A case of Ludwig’s angina, an extensive deep neck infection of odontogenic origin

Introduction

Ludwig’s angina is a serious and potentially life-threatening phlegmon of the floor of the mouth and deep tissues of the neck, originally described by Wilhelm Friedrich von Ludwig in 1836 [1]. The condition is commonly caused by polymicrobial infections of odontogenic origin. Many cases are associated with systemic illnesses, including poor oral health, diabetes mellitus (DM), obesity, hypertension, malnutrition, use of non-steroid anti-inflammatory drugs (NSAIDs), and an immunosuppressed state [2–10].
The infection in Ludwig’s angina can rapidly spread to surrounding tissues and lead to serious complications such as aspiration pneumonia, osteomyelitis of the mandible, sepsis, necrotizing fasciitis, mediastinitis, or airway obstruction [5, 6]. Respiratory compromise is a major complication and may necessitate emergent endotracheal intubation or cricothyroidotomy or tracheostomy [7]. Timely diagnosis and treatment help reduce mortality, complication rate, and length of stay in the hospital. Treatment involves high-dose targeted antibiotic therapy and surgical decompression intervention. Surgical treatment typically involves incision and drainage of purulent material and debridement of infected or necrotic tissue with the goal of improving airway patency. In cases of odontogenic Ludwig’s angina, extraction of diseased teeth is strongly recommended to eliminate the source of infection [5, 10–13].
Literature reports no significant gender predilection for Ludwig’s angina; however, approximately 1/3 of observed cases are associated with systemic illnesses. Hence, immunocompromised patients undergoing chemotherapy or steroid therapy or have diabetes mellitus or HIV infection have a significantly greater risk of fatal outcomes. Herein we present an effective treatment modality for an elderly patient with Ludwig’s angina with atypical odontogenic origin from teeth 33 and 34. This case highlights the importance of prompt and aggressive management of Ludwig’s angina to prevent severe complications and optimize patient outcomes. Proper oral health care, early treatment of carious lesions, and collaboration between physicians and dentists are crucial in preventing Ludwig’s angina. We report the case of Ludwig’s angina of odontogenic origin in an elderly patient with multiple comorbidities successfully treated with repeat surgical intervention and targeted antibiotic therapy.

Case report

A 60-year-old male was admitted to the emergency department with massive swelling of the left side of the face and neck of a 2-week duration. Physical examination revealed diffuse, painful swelling of the left periauricular, submandibular and submental areas, difficulty speaking and swallowing, and paralysis of the left facial nerve. On intraoral examination, multiple carious lesions with visible purulent drainage were observed. The vital signs were stable and there were no signs of respiratory compromise. Multiple comorbidities were noted, including hypertension, congestive heart failure, atrial fibrillation, DM type 2, and osteoarthritis.
Computed tomography (CT) of the neck and craniofacial area showed a phlegmon extending from the oral cavity floor to the subcutaneous and deep tissues of the neck with the involvement of the salivary glands and muscles of mastication. Localized 61 × 22 mm abscess present adjacent to caries-affected teeth 33 and 34, and together with the inflammatory changes in the cortical layer of the mandible suggested that the carious lesions were the starting point of the infection. The airway diameter was decreased to 13 × 11 mm (Figure 1).
Upon admission, empirical antibiotic therapy with 1 g ceftriaxone IV every 12 hours and 500 mg metronidazole IV every 8 hours was initiated and the patient was taken to the operating room for incision and drainage with debridement under general anesthesia. Two incisions, in the submandibular and submental area, were used to drain the purulent material. Samples for microbiological culture and sensitivity testing were obtained and surgical drains were placed. Caries-affected teeth 24, 33, 34 and 48 (FDI World Dental Federation notation) were extracted.
Computed tomography on the second postoperative day revealed a significantly increased extent of the infection, reaching the level of the thyroid cartilage and infiltrating the parapharyngeal space, and further decreased airway diameter (11 × 9 mm). A repeat drainage procedure in general anesthesia was performed. The results of microbiological testing were received, showing the predominant bacteria to be Streptococcus constellatus. An antibiotic regimen consisting of 4.5 g tazobactam and piperacillin IV every 6 hours and 600 mg clindamycin IV every 8 hours was initiated.
On the sixth day of admission, swelling in the periauricular area was observed, along with an increase in the white blood cells (WBC) count and a slower decrease in C-reactive protein (CRP) levels (Figure 2). The patient then underwent surgical decompression under local anesthesia. Standard wound and drain care were continued postoperatively and the patient started improving significantly. On the ninth day of admission, the extent of the infection decreased. The patient continued to improve and was released 18 days after the admission in stable condition with a 7-day course of oral clindamycin.

