Laryngostenosis

LARYNGOSTENOSIS, narrowing of the larynx, does not represent a specific disease but is a symptom encountered in many diseases of both the larynx itself and its neighboring organs; therefore, external and internal stenoses are distinguished. In external stenoses, some pathological process, developing next to the larynx, leads to its compression and the narrowing of its lumen, causing edema or infiltration within it; this occurs with abscesses and neoplasms in the region of the pharynx, tonsils, and root of the tongue, with deep phlegmons of the neck, Ludwig's angina, and goiter. Internal stenoses of the larynx are traumatic, inflammatory (acute laryngitis, edema, perichondritis, abscesses, chronic laryngitis, cicatricial changes, syphilis, and tuberculosis), nervous (spasms and paralyses), and neoplastic (benign and malignant). Stenoses of the larynx cause quite specific changes in the body, regardless of the type of disease, which are related to the restricted access of air to the lungs. At first glance, it would seem that the first and most natural consequence of such a decrease in air inflow to the lungs would be a disturbance of blood gas exchange, a lack of O₂ in it, and an excess of CO₂. This is how older authors (Pieniazek) viewed the matter. However, more recent experimental works (Kohler, Grossman, Sulger, Nissen) depict the phenomena occurring during airway stenosis somewhat differently: they state that with each breath, which is deeper and more prolonged in cases of stenosis, more air enters the lungs than in the normal state. The blood circulating in the lungs comes into contact not only with a larger quantity of air but also under greater intrapulmonary pressure (due to the difficulty of exhaling), as a result of which more complete oxidation of the blood occurs. The more sharply the stenosis is expressed, says Grossman, and the greater the difficulty in breathing, the more thoroughly the oxidation of the blood takes place. Kohler explains the death of experimental animals not by the accumulation of CO₂ in the blood, but by secondary changes in the state of the lungs and heart; upon autopsy, he found sharp dilation of both chambers of the heart, intense hyperemia of the lungs, and vesicular and interlobular pulmonary emphysema. According to Grossman, the essence of the process in question is that deeper respiratory movements cause stronger irritation of the vagus nerve and slow down cardiac contractions; the cardiac chamber becomes overfilled with blood, and to push it through, the heart must expend more and more force, which quickly exhausts it and leads to death. On the part of the lungs during laryngeal stenosis, emphysema is observed, which, according to Pieniazek, occurs because during forced inhalation, more air enters the lungs than is removed during passive exhalation. Grossman explains the appearance of emphysema by the fact that increased pressure in the pulmonary artery leads to the dilation of the alveoli. The development of pathological changes in the body during laryngostenosis depends on the speed of the stenosis's development; with gradually, slowly developing narrowings, the body as if becomes accustomed to and adapts to the created situation, and compensation can last for years; with suddenly or very rapidly and sharply occurring stenoses, asphyxia can occur immediately. Strong, well-nourished people tolerate insufficient air inflow to the lungs worse than weakened, emaciated patients. Laryngostenosis is better tolerated by adults than by children. The appearance of cyanosis does not always indicate the onset of asphyxia; it can temporarily appear in adults during muscular exertion (coughing) and may not appear in children even during complete asphyxia. Pathological-anatomical changes of the larynx during stenoses are extremely diverse and depend on the etiological factor; the mucous membrane at the site of the stenosis is in a state of more or less sharply expressed catarrh. On the swollen, inflamed mucous membrane, due to its reduced resistance, desquamation of the epithelium and superficial erosions can occur from various trivial causes (e.g., coughing), and then granulation tissue can form in these places. The regression of granulations and the healing of ulcers are accompanied by the development of cicatricial tissue, which is especially dense in diphtheria and syphilis and possesses the ability to shrink significantly and narrow the laryngeal lumen. In the muscular apparatus of the larynx, atrophic processes occur from disuse, and degenerative processes occur depending on the infection that caused the stenosis (diphtheria, typhus, Zenker's degeneration of muscles, syphilis, etc.). Symptoms. The most constant and early symptom of laryngeal narrowing is a peculiar noise during breathing—stenotic noise; with small, incipient narrowings, it occurs only during exertion (fast walking, climbing stairs) and during deep breathing, later also during quiet breathing, and always during exhalation. The intensity of the noise increases with the intensification of the stenosis. The voice in laryngostenosis changes: it becomes hoarse and soundless; the only exception is stenoses from the median position of the vocal cords during paralysis of the posterior cricoarytenoid muscles, in which the voice is preserved. In tracheal stenoses, the voice does not change. With progressive stenosis, inhalation begins to suffer; exhalation changes almost not at all; inhalation is prolonged; the ratio of the number of inhalations to the pulse, which is normally 1:4, falls to 1:6 in cases of stenosis. In the vascular system, significant tension and an increase in the pulse wave are observed with a decrease in the pulse rate; during inhalation, the pulse curve drops sharply, and the pulse loses its tension; during exhalation, the pulse curve rises and the tension is restored. In the period of decompensation, retraction of the compliant parts of the chest wall, cooling, and cyanosis of the extremities and face are observed during inhalation. The diagnosis of laryngostenosis based on the symptoms just described is made very easily; but it