Mpilo Medical Journal

Volume 1, No 3, January 1999.

Editor: Predrag M. Maksimovich, MD, DDS, ENT.

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Predrag M. Maksimovich


Ludwig's Angina (Angina Ludovici)

Cellulitis of the Floor of the Mouth

(Compiled by Predrag Maksimovich)


A rapidly spreading, bilateral, indurated cellulitis occurring in the floor of the mouth without abscess formation or lymphatic involvement.


The disease process referred to as Ludwig's angina was formally described in 1836 by Wilhelm Friedrich von Ludwig when he reported on five patients in whom a rapidly progressive soft tissue infection developed, involving the submandibular space and floor of the mouth. Several of these patients died of acute airway obstruction and asphyxiation. Although his original description accurately described the disease process and relevant findings, he erroneously felt that he was dealing with a new form of neck inflammation that was infectious and occurring in an epidemic fashion.
Ludwig's angina, with its potential for airway obstruction, has probably been known since antiquity with references by Hippocrates, Galen, Caelsius, and others under a variety ofterms such as cyanche, carbunculus gangraenosus, morbus strangulatorius, and angina maligna.


Ludwig's angina is an infection of the floor of the mouth. Floor of the mouth is comprised of sublingual space, submandibular space and submental space. The sublingual and submandibular spaces are separated by the mylohyoid muscle and are connected via the mylohyoid cleft (containing the tail of the submandibular gland, Wharton's duct, lingual nerve, hypoglossal nerve, lymphatics, and several arteries and veins). The floor of the submandibular space is formed by the superficial layer of the deep cervical fascia attaching from the hyoid bone to the mandible. The roof is the mylohyoid muscle while the walls are inner surface of the body of mandible, anterior and posterior bellies of the digastric muscles. There is ready communication across the midline with the opposite sublingual or submandibular spaces. The submental space is bounded by the anterior bellies of the digastric muscle laterally, the mandible anteriorly, mylohyoid superiorly and the hyoid bone inferiorly. Thus, infection may readily spread from the main portion of the submandibular space to the submental space and from there to the opposite side. The space located above the mylohyoid muscle is referred to as the sublingual space and consists of loose connective tissue surrounding the tongue and sublingual gland and, again, this space readily communicates with its counterpart on the opposite side. It is worth mentioning that according to the old anatomical nomenclature the submandibular space was described as being formed by the sublingual, submaxillary and submental spaces. Today, the term submaxillary space is obsolete and is replaced by the term submandibular space while the region formerly termed submandibular space is now described as floor of the mouth.

The floor of the mouth as a whole is bounded by the oral mucosa and tongue superiorly and medially, the mandible anteriorly and laterally, the superficial layer of the deep cervical fascia with its tight attachment to the mandible and hyoid bone laterally and inferiorly, and the hyoid bone inferiorly. The submandibular space, or one of its components, is perhaps the space most commonly involved by significant primary infections of the head and neck. Infections may arise from injuries to the floor of the mouth, sublingual or submandibular gland sialoadenitis, or infections from the roots of the mandibular teeth.

Ludwig's angina is a rapidly spreading cellulitis that usually begins in the submandibular space, resulting from an infected molar, and then rapidly spreads to involve the sublingual space, usually on a bilateral basis. With the mandible and superficial layer of the deep cervical fascia presenting relatively unyielding barriers superiorly and laterally, the tongue is forced upward and posteriorly, giving rise to the severe airway obstruction associated with this condition. Submandibular space infections may also spread posteriorly to the carotid sheath or retropharyngeal space, or both, by crossing the lateral pharyngeal space.

As will be seen, the majority of cases of Ludwig's angina are of dental origin, with the development of a submandibular infection that then progresses to involve the sublingual space. Crucial to this process is the relationship of the mandibular dentition to the attachment of the mylohyoid muscle along the mylohyoid ridge. The anterior teeth and first molars regularly attach superior to the mylohyoid insertion, and infection arising from these tooth roots commonly results in a relatively limited sublingual abscess. The second and third molar roots are routinely below the mylohyoid ridge, and infection presenting on the lingual surface will enter the submandibular space. Additionally, it is important to recognize that the roots of the anterior teeth and first molar approximate the lateral mandibular surface, whereas the second and third molar roots approach the lingual surface of the mandible.

