Complications of trans-sphenoidal surgery.
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Biomedical subjects
Publications and source records attributed to E B Kern.
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The structural relationships of the upper lateral cartilage and the septum form an important anatomic area called the liminal valve, one of three known paired valves of the nose. A small deformity in the region of the liminal valve may cause significant airway obstruction that usually can be relieved by surgery. Eighty percent of the population has alternating congestion and decongestion of the nasal turbinates, a phenomenon know as the nasal cycle. The exact function of this cycle is unknown, although it probably allows the two nasal chambers to act in unison and function as one nose. It is important to recognize the cycle as a normal phenomenon and to differentiate it from pathologic causes of nasal obstruction.
The phenomenon of paradoxical nasal obstruction is described. An understanding of this phenomenon is made possible by the knowledge of the nasal cycle and of the concept of total nasal airway resistance. These topics are reviewed and two patients with paradoxical nasal obstruction are described. Direct observation, rhinomanometric tests and serial tomograms were utilized to substantiate these findings.
A 6-year-old child manifested symptoms and signs of alveolar hypoventilation and signs of cor pulmonale caused by obstruction of the upper airway. These symptoms and signs disappeared after tonsillectomy and adenoidectomy. The relationship of upper airway obstruction to hypoventilation and cor pulmonale is discussed in the hope of renewing interest in this problem and alerting physicians to think of this possiblity early in the evaluation of such patients.
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Changes in the pulmonary mechanics of various animal species have been observed after nasal stimulation. In reviewing the methods of these studies, we found that often the respiratory patterns were not controlled well enough to permit conclusions about changes in resistance and compliance. To further investigate the possibility of a nasopulmonary reflex, we first studied the effect of nasal stimulation on pulmonary mechanics in anesthetized, nonparalyzed dogs. In this group of 35 dogs, we found that nasal stimulation typically produced marked changes in breathing patterns, a large transient increase (150%) in pulmonary airflow resistance, but no change in compliance. This response to nasal stimulation could be abolished by interrupting either the trigeminal or the vagus nerves. In an additional group of 12 anesthetized, paralyzed dogs, we found no changes in resistance or compliance after nasal stimulation. From this observation, we concluded that nasal stimulation produced changes in breathing patterns that led to alterations in resistance without an actual change in the intrinsic behavior of the pulmonary airways.
Fifty human subjects were studied and evaluated utilizing posterior rhinomanometry techniques. The main purpose of the investigation was to study the physiologic dynamic range of nasal resistance so that the data might serve as a baseline, not only for evaluation and diagnosis of pathologic states but also for the assessment of nasal responses to various physiologic, drug-induced, or pathologic challenges. Analysis was divided into two parts: first, the evaluation of the average resistance and average change in resistance for each patient, and second, determination of the maximal amount of change to be expected over 15-minute periods in a healthy subject. These studies give the investigator an idea of the magnitude of change that one might expect in normal physiologic situations, based on the 50 subjects that allowed 1,272 observations for justification of the concept of percent change in nasal resistance and not the value of nasal resistance alone. We concluded that the physiologic change in nasal resistance in a normal individual during a 15-minute interval should be less than 53% of the previous observation of nasal resistance. A change greater than 53% suggests a significant change that cannot be attributed to physiologic variability.
The response of nasal airway resistance (Rn) to various degrees of hypoxia and hypercapnia was measured in six subjects using active posterior mask rhinomanometry. All resistances were computed during expiration at the flow rate of 0.5 liter/sec. Hypercapnia, induced by breathing gas mixtures of various contents of carbon dioxide, significantly decreased Rn (P less than 0.05, Wilcoxon signed rank test). The reduction in Rn was proportional to the inspired partial pressure of carbon dioxide over a range of 0 to 50 torr. Breathing gas mixtures of high and low contents of oxygen produced no significant change in Rn (P less than 0.05, Wilcoxon signed rank test). These results indicate that the nasal airway is actively involved in the respiratory response to hypercapnia but not to moderate hypoxia.
The resistance of the larynx to airflow was measured during hypercapnia, hypoxemia, and stimulation of peripheral chemoreceptors by sodium cyanide and phenyl diguanide in 15 dogs anesthetized with alpha-chloralose (80 mg/kg). Laryngeal airway resistance (R1x) was obtained by measuring the pressure difference between the subglottic region and the mouth while a constant flow of humidified air was passed through the larynx. During spontaneous respiration, R1x varies with the phase of the respiratory cycle: R1x is high during expiration (mean +/- SEM = 0.79 +/- 0.19 cm H2O/L/sec) and falls just before inspiration (0.49 +/- 0.14 cm H2O/L/sec) and remains low until the end of inspiration. Hypercapnia, hypoxemia, and chemoreceptor stimulation each stimulated respiration and simultaneously decreased R1x during both inspiration and expiration. Chemoreceptor stimulation with phenyl diguanide (100 microgram/kg) and sodium cyanide (100 microgram/kg) produced similar decreases in R1x whether injected into the right atrium or left ventricle, indicating that these agents are not stimulating pulmonary receptors. The decrease in R1x during stimulation of chemoreceptors will decrease the work of ventilation. This study suggests that the control of ventilation involves the active regulation of the resistance of the laryngeal airway.