Laryngospasm

LARYNGOSPASM, laryngospasmus (from Latin larynx—larynx and spasmus—contraction, convulsion), spasmodic contraction of the glottis; it represents a frequent, most typical manifestation of the overt form of spasmophilic diathesis and is one of the three main types of convulsions associated with it (laryngospasm, eclampsia, and tetany). In mild cases, laryngospasm is detected in the form of labored breathing due to involuntary spasmodic contraction of the laryngeal muscles and is expressed by a sonorous or groaning, pulling, sobbing, loud inspiration; this inspiration resembles the crowing of a rooster and appears during any excitement of the child, crying, laughing, and sometimes without any cause. Such sounds during laryngeal spasm are audible from a distance, give the physician reason to look for spasmophilia, and are so characteristic that they can hardly be confused with anything else. Mild convulsions of the glottis, if not paid attention to, can recur and be replaced by severe attacks threatening the child's life. In typical cases, suddenly in a healthy-looking child, in a state of complete well-being or sometimes after screaming, crying, or coughing, the face turns pale, the head is thrown back, a deep, noisy, whistling inspiration appears, indicating difficult air intake through the spasmodically narrowed larynx. The child unsuccessfully tries to take a series of breaths, but breathing stops—apnea (inspiratory). At the same time, the neck muscles are tense, the mouth is open, individual movements appear in the lower jaw, the gaze is fixed, with an expression of fear, the eyeballs are red and protruding, the eyelids are open, the pupil does not react to light, and severe cyanosis sets in. The arms hang helplessly or are straightened and are in a state of severe rigidity, the skin is covered with cold sweat, consciousness is briefly impaired, urine and feces are passed involuntarily, the pulse is barely palpable, strongly accelerated; sometimes there are twitchings at the corners of the mouth and eyes. The epigastric region is often protruding and hard due to the simultaneous spasm of the diaphragm and abdominal muscles; temperature is normal. The impression is created that the child may suffocate and death is inevitable; but suddenly the laryngeal spasm ceases, a sharp inspiratory sound appears, then individual expiratory movements arise, consciousness returns, breathing is restored and assumes its normal rhythm. After a severe seizure, the child becomes somewhat lethargic, drowsy, as if stunned, but soon calms down, feels well, and returns to play. The subsequent state of sleep does not always occur; if it does occur, it usually lasts only a short time. A laryngospasm attack can cease at any moment and at any stage of its development. Convulsion of the respiratory muscles sometimes occurs without the involvement of the laryngeal muscles, when expiratory dyspnea and cessation of breathing in the expiratory phase (expiratory apnea) appear; it can occur unnoticed by others and lead to death. General convulsions in children can alternate with spasms of the glottis or join them as a consequence of CO₂ poisoning. Seizures of laryngospasm last from a few seconds to one minute, but their frequency, strength, and duration vary greatly. In some, they may recur 1-2 times in a few days, in others there are 2-3 seizures per day, in other children the number of seizures per day reaches 13-15-20 or more. Laryngospasm usually appears no earlier than the 3rd month of life and is not encountered after 2 years, whereas other symptoms of spasmophilia (eclampsia, carpopedal spasms) occur, albeit rarely, even after 2 years. Seizures arise during the day, less often at night upon waking with a scream. The time of their appearance often relates to the end of winter and the first months of spring. The etiological factor for laryngospasm is the spasmophilic soil with its increased nervous excitability and tendency to spasms. Hence it is understandable that laryngospasm attacks in a large number of cases arise in connection with various external factors (fright, psychic excitement, laughter, crying, trauma, etc.). A trigger for the manifestation of laryngospasm can be an overfilled stomach, infection, intoxication, high temperature. Laryngospasm is encountered almost exclusively in rachitic, anemic, nervous children and those suffering from prolonged nutritional disorders; all these states are undoubtedly accompanied by an increase in nervous excitability. Simpson believes that in some cases the child reacts to external stimuli (exogenous factors) by using a motor reflex that has become habitual along well-trodden paths. Laryngospasm occurring in various diseases (measles, croup)—see the corresponding diseases. Pathological anatomy: there are no changes in the larynx; its mucous membrane is normal, and everything boils down to the spasmodic contraction of the laryngeal muscles under the influence of nerve impulses. The course of laryngospasm is usually chronic. The strength and frequency of seizures slowly increase, remain at their peak for some time, and then gradually decrease. Thus, in the course of laryngospasm, 3 periods can be distinguished: increase, high state, and disappearance of laryngeal spasms. The course depends on the underlying ailment. Mild seizures can last for several days and weeks with a tendency to relapse. Under the influence of treatment, laryngospasm seizures weaken and are stopped. The diagnosis of laryngospasm is not difficult, as laryngospasm serves as a characteristic, although not mandatory, sign of spasmophilia and should prompt a search for other symptoms of this diathesis (Chvostek, Trousseau, Erb, Lust, Maslov signs, etc.). Typical laryngospasm seizures are characteristic only of spasmophilia, which is why their confirmation is sufficient for making a diagnosis. Laryngospasm must be distinguished from similar conditions: 1) congenital stenosis of the larynx (stridor laryngis congenitus); the anamnesis (onset from birth, laryngospasm not earlier than 3 months!) makes it possible to differentiate these diseases; 2) affective respiratory seizures, appearing in neuropathic children