Urgent management of ludwig’s angina. A systematic review of maxillofacial and otolaryngological interventions

Nº de DOI: 10.34896/RSI.2026.96.92.001

 

AUTHORS

1. Jeovany Alfredo Caceres Maradiaga. General Practitioner. Attached to the Esmeraldas Rioverde Health District 08D01. Graduate of the Rómulo Gallegos National Experimental University of the Central Plains. (Esmeraldas-Ecuador). https://orcid.org/0009-0000-6190-7819
2. Patricio Wladimir Coba Moreno. ⁠General Dentist. Attached to ⁠Kinemedical Sur. Graduate of the Central University of Ecuador. (⁠Quito-Ecuador). https://orcid.org/0009-0004-3922-9854
3. Allison Paulette Intriago Sabando. General Practitioner. Attached to Private Clinics of Ecuador. Graduate of the Central University of Ecuador. (Quinindé-Ecuador). https://orcid.org/0009-0000-7023-4978
4. David Sebastian Chicaiza Robalino. ⁠ General Dentist. Attached to Private Clinics in Ecuador. Graduate of the University of the Americas. (Quito-Ecuador). https://orcid.org/0009-0001-3542-7843
5. Anthony Josue Campos Reyes. ⁠ General Dentist. Attached to Private Clinics in Ecuador. Graduate of the University of the Americas. (Quito-Ecuador). https://orcid.org/0009-0006-1850-4049

 

SUMMARY

It is concluded that the reduction in mortality, which historically reached 50% and currently stands below 5%, is the direct result of an interprofessional approach integrating hemodynamic stabilization, broad-spectrum antibiotic therapy, and timely surgical debridement.

KEY WORDS

Ludwig’s angina, deep neck space infections, airway management, multidisciplinary approach and odontogenic infections.

RESUMEN

Se concluye que la reducción de la mortalidad —que históricamente alcanzó el 50 % y actualmente se sitúa por debajo del 5 %— es el resultado directo de un enfoque interprofesional que integra la estabilización hemodinámica, la antibioterapia de amplio espectro y el desbridamiento quirúrgico oportuno.

PALABRAS CLAVE

Angina de Ludwig, infecciones de los espacios profundos del cuello, manejo de la vía aérea, enfoque multidisciplinario e infecciones de origen odontogénico.

INTRODUCTION

Ludwig’s angina represents one of the most critical infectious emergencies in the fields of maxillofacial surgery and otorhinolaryngology, characterized by a bilateral, gangrenous, and rapidly progressive cellulitis affecting the submandibular, sublingual, and submental spaces. The objective of this systematic review is to analyze current urgent management protocols, with special emphasis on airway protection and multidisciplinary coordination. An exhaustive search was conducted in databases such as PubMed, Google Scholar, and ScienceDirect, selecting recent studies addressing etiopathogenesis, diagnostic imaging, and surgical interventions. The main findings highlight that over 90% of cases have an odontogenic origin, particularly involving the second and third mandibular molars¹. Early identification of cardinal signs, such as woody induration of the floor of the mouth and tongue elevation, is decisive for survival. Airway management is established as the absolute priority, with awake fiberoptic intubation recommended as the gold standard to prevent acute respiratory collapse².

OBJECTIVE

The main aim of this paper is to analyse and summarise the emergency management protocols for Ludwig’s angina.

METHODOLOGY

For the preparation of this systematic review, a structured search protocol was implemented to identify highly relevant and current scientific literature. The databases consulted included PubMed, ScienceDirect, Google Scholar, and the Cochrane Library. Health Sciences Descriptors (DeCS) and MeSH terms were used, combined with Boolean operators, such as «Ludwig’s Angina,» «Deep Neck Space Infections,» «Airway Management,» «Multidisciplinary Approach,» and «Odontogenic Infections.»

The search was mainly limited to articles published in the last ten years to ensure that recommendations reflect contemporary clinical practices and current antimicrobial resistance patterns. Studies in English and Spanish were included, ranging from highly educational clinical case reports to systematic reviews and retrospective cohort studies.

Inclusion criteria focused on research detailing the management of Ludwig’s angina in adult and pediatric patients. Priority was given to studies analyzing interdisciplinary coordination and the results of different airway control techniques. Likewise, papers evaluating systemic complications, such as mediastinitis and septic shock derived from deep cervical infections, were included.

