Phlegmon of the peri-myndalic space and floor of the mouth: causes, symptoms, diagnosis, treatment

Phlegmon of the perimygdalitis space in the lingual tonsil usually develops within 6-8 days, and against the background of antibiotic therapy, the maturation of the abscess can be delayed for up to 2 weeks, after which it opens on its own, and all signs of perimygdalitis of the lingual tonsil disappear within 4-5 days.

Diagnostics in typical cases with acute onset, obvious signs of catarrhal inflammation and development of unilateral infiltrate with subsequent abscess formation does not cause much difficulty. In case of sluggish course, moderate pain syndrome and unclear acute inflammatory signs, the final diagnosis is not always possible from the first day of the disease. In this case, periamgdalitis of the lingual tonsil should be differentiated from sarcoma and gumma of the lingual tonsil, interstitial glossitis, as well as from phlegmon of the sublingual-thyroepiglottic space.

Treatment in most cases is non-surgical (sulfonamides, antibiotics), which, if prescribed early, can ensure the reverse development of the inflammatory process without suppuration. This is facilitated by physiotherapeutic procedures (UHF, laser therapy), as well as ultraviolet irradiation of blood, polymicrobial vaccination and other immunomodulatory methods. In some cases, with increasing suffocation, tracheotomy may be indicated.

An abscess (phlegmon) is opened when its spontaneous emptying is delayed and clinical signs increase. After opening the abscess, antibacterial treatment is continued for another 3 days.

Phlegmon of the floor of the mouth (Ludwig's angina) is a putrefactive-necrotic phlegmonous process, the etiological factors of which are anaerobic streptococci,

Fusospirochetal association bacteria (B. fusiformis, Spirochaeta buccalis), as well as staphylococcus, E. coli, etc. A number of authors do not exclude a certain role in the development of this disease and anaerobic clostridial microbiota. The source of Ludwig's angina in the overwhelming majority of cases are lower carious teeth, gangrenous pulpitis, periodontitis; less often, the infection can enter the tissue of the floor of the oral cavity from the crypts of the palatine tonsils or occur as a complication during the removal of a pathologically altered tooth.

Pathological anatomy. The pathological picture is characterized by extensive necrosis of the cellular tissue, pronounced edema of the surrounding tissues and enlargement of the regional lymph nodes, often necrosis of the muscles located here (mm. hyoglossus, mylohyoideus, venter anterior m. digastrici), the presence of gas bubbles and a sharp putrid odor. The preserved tissues at the incision site are dry, dense, and bleed little. Instead of pus, only a small accumulation of ichorous fluid the color of meat slops is found. As noted by A. I. Evdokimov (1950), the absence of a tendency to purulent melting of the affected tissues is an essential feature of Ludwig's angina, as a nosological form, distinguishing it from banal phlegmons of the floor of the oral cavity, which are characterized by abundant purulent formation and which are incorrectly classified as Ludwig's angina.

Symptoms and clinical course. The onset of the disease is manifested by chills, malaise, headache, pain in the floor of the mouth when swallowing, loss of appetite, insomnia due to increasing bursting pain in the inflammation site. Body temperature rises slowly and only by the 3rd day reaches 39°C and above. The course of the disease is usually severe and only in some cases is of moderate severity.

A typical early manifestation of Ludwig's angina is swelling in the area of the submandibular salivary gland, characterized by a woody density. From here, the inflammatory process in severe cases quickly spreads to the entire area of the floor of the mouth and, descending to the neck, is concentrated in the subcutaneous tissue. On the neck, the edema extends to the collarbones, upwards it first covers the lower half of the face, then spreads to the entire face and eyelids. The skin above the lesion is unchanged in the first 2-3 days, then it becomes pale, then redness and individual bluish-purple and bronze-colored spots appear, typical of anaerobic infection.

Swelling of the tissues of the floor of the mouth causes narrowing of the entrance to the pharynx, the voice becomes hoarse, speech is slurred, swallowing is painful and difficult. The tissues in the sublingual region swell and rise (second tongue symptom), the mucous membrane above them is covered with fibrinous plaque. The tongue is enlarged, dry, covered with a dark brown plaque, slightly mobile, located between the teeth. The mouth is half-open, a putrid odor is felt from it. The face is pale with a cyanotic or earthy tint, expresses fear, the pupils are dilated. Breathing is intermittent, rapid, the patient feels a lack of air. The patient's position is forced, half-sitting.

The general condition of the patient progressively worsens with each passing day, there are stunning chills and profuse sweating, clouded consciousness, delirium. At the same time, the hemoglobin content drops, with pronounced leukopenia, a sharp shift in the leukocyte formula to the left is noted. With increasing general weakness, decreased cardiac activity and a picture of general sepsis, death can often occur by the end of the first, less often the second week.

Complications: pneumonia and lung abscess, asphyxia, mediastinitis, etc.

Prognosis. In the pre-antibiotic period, mortality reached 40-60%, the prognosis was serious. At present, the prognosis can be considered favorable.

Treatment. Early wide and deep intraoral incisions of the lesions are made, submandibular spaces are opened in case of infiltration of the entire space of the floor of the oral cavity and other surgical interventions on the anterior surface of the neck. The wounds are carefully drained with thin rubber strips. During dressings, they are washed with antiseptic solutions and appropriate antibiotics. Use of antigangrenous serums (Antiperfringens, Antiocdematiens, Antivibrionseptic), broad-spectrum antibiotics, especially active against anaerobes, sulfonamides. Intravenous transfusion of UV-irradiated blood, administration of urotropin, calcium chloride are prescribed; in case of severe leukopenia - leukocyte mass. Drugs that enhance immunity, multivitamins, increased doses of ascorbic acid are also used. Oral care is of great importance. The diet is predominantly plant-milk, plenty of fluids. Bed rest must be observed until the necrotic tissue is completely rejected and body temperature returns to normal.