Ludwig's angina usually develops from dental or periodontal infection, especially of the 2nd and 3rd mandibular molars. It may occur in association with problems caused by poor dental hygiene (i.e. gingivitis and dental sepsis), tooth extractions, or trauma (i.e. fractures of the mandible, lacerations of the floor of the mouth, peritonsillar abscess).

Although not a true abscess, Ludwig's angina resembles one clinically and is treated similarly. Untreated, it may be fatal.

The major manifestations are pain in the area of the involved tooth; severe, tender induration of the submandibular region; trismus; dysphonia; drooling and inability to swallow; and dyspnea and stridor from laryngeal edema and tongue elevation. Fever, chills, and tachycardia are usually present. X-rays of the head and neck are useful to assess the degree of soft-tissue swelling and airway obstruction.


Ludwig's angina occurs most commonly in young adults with periodontal disease. Formerly, Ludwig's angina had been ascribed to an infectious source with an epidemic occurrence. However, it now appears that the reported occurrences of clusters of Ludwig's angina are most likely the result of pseudo-Ludwig's anginas secondary to suppurative lymphadenitis in cases of scarlet fever, diphtheria, or measles. Tschiassny, in an extensive review of the literature and detailed anatomic studies, demonstrated that the majority of Ludwig's angina cases are the result of abscesses second or third molar teeth with penetration into the submaxillary space below the mylohyoid ridge and initiation of a cellulitis. He found that a dental cause was responsible in 75 to 80 per cent of cases, followed by penetrating injury of the floor of the mouth (stab wound, gunshot wound, horse kick, and so on), with mandibular fractures accounting for the rest of the cases. It is interesting to note that extraction of a diseased molar will often initiate the infection, and Tschiassny speculated that the injection of local anaesthetic may seed the submandibular space. Patterson noted that 85 per cent of their cases were related to a dental pathological condition, with 40 per cent of the cases following extraction of a diseased molar. The remaining cases were in children younger than 3 years of age in whom no clear cause could be demonstrated.

The infection is often caused by a hemolytic streptococcus, although the infection may be a mixture of aerobic and anaerobic organisms, which may account for the presence of gas in the tissues. Chills, fever, increased salivation, stiffness in tongue movements, and an inability to open the mouth herald the infection. Thickness is found in the floor of the mouth, and the tongue is elevated. Tissues of the neck become boardlike.

The patient develops a toxic condition, and respiration becomes difficult.

The larynx is edematous.

Microbiological Features

Since most cases of Ludwig's angina are related to a dental cause, it is not surprising that the bacterial cultures mirror the oral flora. The compilation of accurate microbiologic data has been complicated by the fact that most patients have had at least several doses of antibiotics by the time surgical treatment is performed and the additional fact that a number of infections resolve with conservative treatment and no surgical drainage and, thus, no specimen is obtained. It is clear that these infections are almost always the result of mixed flora, involving both aerobes and anaerobes. The most commonly reported aerobes are alpha-hemolytic streptococci, followed by Staphylococcus. The data on anaerobic cultures are more difficult to interpret because of the presence of prior antibiotic therapy and the difficulty in culturing anaerobic organisms. The normal oral flora typically contains Peptostreptococcus, Peptococcus, Fusobacterium nucleatum, Bacteroides melanogenicus, B. oralis, Veillonella, and Spirochaeta. This combination of aerobic and anaerobic organisms gives rise to a synergistic effect caused by the production of endotoxins such as collagenase, hyaluronidase, and proteases, the combination of which promotes a rapidly progressive infection with the clinical features of tissue necrosis, local thrombophlebitis, putrid odor, and gas formation. As a rule, gram-negative organisms do not play a significant role in Ludwig's angina, although Haemophilus influenza, Escherichia coli, and Pseudomonas have all been reported.

