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Ludwig’s angina is a life-threatening, rapidly progressive deep neck infection that poses an immediate risk to the airway. It is usually characterized by diffuse cellulitis of the submandibular, sublingual, and submental spaces, which can lead to sudden airway obstruction due to elevation of the floor of the mouth and posterior displacement of the tongue. Despite recent advances in anti-microbial therapy, imaging techniques, and advanced critical care, delays in recognition and inappropriate airway interventions continue to contribute significantly to increased morbidity and mortality. This chapter provides an intensive care-focused overview of Ludwig’s angina, emphasizing early clinical recognition, diagnostic modalities and challenges, and time-sensitive airway decision-making. Contemporary airway management techniques, including awake fiberoptic intubation, video laryngoscopy, high-flow nasal oxygenation, and surgical airway techniques, are discussed in depth, along with emerging newer adjuncts such as airway ultrasound, disposable flexible endoscopes, and cognitive aids for crisis management. The importance of multi-disciplinary team collaboration – combining airway control (anaesthesia), anti-microbial therapy (infectious disease), surgical drainage (head and neck surgery), and vigilant critical care monitoring (intensivist) – is highlighted to guide clinicians in preventing catastrophic airway failure and improving patient outcomes.
Department of Obstetric Anaesthesia, Women’s Wellness and Research Center (WWRC), Hamad Medical Corporation, Doha, Qatar
Ashish Kumar
Department of Anaesthesia, ICU and Perioperative Medicine, HGH, Hamad Medical Corporation, Doha, Qatar
Zakria Attique
Department of Anaesthesia, HGH, Hamad Medical Corporation, Doha, Qatar
Muhammad Abubaker
Department of Anaesthesia, HGH, Hamad Medical Corporation, Doha, Qatar
Zara Muhammad Nayyar
Department of Anaesthesia, HGH, Hamad Medical Corporation, Doha, Qatar
Aneesa Kuzhichalil
Department of Respiratory Therapy, HGH, Hamad Medical Corporation, Doha, Qatar
*Address all correspondence to: drsanghamitrapadhy@gmail.com
1. Introduction
Ludwig’s angina remains one of the most dramatic and unforgiving airway emergencies encountered in intensive care medicine, anaesthesiology, and emergency practice. Although first described nearly two centuries ago, it continues to challenge modern clinicians because its danger lies not in obvious airway obstruction at presentation but in its potential for rapid deterioration and unpredictable progression, leading to complete airway collapse. The defining pathological process is a rapidly spreading cellulitis of the floor of the mouth and submandibular spaces, which can convert a stable-appearing airway into a cannot-ventilate, cannot-intubate situation within minutes. Contemporary airway management principles are, therefore, central to outcome improvement [1–3].
In the ICU, Ludwig’s angina lies at a unique intersection of infection, airway anatomy, and physiology. Unlike many causes of acute airway compromise, Ludwig’s angina usually presents without early stridor or hypoxaemia. Patients may initially seem comfortable, speaking in full sentences while harbouring extensive sublingual and submandibular oedema that severely narrows the oropharyngeal lumen. This deceptive presentation contributes to delayed diagnosis, delays in airway intervention, and catastrophic deterioration during sedation, induction of anaesthesia, positioning, or diagnostic procedures, particularly in critically ill patients [4, 5].
Historically, the mortality rate of Ludwig’s angina exceeded 50% in the pre-antibiotic era. With the advent of anti-microbial therapy, modern imaging, and timely surgical drainage, mortality has fallen dramatically; however, contemporary deaths still occur almost exclusively due to airway failure or sepsis-related complications. Modern fatalities are often iatrogenic, arising from the loss of spontaneous ventilation during attempted airway control. This underscores the central premise of this chapter: in Ludwig’s angina, airway management is not merely a procedural skill but a strategic, physiology-driven process that must be anticipated early and executed deliberately.