aged 1-5 years and caused mainly by furious screaming and excitement with cessation of breathing in the expiratory phase with phenomena of cyanosis, loss of consciousness, etc.; 3) stridor during enlargement of the thymus gland (characterized by rapid alternation of stridor and free breathing with a clear voice); 4) inflammatory spasms of the vocal cords (differ from laryngospasm by the duration of the seizures, whereas laryngospasm seizures are usually instantaneous). The prognosis for laryngospasm is generally favorable, but it should be made with caution. Mild cases of laryngospasm as a rule end in recovery. Severe, frequent, and prolonged attacks of laryngeal spasm pose a danger to life, and in unfavorable cases, the child may die during one of the first paroxysms from heart paralysis, which is more often noted in children with exudative diathesis, lymphatics, and pasty children (Escherich). The addition of general convulsions, complications with pneumonia, or diarrhea worsens the prognosis. Artificial feeding reduces the chances of recovery. In general, any laryngospasm attack puts the child's life in danger, especially since a severe one can always follow a mild attack. Prophylaxis is aimed at preventing the possibility of recurrence of seizures by protecting the child from agitation, establishing an appropriate regimen, nutrition, and eliminating the underlying disease, i.e., preventing rickets, anemia, nervous and intestinal diseases as the soil for the appearance of laryngospasm. The main tasks of therapy boil down to the symptomatic elimination of the danger of the seizures themselves and to the treatment of spasmophilia and rickets. In mild cases of laryngospasm, any intervention is unnecessary. In a severe attack, if it begins to take on a prolonged character, one should sprinkle the child's face and chest with cold water, pull out the tongue, press its root with a finger, inject camphor under the skin, and attempt to perform artificial respiration. Bendix recommends supporting the forehead of the sitting child with one hand and moderately patting the interscapular region with the other, gradually increasing and accelerating the tempo of movements. In case of asphyxia, besides artificial respiration, the use of electric current, intubation, or tracheotomy (Pott) are recommended, but the benefit of these measures is often doubtful, as the child dies from collapse, not from suffocation. Excitation of cardiac activity is of great importance in view of the possibility of its cessation. For this purpose, cardiac agents are widely used in the form of subcutaneous injections (camphor, Cardiazol, caffeine), heart massage. To stop the seizure, it is possible to administer an enema of chloral hydrate (0.3-0.5 per dose) as soon as possible. A good effect is given by a single subcutaneous injection of Luminal-natrium at 0.1 in an aqueous solution. In threatening cases of laryngospasm, the physician uses chloroform anesthesia or injects an 8% solution of magnesium sulfate at a rate of 0.2 per 1 kg of weight (10-15 cm³) (see Spasmophilia). It is necessary to pay attention to diseases that create a predisposition to laryngospasm (rickets, anemia, nutritional disorders, etc.). It is important, in the presence of laryngospasm, to widely implement hygienic measures (use of air, light, etc.). A. Popov.

Laryngospasm is also encountered in adults as a secondary phenomenon (see also Larynx, pathology). Laryngospasm in adults manifests in the form of suddenly occurring seizures of tonic convulsions of the respiratory muscles and the muscles constricting the glottis: a typical symptom of laryngospasm is wheezing; the duration of the seizure varies, but it is usually very short, lasting a few seconds, thanks to which patients are able to endure the asphyxia that always accompanies laryngospasm without particularly serious consequences. This condition in adults in the majority of cases appears reflexively during diseases of various organs located in areas adjacent to those through which the inferior laryngeal nerve (recurrent) passes, and primarily during lesions of the bronchial glands, large vessels (aortic arch, right subclavian artery), beneath which the recurrent nerve passes on its way to the larynx, as well as the esophagus. Furthermore, laryngospasm can manifest in the form of a reflex from distant organs (disease of the uterus); in subjects with a neuropathic constitution, laryngospasm is encountered more frequently. Sometimes laryngospasm is observed in hydrocephalus. Literature—see the corresponding chapters of the main manuals cited in the literature for the article Larynx. 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 the organs adjacent to it; 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 in it; this occurs with abscesses and neoplasms in the region of the pharynx, tonsils, root of the tongue, with deep phlegmons of the neck, Ludwig's angina, and with goiter. Internal stenoses of the larynx can be traumatic, inflammatory (acute laryngitis, edema, perichondritis, abscesses, chronic laryngitis, cicatricial changes, syphilis, and tuberculosis), nervous (spasms and paralyses), and neoplasms (benign and malignant). Stenoses of the larynx cause quite specific changes in the organism, regardless of the type of disease, which are related to the restriction of air access to the lungs. At first glance, it would seem that the first and most natural consequence of such a reduction in the inflow of air 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 old authors (Pieniazek) viewed this matter. However, more recent experimental works (Kohler, Grossman, Sulger, Nissen) depict the phenomena occurring during stenosis of the respiratory tract somewhat differently: they state that with each breath, which is deeper and longer during stenoses, more air enters the lungs than in the normal state. The blood circulating in the lungs comes into contact not only with a larger amount of air but also under higher 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 occurs. Kohler explains the death of experimental animals not by the accumulation of CO₂ in the blood, but by a secondary change in the state of the