Clinical Features

The clinical picture of Ludwig's angina is typically that of a young man with poor dentition that presents with a history of increasing oral or neck pain and swelling. Frequently, the patient's symptoms are unilateral, but they soon progress to involve both sides. As the infection progresses, there is increasing edema and induration of both the external perimandibular region and the floor of the mouth. The soft tissues of the floor of the mouth become tremendously swollen and, as a result of the relatively unyielding superficial layer of the deep cervical fascia and mandible, the expansion progresses superiorly and posteriorly. This expansion has the effect of thrusting the tongue posteriorly and superiorly with approximation of the palatal vault. There is increasing neck rigidity, trismus, odynophagia and, eventually, drooling. The temperature is typically elevated in the 100 to 102 F range, and 104 F is not uncommon.

As the swelling progresses, there is increasing encroachment upon the airway, and the patient assumes an erect posture with tachypnoea. Dyspnea and stridor signal the imminent danger of airway obstruction. This is truly a desperate situation because visualization of the larynx by conventional techniques is impossible, and attempts at intubation may actually precipitate airway obstruction. Similarly, a tracheostomy is extremely difficult because of the inability of the patient to lie supine and the presence of significant neck edema. The point to stress is the rapidity with which this process may occur; many case reports detail a progression from onset of symptoms to respiratory obstruction within the space of 12 to 24 hours.

Physical Examination

The physical examination typically shows fever, tachycardia, and variable degrees of respiratory obstruction with dysphagia and drooling.

The submandibular and submental regions are tense, swollen, and tender. The floor of the mouth is tense and indurated, with massive mucosal swelling and pouting of soft tissue over the edges of the lower teeth. Fluctuance is unusual. The tongue is pushed superiorly, and there is marked trismus.

Indirect examination of the larynx is, at best, difficult and usually impossible. Nasopharyngeal fiberoptic examination will reveal the presence of a greatly enlarged base of the tongue pushing the epiglottis posteriorly; the supraglottis and endolarynx are normal in appearance.

Laboratory and Radiologic Examination

The diagnosis and treatment of Ludwig's angina are based on the clinical parameters outlined; laboratory and radiologic studies offer only supporting evidence. Typically, the white blood cell count is moderately to markedly elevated in the range of 15,000 to 20,000, with a marked shift to the left. X-ray studies will show soft tissue edema, occasionally gas, and posterior displacement of the tongue with airway encroachment. Because of the fact that these infections are often odontogenic, panoramic tomography may be helpful in determining the site of origin for the infection and may aid in planning the treatment regimen.


Since Ludwig's original description, a variety of inflammatory conditions related to the floor of the mouth have been labeled Ludwig's angina (Table 1), but in reality many would most appropriately be termed pseudoangina ludovici. These pseudo-Ludwig's angina are more limited infections that involve only the sublingual space, the submandibular lymph nodes, the submandibular gland, or the submental space, or they are abscesses involving one or more of these spaces. Ludwig's original description was of a disease process that was a "gangraenous induration of the connective tissues of the neck which advances to involve the tissues which cover the small muscles between the larynx and the floor of the mouth". There is a general consensus in the literature that to qualify as a true Ludwig's angina, the following features should be present: (1) a spreading cellulitis with no specific tendency to form abscesses, (2) involvement of both submaxillary and sublingual spaces, usually bilaterally, (3) spread by direct extension along fascial planes and not lymphatics, (4) involvement of muscle and fascia but not submandibular gland or lymph nodes, and (5) origination in the region of the submaxillary space with progression to involve the sublingual space and floor of the mouth.

Table 1. Criteria for Diagnosis of Ludwig's Angina

Rapidly progressive cellulitis; not an abscess

Develops along fascial planes with direct extension; does not involve lymphatic spread

Does not involve submandibular gland or lymph nodes

Involves both sublingual and submaxillary spaces and is usually bilateral

Ludwig's angina may be described as an overwhelming, generalized septic cellulitis of the submandibular region. Although not seen often, Ludwig's angina, when it does occur, usually is an extension of infection from the mandibular molar teeth into the floor of the mouth, since their roots lie below the attachment of the mylohyoid muscle. It is usually observed after extraction.