This chapter adopts an ICU-focused, pragmatic approach rather than a purely surgical or infectious disease perspective. Emphasis is placed on the early recognition of high-risk features, the avoidance of precipitous airway interventions, and structured multi-disciplinary decision-making for critically ill patients with limited physiological reserve. Emerging technologies and newer adjuncts, such as high-flow nasal oxygenation (HFNO), airway ultrasound, disposable flexible bronchoscopes, and cognitive aids, are all integrated into a modern airway management framework.
Ludwig’s angina is uncommon, and its true incidence is difficult to ascertain due to variability in diagnostic criteria and reporting practices. Most contemporary series originate from tertiary referral centres and ICUs, suggesting that milder cases may go unrecognized or be managed before progression. Despite its rarity, the condition carries a disproportionate morbidity risk because it frequently affects patients with comorbidities that impair immune response and physiological reserve.
Odontogenic infection remains the predominant aetiology, accounting for approximately 70–90% of cases, most commonly arising from second and third mandibular molars due to their anatomical relationship with the submandibular and sublingual spaces. Polymicrobial infection involving aerobic and anaerobic oral flora is typical. Non-odontogenic causes, although less common, include mandibular fractures, oral lacerations, penetrating trauma, submandibular sialadenitis, and iatrogenic injury following dental or otolaryngological procedures.
Patient-related risk factors include diabetes mellitus (most common), alcoholism, malnutrition, chronic kidney disease, malignancy, steroid use, pregnancy, and poor dental hygiene. Immunocompromised patients demonstrate more aggressive disease and higher rates of systemic complications [6]. In pregnant patients, physiological airway oedema and reduced functional residual capacity may accelerate decompensation. Delayed presentation and inadequate outpatient care further reduce the margin for safe airway intervention (Table 1).
Category
Details
Odontogenic sources
Second and third mandibular molar infections, periodontal disease.
The pathophysiology of Ludwig’s angina is associated with the unique anatomy of the floor of the mouth and deep cervical fascial planes. The sub-mandibular space, which is divided by the mylohyoid muscle into the sublingual space superiorly and the submaxillary space inferiorly, allows infection originating in these mandibular molars to spread rapidly through these contiguous compartments, typically involving both sides of the neck in a symmetrical fashion.
Unlike other abscess-forming infections, early Ludwig’s angina is predominantly cellulitic. This distinction is clinically crucial: diffuse oedema and induration, rather than localized pus, drive airway compromise, and progressive swelling elevates the floor of the mouth, displaces the tongue posteriorly, and reduces oropharyngeal volume. Even small increases in soft tissue thickness can cause exponential increases in airway resistance, particularly during supine positioning or sedation, especially in critically ill patients [4, 5] (Figure 1).
Figure 1.
Fascial space involvement in Ludwig’s angina highlights the mechanism of airway compromise caused by progressive soft tissue oedema rather than abscess formation.
Venous and lymphatic obstruction further exacerbate oedema, creating a vicious cycle of swelling and airway narrowing. Importantly, laryngeal structures may remain relatively unaffected in the early phase of the disease, leading to a false sense of security during indirect laryngoscopy or early fiberoptic evaluation. Loss of pharyngeal muscle tone during the induction of anaesthesia can abruptly convert a marginal airway into a completely obstructed one.
From a physiological standpoint, patients with Ludwig’s angina often have reduced apnoea tolerance due to sepsis, pain-related tachypnoea, and decreased functional residual capacity. In critically ill patients, even brief interruptions in ventilation can result in rapid desaturation, emphasizing the importance of maintaining spontaneous breathing whenever possible.
The clinical presentation of Ludwig’s angina evolves along a continuum, and early recognition, which is essential to prevent catastrophic airway events, is crucial. Initial symptoms are often non-specific and include dental pain, sore throat, fever, malaise, and neck swelling. As the infection progresses, patients develop dysphagia, odynophagia, trismus, and a characteristic firm swelling of the submandibular region.
