Exhaled nitric oxide and lung function after moderate normobaric hyperoxic exposure.

INTRODUCTION: Pulmonary oxygen toxicity is associated with inflammatory responses in the airways and alveoli. The purpose of this study was to investigate whether the changes in exhaled nitric oxide (FE(NO)) after exposure to normobaric hyperoxia (NBO), 100% oxygen (O2) at 1 atmosphere absolute (atm abs) for 90 minutes, are associated with changes in lung function. METHODS: Eighteen healthy non-smoking subjects were exposed to NBO breathing 100% oxygen and to breathing ambient air, both for 90 minutes on separate days and in random order. Dynamic and static lung volumes, maximal expiratory flow rates, distribution of ventilation including closing volume and slope of phase III of the nitrogen washout curve (delta N2), diffusion capacity (D(L)CO) and FE(NO) were measured before and after the exposures. RESULTS: The mean reduction in FE(NO) was 20% (SD = 20) after the NBO exposure (p < 0.001). Static and dynamic lung volumes, maximal expiratory flow rates, DLCO and distribution of ventilation were unchanged. No association was found between the changes in the lung function variables and the change in FE(NO). DISCUSSION: Unchanged indices of distribution of ventilation and maximal expiratory flow rates indicate no small airways' dysfunction, and unchanged DLCO suggests preserved gas transfer in the lung despite a significant reduction in FE(NO). FE(NO) might be an index of oxygen exposure, but further studies over a wide range of oxygen exposures are necessary to establish the role of FE(NO) as a marker of pulmonary oxygen toxicity.

Closing capacity and gas exchange in chronic heart failure.

BACKGROUND: Although it is commonly assumed that pulmonary congestion and edema in patients with chronic heart failure (CHF) promotes peripheral airway closure, closing capacity (CC) has not been measured in CHF patients. PURPOSES: To measure CC and the presence or absence of airway closure and expiratory flow limitation (FL) during resting breathing in CHF patients. METHODS: In 20 CHF patients and 20 control subjects, we assessed CC, FL, spirometry, blood gas levels, control of breathing, breathing pattern, and dyspnea. RESULTS: The patients exhibited a mild restrictive pattern, but the CC was not significantly different from that in control subjects. Nevertheless, airway closure during tidal breathing (ie, CC greater than functional residual capacity [FRC]) was present in most patients but was absent in all control subjects. As a result of the maldistribution of ventilation and the concurrent impairment of gas exchange, the mean (+/- SD) alveolar-arterial oxygen pressure difference increased significantly in CHF patients (4.3 +/- 1.2 vs 2.7 +/- 0.5 kPa, respectively; p < 0.001) and correlated with systolic pulmonary artery pressure (r = 0.49; p < 0.03). Tidal FL is absent in CHF patients. Mouth occlusion pressure 100 ms after onset of inspiratory effort (P0.1) as a percentage of maximal inspiratory pressure (Pimax) together with ventilation were increased in CHF patients (p < 0.01 and p < 0.005, respectively). The increase in ventilation was due entirely to increased respiratory frequency (fR) with a concurrent decrease in Paco2. Chronic dyspnea (scored with the Medical Research Council [MRC] scale) correlated (r2= 0.61; p < 0.001) with fR and P0.1/Pimax. CONCLUSIONS: In CHF patients at rest, CC is not increased, but, as a result of decreased FRC, airway closure during tidal breathing is present, promoting the maldistribution of ventilation, ventilation-perfusion mismatch, and impaired gas exchange. The ventilation is increased as result of increased fR, and Pimax is decreased with a concurrent increase in P0.1, implying that there is a proportionately greater inspiratory effort per breath (P0.1/Pimax). These, together with the increased fR, are the only significant contributors to increases in the MRC dyspnea score.

Airway occlusion assessed by single breath N2 test and lung P-V curve in healthy subjects and COPD patients.