Discussion

Ludwig’s angina is a rare, rapidly-progressing infection that most commonly arises in the oral cavity and spreads to the submandibular, sublingual, submental, and parapharyngeal spaces. The infection causes significant bilateral swelling of the soft tissues of the neck and displacement of the tongue, which may lead to compression of the airway [8]. Prompt recognition and aggressive treatment of Ludwig’s angina are crucial in preventing respiratory complications and led to the full recovery of the patient in this case.
Poor oral hygiene and inadequately managed dental infections are major predisposing factors of Ludwig’s angina. The origin of the infection is odontogenic in 73–85% of cases [3, 4, 6]. Molar teeth, particularly the second and third lower molars, were found to be the source of the infection in the majority of patients [1]. Infections arising from premolar teeth have also been reported [9]. In our patient, infection is thought to have arisen from the extensive caries of the lower canine and first lower premolar teeth. Ludwig’s angina may also develop due to penetrating injuries, dental or surgical procedures, mandibular fractures, submandibular sialadenitis or sialolithiasis, or skin infection [2].
Comorbidities are frequently associated with Ludwig’s angina and may affect the course and severity of the infection. The medical history of our patient included poorly controlled DM type 2, obesity, cardiovascular disease, and osteoarthritis treated with NSAIDs, all of which may have contributed to the severity of the infection. Hyperglycemic environment is known to increase the overall risk of infections, primarily due to immune dysregulation. Bidirectional, reciprocal relationship between DM and dental disease has been reported and may further increase the incidence of Ludwig’s angina in diabetic patients. Possible pathogenetic mechanism includes caries development due to reduced salivary flow rate caused by hyperglycemia and high intake of cariogenic foods in patients with frequently co-occurring DM type 2 and obesity [11].
Ludwig’s angina is caused by polymicrobial infections in majority of cases. The most commonly isolated pathogens include Streptococcus viridans, Streptococcus pyogenes, Staphylococcus epidermidis, Staphylococcus aureus and Peptostreptococcus species [2, 4]. In this case, the microbiological culture yielded Streptococcus constellatus, a part of normal oral flora and an opportunistic pathogen. Deep neck infections due to Strep. constellatus have been reported in the literature and are thought to be associated with an odontogenic source of infection [10, 12].
The most common symptoms of Ludwig’s angina include malaise, fever, dysphagia, odynophagia, trismus, and respiratory distress. On physical examination, the submandibular and neck area may be severely edematous and painful [13]. In our case, extensive swelling of the face and neck was present, but did not lead to airway compromise. The patient continued to be closely monitored for any signs of respiratory difficulty until the edema subsided.
Diagnosis of Ludwig’s angina is mainly clinical, but imaging studies are usually required to determine the extent of the infection and aid in evaluating the patency of the airway. Computed tomography with contrast is usually the preferred modality due to wider availability, however, MRI may be used to better evaluate soft tissues [13]. In emergency situations, ultrasonographic examination may be helpful to assess the spread of the infection [14].
Treatment of Ludwig’s angina typically involves antibiotic therapy and surgical intervention. If there is any suspicion of respiratory compromise, airway control is the first step in medical management as asphyxiation is the leading cause of death [6]. Early initiation of antibiotic therapy is crucial. Empiric broad-spectrum antibiotics are used upon admission of the patient and the regimen is adjusted after the results of microbiological testing become available. In the reported case, ceftriaxone plus metronidazole were used initially and later changed to a targeted antibiotic regimen consisting of tazobactam-piperacillin combination plus clindamycin, effective against Strep. constellatus and recommended for use in immunosuppressed patients with Ludwig’s angina. Other options include ampicillin-sulbactam for immunocompetent patients, and cefepime plus metronidazole or carbapenems for immunocompromised patients [13]. Intravenous dexamethasone may be added to reduce edema, but its use is not recommended routinely [15].
There is no consensus on the necessity of surgical intervention, but surgical drainage may be indicated if the localized collection of purulent material is identified or if medical therapy is ineffective [5]. In our case, repeat surgical decompression was necessary to control the infection. Due to the aggressive nature of Ludwig’s angina and its potential to spread to multiple anatomical compartments, complete drainage during the initial procedure is challenging, and can lead to recurrence of abscesses and rapid disease progression, requiring multiple surgeries.
Prevention of Ludwig’s angina involves primarily dental care, early recognition and treatment of carious lesions and dental infections, and collaboration between physicians and dentists, to decrease the incidence of odontogenic deep neck infections. Effective management of predisposing systemic conditions, such as DM, may also aid in the prevention of dental and deep neck infections.
In conclusion, Ludwig’s angina is a serious condition requiring prompt recognition and treatment. Our case highlights the importance of early initiation of targeted antibiotic therapy and surgical decompression to help prevent complications and optimize patient outcomes. Preventive measures consisting of management of systemic illnesses and proper dental care are crucial in reducing the incidence and severity of Ludwig’s angina.

Funding

No external funding.

Ethical approval

Not applicable.

Conflict of interest

The authors declare no conflict of interest.

References