Classic late findings include stridor, cyanosis, and overt respiratory distress – representing pre-terminal airway compromise and should not be awaited before intervention. More subtle signs, including elevation or firmness of the floor of the mouth, inability to tolerate the supine position, drooling due to impaired secretion handling, and a muffled or ‘hot potato’ voice, are often more predictive of impending airway failure.
Trismus is particularly important from an airway planning perspective, as it limits mouth opening, making access for direct or video laryngoscopy quite difficult and predicts difficulty with rescue techniques. Rapid progression of neck swelling over hours, rather than days, should heighten concern for the aggressive nature of the disease and prompt early multi-disciplinary involvement, consistent with difficult airway recommendations [1–3].
In the ICU, clinicians must also recognize systemic red flags such as tachypnoea, hypoxaemia, hypotension, rising lactate levels, and altered mental status, which may reflect sepsis-related physiology that dramatically reduces the patient’s tolerance for airway manipulation. In such patients, even brief hypoventilation during airway attempts may precipitate cardiovascular collapse [7] (Table 2).
Clinical feature
Airway implication
Floor-of-mouth elevation
Posterior tongue displacement, airway narrowing
Trismus
Limited access for laryngoscopy
Drooling/inability to handle secretions
Impending airway obstruction
Muffled (‘hot potato’) voice
Supraglottic oedema
Stridor
Late sign of critical airway compromise.
Hypoxemia or tachypnoea
Reduced apnoea tolerance
Table 2.
Clinical warning signs that should prompt immediate airway planning and specialist involvement.
Ludwig’s angina diagnosis is primarily clinical – airway stabilization should always supersede diagnostic testing. In a patient with high-risk features, imaging must never delay airway control. Once the airway is secured, contrast-enhanced CT of the neck is the imaging modality of choice to delineate the extent of infection, identify abscess formation, and guide surgical drainage. CT findings generally consist of diffuse soft tissue swelling of the submandibular and sublingual spaces, fat stranding, and gas formation in severe cases. Importantly, the lack of an isolated abscess does not preclude serious disease, since cellulitis can be enough to lead to life-threatening airway compromise. Bedside ultrasound is an emerging adjunct in the ICU. It can help identify disrupted anatomy, evaluate the thickness of soft tissue oedema, and identify the cricothyroid membrane in anticipation of a surgical airway. Ultrasound does not replace CT but provides instant clinical information and doesn’t require patient transport. Laboratory investigations frequently show leukocytosis, increased inflammatory markers, and metabolic derangements suggestive of sepsis. When possible, blood cultures are obtained before antibiotic administration, but empiric therapy should not be deferred. Microbiological cultures collected from surgical drainage typically demonstrate polymicrobial infection with a combination of aerobic and anaerobic oral flora. Early involvement of anaesthesia, otolaryngology, maxillofacial surgery, and critical care teams is a diagnostic and therapeutic imperative. Ludwig’s angina should be managed as a collaborative airway emergency rather than as a single-speciality problem.
6. Principles of airway management in Ludwig’s angina
Airway management in Ludwig’s Angina is quite unlike routine tracheal intubation in the intensive care unit. The focus here is on airway management, preserving spontaneous ventilation while avoiding manoeuvres that could induce sudden, full obstruction [1, 2, 5]. In contrast to laryngeal oedema or bronchospasm, airway compromise in Ludwig’s angina occurs through progressive extrinsic compression and distortion of upper airway anatomy. Therefore, the loss of muscle tone triggered by sedative and neuromuscular blocking agents can lead to immediate and irreversible airway collapse [1–3]. Having a clearly defined and early organized airway plan needs to be shared among the anaesthesia, critical care, and surgical teams. Such a comprehensive plan should feature initial tactics, rescue pathways, and specific parameters for escalation to a surgical airway. Restricting airway attempts is important, as repeated instrumentation furthers oedema, bleeding, and secretion burdens, rapidly turning a difficult airway into an impossible one (Figure 2). Positioning plays an important role. With patients generally upright to keep airways open, supine positioning should be avoided whenever possible. Supplemental oxygen, ideally HFNO, should also be initiated early to enhance oxygen reserve and mitigate hypoxaemic risk during airway manipulation.