This infection differs from other types of postextraction cellulitis in several ways. First, it is characterized by a brawny induration. The tissues are boardlike and do not pit on pressure. No fluctuance is present. The tissues may become gangrenous, and when cut, they have a peculiar lifeless appearance. A sharp limitation is apparent between the involved tissues and the surrounding normal tissues.

Second, three fascial spaces are involved bilaterally: submandibular, submental, and sublingual spaces. If the involvement is not bilateral, the infection is not considered a Ludwig's angina.

Third, the patient has a typical open-mouth appearance. The floor of the mouth is elevated, and the tongue is protruded, making respiration difficult. Two large potential fascial spaces are at the base of the tongue, and either or both are involved. The deep space is located between the genioglossus and geniohyoid muscles; the superficial space is located between the geniohyoid and mylohyoid muscles. Each space is divided by a median septum. If the tongue is not elevated, the infection is not >considered a true Ludwig's angina.

Pathognomonic for Ludwig's angina is the sign of cock's crest. Sometimes unilaterally but usually bilaterally the floor of the mouth is red and swollen and a streak of yellow fibrin covers sublingual carunculae so that it looks as if a cock is protruding his red head with a yellow crest from below the tongue. It can be stated safely that if the mucosa of the floor of the mouth is normal there is no Ludwig's angina.


Treatment of Ludwig's angina depends on the stage of disease when the patient presents. Actually, Ludwig's angina is a spectrum of conditions, ranging from a periapical abscess and mild cellulitis in its early stage to massive sepsis with airway obstruction later on. Treatment may be tailored to the status of the individual patient, with the understanding that this disease may progress very rapidly, and if initial steps are not successful, more radical means must be employed. In the early stages of Ludwig's angina, with unilateral mild swelling and edema, simple intravenous antibiotics and supportive measures may be sufficient. This is often coupled with extraction of the inciting tooth, if it is identifiable. If the patient presents with more advanced disease or the disease progresses to bilateral swelling, dysphagia with drooling, or any symptoms of airway compromise, early airway intervention, in a controlled fashion, is advocated rather than waiting until emergency procedures are required.

Surgical treatment is directed at securing an airway and providing surgical drainage. The choice of airway management rests on the experience and availability of the treating personnel. Although airway management by nasotracheal intubation, with or without fiberoptic assistance, is well described in the literature, it should be borne in mind that airway manipulation may precipitate acute obstruction and, thus, a tracheostomy set should always be available. Because of the possibility of postoperative extubation, and the difficulty of reintubation, conversion to a tracheostomy is generally advocated for postoperative airway management. If intubation is not possible, a tracheostomy under local anaesthesia, often with the patient sitting upright, is required. This may be complicated by the presence of significant edema in the neck. Those patients with a rapidly deteriorating airway may require a cricothyroidotomy.

Once the airway is established, surgical drainage is performed.

Drainage consists of a wide surgical decompression of the suprahyoid region. Generally, the infectious process is bilateral, and the approach is through a median, horizontal incision three to four fingerbreadths below the mandibular margin. The length of the incision may be variable, but generally it crosses to the submandibular region bilaterally. The mylohyoid muscle is split in the midline, and drainage is established both medially and laterally. Often, the side on which the infection started needs to be explored with decompression of the submandibular capsule and blunt dissection to the mandibular margin. The tissues have been described as having a peculiar "salt pork" appearance, with woody induration, watery edema, and little bleeding. Gross purulence is rarely encountered at the time of exploration but will often drain from the wound several days after decompression. Multiple drains are placed, and the wounds are left open.

The choice of antibiotics must be tailored to the individual patient, but high-dose penicillin (12 to 16 million units/day) is considered the drug of choice. Chloramphenicol and clindamycin are alternate possibilities, especially in penicillin-allergic patients. In immunocompromised patients, consideration should be given to providing broader coverage for the possibility of gram-negative anaerobic organisms and penicillin-resistant staphylococci.


Ludwig's original description reported a 60 per cent mortality rate, whereas Patterson's recent report had a 0 per cent mortality rate. The major cause of death in Ludwig's angina is acute airway obstruction, and the most effective means of preventing it include careful monitoring of the patient with intervention at the earliest sign of airway compromise.