PURPOSE: To determine whether the analysis of the slow expiratory transpulmonary pressure-volume (PL-V) curve provides an alternative to the single-breath nitrogen test (SBN) for the assessment of the closing volume (CV). METHODS: SBN test and slow deflation PL-V curve were simultaneously recorded in 40 healthy subjects and 43 COPD patients. Onset of phase IV identified CV in SBN test (CVSBN), whereas in the PL-V curve CV was identified by: a) deviation from the exponential fit (CVexp), and b) inflection point of the interpolating sigmoid function (CVsig). RESULTS: In the absence of phase IV, COPD patients exhibited a clearly discernible inflection in the PL-V curve. In the presence of phase IV, CVSBN and CVexp coincided (CVSBN/CVexp=1.04±0.04 SD), whereas CVsig was systematically larger (CVsig/CVexp=2.1±0.86). CONCLUSION: The coincidence between CVSBN and CVexp, and the presence of the inflection in the absence of phase IV indicate that the deviation of the PL-V curve from the exponential fit reliably assesses CV.

Techniques for assessing small airways function: Possible applications in asthma and COPD.

In recent years special interest has been expressed for the contribution of small airways in the pathophysiology, clinical manifestations and treatment of asthma and COPD. Small airways contribute little to the total respiratory resistance so that extensive damage of small airways may occur before the appearance of any symptoms, and this is the reason why they are characterized as the "silent zone" of airways. Furthermore, the peripheral localization of the small airways and their small diameter constitutes difficult their direct assessment. Thus, they are usually studied indirectly, taking advantage of the effects of their obstruction, such as premature closure, air trapping, heterogeneity of ventilation, and lung volume dependence of airflow limitation. Today, several heterogeneous methods for the assessment of small airways are available. These can be either functional (spirometry, plethysmography, resistance measurements, nitrogen washout, alveolar nitric oxide, frequency dependence of compliance, flow-volume curves breathing mixture of helium-oxygen) or imaging (mainly through high resolution computed tomography). The above-mentioned methods are summarized in Table 1. However, no method is currently considered as the "gold standard" and it seems that combinations of tests are needed. Furthermore, it is not clear whether the small airways are affected in all patients with asthma or COPD and their clinical significance remains under investigation. Well-designed future studies with large numbers of patients are expected to reveal which of the methods for assessing the small airways is the most accurate, reliable and reproducible, for which patients, and which can be used for the evaluation of the effects of treatment.

Contributions of lower limb and abdominal compression to ventilation inhomogeneity in hypergravity.

Gravito-inertial load in the head-to-foot direction (Gz) and compression of the lower body half by an anti-G suit (AGS) are both known to influence ventilation distribution in the lungs. To study the interaction of Gz and AGS and to asses the separate contributions from lower limbs and abdominal compressions to large and small-scale ventilation inhomogeneities nine males performed SF6/He vital capacity (VC) single-breath washouts at 1, 2, and 3 Gz in a centrifuge, with abdominal and/or lower limbs compressions. SF6/He and (SF6-He) phase III slopes were used for determination of overall and small-scale ventilation inhomogeneity. Closing volume and phase IV height were used as measures of large-scale inhomogeneity. VC decreased marginally with G-load but markedly with lower limbs compression. Small-scale ventilation inhomogeneity increased slightly with G-load, but substantially with AGS pressurization. Small-scale ventilation inhomogeneity increased with AGS pressurization. Large-scale inhomogeneity increased markedly with G-load. Translocation of blood to the lungs might be the key determinant for changes in small-scale ventilation inhomogeneity when pressurizing an AGS.

Single-breath, room-air method for measuring closing volume (phase 4) in the normal human lung.

The purpose of this study was to evaluate a new method to measure closing volume (CV). This new method does not require oxygen or inert gases to be inhaled to obtain the onset of phase 4. Because there are regional differences in the concentrations of the resident alveolar gases (O2, CO2, and N2), there should be an abrupt change in the concentration of these gases at the terminal portion of a prolonged expired vital capacity (VC) that marks the onset of phase 4. Nine normal healthy subjects, 30 to 65 years of age, inspired room air from residual volume (to mimic the maneuver of the standard single breath N2 (SBN2) washout test) to total lung capacity. During the expiration (flow constant at 250 ml.s-1) following a 10-s breath hold at total lung capacity, the exhaled gas was analyzed with a mass spectrometer for fractions of O2, CO2, and N2. Although the onset of phase 4 can be shown as the change in concentration of any of the three alveolar resident gases, oxygen was selected because (1) it demonstrates a greater apex to base concentration gradient than that found with CO2 and N2, and (2) a clear identification of the onset of phase 4 (minimum value of O2 fraction). With this method, the mean +/- SEM of CV was 16.8 +/- 1.52 percent (CV x 100/VC). No significant difference was found among the room air method, SBN2 method, and the helium bolus technique.