Figure 2.
Airway decision-making algorithm in Ludwig’s angina is referenced here to emphasize early identification of high-risk features, avoidance of rapid sequence induction, and prioritization of awake techniques.
Box 1: This vignette highlights the importance of early airway recognition, the avoidance of rapid sequence induction, and multi-disciplinary coordination in preventing catastrophic airway loss.
When delay is dangerous: A 54-year-old man with poorly controlled diabetes presented with a 48-hour history of dental pain, progressive neck swelling, and dysphagia. On arrival to the ICU, he was upright, tachypnoeic, and unable to tolerate the supine position. Examination revealed firm bilateral submandibular swelling, an elevated floor of the mouth, and a muffled voice without stridor. Recognizing high-risk features, the team initiated HFNO and assembled anaesthesia, ENT, and critical care teams. Awake fiberoptic intubation was performed with minimal sedation, preserving spontaneous ventilation. Post-intubation CT confirmed extensive bilateral submandibular cellulitis without abscess. Broad-spectrum antibiotics were started, followed by surgical drainage. The patient was extubated successfully on ICU Day 4 after resolution of oedema and discharged without airway complications.
Awake airway management represents the cornerstone of safe practice in advanced Ludwig’s angina. These techniques preserve spontaneous ventilation, allow continuous neurological assessment, and provide an opportunity to abort the procedure if airway patency deteriorates.
7.1 Awake fiberoptic intubation
Awake fiberoptic intubation is widely regarded as the technique of choice by experienced hands [2, 8] (Figure 3). The flexible bronchoscope permits navigation around distorted anatomy and avoids the need for alignment of the oral, pharyngeal, and laryngeal axes. Patient and airway preparation is critical and often determines success more than technical skill.
Figure 3.
Awake fiberoptic intubation setup in the ICU illustrates optimal patient positioning, monitoring, oxygen delivery, and team arrangement for this high-risk procedure.
Topical anaesthesia of the nasal passages, oropharynx, and larynx should be achieved using lidocaine sprays, gels, or nebulization. Anti-sialagogues may be administered judiciously to improve visualization. Sedation, if used, should be minimal and titrated carefully; excessive sedation risks hypoventilation and loss of airway tone.
Patient cooperation is essential. Clear communication, reassurance, and maintenance of a calm environment improve success rates. The procedure should be abandoned immediately if oxygenation worsens or airway obstruction progresses. Guidelines for awake tracheal intubation emphasize meticulous topical anaesthesia, cautious sedation, and readiness to abandon attempts if deterioration occurs [2].
7.2 Awake video laryngoscopy
Awake video laryngoscopy may be considered in selected patients with preserved mouth opening and minimal floor-of-mouth elevation. While video laryngoscopy improves glottic visualization compared to direct laryngoscopy, it does not bypass supraglottic distortion and is, therefore, less reliable in advanced disease [1]. Its role should be limited to carefully selected cases with immediate backup plans in place.
Adjunctive strategies are critical in reducing the physiological stress of airway management. HFNO improves pre-oxygenation, provides apnoeic oxygenation, and may decrease the risk of rapid desaturation during airway manipulation [9, 10]. Airway ultrasound has emerged as a valuable bedside tool for identifying the cricothyroid membrane, assessing soft tissue oedema, and guiding emergency surgical airway placement (Table 3). For patients with distorted neck anatomy, pre-procedural ultrasound mapping can speed up the time to airway access. Cognitive aids, checklists, and designated airway carts minimize human error in stressful conditions. Disposable flexible bronchoscopes offer rapid availability and reduce concerns regarding equipment contamination or malfunction [3–5].