Studies addressing superficial neck infections without involvement of the submandibular or sublingual spaces were excluded. Articles with unclear methodology, those not available in full text, or those presenting duplicate data from patient series already reported in other larger publications were also discarded.

The quality of the evidence was evaluated using standardized tools according to each study’s design. For systematic reviews, rigor levels in data synthesis were considered, while for observational studies, sample size and clarity in defining outcome variables, such as intubation success rate or hospital mortality, were analyzed.

Data extraction was performed systematically, collecting information on predominant etiology, most frequent microorganisms, key radiological findings, and pharmacological and surgical treatment protocols. Special attention was paid to the differentiation between true Ludwig’s angina and conditions that may mimic it, such as traumatic sublingual hematoma, to ensure that diagnostic recommendations were accurate.

RESULTS

Ludwig’s angina is a severe infection of the deep neck spaces that, despite advances in antimicrobial therapy, continues to pose a vital challenge in emergency departments. Originally described by Wilhelm Frederick von Ludwig in 1836, this entity is defined as a rapidly spreading cellulitis that does not respect lymphatic barriers but rather extends through fascial planes¹. Its polymicrobial nature and its capacity to compromise the airway within hours make it a pathology of high diagnostic and therapeutic complexity.

In the pre-antibiotic era, the mortality rate associated with this condition was alarmingly high, often exceeding half of the diagnosed cases. In modern clinical practice, although the incidence has decreased due to improved oral hygiene and access to dental treatments, the severity of complications remains significant³. Among these, necrotizing descending mediastinitis stands out—a fulminant complication that occurs when the infection progresses into the chest through the retropharyngeal or prevertebral space⁴.

Successful management of Ludwig’s angina requires a coordinated response among specialists in maxillofacial surgery, otorhinolaryngology, anesthesiology, and intensive care. The complexity lies in the fact that massive soft tissue edema of the neck and floor of the mouth not only mechanically obstructs the pharynx but also distorts the laryngeal anatomy, hindering conventional intubation maneuvers⁵. Therefore, the approach must be proactive, prioritizing airway safety before the patient presents signs of respiratory exhaustion.

This systematic review aims to synthesize the most recent evidence on intervention strategies, evaluating everything from the utility of new imaging techniques to selection criteria for surgical drainage. By consolidating this knowledge, we seek to provide a clear guide for the clinician facing this emergency, optimizing response times and minimizing the risks of long-term sequelae or fatal outcomes.

Anatomical Considerations and Etiopathogenesis:

Anatomy of the submandibular, sublingual, and submental spaces:

Understanding Ludwig’s angina is impossible without a detailed analysis of the anatomy of the suprahioid region. The affected area comprises a complex system of fascial spaces that communicate freely with each other. The mylohyoid muscle acts as the central anatomical component in this pathology, functioning as a diaphragm that divides the submandibular space into two compartments: the sublingual space above and the submandibular space proper below¹.

The sublingual space contains the sublingual gland, Wharton’s duct, and the lingual and hypoglossal nerves. The submandibular space, located inferiorly to the mylohyoid, houses the submandibular gland and lymph nodes. For its part, the submental space is located in the midline, between the anterior bellies of the digastric muscles. Because the mylohyoid muscle has an incomplete posterior insertion, there is a direct communication route that allows the infection to spread rapidly from one space to another, resulting in characteristic bilateral and symmetrical inflammation².

Pathophysiology of cellulitic infection spread:

Unlike other cervical abscesses that tend to form localized collections, Ludwig’s angina behaves as an aggressive and gangrenous cellulitis. The infection spreads by continuity through fascial planes rather than via lymphatic routes¹. This progression generates massive soft tissue edema which, being confined by dense cervical fascia and the mandible, exerts considerable internal pressure.

The most critical consequence of this tissue expansion is the superior and posterior displacement of the tongue. Since the floor of the mouth is limited inferiorly by the mylohyoid muscle and laterally by the mandible, the only path for edema expansion is upwards and backwards, which inevitably occludes the oropharynx and mechanically compromises the airway³. Furthermore, inflammation can extend toward the hyoid bone and epiglottis, increasing the risk of laryngospasm and total obstruction.

Etiological factors: odontogenic origin vs. other causes:

In the vast majority of cases, approximately between 70% and 90%, Ludwig’s angina has an odontogenic origin⁶. The infection usually originates in the second or third lower molar. This is due to an anatomical peculiarity: the roots of these molars often extend below the insertion line of the mylohyoid muscle on the internal face of the mandible. Therefore, an apical infection in these teeth breaks the lingual bone cortex and directly accesses the submandibular space¹.

