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Summary Table

Feature	Details
Risk Factors	Recent dental infection or procedure (especially involving mandibular 2nd/3rd molars), poor dental hygiene, diabetes mellitus, immunosuppression (HIV/AIDS, alcoholism, malnutrition), oral trauma, tongue or lip piercings
Etiology	Polymicrobial odontogenic infection spreading to the submandibular space; mixed aerobic-anaerobic flora including Streptococcus viridans, Staphylococcus aureus, and Bacteroides species
Patient Presentation	Rapidly worsening neck swelling, mouth pain, dysphagia, drooling, muffled "hot potato" voice, trismus, fever
Classic Physical Exam	Bilateral, firm ("woody"), tender submandibular swelling; elevated and posteriorly displaced tongue; floor of mouth induration; no fluctuance early on; patient may be sitting upright, leaning forward, or in a "sniffing" position to maintain airway
Key Diagnostic Results	Primarily a clinical diagnosis; CT neck with IV contrast shows diffuse soft tissue enhancement and gas tracking in the submandibular, sublingual, and submental spaces; leukocytosis on CBC
Management	Immediate airway assessment and securing (fiberoptic nasal intubation or surgical airway preferred over oral intubation); IV broad-spectrum antibiotics (ampicillin-sulbactam or clindamycin + penicillin); early surgical consultation for incision and drainage if no improvement or abscess formation
Keywords	"Woody" submandibular induration, elevated tongue, floor of mouth swelling, bilateral neck swelling after dental infection, airway emergency, "hot potato" voice

1. Pathophysiology

Ludwig's angina is a rapidly progressive bilateral cellulitis involving three fascial spaces of the floor of the mouth: the sublingual, submandibular, and submental spaces. Unlike a discrete abscess, this is a diffuse, spreading infection without well-defined walls of pus in its early stage. This distinction is critical because the lack of fluctuance early on can mislead clinicians into underestimating the severity.

The infection originates most commonly from the mandibular 2nd and 3rd molars. This is an anatomic inevitability rather than coincidence: the roots of these teeth penetrate below the mylohyoid line, placing their apices directly adjacent to the submandibular space. When a periapical abscess forms at these root tips, bacteria gain direct access to the submandibular space and rapidly spread through the loose connective tissue of the floor of the mouth. Because fascial planes in this region communicate freely across the midline, the infection becomes bilateral early.

The key danger of Ludwig's angina is airway compromise through tongue displacement. As infection and edema expand within the sublingual and submandibular spaces, the tongue is pushed superiorly and posteriorly, progressively obstructing the oropharynx. The swelling is characteristically described as "woody" induration, meaning the tissue is board-like and non-compressible, reflecting diffuse cellulitis rather than a fluid-filled abscess. This firmness also means that simply aspirating or draining a single collection will not resolve the problem.

Additional life-threatening complications arise when the infection tracks along cervical fascial planes into the mediastinum (descending necrotizing mediastinitis), the carotid sheath (internal jugular vein thrombosis, carotid artery erosion), or the retropharyngeal space. These pathways explain why untreated Ludwig's angina carries a historically high mortality rate and why airway management takes absolute precedence over all other interventions.

The polymicrobial nature of the infection reflects the normal oral flora: aerobic organisms (primarily Streptococcus viridans group) initiate tissue invasion, while anaerobes (Bacteroides, Peptostreptococcus, Fusobacterium) thrive in the necrotic, low-oxygen environment that follows. This mixed flora dictates the choice of antibiotics covering both aerobic and anaerobic organisms.

2. Classification and Clinical Manifestation

Ludwig's angina itself is not formally subclassified by stage in the way many diseases are, but its clinical progression and relationship to other deep neck space infections is highly testable. The table below distinguishes the involved anatomic compartments and their clinical correlates.

