Parotitis

PAROTITIS, inflammation of the parotid gland. Infectious, or secondary, parotitis arises as a result of local processes or general infectious diseases. The former include: 1) foreign bodies in the gland duct, leading to ascending infection and damage to the gland parenchyma; 2) inflammatory processes in neighboring organs (purulent cervical lymphadenitis); and 3) various types of stomatitis, especially mercurial. Finally, trauma and wounds can also cause extensive and life-threatening purulent parotitis. Parotitis arising in connection with local inflammatory processes, in contrast to parotitis observed during infectious diseases, usually runs a more favorable course and has a good prognosis. As for parotitis during infectious diseases, it is observed as a severe complication in typhus, scarlet fever, pneumonia, influenza, smallpox, epidemic encephalitis, cholera, and sepsis. Isolated cases of gonorrheal parotitis have been described. Infectious parotitis also includes postoperative parotitis, which is of great interest in the daily work of surgical departments. Mention should also be made of parotitis encountered in severely mentally ill patients. A particularly frequent complication is parotitis in typhus, predominantly in epidemic typhus, which is characterized by the following statistical data: 1) parotitis occurs in epidemic typhus in 4.7% of all cases; 2) in typhoid fever, in 1.2%; 3) in relapsing fever, in 0.8%. A large percentage of cases fall to women (63%). Children are rarely affected (Kartashov). Of all surgical complications in epidemic typhus, 16% are cases of parotitis. In other diseases mentioned above, parotitis is encountered much less frequently, usually in the form of isolated cases. Etiology and pathogenesis. In the pus during parotitis, Staphylococcus aureus is most often found, less often Staphylococcus albus and streptococcus. Kartashov isolated a special Gram-positive microbe from the pus in typhus-associated parotitis, belonging to the type Micrococcus tenuis. In isolated cases, pathogens of the infectious disease that had been complicated by parotitis were found (typhoid bacillus, Yanovsky). The question of the routes of infection penetration into the parotid gland is still controversial. Three possible routes should be pointed out: 1) hematogenous, 2) lymphogenous, and 3) stomatogenous. Pathological-histological studies do not provide direct indications of the hematogenous route of infection penetration into the gland. In microscopic preparations, bacteria are detected not in the capillaries of blood vessels or in the surrounding tissue, but in the form of clusters in the alveolar branches of the gland and in the excretory ducts (Orth, Hanau). The unilateral nature of the lesion, the rarity of parotitis in general septic processes, as well as bacteriological data, also somewhat diminish the significance of the hematogenous route of bacterial introduction. The second route, lymphogenous, also cannot play a decisive role in the penetration of microbes into the parotid gland. The main collectors of lymph from the oral cavity and nose are the lymph nodes located in the submandibular triangle, and not those present on the periphery and in the stroma of the gland. The latter collect lymph coming only from a small section of the nasopharynx. Thus, the possibility of infection entering via lymphatic pathways is limited. It should also be noted that infectious parotitis is rare in children, despite the fact that they have a well-developed lymphatic system here. The stomatogenous route of infection introduction is obviously the most frequent and important. A decrease in saliva secretion during febrile diseases as a result of high temperature, low fluid intake, a decrease in taste stimuli, and the absence of chewing movements, with the constant presence of microbes in the lower part of Stensen's duct, creates favorable conditions for ascending infection. In this regard, one must take into account the often insufficient oral hygiene in severe patients, the presence of a large number of carious teeth, the possibility of a qualitative change in saliva in the sense of a decrease in its bactericidal properties, as well as an increase in bacterial virulence due to the weakening of the organism by severe infection. All these factors create very favorable conditions for the development of stomatogenous infection and its penetration into the gland. Somewhat contradicting this position is the frequent finding in pus during parotitis of pure cultures of Staphylococcus aureus without an admixture of other oral bacteria, as well as the absence of putrefactive phenomena, which are so characteristic of oral infection. In infectious diseases, the parotid gland is affected much more often than other salivary glands. The special location of this gland, surrounded by a dense fascia and compressed between the mastoid process and the angle of the lower jaw, presents favorable conditions for vascular disorders and thereby creates a kind of locus minoris resistentiae (Davydovsky). On the other hand, the thin saliva of the parotid gland, unlike that of other salivary glands, does not contain mucin and therefore, according to Herzen, does not possess the ability to agglutinate bacteria and thus prevent their advancement. The comparative frequency of parotitis in epidemic typhus may be due, on the one hand, to the exhaustion of patients even before the disease (observations on epidemics of specifically famine typhus point to a large number of complications of this kind), and, on the other hand, by virtue of organic changes in the secretory nerves and salivary centers of the medulla oblongata, a sharp decrease in the secretion of salivary glands of a functional nature is possible, as well as a qualitative change in this secretion. Furthermore, in epidemic typhus, due to the particularly prolonged fever, anorexia, and unconscious state, the function of the gland must undoubtedly suffer even more significantly (Davydovsky). Pathological anatomy. Parotitis is distinguished as: 1) catarrhal ("serous" parotitis according to Davydovsky), which represents only edema of the gland; 2) purulent; and 3) gangrenous. The first and third forms are rare. Most