Adjunct
Role in airway management
High-flow nasal oxygenation
Improves oxygenation, prolongs safe apnoea time
Airway ultrasound
Identifies anatomy, oedema, and the cricothyroid membrane
Disposable flexible bronchoscope
Rapid deployment for awake intubation
Cognitive aids/checklists
Reduces human error during crisis
Vasopressor support
Maintains haemodynamic stability during airway intervention
Table 3.
Adjuncts to improve safety during airway management summarizes tools that enhance procedural success and patient safety.
Failure of awake airway techniques mandates immediate escalation of airway techniques rather than repeated attempts. Repeated laryngoscopy or bronchoscopy can lead to trauma, bleeding, and oedema rapidly worsening airway conditions. Supraglottic airway devices may provide transient oxygenation but should not be relied upon as definitive solutions due to poor seal and risk of displacement [1, 5]. Difficult airway guidelines emphasize early transition to rescue pathways rather than persistence with failing techniques [1, 3].
Early activation of surgical airway pathways is essential. A low threshold for awake tracheostomy or emergency cricothyrotomy should be maintained, particularly in the presence of worsening hypoxaemia, agitation, or anatomical progression. Figure 4 below shows a brief comparison between these twosurgical pathways.
Figure 4.
Surgical airway options in Ludwig’s angina provide a comparative overview of rescue techniques and their indications.
Airway management is not enough by itself for Ludwig’s angina. Early empiric broad-spectrum intravenous antibiotics should be initiated in a timely manner and cannot be delayed for microbiological confirmation. Therapy must also include coverage for aerobic and anaerobic oral bacteria, namely Streptococcus species, Staphylococcus aureus, and anaerobes such as Bacteroides and Fusobacterium. Common empiric regimens used in ICU settings include a beta-lactam/beta-lactamase inhibitor combination or a third-generation cephalosporin with metronidazole. Clindamycin combined with a fluoroquinolone is indicated for patients with a penicillin allergy. Antibiotic usage should be titrated based on culture results as well as clinical response. Early surgical involvement is essential in rapidly progressing deep neck infections [8].
Descending necrotizing mediastinitis represents a severe complication, requiring aggressive multi-disciplinary management [11].
11. Medical management and sepsis control
Control of the airway alone is not enough to manage Ludwig’s angina. Early empiric broad-spectrum IV antibiotics are mandatory and should not be delayed for microbiological confirmation [6] (Table 4). Therapy needs to encompass both aerobic and anaerobic oral flora, including Streptococcus species, Staphylococcus aureus, and anaerobes like bacteroides and fusobacterium.
Clinical scenario
First-line regimen
Alternative (penicillin allergy)
Notes
Community-acquired, hemodynamically stable
Ampicillin–sulbactam IV
Clindamycin + levofloxacin
Coverage for oral streptococci and anaerobes
Severe infection or sepsis
Piperacillin–tazobactam IV
Meropenem
Broad-spectrum coverage, including anaerobes and gram-negative organisms
MRSA risk factors present
Add vancomycin
Add linezolid
Adjust based on local resistance patterns
Immunocompromised host
Carbapenem-based regimen
Carbapenem + vancomycin
Early infectious disease consultation advised
Table 4.
Antibiotic regimens for Ludwig’s angina summarize commonly used empiric and targeted antimicrobial strategies.
Common empiric formulations include a beta-lactam/beta-lactamase inhibitor combination or a third-generation cephalosporin along with metronidazole. For patients who are allergic to penicillin, clindamycin combined with a fluoroquinolone may be prescribed. Antibiotic treatment should be adjusted based on culture results and clinical response. Therapy should be tailored according to cultures and clinical response [6].
Sepsis management follows the principles of the Surviving Sepsis Campaign, including early resuscitation, vasopressor support, lactate monitoring, and timely source control [7].
