Chief Complaint: “My mouth and neck hurt”
HPI: 20 yr old Spanish speaking only male with no reported PMH. The patient arrived initially to a community Emergency Department at 0300for evaluation of neck pain.
The patient reported onset of “mouth pain” approximately 5-6 days prior to day of evaluation. He noted steady progression of pain intensity with rapid progression in the 24 hours preceding evaluation. In the past 24 hours he noted onset of anterior neck skin erythema with associated swelling. Several hours prior to arrival he attempted to lay down and felt it was more difficult than usual to breath. Upon arrival to the ED the patient was alert but appeared in significant distress with a report of 10/10 pain greatest in the right submandibular and anterior neck region. He stated that pain was exacerbated by rotation of the neck, tongue protrusion, and speaking. He denied drooling, breathing difficulty, neck trauma, other adenopathy, fever, chills, or similar event in the past.
FM/SH/ROS: Non contributory
Vital signs: 38.2, HR 120’s, BP 155/82, RR 28, SpO2 98% on RA.
On examination the patient was alert but in significant distress. He was seated up right and diaphoretic. Neck exam revealed significant swelling of the upper anterior neck; greater on the right versus left; exquisitely tender to palpation. Overlying skin erythema which is warmth; there was no crepitus, fluctuance, or induration. Tongue appeared elevated with sublingual edema and pooling of secretions. No stridor. Low respiratory tract clear.
NP Scope: Edematous epiglottis with visible cords and patent airway
Laboratory: WBC’s 23,000; neutrophils 22,000.
Imaging: CT with angiography - two submandibular fluid collections, the largest 3.3 cm x 1 cm.
Clinical Course: While in the community ED, he had continued to maintain his airway and was handling his secretions. With concern for deep space neck infection fluid resuscitation and Unasyn were initiated. With predicted progression of airway compromise, consultation with ENT at an academic center was placed. In agreement, the patient was transferred, directly proceeding to the O.R. for awake tracheostomy. Once airway stability was obtained, examination revealed purulence emanating from molar # 18 with perforation of the lingual palate. The patient ultimately underwent tooth extraction, transoral drainage of the sublingual and submandibular spaces with continued oral drain and admission for monitoring and IV antibiotics.
With the advent of antibiotics mortality exceeded 50%. With improved dental care, deep space infections are a rare occurrence. Yet, when present, the represent a diagnostic challenge with potential for fatal outcomes.
Ludwig’s angina was described first in 1836 by German physician, Wilhelm Frederick von Ludwig as a rapidly and frequently fatal progressive gangrenous cellulitis and edema of the soft tissues of the neck and floor of the mouth. Prior to antibiotics, swelling frequently led to respiratory obstruction and death; thus, the term angina was added to the description which arises from angere meaning “to strangle”.
“Ludwig’s” is often loosely applied to deep space neck infections but should be limited to those infections which are: bilateral, involves the submandibular space (including both the sublingual and submylohyoid spaces), originates in the floor of the mouth, and is associated with rapid spread; often with a brawny cellulitis.
Most commonly these patients present with sore throat (73%) followed by odynophagia (62.8%). Painful neck swelling, tooth pain, dysphagia, dyspnea, fever, and malaise are the most common complaints. Neck swelling and a protruding or elevated tongue are seen in the vast majority. Stridor, trismus, cyanosis, and tongue displacement suggest an impending airway crisis. Edema and induration of the anterior neck, often with cellulitis, may be present in advanced cases. Early signs and symptoms of obstruction may be subtle. Airway compromise is always synonymous with the term Ludwig’s angina, and it is the leading cause of death. Therefore, airway management is the primary therapeutic concern
In order to understand this condition a review of anatomy is key. Many subcutaneous abscesses we in the Emergency Department are fluctuant with purulent discharge. Why doesn’t this occur in Ludwig’s? The superficial layer of the deep cervical fascia (SLDCF) is an essential structure in understanding deep space infections of the neck. The SLDCF generally forms the outer margin of odontogenic deep space neck infections. The tenacity of this fascia prevents the egress of pus toward the skin until neck infections are quite late. The result is that because of the barrier of the SLDCF, infections will expand to the point of descending toward the mediastinum, ascending to the lateral pharynx and masticator spaces, or will expand to the point of causing airway obstruction. Understanding the SLDCF is essential to understanding the pathway of infection. Clinically, this means you may see significant cellulitis, occasionally with serosanguinous fluid, but no frank pus. The sagittal image in the figure below highlights this fascia in red:
The submandibular space is limited by the oral mucosa of the floor and below by the superficial layer of the deep cervical fascia; this extends from the mandible to the hyoid bone. Myolohyoid muscles divide the space into the sublingual (superior) and submaxiallary (inferior) spaces.