often (in 75%) purulent parotitis occurs. In microscopic studies, one usually finds in the small and medium excretory ducts of the gland (especially in the section of secretory tubes) an abundant accumulation of leukocytes and desquamation of the duct epithelium; the walls of the ducts are eroded in places, with purulent infiltration spreading to the stroma of the gland. Individual sections of the gland parenchyma are in a state of necrobiosis or amorphous decay (in areas of diffuse infiltration). Clinical picture and course. Parotitis arises in epidemic typhus in the second half of the disease, between the 15th and 25th day; in typhoid fever, between the 14th and 25th day; in relapsing fever, between the 21st and 25th day, usually after the second attack (Hesse); in influenza, on the 13th–14th day; in pneumonia, on the 9th–10th day. There is an indication of the onset of parotitis after epidemic typhus on the 57th and 63rd day (Kartashov). The lesion in infectious parotitis is most often unilateral. In bilateral processes, one side becomes ill first, then, after 4–5 days, the other. Some time after the onset of the underlying disease, a sudden rise in temperature and a sharp deterioration in the general condition occur: sharp pains appear in the area of the inflamed gland, radiating to the ear, the temporal region, and the head; there is ringing in the ear, sometimes some weakening of hearing, and occasionally a temporary paresis of the facial nerve. Swallowing and opening the mouth are so painful that patients refuse food. There is dryness in the mouth. Patients become restless. Soon, swelling appears in the area of the affected gland, spreading from the middle of the cheek to the neck. The edema often spreads to the scalp and even to the opposite side of the face. The face takes on a characteristic expression, especially in bilateral lesions. With the increase in swelling, all complaints and shooting pains become more intense due to a sharp increase in pressure on the unyielding and tense fascia of the gland. Movements of the lower jaw are barely possible, and breathing is difficult. The skin is reddened, immobile, and edematous. Superficial veins are dilated, and the complexion is bluish-purple due to the compression of large venous trunks. Often, there is a picture of rapidly progressing phlegmon. All these phenomena increase until the 3rd–4th day, after which either symptoms of regression and subsidence of the process appear, or, most often, signs of suppuration. Detecting fluctuation during suppuration, thanks to the dense and unyielding fascia covering the gland, is sometimes difficult. Often, pus breaks through into the external auditory canal in the absence of clear signs of fluctuation on the cheek. In such cases, one must judge the suppuration of the gland by the increasing swelling and rising temperature during a progressive deterioration of the general condition. In favorable cases, the process resolves within 1–2 weeks; only an enlargement and induration of the gland remain for a more or less prolonged time. If it results in suppuration, the disease takes a prolonged course, sometimes accompanied by extensive destruction of the parotid gland. Cases of death with symptoms of sepsis are not uncommon. Complications. The capsule of the gland, formed from several fascial layers, has two weak points; one of them is located at the apex of the pharyngeal process of the gland: here there is an opening in the fascial capsule, creating a direct connection between the gland and the adjacent tissue of the cervical neurovascular bundle.

Pus can easily break through this opening and descend along the vessels to the mediastinum. The resulting phlegmonous parapharyngitis and mediastinitis quickly lead to the death of the patient. A second unprotected area is located along the lower surface of the external auditory canal. Here, the fascia does not cover the gland and passes directly onto the periosteum of the tympanic part of the temporal bone. In this place, pus can destroy the membranous-cartilaginous part of the external auditory canal and exit outward. In this process, there are occasionally cases of purulent inflammation of the middle ear with all its consequences. Thromboses of the jugular veins and cerebral sinuses are also observed (Smith, Bloxam). Cases of severe venous and arterial hemorrhages have been described (Nelaton, Gilette) due to the destruction of vessel walls by the purulent process. Paralyses of the facial nerve are also possible due to its destruction. Herzen admits the possibility of paralysis of the soft palate in typhus-related parotitis as a result of ascending neuritis of the nerves innervating the muscles of the soft palate. The diagnosis of parotitis does not present great difficulties. When, during an infectious disease, swelling of the parotid gland appears with a characteristic picture of inflammation and corresponding complaints of the patient, the diagnosis of parotitis does not cause doubts. It is important to establish the nature of the process and the time of abscess formation, which is necessary for determining treatment methods and timely surgical intervention. The prognosis depends to a large extent on the state of the patient's strength and on the severity of the general infection against the background of which parotitis develops. The process rarely shows a tendency toward regression; usually, a severe purulent inflammation develops, requiring surgical intervention. In gangrenous parotitis and in most of the complications mentioned above, the prognosis is always poor. In uncomplicated cases, the highest percentage of mortality is given by typhus-related parotitis, especially in bilateral lesions. Parotitis that develops at the very height of the disease worsens the course of the underlying disease and clouds the prognosis. Parotitis that develops after the crisis (in typhus) is less dangerous. Mortality in typhus-related parotitis increases in connection with the increase in the age of patients. According to Kartashov's data, parotitis gives from 4 to 30 years - 8%, from 30 to 40 years - 14%, from 40 to 50 years - 33%, and from 50 years and above - 45% mortality. The average mortality in typhus-related