Tracheal dead space influences regional ventilation measurement in dogs.

The lung volume at which airway closure begins during expiration (closing volume, CV) can be measured 1) with a radioactive bolus inspired at residual volume (RV) and 2) with the single-breath N2 elimination test. In previous studies in dogs, we observed that N2 CV was systematically larger than 133Xe bolus CV (Xe CV) [N2 CV %vital capacity (VC) = 35 +/- 2.3 (SE) vs. Xe CV %VC = 24 +/- 2.2, P less than 0.01]. Because the regional RV in the dog is evenly distributed throughout the lung and all airways closed at RV, N2 CV is related to the regional distribution of the tracheal N2; differences between N2 and Xe CV could then be related to the size of the inhaled dead space. Simultaneous measurements of Xe and N2 CV were performed at various sites of Xe bolus injection while the regional distribution of the bolus was measured. Injections at the level of the carina increased Xe CV to a value (30 +/- 1.4%VC) near simultaneous N2 CV (32 +/- 1.5%VC) and increased the unevenness of regional distribution of the Xe bolus. The difference between N2 and Xe CV is then the result of the size of the inspired tracheal dead space. Moreover, comparisons between different values of Xe CV require injections of the boluses at the same distance from the carina.

Surfactant effects in model airway closure experiments.

The capillary instability that occurs on an annular film lining a tube is studied as a model of airway closure. Small waves in the film can amplify and form a plug across the tube. This dynamical behavior is studied using theoretical models and bench-top experiments. Our model predicts the initial growth rate of the instability and its dependence on surfactant effects. In experiments, an annular film is formed by infusion of water into an initially oil-filled glass capillary tube. The thickness of the oil film varies with the infusion flow rate. The instability growth rate and closure time are measured for a range of film thicknesses. Our theory predicts that a thinner film and higher surfactant activity enhance stability; surfactant can decrease the growth rate to 25% of its surfactant-free value. In experiments, we find that surfactant can decrease the growth rate to 20% and increase the closure time by a factor of 3.8. Functional values of a critical film thickness for closure support the theory that it increases in the presence of surfactant.

A novel interpretation of closing volume based on single-breath nitrogen washout curve simulation.

Although closing volume is regarded as a clinical test for the early detection of peripheral airway closure, its grounds are not clear. There have been no simulation studies for phase IV in the single-breath nitrogen washout (SBNW) curve, even though several mathematical models for phase III have been proposed. We modeled the lung tissue deformation during slow expiration in which the tissue was regarded as a porous elastic body similar to a sponge. We assigned the maximum tissue density of lung parenchyma over which the lung tissue could not be contracted according to several experimental reports in literature. SBNW curves were then simulated by computing expired air volume and nitrogen concentration for respective acini in the lung model. The simulated SBNW curves well reproduced phase IV, cardiac oscillation, and its postural changes. We found that the higher lung compliance increased closing volume, but decreased residual volume. The smaller maximum tissue density generated larger closing volume and larger residual volume. It suggested that phase IV reflected the alveolar contractility, and the increase of closing volume in emphysema could be explained by an insufficient contraction of alveoli. We also found that the distribution of maximum tissue density affected the onset of Phase IV. A constant value of density generated a clear onset, but a wide distribution of it corresponding to peripheral airway closure obscured it. We suggest that the airway closure was not necessary for phase IV appearance in both normal and emphysematous lung.

Closing volume: a reappraisal (1967-2007).

Measurement of closing volume (CV) allows detection of presence or absence of tidal airway closure, i.e. cyclic opening and closure of peripheral airways with concurrent (1) inhomogeneity of distribution of ventilation and impaired gas exchange; and (2) risk of peripheral airway injury. Tidal airway closure, which can occur when the CV exceeds the end-expiratory lung volume (EELV), is commonly observed in diseases characterised by increased CV (e.g. chronic obstructive pulmonary disease, asthma) and/or decreased EELV (e.g. obesity, chronic heart failure). Risk of tidal airway closure is enhanced by ageing. In patients with tidal airway closure (CV > EELV) there is not only impairment of pulmonary gas exchange, but also peripheral airway disease due to injury of the peripheral airways. In view of this, the causes and consequences of tidal airway closure are reviewed, and further studies are suggested. In addition, assessment of the "open volume", as opposed to the "closing volume", is proposed because it is easier to perform and it requires less equipment.