lungs and heart; during 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 lies in the fact that deeper respiratory movements cause stronger irritation of the vagus nerve and slow down cardiac contractions; the cardiac cavity becomes overfilled with blood, to push which the heart must expend more and more force, which quickly exhausts it and leads to death. On the part of the lungs during laryngeal stenoses, emphysema is observed, which, according to Pieniazek, occurs because more air enters the lungs during forced inhalation than is removed during passive exhalation. Grossman explains the appearance of emphysema by the fact that increased pressure in the pulmonary artery leads to dilation of the alveoli. The development of pathological changes in the organism during laryngostenosis depends on the speed of the development of the stenosis; with gradually, slowly developing narrowings, the organism as if gets used to and adapts to the created situation, and compensation can last for years; with suddenly or very quickly 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 insignificant 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 strongly and narrow the lumen of the larynx. 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, typhoid, Zenker's degeneration of muscles, syphilis, etc.). Symptoms. The most constant and early symptom of narrowing of the larynx is a peculiar noise during breathing—stenotic noise; with small, beginning 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 exceptions are stenoses from the median position of the vocal cords during paralysis of the posterior cricoarytenoid muscles, in which the voice is preserved. With stenoses of the trachea, the voice does not change. With progressive stenosis, inhalation begins to suffer, while exhalation remains almost unchanged; inhalation is prolonged; the ratio of the number of inhalations to the pulse, which is normally 1:4, falls to 1:6 in stenoses. In the vascular system, significant tension and an increase in the pulse wave are observed with a decrease in the number of pulse beats; during inhalation, the pulse curve drops sharply, and the pulse loses its tension; during exhalation, the pulse curve rises and the tension is restored. During the period of decompensation, retraction of the compliant areas 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 only 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, 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 stenosis of the larynx, but with it, exhalation is difficult, whereas with stenoses of the larynx and trachea, inhalation is disturbed. The character of the stenosis can be established by the laryngoscopic picture and examination through the tracheotomy opening. Laryngoscopy in some diseases gives quite definite, characteristic pictures. Thus, with acute stenosis from edema of the larynx (congestive or inflammatory), soft tumors of a transparent, grayish appearance are observed on the aryepiglottic folds, false vocal cords, and the epiglottis. With subglottic laryngitis, thick red rolls appear directly below the true vocal cords. With chronic stenoses after typhoid fever in tracheotomized patients, the larynx loses its contours, and the entrance to the larynx is filled with red, thickened mucous membrane, representing as it were a continuation of the aryepiglottic folds. With stenoses after typhus, the picture is different: the contours of the larynx are more or less preserved, it is possible to distinguish the true vocal cords from the false ones, the aryepiglottic fold is expressed, the arytenoid cartilages are thickened and immobile, and their apices are rounded. The lumen of the larynx is closed by thickened red true vocal cords touching each other along 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. With 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 is similar to the picture in ankylosis of the arytenoid.

The treatment of acute stenoses is determined by the disease that caused the stenosis, but besides this, there are also some measures that can be useful in any stenosis regardless of its etiology. In the first place are the long-known agents—narcotics: morphine (for children 0.0025 per year of age) and chloroform; patients calm down, 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 main treatment to take effect, e.g., serum for diphtheria. The beneficial effect of narcotics is explained by the fact that in any inflammatory process in the larynx, a reflex spasm of the laryngeal muscles occurs, which increases the stenosis. The most essential and inevitable measure, when stenosis begins to turn into asphyxia, is surgical intervention—tracheotomy or intubation (see). Chronic stenoses are divided into two groups regarding treatment: one includes cases where the narrowing is caused by scars or infiltrates from perichondritis—organic stenoses; the second—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 area by repeated introduction 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 hold up in practice, mainly because it turned out that the laryngeal lumen, sufficient for free breathing achieved by dilation, soon narrowed again after the cessation of dilation, and that to obtain a more lasting result, a long 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 drawbacks. It is soft, elastic, completely fills the lumen of the airway, 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: cutting the recurrent nerve to convert the incomplete paralysis of the m. postici causing the stenosis into a complete one (Ruault), in which the glottis widens; replacing the paralyzed muscle with a healthy one (Rethi, Marschik); pulling up and fixing the true vocal cord to the thyroid cartilage with a suture (Payr, Perekalin, Galebsky); excision of the vocal cords (Citelli, A. Ivanov); enucleation of the arytenoid cartilage (A. Ivanov), etc. Most of the listed methods now have purely historical and theoretical interest; they did not enter practice because the authors themselves did not obtain the desired results. It is most practical to view paralyzed, immobile vocal cords as scars and to apply the same operation of laryngostomy to functional stenoses.