parotitis is 20-25%. Postoperative parotitis belongs to rare complications (0.5%). Most often (in 75%) it occurs after operations in the abdominal cavity. According to the collective statistics cited by Opokin and Heineke, in 72% of cases, parotitis occurred after operations on the female genital sphere, which was explained by the reflex connection between these organs. Later statistics (Zilberman and Kagan), while also pointing to the frequency of parotitis after laparotomies, do not confirm the data of Opokin and Heineke. Predisposing factors for postoperative parotitis can be considered: 1) a decrease in the secretory activity of the glands under the influence of preoperative fasting and restriction of fluid intake after the operation, 2) insufficiently careful wiping of the mouth during the operation, pulling out the tongue with the infliction of abrasions, wounds, etc., 3) traumatization of the parotid gland during insufficiently skillful holding of the lower jaw during anesthesia, and 4) negligence in the care of the oral cavity after the operation. The influence of various types of anesthesia as a predisposing factor has not been clarified. One of the causes of a more constant nature should be recognized, according to the experiments of I. P. Pavlov, as a reflex decrease or temporary cessation of saliva secretion after laparotomies. A disease of parotitis is noted relatively often in patients for whom nutrition through the mouth is sharply limited or completely stopped (in cases of bleeding stomach ulcers, etc.). Cases of parotitis after gunshot wounds have been described ("post-traumatic" parotitis of Larin). These data testify to the predominance of stomatogenic infection in postoperative parotitis. Some authors (Zilberman and Kagan) do not exclude the possibility of hematogenous infection, assuming that the abundance of anastomoses between the vessels of the masseter muscle and the parotid gland contributes, during contraction of the masseter muscle, to the settling of an infected embolus in the gland and the development of postoperative parotitis. According to Frankel, the mechanism of the onset of postoperative parotitis is analogous to that in postoperative thrombophlebitis. Postoperative parotitis occurs most often on the 4th-5th day after the operation with a sudden increase in temperature and a sharp deterioration in the general condition. Subsequently, the forms of the clinical picture and the course of the disease differ little from the picture of parotitis described above. Parotitis usually does not affect the healing processes of the surgical wound. The prevention of infectious parotitis is basically reduced to careful care of the oral cavity. It consists of carefully wiping the oral cavity of weakened patients with a finger wrapped in soft gauze moistened in a weak solution of citric acid (Herden), Kalii hypermanganici, etc. This measure leads simultaneously to an increase in saliva secretion. Rinsing the mouth with weak antiseptic solutions (Sol. Kalii hypermanganici-2.5 : 50.0; a few drops per glass of boiled water until it turns the color of red wine; 2% solution of boric acid, etc.). In the absence of contraindications, it is necessary to prescribe sufficient fluid intake by mouth. In surgical practice, before the operation, the oral cavity must be brought into complete order by brushing teeth and multiple rinses. After the operation, one must avoid, if possible, restricting fluid intake by mouth. Treatment of parotitis at the beginning of the disease, in the absence of signs of suppuration, should be reduced to the application of heat, mainly in the form of hot warming compresses, changed 3-4 times during the day. This measure, by causing hyperemia, contributes to the resolution of the process, gives a pleasant sensation of warmth, and significantly reduces pain. Dry heat and, in particular, light procedures (blue lamp, Sollux) have an equally favorable effect, with the help of which it is sometimes possible to arrest the acute phenomena of parotitis. Upon the appearance of signs of suppuration (mainly fluctuation), it is necessary to make an incision and release the pus. Early incisions do not make it possible to open all purulent foci, which may subsequently require multiple additional incisions. After early incisions, persistent salivary fistulas are observed (Herzen). Defenders of early operations (Hesse) believe that the performed incision should prevent the penetration of the purulent process deep inside and prevent perforation into neighboring organs. Furthermore, after the incision of the strongly tense fascia of the gland, the unbearable pain weakens. Ultimately, the question of the timing of intervention is decided individually in relation to each separate case, depending on the severity of the lesion and the general condition of the patient. Most surgeons still resort to incisions in the presence of clear signs of suppuration. One must operate under general anesthesia. Incisions should be made in a direction parallel to the course of the branches of the facial nerve, for example: a horizontal incision under the angle of the lower jaw, an incision below the earlobe along the line connecting the latter with the corner of the mouth, etc. Herzen makes two incisions: the first is vertical, 1 cm medial to the external auditory canal, parallel to the temporal artery and the n. auriculo-temporalis to the place of attachment of the earlobe to the skin of the face; the second incision is behind the angle of the lower jaw, parallel to the stylohyoid muscle. These incisions provide good access to the pharyngeal process and are located on the periphery of the gland, where there are no excretory ducts of significant size. After dissecting the fascia of the gland, one must enter its tissue by blunt dissection, without making rough manipulations to avoid damaging large vessels; it is necessary to penetrate with a finger to the pharyngeal process of the gland; loose tamponade. After the operation, final healing usually occurs in 4-6 weeks. As possible postoperative complications, one should note: 1) persistent salivary fistulas, 2) paralyses of the facial nerve (not often), and 3) as a rare complication, hyperhidrosis parotidea.