Sepsis management follows standard critical care principles, including early fluid resuscitation, vasopressor support when indicated, lactate monitoring, and source control through surgical drainage. Corticosteroids may be considered to reduce airway oedema, but evidence remains limited, and their use should not delay definitive airway or surgical management.
12. Intensive care management after airway securing
Following airway stabilization, patients require close ICU monitoring due to the risk of ongoing oedema, infection progression, and systemic complications. Mechanical ventilation strategies should include lung-protective ventilation, particularly in septic patients who are at high risk of developing acute respiratory distress syndrome.
Sedation should be minimized whenever possible to facilitate neurological assessment and early mobilization.
Daily evaluation of airway oedema is essential prior to considering extubation. A cuff leak test, flexible endoscopic assessment, or airway ultrasound may assist in determining readiness for extubation.
Nutritional support, glycaemic control, and thromboprophylaxis form integral components of comprehensive ICU care. Multi-disciplinary rounds involving intensivists, anaesthesiologists, surgeons, and infectious disease specialists improve coordination and outcomes [4, 5].
13. Complications and outcomes
Despite major modern advances, Ludwig’s angina continues to carry significant risk and airway-related complications, which include sudden obstruction, failed intubation, and prolonged mechanical ventilation. Infectious complications may include mediastinitis, necrotizing fasciitis, septic shock, and multi-organ failure [11].
Even though mortality rates have decreased subst-ally with early airway intervention and antibiotic therapy, they remain elevated in patients with delayed presentation, immunosuppression, or inadequate source control. Early recognition, decisive airway management, and multi-disciplinary care are the strongest predictors of favourable outcomes.
14. Special populations
Certain classes of populations, such as paediatric, pregnant, immunocompromised, or elderly patients, require a tailored approach to airway and critical care management in Ludwig’s angina due to altered anatomy, physiology, or disease trajectory.
14.1 Pregnant patients
Pregnancy introduces physiological airway oedema, reduced functional residual capacity, and increased oxygen consumption, all of which shorten safe apnoea time. Supine positioning may worsen both airway patency and uteroplacental perfusion. Awake airway techniques with left uterine displacement and early obstetric consultation are recommended. Awake techniques are particularly advised in high-risk airways [1, 2]. Foetal monitoring should be considered once maternal stabilization is achieved.
14.2 Paediatric patients
Children may deteriorate more rapidly due to smaller airway calibre and limited physiological reserve. Anxiety and lack of cooperation often preclude awake techniques, increasing reliance on experienced paediatric anaesthesiology and early surgical airway consideration. Lower thresholds for ICU admission and airway intervention are warranted. Management principles align with paediatric difficult airway frameworks [12].
14.3 Immunocompromised and elderly patients
Immunosuppressed patients often present late with atypical signs and have higher rates of polymicrobial infection and sepsis. Elderly patients may exhibit blunted inflammatory responses yet decompensate quickly. In both groups, early imaging after airway control and aggressive source management is essential. The higher risk of polymicrobial infection and sepsis necessitates early imaging and aggressive management [6].
15. Conclusions
Ludwig’s angina is an airway emergency masquerading as a neck infection. Early recognition, avoidance of precipitous airway interventions, and preference for awake airway techniques are central to safe management. A structured, multi-disciplinary ICU approach is essential to prevent catastrophic airway failure and improve survival.
Acknowledgments
The authors acknowledge the contributions of the intensive care, anaesthesia, otolaryngology, respiratory therapy, and maxillofacial surgery teams involved in the management of patients with deep neck infections.
Use of AI as assistive technology for language enhancement, formatting support, creation of figures, etc., was undertaken.
Conflict of Interest
The authors declare no conflict of interest.
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Written By
Sanghamitra Padhy, Ashish Kumar, Zakria Attique, Muhammad Abubaker, Zara Muhammad Nayyar, Aneesa Kuzhichalil
Submitted: 07 February 2026Reviewed: 09 February 2026Published: 30 July 2026
Open access peer-reviewed chapter - ONLINE FIRST
