (Figure 1). However, many risk factors for SDB/OSA, such as obesity and male gender, are the same as for hypertension and cardiovascular disease.3 Thus, only recently has there been converging evidence that SDB is a risk factor for their development.4–6 Moreover, there is increasing information to indicate that SDB/OSA is linked to metabolic, vascular, hematologic, and genetic markers associated with increased cardiovascular disease risk. In addition, central sleep apnea (CSA), another form of SDB, appears to be an important factor that influences morbidity and mortality among those with heart failure (HF). Nevertheless, responsible mechanisms, the role of SDB as a risk factor “independent” of associated comorbidities, and whether treatment of SDB will mitigate this risk are unknown and remain to be determined. Figure 1. This illustrates the range of cardiovascular diseases and potential mechanisms that may be associated with sleep-disordered breathing. As illustrated in this figure, there is likely an interaction between multiple potential mechanisms, particularly in individuals who may have a genetic susceptibility for sleep-disordered breathing. This report summarizes the proceedings of a workshop sponsored by the National Center on Sleep Disorders Research and the National Heart, Lung, and Blood Institute on September 12 to 13, 2002, to assess a broad array …

Isoflurane facilitates hiccup-like reflex through gamma aminobutyric acid (GABA)A- and suppresses through GABAB-receptors in pentobarbital-anesthetized cats.

The mechanism by which volatile anesthetics exert inconsistent effects on hiccups is unknown. We elicited a hiccup-like reflex by mechanical stimulation of the dorsal epipharynx in mechanically ventilated cats. The magnitude of the hiccup-like reflex was measured as the peak negative esophageal pressure (nPes) generated against an occluded airway. First, we examined the effects of different end-expiratory concentrations of isoflurane on nPes. Second, we determined the effects of 1.0 minimum alveolar anesthetic concentration of isoflurane on nPes after a peripherally restricted gamma aminobutyric acid (GABA)(A)-receptor antagonist, bicuculline methiodide (BM), a GABA(B)-receptor antagonist, CGP 35348, a peripherally restricted GABA(B)-receptor antagonist, CGP 54626, or saline had been administered IV. Third, BM, CGP 35348, or artificial cerebrospinal fluid was administered intracisternally before 1.0 minimum alveolar anesthetic concentration of isoflurane exposure. During isoflurane anesthesia, nPes was inversely proportional to the end-expiratory isoflurane concentration. The rank order of nPes values obtained after IV drug pretreatment and isoflurane exposure was BM < saline < CGP54626 < CGP35348. After intracisternal drug pretreatment and isoflurane administration, the order of nPes was BM < artificial cerebrospinal fluid < CGP35348. Isoflurane modulates the hiccup-like reflex in opposite directions through both central and peripheral GABA(A) and GABA(B) receptors, with the net effect being a dose-dependent suppression. Isoflurane facilitated the hiccup-like reflex through activation of central and peripheral gamma aminobutyric acid (GABA)(A) receptors but suppressed it via activation of central and peripheral GABA(B) receptors. The net result was that the hiccup-like reflex was inhibited in proportion to the alveolar isoflurane concentration.

Lateral Neck Radiography versus Direct Video Rhinoscopy in Assessing Adenoid Size

To evaluate the usefulness of adynamic lateral neck radiographs and dynamic video rhinoscopy in assessing adenoid size and the relationship of these methods to associated symptoms and thus the severity of the disease. Children with suspected adenoid hypertrophy underwent standard lateral neck soft tissue radiographs: the percentage of airway occlusion, adenoid to nasopharynx (AN) ratio, airway to soft palate ratio, and adenoid thickness were assessed by a radiologist. The percentage of airway closure was assessed by direct fibre-optic rhinoscopy in an ear, nose, and throat clinic. Associated clinical symptoms were assessed by parents using a standardized questionnaire, evaluating the severity of symptoms (snoring, sleep apnea, mouth breathing, and otitis media) to give a total symptom score out of 16. Nonparametric statistical analysis using Spearman's correlation coefficients was performed on 32 patients. There was a weak correlation, which approaches significance, between the percentage of airway occlusion assessed by fibre-optic rhinoscopy and the total symptom score (r = .344, p = .054). However, this correlation becomes significant when the frequency of otitis media is omitted (r = .367, p = .039). There was also a significant correlation between airway occlusion assessed by rhinoscopy and the percentage of airway occlusion as determined by lateral neck radiography (r = .431, p = .014). There was no correlation between any of the measurements taken by lateral soft tissue neck radiography and total symptom score. Dynamic video rhinoscopy is more accurate at assessing adenoid hypertrophy, and the percentage of airway occlusion, as estimated by video rhinoscopy, is better correlated to the severity of symptoms than are values obtained by lateral neck radiography.

Colin Andrew Ramsay, MD, FRCP (June 11, 1936−April 24, 2003)

“Bolus death” or “Café Coronary syndrome” refers to death due to asphyxia caused by an occlusion of the upper airways due to food. In this kind of asphyxia, the food bolus obstructs the larynx or the bronchial branches. This kind of event often affects subjects with acute intoxication due to alcohol or drugs, or with edentulism and with neurological or psychiatric diseases.An elderly woman, suffering from schizophrenia, was found dead in her house due to food bolus asphyxia. The post-mortem toxicological analysis on the deceased’s biological fluids revealed the presence of tricyclic antidepressants, antipsychotics and neuroleptics. Study of the oral cavity showed the presence of partial edentulism and periodontal disease.We hypothesize that this kind of asphyxia in adults can be prevented. We believe that there are two major preventable factors: edentulism and salivation disorders in elderly and neuropsychiatric patients. The primary prevention of these pathologies would deal with the basic physician, similarly to other screenings already effectively in place.It is possible to prevent fatal asphyxia in subjects who suffer from this kind of diseases through appropriate screening. This prevention strategy would greatly reduce the amount of choking deaths in adults.

Effect of ischemia and reperfusion without airway occlusion on vascular barrier function in the in vivo mouse lung.

Ischemia-reperfusion (I/R) lung injury causes increased vascular permeability and edema. We developed an in vivo murine model of I/R allowing measurement of pulmonary vascular barrier function without airway occlusion. The left pulmonary artery (PA) was occluded with an exteriorized, slipknotted suture in anesthetized C57BL/6J mice. The effect of ischemic time was determined by subjecting mice to 5, 10, or 30 min of left lung ischemia followed by 150 min of reperfusion. The effect of reperfusion time was determined by subjecting mice to 30 min of left lung ischemia followed by 30 or 150 min of reperfusion. Changes in pulmonary vascular barrier function were measured with the Evans blue dye (EBD) technique, dual-isotope radiolabeled albumin (RA), bronchoalveolar lavage (BAL) protein concentration, and wet weight-to-dry weight ratio (WW/DW). Increasing left lung ischemia with constant reperfusion time or increasing left lung reperfusion time after constant ischemic time resulted in significant increases in left lung EBD content at all times compared with both right lung values and sham surgery mice. The effects of left lung ischemia on lung EBD were corroborated by RA but the effects of increasing reperfusion time differed, suggesting binding of EBD to lung tissue. An increase in WW/DW was only detected after 30 min of reperfusion, suggesting edema clearance. BAL protein concentrations were unaffected. We conclude that short periods of I/R, without airway occlusion, increase pulmonary vascular permeability in the in vivo mouse, providing a useful model to study molecular mechanisms of I/R lung injury.

Selective Bronchography

Selective Bronchography