Anatomic Spaces Involved

Space	Boundaries	Clinical Sign When Involved
Sublingual	Between the oral mucosa superiorly and the mylohyoid muscle inferiorly	Elevation of the tongue, floor of mouth swelling visible intraorally
Submandibular	Between the mylohyoid muscle superiorly and the superficial layer of deep cervical fascia inferiorly	Firm, tender swelling below the mandible, externally visible neck fullness
Submental	Midline space between the anterior bellies of the digastric muscles	Submental fullness, "double chin" appearance, chin-to-hyoid firmness

Progression of Clinical Manifestations

Stage	Features
Early	Unilateral dental pain, mild submandibular tenderness, low-grade fever; may mimic simple dental abscess
Established	Bilateral submandibular swelling with "woody" induration, trismus, dysphagia, odynophagia, drooling, fever, elevated tongue on intraoral exam
Advanced / Pre-arrest	Stridor, inability to swallow secretions, tripod positioning or "sniffing" posture, tachypnea, cyanosis, muffled voice progressing to inability to speak; signs of sepsis (tachycardia, hypotension, altered mental status)
Complicated	Spread to parapharyngeal or retropharyngeal space (posterior pharyngeal wall bulging), descending mediastinitis (chest pain, widened mediastinum), Lemierre syndrome if internal jugular vein thrombophlebitis develops, airway loss

Classic Clinical Features as Exam Cues

Clinical Feature	What It Signals
"Woody" or "brawny" submandibular swelling	Cellulitis, not abscess (no fluctuance)
Tongue elevation and protrusion	Sublingual space involvement, impending airway loss
Bilateral involvement	Rules out simple unilateral submandibular abscess
Trismus	Involvement of muscles of mastication or pterygoid space extension
Drooling and dysphagia	Inability to manage secretions from oropharyngeal compromise
"Hot potato" voice	Supraglottic soft tissue edema affecting phonation

3. Diagnostic Workup

Test	Role	Key Findings
Clinical examination	Best initial assessment	Bilateral submandibular "woody" induration, elevated tongue, floor of mouth swelling
CT neck with IV contrast	Best imaging study	Diffuse soft tissue stranding and enhancement in submandibular/sublingual/submental spaces, possible gas tracking, identifies drainable abscess collections if present
Panoramic dental radiograph	Identify odontogenic source	Periapical lucency at the mandibular molar roots
CBC with differential	Assess systemic response	Leukocytosis with left shift
Blood cultures	Identify bacteremia	Obtain before antibiotics if patient is septic; often polymicrobial
Wound/aspirate culture	Guide targeted therapy	Aerobic and anaerobic cultures from surgical specimens when drainage is performed
Lateral neck radiograph	Rapid bedside screening	Soft tissue swelling anterior to the cervical spine, possible airway narrowing (limited sensitivity)

Ludwig's angina is fundamentally a clinical diagnosis. When a patient presents with bilateral submandibular swelling that is firm and non-fluctuant, a history of dental disease, and signs of oropharyngeal compromise (elevated tongue, drooling, trismus), the diagnosis should be made at the bedside. The first priority is always airway assessment, not imaging.

CT of the neck with IV contrast is the imaging study of choice once the airway is secured. Its primary role is not to "confirm" Ludwig's angina (which is already diagnosed clinically) but rather to define the extent of disease, identify whether an organized drainable abscess has formed within the cellulitis, detect gas formation suggesting necrotizing infection, and evaluate for extension into the parapharyngeal space, retropharyngeal space, or mediastinum. On CT, expect to see diffuse enhancement and fat stranding in the submandibular region without a well-defined rim-enhancing collection in early disease. If a rim-enhancing fluid collection is present, that signals abscess formation requiring surgical drainage.

A panoramic dental radiograph (orthopantomogram) should be obtained when the patient is stable to identify the offending tooth. Periapical radiolucency around the roots of the lower second or third molar is the classic finding, and this tooth will ultimately need extraction as part of definitive source control.

Blood cultures should be drawn before initiating antibiotics, particularly in septic patients. However, do not delay antibiotic administration to wait for culture results. Wound cultures (aerobic and anaerobic) are obtained during surgical drainage and are more likely to yield the causative organisms than blood cultures.