Review of cultures have demonstrated odontogenic infection in approximately 60-85% of those with this presentation.
These are frequently polymicrobial with most related to the second or third mandibular molar teeth. Other sources include peritonsillar or parapharyngeal abscesses, mandibular fracture, oral lacerations/piercing, or submandibular sialodentitis. Predisposing factors include: dental carries, recent dental treatment, systemic illnesses such as diabetes mellitus, malnutrition, alcoholism, compromised immune system such as AIDS, and organ transplantation and trauma; up to 50% have no identifiable site of origin. Although as many as 50 to 100 bacterial species may be present on the oral or nasopharyngeal mucosal surface, the typical deep neck space infection includes, on average, five or six bacterial types. As 2/3 of these infections will involve a beta-lactamase producing organism, the most efficacious antimicrobial agents include amoxicillin/clavulanate, ticarcillin/clavulanate, cefoxitin, carbapenem, or clindamycin.
Without intervention, complications may be severe and life threatening with risk of upper airway obstruction, descending mediastinitis, pleural empyema, pericarditis, jugular vein thrombosis, septic shock, and carotid pseudoaneurysm. These may present and proceed with amazing speed (Wang et al), but they can generally be avoided by early recognition and aggressive treatment.
Early recognition of the disease is of paramount importance. Mainstay of treatment is to secure the airway, antibiotic therapy, and often surgical drainage by OMFS or ENT.
Medical management of these patients should begin promptly with intravenous access, fluid resuscitation, and administration of IV antibiotics. Antibiotic therapy should be administered empirically and tailored to culture and sensitivity results.
Computed tomography is the imaging modality of choice for the diagnosis of deep neck space infections.
Airway compromise should not be taken lightly as these infections may progress rapidly. Cases described as “perilous airway”. Direct compression of the airway may arrive from displacement of the tongue posteriorly or secondary to laryngeal edema. These patients should be managed as presumed difficulty airway and are challenging with even when in a relatively controlled O.R. environment. In several studies, up to 75% of patients with Ludwig’s angina required tracheostomy. In a study reviewing 20 attempts at oral intubation, 11 were unsuccessful, failed airways requiring emergent tracheostomy. Involve our colleagues in Anesthesia and ENT early.
Many deep infections of the head and neck require surgical intervention in the form of incision and drainage. Many would argue that when there is an abscess in the deep neck, surgical drainage is mandatory. Depending on the series, surgical drainage is required in 10% to 83% of patients who present with deep neck space infections.
I have every symptom of Ludwigs Angina. In the last 12 months Cardiomyopathy (in a custody issue with my son's dad has hid them I have been sad very sad) I have no other issues I am thin, active eat good. When I cry I can feel my chest squeezing. I also have a fatty tumor in top rt shoulder, and in 2009 I had one removed in neck My entire family was born with bad teeth. From parents. Mine the worst. And since my twins were born I have let mine go worse than bad. Today I was told I need a heart fib. I am 55 yrs old. My heart infraction count us in the teens. I am freaking out. Especially after reading all about it . As I have read tonight
Endocarditis, Ludwig Angina, Sialadenitis, and Madelung Disease all can be caused by sever infection in teeth and gums and I fit the profile for it all. And could this stuff be hereditary? I want to turn my health around and not with a fib or tons of medicine, or be a disabled person. I just know I feel very strong my mouth is the problem. Anyway thank you