Responses of upper-airway dilating muscles and diaphragm activity to end-expiratory pressure loading in anesthetized dogs.

The steady-state responses of upper-airway dilating muscles and diaphragm activity to elevation of lung volume induced by positive end-expiratory pressure loading were studied in 9 pentobarbital-anesthetized dogs with vagus nerves intact. The early and late effects of 5 min of expiratory threshold loads upon upper airway dilating muscle activity (the alae nasi, the genioglossus and the posterior cricoarytenoid) were compared to their effects on diaphragm activity. During resting O2 breathing, application of 5 and 10 cm H2O of positive end-expiratory pressure produced no significant change in the peak electrical activity of the upper-airway dilating muscles and diaphragm (p greater than 0.05). No qualitative differences were found in the upper-airway dilating muscles and diaphragm responses to expiratory threshold loads when the animals breathed 3 or 7% CO2 in O2, compared to when they inspired 100% O2. Furthermore, no differences were found in the electrical activity of the upper-airway dilating muscles and diaphragm at any given end-tidal CO2 when unloaded responses were compared with loaded responses during progressive hypercapnia. However, positive end-expiratory pressure loading caused significant prolongation of expiratory duration, which gradually returned toward control levels when the loads were maintained. In animals who developed periodic breathing by increasing levels of anesthesia, positive end-expiratory pressure loading eliminated the periodicity and made the pattern of breathing regular. Based on these results, it can be concluded that under the conditions of these experiments, increases in lung volume produced by expiratory threshold loads do not reduce the activity of upper-airway dilating muscles. The maintenance of the electrical activity of the upper-airway dilating muscles might be caused by excitatory reflex mechanisms or central habituation.

[Comparative methodologic studies of closing volume and increase in airway resistance volumes]. / Vergleichende methodologische Untersuchungen über das Closing Volume und das Strömungswiderstandsanstiegsvolumen.

The early recognition of obstructive lung diseases plays an important role in the subsequent therapy; the closing volume, determined by means of single-breath oxygen test has been established as a suitable parameter. This technique, however, has not succeeded as a routine method due to prohibitive costs. In a clinical study the closing volume and the easier estimatable so-called flow-resistance elevation volume (Ros-volume-curve parameter obtained from oscilloresistometry/volumetry) were compared and a correlation sought. It could be concluded, that for characterization of small airways diseases the closing volume is a more suitable parameter than the flow-resistance elevation volume.

Closing volume influences the postural effect on oxygenation in unilateral lung disease.

In normal adults, both blood flow and ventilation are distributed preferentially to the dependent lung zones. In adults with unilateral lung disease, arterial oxygenation improves when they are positioned with their good lung down because of improved matching of ventilation and perfusion. When the closing volume is increased, dependent airways are closed during tidal breathing, so that reduced ventilation-perfusion ratio and hypoxia develops and ventilation is preferentially distributed to the upper lung zones. We undertook an observational study on the effects of lateral recumbency on arterial oxygenation in adult patients with unilateral lung disease and tested the hypothesis that oxygenation in lateral recumbency might be influenced by an increase in closing volume. Arterial blood gases were analyzed in the supine, right and left lateral decubitus positions and the AaPO(2) was calculated in 44 randomly selected patients 49.9 +/- 18.7 yr of age with unilateral pneumonia (23 cases) or pulmonary tuberculosis (21 cases). In 26 patients, individual Pa(O(2)) with the normal lung in the dependent position was higher than that with the diseased lung; the opposite was true for 18 patients. The difference in Pa(O(2)) and AaPO(2) between the two positions was statistically significant in both groups. In 16 patients (10 men and six women 49.2 +/- 18.2 yr of age), we measured closing volume and determined the fractional ventilation to each lung by (133)Xe lung scan in the three positions. In these 16 patients, the difference in Pa(O(2)) between the normal and the diseased lung in the dependent position was related significantly to the difference in the fractional ventilation going to the normal lung between the dependent and the supine position (r = 0.642, p = 0. 007). The latter was related significantly to the % predicted closing volume (CV/VC) (r = -0.597, p = 0.015). This study has shown that closing volume, as well as posture, might be involved in determining oxygenation in lateral recumbency in patients with unilateral lung disease.

Recurrent exacerbations in severe asthma are associated with enhanced airway closure during stable episodes.