A critical exam concept: do not send a patient with an unstable airway to the CT scanner. If there is any concern about imminent airway loss (stridor, severe tongue elevation, inability to manage secretions), the airway must be secured first. CT can wait; the airway cannot.

4. Management and Treatment

Priority	Intervention	Details
1. Airway	Secure the airway	Fiberoptic nasotracheal intubation (preferred) or awake tracheostomy; avoid blind oral intubation
2. Antibiotics	IV broad-spectrum empiric therapy	Ampicillin-sulbactam 3 g IV every 6 hours OR Penicillin G 2-4 million units IV every 4-6 hours + Metronidazole 500 mg IV every 8 hours OR Clindamycin 600-900 mg IV every 8 hours (if penicillin-allergic)
3. Surgical consult	Incision and drainage	Indicated when abscess is identified on imaging, when clinical deterioration occurs despite 48 hours of antibiotics, or when gas gangrene/necrotizing infection is suspected
4. Source control	Dental extraction	Extraction of the offending tooth after acute infection is controlled
5. Steroids (adjunctive)	Dexamethasone	8-10 mg IV every 8 hours for 48 hours to reduce edema and potentially avoid surgical airway; evidence is supportive but not definitive
6. Supportive care	ICU monitoring, IV fluids, pain management, NPO if airway concern	Continued reassessment of airway status even after initial stabilization

Airway management is the single most important step and is always the correct "next best step" when a vignette describes a patient with signs of upper airway obstruction. The classic exam scenario presents a patient with worsening bilateral neck swelling, an elevated tongue, stridor, and drooling, then asks what you should do first. The answer is never "order a CT" or "start antibiotics." It is always to secure the airway.

Fiberoptic nasotracheal intubation performed by an experienced operator is the preferred method of definitive airway management. The rationale: trismus and massive lingual swelling make direct laryngoscopy and oral intubation extremely difficult and dangerous. Blind oral intubation attempts risk complete airway obstruction, laryngospasm, and a "cannot intubate, cannot ventilate" scenario. If fiberoptic intubation fails or is unavailable, an awake tracheostomy under local anesthesia is the fallback. A surgical airway setup should always be at the bedside before any intubation attempt.

Empiric IV antibiotics should be started immediately after blood cultures are drawn and the airway is addressed. The regimen must cover gram-positive cocci (streptococci, staphylococci), gram-negative rods, and anaerobes. Ampicillin-sulbactam (Unasyn) 3 g IV every 6 hours is the most commonly recommended single-agent regimen because it provides excellent coverage of oral flora including beta-lactamase-producing anaerobes. An alternative combination is high-dose Penicillin G plus Metronidazole for enhanced anaerobic coverage. For patients with penicillin allergy, Clindamycin 600-900 mg IV every 8 hours is the standard substitute, offering both aerobic gram-positive and anaerobic coverage. Antibiotics are typically continued IV for at least 48-72 hours after clinical improvement, then transitioned to oral therapy (amoxicillin-clavulanate 875/125 mg twice daily) to complete a total course of 10-14 days.

Surgical drainage is not universally required in Ludwig's angina, particularly in the early cellulitic phase when no drainable collection exists. However, surgery becomes necessary when CT reveals an abscess, when clinical deterioration continues despite 48 hours of appropriate antibiotics, or when crepitus or imaging suggests gas gangrene. The surgical approach involves bilateral submandibular incisions with blunt dissection through the mylohyoid to decompress both the submandibular and sublingual spaces.

IV dexamethasone (8-10 mg every 8 hours for 48 hours) is used as an adjunctive measure to reduce airway edema. Some evidence suggests that early steroid use can reduce the need for surgical airway intervention and shorten hospital stays. However, steroids should never replace airway management and should be avoided if there is concern for necrotizing fasciitis, where immunosuppression could worsen outcomes.

