52. Ludwig’s Angina
Definition
Ludwig’s angina is cellulitis of the mouth floor. It expands very rapidly and can spread to other areas of the body, such as the mediastinum or the coccyx, via the myriad tissue planes found within the neck. Ludwig’s angina is potentially fatal.
Incidence
Currently there is no accurate estimate for the frequency at which this severe form of cellulitis occurs.
Etiology
For 100 years after the original description, Ludwig’s angina was generally viewed as a complication of a local anesthetic agent infiltration given for extraction of mandibular molars. The actual pathogenesis is the extension and expansion of a dental abscess into the submandibular space(s). Even today, the majority of Ludwig’s angina cases are initiated by an odontogenic source.
Possible Sources of Ludwig’s Angina
• Brachial cleft anomalies
• Cervical lymphadenitis
• Compound mandibular fracture
• Dental abscesses/infections
• Foreign body aspiration
• Infected malignancy
• IV drug use/abuse
• Lymphalocele
• Mastoiditis with apicitis of the petrous part of the temporal bone and Bezold’s abscess (abscess in the neck with pus tracts deep to the superior portion of the sternocleidomastoid muscle and along the posterior belly of the digastric muscle)
• Necrosis and suppuration of a malignant cervical lymph node or mass
• Oral surgical procedures
• Otitis media
• Penetrating trauma to the oral cavity pharynx
• Salivary gland infection/obstruction
• Sialadenitis
• Thyroiditis
• Tonsillar and pharyngeal infections
Infectious Organisms Associated with Ludwig’s Angina
• Bacteroides melaninogenicus
• Bacteroides oralis
• Escherichia coli
• Fusobacterium nucleatum
• Hemophilus influenzae
• Peptostreptococcus species
• Pseudomonas species
• Spirochaeta species
• Staphylococcus aureus
• Streptococcus pneumoniae
• Streptococcus pyogenes
• Streptococcus viridans
Signs and Symptoms
• Difficulty breathing
• Dysphonia
• Edema of neck, tongue, and the submandibular region
• Fear
• Increased salivation
• Pain
• Protruding tongue
• Trismus
Medical Management
The highest priority for care of a patient with Ludwig’s angina is to ensure a patent airway. This form of cellulitis spreads/expands quite rapidly. Despite the numerous fascial planes within the neck, the expansion of the inflammatory edema is limited by the mandible, hyoid bone, and superficial layer of the deep cervical fascia. As a result, the tongue and mouth floor may be displaced in a superior and posterior direction. The lingual displacement and frequent laryngeal edema can quickly overrun and completely occlude the airway, culminating in death by asphyxiation. Direct laryngoscopy for endotracheal intubation may be extremely difficult or impossible. It may quickly become necessary to have the airway secured surgically via tracheostomy. Such a decision must be made very rapidly to avert fatal sequelae.
If this infectious process has progressed to the point that the airway must be secured by surgical means, the submandibular region and other areas need to be explored. The areas should be incised, irrigated, and drained. Wound cultures should be obtained to identify the causative organism and determine the most appropriate antibiotic to treat the infection. Parenteral antibiotics should be administered until the patient has been afebrile for at least 48 hours. Before antibiotics were available, the mortality with this disease was more than 50%. Early diagnosis and aggressive antibiotic therapy has reduced mortality to less than 2%.
Complications
• Airway obstruction
• Aspiration
• Carotid artery erosion/rupture
• Cranial nerve dysfunction
• Grisel syndrome
• Innominate artery rupture
• Mandibular osteomyelitis
• Mediastinal abscess
• Mediastinitis
• Necrotizing fasciitis
• Osteomyelitis (cervical)
• Pericardial effusion
• Pleural effusion
• Pneumothorax
• Septic emboli
• Septic shock
• Subphrenic abscess
• Thrombosis of internal jugular
Anesthesia Implications
Airway management is the most critical factor. It may be most appropriate and prudent to secure the patient’s airway surgically via awake tracheostomy, using local anesthetic infiltration and minimal or no sedation. Intravenous induction may cause near-instantaneous loss of the patient’s airway. Awake fiberoptic intubation may be preferable to direct laryngoscopy. Instrumentation of the patient’s airway should be held to a minimum because of the additional airway edema that may be evoked by the manipulation. Sedation must be kept at a minimum for the awake fiberoptic attempt. Because of a high potential for continued further expansion of the airway edema, an armored endotracheal tube may be the most appropriate choice to secure the patient’s airway.
It would be wise to keep the patient ventilated by whatever method has been successful—nasotracheal or orotracheal intubation or tracheostomy—and ensure that the patient is sedated and comfortable. Repeated trips to the operating room may be necessary for serial incision and drainage of the infected area. It is important to remember that it will take time for the intravenous antibiotic therapy to become optimally effective.