is not enough to determine the presence of stenosis; it is also necessary to establish its location, character, and etiology. According to Gerhardt, the distinction between laryngeal stenosis and tracheal stenosis is as follows: with a lesion of the larynx, the voice changes, the head is tilted backward, and the larynx rises and falls during breathing; with a lesion of the trachea, the voice is unchanged, the head is tilted forward, and the larynx is immobile even during forced breathing. An asthma attack presents a picture very similar to acute laryngeal stenosis, but in asthma, exhalation is difficult, whereas in stenoses of the larynx and trachea, inhalation is impaired. The character of the stenosis can be established by the laryngoscopic picture and examination through a tracheotomy opening. Laryngoscopy in certain diseases provides quite specific, characteristic pictures. Thus, in acute stenosis from laryngeal edema (congestive or inflammatory), soft, transparent-looking, grayish-colored tumors are observed on the aryepiglottic and false vocal cords and on the epiglottis. In subglottic laryngitis, thick red ridges appear directly below the true vocal cords. In chronic stenoses after typhoid fever in tracheotomized patients, the larynx loses its contours, and the laryngeal inlet is filled with red, thickened mucous membrane, which appears as a continuation of the aryepiglottic folds. In stenoses after typhus, the picture is different: the contours of the larynx are more or less preserved, the true vocal cords can be distinguished from the false ones, the aryepiglottic fold is distinct, the arytenoid cartilages are thickened and immobile, and their apices are rounded. The laryngeal lumen is closed by thickened, red true vocal cords that touch each other at the midline. In other cases, it can be seen that the true vocal cords have suffered less; they sometimes even have a normal white color but remain immobile in the median position due to ankylosis of the cricoarytenoid joint. In bilateral paralysis of the posterior cricoarytenoid muscle, the larynx has a completely normal appearance; only the true vocal cords remain immobile in the median position; such a laryngoscopic picture resembles the picture in ankylosis of the arytenoid. The treatment of acute stenoses is determined by the disease that caused the stenosis, but in addition to this, there are some measures that can be useful in any stenosis regardless of its etiology. In the first place are the long-known remedies—narcotics: morphine (for children 0.0025 per year) and chloroform; patients become calm, breathe more freely, fall asleep, and the attack sometimes disappears for a long time. This pause, a postponement of asphyxia, is used to give time for the primary treatment to take effect, e.g., serum therapy in diphtheria. The beneficial effect of narcotics is explained by the fact that during any inflammatory process in the larynx, a reflex spasm of the laryngeal muscles occurs, which intensifies the stenosis. However, the most essential and inevitable measure, when stenosis begins to progress to asphyxia, is surgical intervention—tracheotomy or intubation (see). Chronic stenoses in terms of treatment are divided into two groups: one includes cases where the narrowing is caused by scars or infiltrates from perichondritis—organic stenoses; the second includes cases with a median position of the vocal cords—functional stenoses.

To eliminate narrowing of the larynx of an organic nature, only two paths are conceivable: one is the gradual dilation of the narrowed site by the repeated introduction into it of instruments of progressively increasing diameter; the second path is the removal, excision of scars and infiltrates causing the narrowing. A great many instruments for dilation have been proposed: Schrotter's rubber bougies, Thost's metal ones, tin bougies, O'Dwyer's tubes, Ilyashenko's lead tube-bougies, laminaria, dilators with one or many branches, rubber tubes, and numerous metal cannulas of the most diverse design. The vast majority of these instruments now have only historical significance: they did not persist in practice mainly because it became clear that the laryngeal lumen, sufficient for free breathing achieved by dilation, narrowed again soon after the cessation of dilation, and that to obtain a more lasting result, a prolonged stay of the dilating bougie in the larynx was necessary. Therefore, combinations of cannulas with bougies appeared, but these combinations also proved impractical: firstly, because hard metal bougies often caused pressure sores, and secondly, because with them the posterior wall of the trachea bulged forward into the angle between the cannula and the bougie and formed a new obstacle that hindered decannulation. The rubber tube does not have these disadvantages. It is soft, elastic, completely fills the lumen of the respiratory tract, and exerts uniform, gentle pressure on all its walls. Recently, it has been gaining more and more adherents and is gradually displacing all other dilating agents. Either a straight tube or a T-shaped one is used. - Excision of scars and infiltrates causing laryngeal stenosis is performed during the operation of laryngostomy (see). To eliminate functional stenoses, a number of operations have been proposed, based on various anatomical and physiological grounds: transection of the recurrent nerve to convert the incomplete paralysis of the m. postici causing the stenosis into a complete one (Ruault), during which the glottis widens; replacement of the paralyzed muscle with a healthy one (Rethi, Marschik); pulling up and fixation by suture of the true vocal cord to the thyroid cartilage (Payr, Perekalin, Galebsky); excision of the vocal cords (Citelli, A. Ivanov); enucleation of the arytenoid cartilage (A. Ivanov), and others. Most of the listed methods now have purely historical and theoretical interest; they did not enter into practice, because the authors themselves did not obtain the desired results. It is most practical to view paralyzed, immobile cords as scars and to apply the same operation of laryngostomy to functional stenoses.