Other less frequent causes include sialadenitis of the submandibular gland, infected mandibular fractures, penetrating wounds in the floor of the mouth, and infections after lingual piercing placement. In the pediatric population, although the odontogenic cause remains prevalent, upper respiratory tract infections and complications from tonsillitis should also be considered³. In rare cases, blunt trauma can generate sublingual hematomas that mimic the clinical presentation of Ludwig’s angina, a condition termed «pseudo-Ludwig’s angina»⁸.

Clinical Diagnosis and Risk Assessment:

Cardinal signs and initial clinical presentation:

The diagnosis of Ludwig’s angina is fundamentally clinical. The classic presentation is characterized by a triad of symptoms: bilateral neck swelling, tongue elevation, and rapid symptom progression. Patients usually present with «woody induration» in the submandibular region, which feels extremely firm to the touch and does not pit¹. This firmness is indicative of high tissue pressure and the cellulitic nature of the infection.

Other common signs include trismus (limited mouth opening), which greatly hinders exploration of the oropharynx, and «hot potato» voice, caused by restricted lingual movement. The patient may present sialorrhea (inability to swallow saliva) and a tripod position to facilitate breathing. Fever, chills, and tachycardia are common systemic manifestations reflecting the inflammatory response to the polymicrobial infection².

Diagnostic criteria and severity scales:

To establish the diagnosis rigorously, Grodinsky’s criteria are usually applied, which include: bilateral involvement of more than one deep space, presence of gangrenous cellulitis with scant or serosanguinous pus, involvement of connective tissues and fascia but not lymph glands, and spread by fascial continuity¹. Severity assessment must be continuous, as the patient’s condition can deteriorate within minutes.

The presence of stridor, cyanosis, or the use of accessory muscles for breathing are indicators of imminent airway obstruction and demand immediate intervention. Laboratory markers, such as elevated C-reactive protein (CRP) and a high neutrophil-to-lymphocyte ratio (NLR), are useful for evaluating the severity of the systemic inflammatory response and predicting the risk of complications such as sepsis².

Diagnostic imaging: utility of computed tomography and ultrasound:

Although the diagnosis is clinical, imaging tests are essential to determine the extent of the infection and plan the surgical approach. Contrast-enhanced computed tomography (CT) is considered the gold standard. CT allows precise visualization of gas in tissues, the formation of fluid collections or abscesses, and the degree of displacement of airway structures². Furthermore, it is crucial for detecting the extension of the infection toward the parapharyngeal space or the mediastinum⁵.

Ultrasound can be a useful tool in the early stages or in pediatric patients to identify drainable collections, but its utility is limited by the presence of tissue gas and the difficulty of evaluating deep spaces behind the mandible⁶. It is important to note that no imaging study should delay securing the airway in a patient with evident respiratory compromise. The risk of sending an unstable patient to the radiology suite is considerable, so stabilization must always precede the acquisition of complex images¹.

Airway Management: The Absolute Priority:

Predictive evaluation of respiratory compromise:

The most common cause of death in Ludwig’s angina is asphyxia due to upper airway obstruction. Therefore, predictive evaluation must be the first step in emergency management. Clinicians must look for signs of «difficult airway» both anatomically and physiologically. Severe trismus, lingual protrusion preventing visualization of the uvula (Mallampati unevaluable), and massive cervical edema are predictors of extremely difficult or impossible conventional orotracheal intubation⁵.

The presence of arytenoid edema on preoperative CT has been identified as a significant risk factor for the need for a surgical airway or prolonged intubation⁵. If the patient presents with inspiratory stridor, this indicates that the airway diameter has been reduced to less than 5 mm, constituting an extreme emergency. In this scenario, any attempt at airway manipulation without proper preparation can precipitate laryngospasm or total collapse of the pharyngeal lumen.

Approach techniques: fiberoptic intubation vs. cricothyroidotomy and tracheostomy:

Airway management in these patients requires careful planning and the presence of experienced personnel. Awake flexible fiberoptic intubation is currently considered the technique of choice¹. This technique allows visualization of the airway while the patient maintains their own muscle tone and protective reflexes, avoiding the soft tissue collapse that occurs following general anesthesia induction.