Tracheostomy (either initially or after intubation) is generally considered the safest means of maintaining an airway. Following acute airway obstruction, the next major potential complication of Ludwig's angina is extension of the infection to the carotid sheath or retropharyngeal space with inferior extension into the mediastinum. Although extension to the mediastinum was formerly common, it is somewhat unusual with present-day surgical drainage and antibiotics. Extension of Ludwig's angina should be suspected if there is persistent or increasing neck edema, spiking temperatures, or persistent leukocytosis. Later findings of mediastinal extension include increasing signs of septic shock with tachycardia and decreasing blood pressure, crepitation of the lower neck, or development of mediastinal crepitation or a mediastinal crunch. The patient with mediastinitis will often report increasing neck pain, chest tightness, and increasing dyspnea. The chest x-ray film may show a widened mediastinum, pericardial air, pulmonary infiltrates, and extrapleural fluid. As mentioned, in the acute phase of Ludwig's angina, there is little or no purulence because of the fact that the infection is developing so rapidly that there is no time for pus to develop; later it is common for purulence to drain from the wounds. It is also possible that isolated, undrained pockets of pus may develop, which may give rise to continuing signs of sepsis. A CT scan of the neck with contrast medium may be most helpful in detecting these residual pockets and directing surgical drainage.

Other complications can include asphyxiation, aspiration pneumonia, lung abscesses, and metastatic sepsis.


1. Paparella, M.: Otolaryngology & Head and Neck Surgery.
2. Kruger, G.: Textbook of Oral and Maxillofacial Surgery.
3. Merck Manual.
4. McMinn, R. M. H.: Last's Anatomy.

Case Reports

Several other patients.

Cystadenocarcinoma of the RT submandibular gland.

Recurrence one year after the first operation.

Cystadenocarcinoma growing for about four years. Notice the ophthalmoplegia.

The patient immediately after LT hemimandibulectomy with exarticulation from the second LT premolar tooth for carcinoma involving LT trigonum retromolare, anterior LT tonsil and LT angle of the mandible. Notice the deviation of the mandible to the left.

Intraoral wound healing mainly per secundam. One vicryl sutur is still visible.

Recurrence in the LT cheek one year after the first operation. Removed with radical parotidectomy.

State after removal of the tumor of the LT lower eyelid and zygomatic area with reconstruction with local rotational flap. Notice the defect of the eyelid, ektropion and scar.

Squamocellular carcinoma destructing the nos and extending per continuitatem to the upper lip, both cheeks and both peri- and submandibular regions.

After partial amputation of the nose and upper lip.

Squamocellular carcinoma destructing almost whole of the body of the mandible.

Primary reconstruction achieved with transpositional regional flap from the neck. Lower cortex of the mandible was retained to keep the space.


A patient from the rural areas treated for a long time for an "eye infection". Alleggedly, eye globe was removed.

An orbital exenteration was performed. A structure similar to a shrunken eye globe was also removed. Histology: carcinoma.

Some six months after the first operation a local recurrence in the temporal region is evident.

LT parotid cystadenocarcinoma.

Scar is visible after a biopsy (sic!!!) performed in other hospital. Superficial parotidectomy was done with preservation of the facial nerve and the scar with the surrounding skin was included with the specimen.

CT scan showed a lesion the size of a fist in the anterior RT frontal lobe.

During the first operation, black masses were removed.
Histology: blastomycosis.
During the second operation the neurosurgeon removed the tumefaction from the anterior lobe.

Sarcoma maxillae.

After the first operation.

Six months later the patient appeared with even greater tumour.

After the second operation.

Pharyngeal fistula after irradiation and total laryngectomy for laryngeal carcinoma.

Reconstruction with Ariyan's pectoralis major musculo-cutaneous flap. Notice the elevation of the Bakamjian's delto-pectoral flap for possible future use.

Incipient necrosis of the flap above the tracheostomy.

Terminal stage of the laryngeal carcinoma with fungiform recurrences.

Plasmacytoma undergoing (unsuccessful) radiotherapy.


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