Dental extraction of the causative tooth is essential for long-term source control but is performed after the acute phase is managed. Leaving the offending tooth in place invites recurrence.

5. Differential Diagnosis and Distractors

Differential	Why It Looks Similar	Key Discriminator
Peritonsillar abscess (quinsy)	Fever, sore throat, trismus, muffled voice, drooling	Unilateral tonsillar swelling with uvular deviation; no submandibular induration; swelling is peritonsillar, not in the floor of the mouth
Submandibular abscess (unilateral)	Submandibular swelling, dental origin, fever	Unilateral, fluctuant swelling; Ludwig's angina is bilateral and "woody" without fluctuance early on
Angioedema	Rapid swelling of the tongue, lips, and floor of mouth; airway compromise	No fever, no dental source, no induration; often associated with ACE inhibitors, allergen exposure, or hereditary C1-esterase inhibitor deficiency; swelling is soft and pitting
Parapharyngeal abscess	Deep neck swelling, fever, dysphagia, trismus	Swelling is posterior and lateral (behind the tonsil), often with medial displacement of the lateral pharyngeal wall on exam; submandibular region is not the primary site
Retropharyngeal abscess	Fever, neck stiffness, dysphagia, drooling, airway compromise	Most common in children under age 6; posterior pharyngeal wall bulging; CT shows pre-vertebral fluid collection; submandibular swelling absent
Epiglottitis	Acute airway obstruction, drooling, fever, muffled voice, tripod positioning	No submandibular swelling; lateral neck radiograph shows "thumbprint sign" (swollen epiglottis); direct laryngoscopy reveals cherry-red epiglottis
Salivary gland infection (submandibular sialadenitis)	Submandibular swelling, pain, fever	Usually unilateral; worsened by eating (salivary stimulation); Wharton duct may express pus on bimanual palpation; no floor-of-mouth elevation
Lemierre syndrome	Oropharyngeal infection progressing to severe sepsis, neck swelling	Starts as pharyngitis/tonsillitis, not dental infection; internal jugular vein thrombophlebitis on CT; septic emboli to lungs; caused by Fusobacterium necrophorum

6. Traps and High-Yield Pearls

The most common way students lose points on Ludwig's angina questions is by choosing to image the patient before addressing the airway. A well-constructed vignette will describe a toxic-appearing patient with bilateral submandibular swelling, an elevated tongue, stridor, and progressive dysphagia, and then offer "order CT neck with contrast" as a tempting answer choice. The correct answer in this setting is always to secure the airway first. No imaging study should delay airway intervention when clinical signs of obstruction are present.

A second classic trap involves confusing Ludwig's angina with a peritonsillar abscess. Both present with trismus, muffled voice, and fever, but the anatomic location is completely different. Vignettes describing floor-of-mouth swelling and bilateral submandibular induration point to Ludwig's angina; vignettes describing unilateral tonsillar bulging with uvular deviation point to peritonsillar abscess. The treatment also diverges: peritonsillar abscess is drained by needle aspiration or incision through the soft palate, while Ludwig's angina requires a submandibular surgical approach when drainage is needed.

Students also stumble on the method of intubation. When a question asks how to secure the airway, do not choose "direct laryngoscopy and orotracheal intubation." The trismus and massive tongue swelling make this approach both technically impossible and dangerous. Fiberoptic nasotracheal intubation or surgical airway (tracheostomy) is the answer.

Finally, remember that Ludwig's angina in its early phase is cellulitis, not abscess. Asking for incision and drainage as the first step is a trap when the CT shows diffuse enhancement without a rim-enhancing collection. In this setting, the correct management is IV antibiotics with close monitoring; surgical drainage is reserved for abscess formation or failure to improve. The core competency being tested is the ability to prioritize airway management in a deep neck infection, correctly identify the anatomic spaces involved, choose the appropriate intubation technique, and sequence the management steps (airway, then antibiotics, then imaging, then consider drainage) in the right order.

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