However, fiberoscopy may fail due to the presence of secretions, blood, or such severe anatomical distortion that it prevents the passage of the device. In such cases, or when compromise is imminent, scheduled tracheostomy or emergency cricothyroidotomy is necessary². It is important to note that performing a tracheostomy in a patient with Ludwig’s angina is technically difficult due to the «bull neck» caused by edema, which increases the distance between the skin and the trachea and hinders the localization of anatomical landmarks. For this reason, some protocols suggest performing tracheostomy under local anesthesia before attempting any other maneuver if obstruction is critical.

Management protocols in the intensive care unit:

Once the airway is secured, the patient must be transferred to the intensive care unit (ICU) for close monitoring. ICU management focuses on hemodynamic stabilization, administration of intravenous antibiotics, and surveillance of infection progression. In patients who have been orotracheally intubated, it must be considered that deep tissue edema may take several days to resolve, making premature extubation a major risk⁵.

ICU protocols also include the management of protective mechanical ventilation and the prevention of secondary complications such as aspiration pneumonia, which is common due to pre-existing dysphagia and sialorrhea. Coordination with the surgical team is vital to decide when to perform control CT scans if the patient does not show clinical improvement, looking for undetected extensions of the infection. Early nutritional support and strict glycemic control are equally fundamental, especially in diabetic patients, who present a higher risk of necrotizing infections and more turgid disease progression⁹.

Antimicrobial Treatment and Pharmacological Support:

Prevalent microbiology and resistance patterns:

Ludwig’s angina is typically a polymicrobial infection reflecting the normal flora of the oral cavity. Microorganisms most frequently isolated include viridans group streptococci, Staphylococcus aureus, and a variety of anaerobes such as Bacteroides, Fusobacterium, and Peptostreptococcus⁶. This bacterial synergy is responsible for the rapid tissue destruction and characteristic gas production of the disease.

In recent years, an increase in the prevalence of resistant strains has been observed, including methicillin-resistant Staphylococcus aureus (MRSA) and extended-spectrum beta-lactamase (ESBL) producing bacteria, especially in patients with previous hospitalizations or chronic comorbidities². Furthermore, in immunocompromised or diabetic patients, gram-negative pathogens such as Klebsiella pneumoniae may appear, which is associated with a higher incidence of abscess formation and systemic complications⁹.

Broad-spectrum empirical antibiotic therapy regimens:

The immediate initiation of intravenous antibiotic therapy is crucial and should not be delayed waiting for culture results. The empirical regimen must cover both aerobic gram-positives and strict anaerobes. A commonly used combination is ampicillin-sulbactam or clindamycin combined with a third-generation cephalosporin¹. In cases where MRSA is suspected, the addition of vancomycin or linezolid should be considered.

For patients with severe septic conditions or risk factors for resistance, the use of carbapenems (such as meropenem) provides robust coverage against a wide range of pathogens, including gram-negative anaerobes². Once culture and antibiogram results are available, therapy should be de-escalated to a more targeted regimen to minimize selective pressure and side effects. Treatment duration usually extends for 2 to 3 weeks, depending on clinical response and resolution of collections on control images.

Use of corticosteroids and adjuvant therapies in the acute phase:

The role of corticosteroids in Ludwig’s angina is a subject of debate, although many protocols include them to help reduce soft tissue edema and improve mouth opening. Dexamethasone administration can facilitate airway visualization during intubation maneuvers and potentially reduce the need for a surgical airway in selected cases¹. Nonetheless, corticosteroids should not be considered a substitute for airway protection or surgical drainage.

Other adjuvant therapies include aggressive blood glucose control in diabetic patients, as hyperglycemia compromises neutrophil function and promotes bacterial spread³. The use of antifibrinolytics has been reported in specific cases where inflammation is secondary to hematomas (pseudo-angina), but its use is not standard in infectious angina⁸. Hemodynamic support with fluid therapy and vasopressors is essential in patients presenting signs of septic shock to maintain organ perfusion.

Surgical Intervention: Debridement and Drainage:

Despite advances in antibiotic therapy, surgical intervention remains the pillar of treatment for cases of Ludwig’s angina presenting purulent collections or lack of response to initial medical management. The primary objective of surgery is not only the evacuation of pus but the decompression of tense anatomical spaces that threaten airway patency¹⁰.