Excessive airway narrowing is a cardinal feature of asthma, and results in closure of airways. Therefore, asthmatic patients in whom airway closure occurs relatively early during expiration might be prone to severe asthma attacks. To test this hypothesis, we compared closing volume (CV) and closing capacity (CC) in a group of asthmatic patients with recurrent exacerbations (more than two exacerbations in the previous year; difficult-to-control asthma), consisting of 11 males and two females, aged 20 to 51 yr, with those in a group of equally severely asthmatic controls without recurrent exacerbations (stable asthma) consisting of 13 males and two females aged 18 to 52 yr. Both groups used equivalent doses of inhaled corticosteroids and were matched for sex, age, atopy, postbronchodilator FEV(1), and provocative concentration of methacholine causing a 20% decrease in FEV(1). They were studied during a clinically stable period of their disease. The patients inhaled 400 microg salbutamol via a spacer device, after which TLC and RV were measured by multibreath helium equilibration, together with the slope of Phase 3 (dN(2)), CV, and CC, by single-breath nitrogen washout. CV and CC were expressed as ratios of VC and TLC, respectively, and all data are presented as % predicted (mean +/- SEM). There was no difference in TLC in patients with difficult-to-control asthma and those with stable asthma (106.7 +/- 4.0% predicted versus 101.7 +/- 4.3% predicted, p = 0.40), RV (113.1 +/- 7.8% predicted versus 100.9 +/- 7.1% predicted, p = 0.26), or dN(2) (142.7 +/- 16.3% predicted versus 116.0 +/- 20.2% predicted, p = 0.23). In contrast, CV and CC were increased in the patients with difficult-to-control asthma as compared with the group with stable asthma (CV: 159.5 +/- 26.8% predicted versus 98.8 +/- 12.5% predicted, p = 0.024; CC: 114.0 +/- 6.4% predicted versus 99.9 +/- 3. 6% predicted, p = 0.030). These findings show that asthmatic individuals with recurrent exacerbations have increased CV and CC as compared with equally severely asthmatic but stable controls, even after bronchodilation during well-controlled episodes. The findings imply that airway closure at relatively high lung volumes under clinically stable conditions might be a risk factor for severe exacerbations in asthmatic patients.

Is ventilation during maximal exercise limited by dynamic airway closure?

A study was undertaken to find if the reason why horses hypoventilate when running is that they experience expiratory flow limitation due to dynamic airway closure. To test this hypothesis, we measured peak expiratory flows on a Thoroughbred galloping on a treadmill and hypoventilating and compared those flows with the peak dynamically-limited flow that the same horse could achieve during a forced expiratory flow-volume manoeuvre. At the approximate lung volumes at which the horse was ventilating while running, it did not appear to be mechanically limited and appeared to have reserve capacity available potentially to increase its expiratory flow.

Differences in airway closure between normal and asthmatic subjects measured with single-photon emission computed tomography and technegas.

The absence of a maximal dose-response plateau as well as gas trapping and increases in closing capacity (CC) suggest that increased airway closure is an important mechanical abnormality of asthmatic airways. We compared the extent and distribution of airway closure in 13 normal and in 23 asthmatic subjects. Airway closure (LVclosed) was measured with single-photon emission computed tomography (SPECT) and an inhaled Technegas bolus as the percentage of lung volume without Technegas (LVtrans), and with CC, using nitrogen washout. LVclosed was compared in the apical, middle and lower zones, each being of equal vertical height. Values of mean LVclosed +/- 95% confidence interval (CI) were similar in normal (30 +/- 6.0% LVtrans) and asthmatic subjects (30 +/- 7.8% LVtrans). In normal subjects, LVclosed correlated with both age (r = 0.89, p < 0. 01) and CC (r = 0.86, p < 0.01), was more extensive in the lower zone (58 +/- 18.8% LVtrans, p < 0.01) than in the middle and upper zones (17 +/- 8.7% and 26 +/- 8.2 LVtrans, respectively), and increased with age in both the middle and lower zones (r = 0.94 and r = 0.90, respectively, p < 0.01). In asthmatic subjects, LVclosed did not correlate with age; was greatest in the lower zone, intermediate in the middle zone, and lowest in the apical zone (59 +/- 13.2%, 22 +/- 5.8%, and 12 +/- 4.4% LVtrans, respectively, p < 0. 01); and correlated weakly with age in the middle zone only (r = 0. 46, p < 0.05). We conclude that there is a predictable pattern of airway closure in normal subjects and that it is primarily influenced by pulmonary elastic recoil. This pattern is lost in asthmatic subjects. This may be explained by an increased range of closing pressures and a patchy distribution of airway closure, probably secondary to allergic inflammation.

