Ludwig's Angina

ANGINA LUDOVICI, the acute septic inflammation of the cellular tissue in the submandibular region of the neck described in 1836 by Dr. Ludwig (Ludwig, Stuttgart). He considered the disease itself as a phlegmon in the region of the submandibular salivary gland with a tendency to putrid necrosis of the tissue. Since then this disease has become known under the name A. L. However, it was also described by Hippocrates, Galen, Celsus, and others. The inflammatory process develops in the bed of the submandibular salivary gland. The bed is bounded above by the muscul. mylo-hyoideus and the edge of the lower jaw, below by the digastric muscle and the hyoid bone. In front, this bed is covered by the superficial fascia of the neck, which, attaching itself to the hyoid bone, goes upward to the face. At the edge of the lower jaw it merges with the fascial covering of the surface of the m. mylo-hyoideus; on the side it gives a process inward, by which the bed of the gland is separated from the retromandibular bed, connecting with it along the course of the blood vessels. Behind, this submandibular receptacle is open, has no limitation, and communicates below with the large connective tissue spaces of the neck; above, through the interval between the posterior edge of the musculi mylo-hyoidei and the anterior surface of the musculi hyo-glossi, it passes into the regio sublingualis. The submandibular bed contains the submandibular salivary gland, covered by its capsule, lymph glands, and vessels, blood vessels and nerves. The process of the submandibular gland together with its duct penetrates into the fissure between the edge of the musculi mylo-hyoidei and the surface of the musculi hyo-glossi and reaches the posterior end of the glandulae sublingualis. By this path a direct communication is established between the regio submaxillaris and the regio sublingualis. The cellular tissue of the submandibular bed is usually infected secondarily. The primary focus of infection is located in the oral cavity (caries teeth, crypts of tonsils, ulcers of the pharynx and floor of the mouth, alveolar necroses, etc.). The causative agent of the inflammation is apparently most often streptococcus, but inflammation can be caused by other microorganisms (staphylococcus, pneumococcus, intestinal bacillus, etc.). Of 106 collected cases, Thomas found indications of bacteriological investigation only in 18 cases: in 6 cases streptococcus was found, in 8 cases streptococcus together with staphylococcus or pneumococcus, in 2 cases only staphylococcus, in one case only pneumococcus, and in one case an undefined bacillus. From the primary focus, infection spreads to the cellular tissue of the submandibular bed either by gradual progression or along lymphatic paths. There are indications that infection from the oral cavity can also pass here along the duct of the submandibular salivary gland. Regardless of the location of the primary focus, infection, penetrating into the submandibular bed, causes phlegmonous inflammation there. A hard, progressive phlegmon develops, which has no tendency to pus liquefaction. The process involves the submandibular salivary gland, muscles, floor of the mouth and tongue, cellular tissue of the neck, pharynx and larynx. Edema develops, which spreads more or less quickly to the face up to the zygomatic arch, to the chin and to the neck up to the clavicle. The edema captures the gums, the region of the sublingual salivary glands, the tongue, which usually reaches enormous sizes, and can also spread to the pharynx and larynx. In rare cases, the process begins with inflammation of the cellular tissue in the regio sublingualis and then passes to the cellular tissue of the submandibular bed. With the development of the process, fetor appears from the mouth, speech, swallowing, and even breathing become difficult. The inflammatory process can pass from one side to the other, can spread to the mediastinum, and can lead to inflammation of the lungs and pleura. The general condition is usually severe: irregular septic temperature (up to 39–40°), poor well-being, headaches, loss of appetite, insomnia. According to the observations of the authors, the disease is especially susceptible to young people aged 16–30, since carious teeth occur most frequently in this age. Men apparently get sick more often than women. Thus, according to Thomas, of 106 cases there were 76 men, 20 women, and in 10 cases the sex was not noted. The prognosis is severe: Thomas, on 106 cases, reports recovery in 63 cases, death in 43 cases (40.56%). The main cause of the fatal outcome is the transition of the inflammatory process to the pharynx and larynx. The worst prognosis occurs when the inflammatory process begins in the regio sublingualis, since in such cases the pharynx and larynx are captured especially quickly. The same significance has the too rapid spread of the process from the submandibular bed to the floor of the mouth. Treatment. First of all, for the purpose of prevention, it is necessary to propagate oral hygiene. Dentists before extracting teeth must carry out disinfection of the oral cavity with antiseptic solutions most carefully, since cases have been described in which A. L. developed after injecting cocaine around a carious tooth and extracting it. In the developed disease, anti-streptococcal serum is applied, but without great results. Therefore, if the diagnosis is established exactly, a wide and deep incision through the submandibular bed should be made, and with extensive damage also along the midline between the chin and the hyoid bone, penetrating through the musculus mylo-hyoideus as far as the mucous membrane of the oral cavity. Usually turbid putrid fluid is released, and sometimes gas as well. Some surgeons, during these incisions, remove the submandibular salivary gland, others incise its capsule. In case of acute difficulty of breathing, tracheotomy must be performed. In view of the possibility of thrombosis of the venae jugularis and, consequently, embolism, patients in the postoperative period should not leave bed early and should be discharged only when acute inflammatory phenomena (infiltrate, high temperature, etc.) have passed.