Indications and optimal timing for surgical decompression:

The decision to intervene surgically must be based on a rigorous clinical evaluation and radiological findings. Absolute indications include the presence of a fluid collection detectable by computed tomography (CT), imminent airway compromise, suspicion of necrotizing fasciitis, or lack of clinical improvement after 24 to 48 hours of intensive antibiotic treatment¹¹. Literature reports that approximately 81% of patients with deep neck infections require open surgical drainage as part of their definitive management¹⁵.

Intervention time is a critical prognostic factor. A delay in drainage can allow the infection to progress toward the parapharyngeal space and, subsequently, to the mediastinum, exponentially increasing mortality¹⁶. In Ludwig’s angina, the «woody cellulitis» phase may precede frank abscess formation; at this stage, decompression via wide incisions can prevent mechanical asphyxia by allowing edematous tissues to expand outward instead of compressing the oropharynx¹⁷.

Surgical approaches from the maxillofacial surgery perspective:

From the perspective of maxillofacial surgery, the approach focuses on eliminating the source of infection and accessing the submandibular, sublingual, and submental spaces. Given that most cases have an odontogenic origin (especially lower second and third molars), extraction of the affected dental organs is a mandatory step to prevent recurrences¹¹.

The standard procedure usually involves a wide transverse cervical incision («apron» or bilateral submandibular incision) allowing communication of the affected spaces. Blunt dissection is performed to connect the sublingual space with the submandibular space through the mylohyoid muscle, ensuring complete decompression of the floor of the mouth¹³. It is essential to leave Penrose-type drains or closed suction systems to allow continuous egress of debris and purulent material during the immediate postoperative period¹².

Management of deep cervical spaces by otorhinolaryngology:

The participation of the otorhinolaryngologist is vital when the infection extends beyond the limits of the floor of the mouth. Access to the parapharyngeal and retropharyngeal spaces requires detailed knowledge of deep cervical anatomy to avoid injury to vital structures such as the carotid sheath and cranial nerves¹¹. In situations where extension to the upper mediastinum is confirmed, the otorhinolaryngologist can perform a cervical mediastinoscopy to drain collections localized above the fourth thoracic vertebra¹².

Furthermore, airway management via scheduled tracheostomy is often the responsibility of the otorhinolaryngology team. In patients with severe anatomical distortion of the neck and extreme trismus, tracheostomy under local anesthesia may be the safest option before proceeding to extensive surgical debridement, thus avoiding the risks of a failed difficult intubation¹².

Complications and Postoperative Management:

Ludwig’s angina is a pathology with a high potential for systemic and regional complications that can lead to permanent sequelae or the death of the patient. Postoperative management in an intensive care unit (ICU) is essential for continuous surveillance of disease progression.

Necrotizing descending mediastinitis and other systemic complications:

The most feared complication of Ludwig’s angina is descending necrotizing mediastinitis (DNM). This occurs when the infection crosses the retropharyngeal space or the «danger» space into the chest, taking advantage of the negative intrathoracic pressure during inspiration¹¹. DNM is associated with a mortality rate that can exceed 25%, even with aggressive treatment¹⁶. Signs of suspicion include retrosternal pain, persistent dyspnea, and mediastinal widening on chest X-ray.

Other serious complications include internal jugular vein thrombosis (Lemierre’s syndrome), carotid artery erosion, brain abscess, and severe sepsis with multi-organ failure¹⁸. Hematogenous spread can lead to cavernous sinus involvement, especially if the infection progresses through deep venous plexuses, representing an additional neurosurgical and ophthalmological emergency¹³.

Postoperative care and control of the source of infection:

Following surgery, the patient must remain monitored in the ICU to ensure hemodynamic stability and airway patency. Control of the source of infection involves not only the initial surgery but also frequent local dressings and, occasionally, programmed re-interventions («second-look») to ensure no residual collections exist¹². The use of vacuum sealing drainage (VSD) systems in cervical incisions has shown promising results, potentially shortening ICU stay and facilitating tissue granulation, although it does not always improve the final prognosis in cases of advanced DNM¹⁶.

Early enteral nutrition is fundamental to support the immune response, often administered via a nasogastric tube if oropharyngeal edema prevents normal swallowing. Likewise, strict surveillance of blood glucose levels must be maintained, given that poor metabolic control is a major risk factor for tissue necrosis progression¹³.