Contribution of body habitus and craniofacial characteristics to segmental closing pressures of the passive pharynx in patients with sleep-disordered breathing.

Obesity and craniofacial abnormalities may contribute to the pathogenesis of obstructive sleep apnea. The purpose of this study was to evaluate the influence of body habitus and craniofacial characteristics on types of pharyngeal closure. The types of pharyngeal closure were determined by endoscopic evaluations of closing pressures of the passive pharynx in 54 paralyzed and anesthetized patients with sleep-disordered breathing (SDB). Assessment of craniofacial characteristics of the SDB patients and 24 normal subjects were made by lateral cephalometry. As compared with normal subjects, SDB patients demonstrated receded mandibles and long lower faces with downward mandible development. SDB patients with positive closing pressures at both the velopharynx and oropharynx (VP + OP group) demonstrated smaller maxillas and mandibles than those with positive closing pressures at the velopharynx only (VP-only group). Obesity was more prominent in the VP-only group than in the VP + OP group. Our results suggest that obesity and craniofacial abnormalities contribute synergistically to increases in collapsibility of the passive pharyngeal airway in patients with SDB. Furthermore, the relative contribution of obesity and craniofacial anomaly appears to determine the type of pharyngeal closure in SDB.

Efecto de hemodilución y drogas vasoactivas sobre la presión crítica de cierre / Effect of hemodilution and vasoactive agents on the critical closing pressure

La presión crítica de cierre se atribuye a colapso microvascular, debido a vasoconstricción o a presión perivascular elevada. Las características físicas no newtonianas de la sangre podrían ser también importantes. Para establecer si cambios de la viscosidad sanguínea afectan a la presión crítica, se estudió el efecto de hemodilución aguda normovolémica. Se usaron once perros anestesiados con pentobarbital y ventilados mecánicamente, a los cuales se midió presión arterial central y péríférica con catéteres Millar, y flujo mediante transductor electromagnético en aorta proximal. La presión crítica de cierre se midió por extrapolación del decaimiento exponencial de la presión atierial luego de ocluir la aorta por 3 segundos. Se realizaron mediciones control y luego de administrar fenilefrina y nitroprusiato. Luego se realizó hemodilución sustituyendo 30 a 35 ml/kg de sangre con suero fisiológico, disminuyendo el microhematocrito desde 39 ñ 11 por ciento a 26 ñ 5 por ciento. Luego se repitieron las mediciones y las drogas vasoactivas. Fenilefrina aumentó y nitroprusiato disminuyó la presión crítica de cierre, antes y después de hemodilución. La presión crítica disminuyó con la hemodilución de 44 ñ 8 a 35 ñ 7 mmhg (p<0,05). El gasto cardíaco promedío aumentó 70 por ciento, con disminución proporcional de la resistencia vascular. La disminución de la presión crítica de cierre frente a la hemodilución aguda normovolémica sugiere que ésta resulta en parte de las características físicas de la sangre. Sin, embargo, cambios de tono vascular también la afectan, por lo que su origen es probablemente multifactorial

Pseudo-obstruçäo nasolacrimal na infância / Pseudonasolacrimal obstruction in infancy

Avaliamos 22 crianças de 6 meses a 8 anos de idade, portadoras e pseudo-obstruçäo nasolacrimal (PONL). A PONL ocorreu mais frequentemente no sexo feminino (68,2 por cento). A queixa e epífora foi esporádica, geralmente associada à processos obstrutivos de vias aéreas superiores. A dacriocistografia (DCG) mostrou vias lacrimais pérveas em todas as crianças e alteraçöes nasais, como hipertrofia de cornetos (77,3 por cento), velamento dos seios da face (18,2 por cento), desvio do septo nasal (18,2 por cento), espessamento mucoso dos seios da face (13,6 por cento) e dilataçäo do saco lacrimal (13,6 por cento). Os auotres sugerem que se pense na PONL quando se tem epífora esporádica, DCG com VL pérveas e sinais obstrutivos nasais