Prognostic factors and reduction of hospital mortality:

The prognosis for Ludwig’s angina has improved significantly since the pre-antibiotic era, but mortality remains linked to specific factors. Early diagnosis and timely intervention are the most important determinants for a favorable outcome¹⁶. Factors such as advanced age, presence of diabetes mellitus, hypertension, and delay in seeking medical attention correlate with longer hospital stays and complications¹⁶.

The implementation of multidisciplinary protocols integrating rapid imaging evaluation (CT) and immediate airway stabilization has proven to be the most effective strategy for reducing hospital mortality¹². Public education on oral hygiene and timely treatment of dental caries remains the most relevant primary prevention measure to avoid the occurrence of this potentially fatal pathology¹⁷.

DISCUSSION

The management of Ludwig’s angina represents one of the most complex challenges in emergency medicine and head and neck surgical specialties. Despite the availability of advanced technology, the essence of therapeutic success lies in rapid clinical judgment and coordinated intervention.

When analyzing international literature, there is almost unanimous consensus that contrast-enhanced computed tomography is the «gold standard» for diagnosis and surgical planning, allowing precise identification of affected spaces and possible mediastinal extension^{11, 15}. However, a clinical controversy arises regarding imaging timing: in patients with imminent respiratory compromise, transfer to the radiology suite can be dangerous. In these cases, bedside ultrasound emerges as a useful tool to identify drainable collections and guide intervention without mobilizing the unstable patient¹⁹.

Regarding airway management, while some centers advocate for awake fiberoptic intubation as the first option, others suggest that in advanced stages of Ludwig’s angina, tracheostomy under local anesthesia should be considered earlier to avoid laryngeal trauma and laryngospasm associated with multiple failed intubation attempts¹².

Ludwig’s angina is, by definition, a disease that blurs the boundaries between maxillofacial surgery and otorhinolaryngology. Coordination between these teams, along with intensive care and radiology specialists, is fundamental¹¹. Reviewed evidence suggests that centers using a team approach for managing deep neck infections obtain better results, especially in early detection of complications such as mediastinitis¹⁶.

This synergy allows that, while the maxillofacial surgeon addresses the odontogenic focus and anterior spaces, the otorhinolaryngologist secures the airway and monitors parapharyngeal extension. This cooperative work model optimizes surgical times and ensures that all anatomical compartments at risk are properly evaluated and treated¹².

A significant limitation identified in this review is the scarcity of randomized clinical trials on Ludwig’s angina management. Most available evidence comes from retrospective observational studies and case series, which limits the strength of recommendations in areas such as corticosteroid use or exact surgical drainage timing¹⁵. There is a need for multi-center studies evaluating the efficacy of new technologies, such as video-assisted thoracoscopic surgery (VATS) for managing mediastinal extension, compared to traditional open approaches¹⁶.

Additionally, the role of ultrasound in airway management and abscess detection in the emergency setting requires broader validation to be formally integrated into triage protocols¹⁹. Future research should also focus on developing more precise risk scales combining clinical parameters and inflammatory biomarkers to predict which patients will progress toward necrotizing forms of the disease¹³.

CONCLUSIONS

1. Ludwig’s angina remains a high-priority medical-surgical emergency demanding a high index of clinical suspicion. Although its incidence has decreased due to improved oral health and antibiotic access, its presentation remains potentially lethal due to the speed with which it can occlude the upper airway. Successful management is based on three non-negotiable pillars: early and safe airway securing, broad-spectrum intravenous antibiotic therapy, and timely surgical debridement for cervical space decompression.
2. The integration of multidisciplinary teams composed of maxillofacial surgeons, otorhinolaryngologists, and intensivists is the determining factor in reducing complication rates, especially descending necrotizing mediastinitis. The use of computed tomography as the primary diagnostic tool and the adjuvant support of corticosteroids have optimized clinical outcomes. Nonetheless, prevention through proper treatment of primary odontogenic infections remains the most effective strategy to mitigate the impact of this severe pathology on public health. This coordination between specialists allows for early surgical intervention and aggressive airway management, critical elements given that the infection can progress rapidly from the submandibular spaces into deeper cervical structures. Precise identification of initial oropharyngeal or odontogenic foci is fundamental, as lack of timely control facilitates the spread of cellulitis into the mediastinum, drastically raising mortality risk. Therefore, anatomical delimitation via imaging studies and expeditious surgical debridement constitute the basis of the therapeutic protocol to avoid respiratory obstruction and systemic sepsis.

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