60 yo femal with neck pain

[pbruss]

60 yo female brough in by husband for neck pain for past few days. that is the only history they can give.

on examshe is lethargic, hypoxic, tachy and hyoptensive. she has an ae of redness and swelling that extends from her chin to her sternal notch that warm and tender.

her ct scanis attached. what is the next step in treatment?

A. emergent ENT eval
B. Unasyn 3 g iv
C. fiberoptic intubation
D. Unasyn 3g and Clinda 600mg iv
E. emergent placment of left chest tube

Attachments:

[Bjs04f]

C- lots of gas and soft tissue swelling concerning for ludwigs, need that airway

[mwiepking]

Agree with C, then D (ampicillin/sulbactam and clindamycin) for antibiotics while you're doing that or once you've got the airway in.

[kemple]

Agree with Brando on this one, looks like there is already some airway compromise I would tube before it's too late. Then I would get ENT to lance them. However, while waitig for ENT I would go ahead and start the abx.

[pbruss]

spot on. this was a bad Ludwig's that we intubated then gave unasyn and clinda. i have to say i was very impressed with Bahhur who did the intubation. see below for up to date for review

Submandibular space infections (Ludwig's angina)
Author
Anthony W Chow, MD, FRCPC, FACP
Section Editor
Stephen B Calderwood, MD
Deputy Editor
Anna R Thorner, MD
Disclosures: Anthony W Chow, MD, FRCPC, FACP Nothing to disclose. Stephen B Calderwood, MD Consultant/Advisory Boards: Pulmatrix [Inhaled antimicrobial products (Not currently released)]. Patent Holder: Vaccine Technologies [Cholera (Cholera vaccines)]. Equity Ownership/Stock Options: PharmAthene [Biodefense (Anthrax)]. Anna R Thorner, MD Employee of UpToDate, Inc.
Contributor disclosures are reviewed for conflicts of interest by the editorial group. When found, these are addressed by vetting through a multi-level review process, and through requirements for references to be provided to support the content. Appropriately referenced content is required of all authors and must conform to UpToDate standards of evidence.
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All topics are updated as new evidence becomes available and our peer review process is complete.
Literature review current through: Jul 2014. | This topic last updated: Sep 17, 2013.
INTRODUCTION — Ludwig's angina is a bilateral infection of the submandibular space that consists of two compartments in the floor of the mouth, the sublingual space and the submylohyoid (also known as submaxillary) space (figure 1). It was first described by the German physician, Wilhelm Frederick von Ludwig in 1836. This infection most commonly arises from an infected second or third mandibular molar tooth. It is an aggressive, rapidly spreading cellulitis without lymphadenopathy with potential for airway obstruction and requires careful monitoring and rapid intervention for prevention of asphyxia and aspiration pneumonia.

The anatomy, microbiology, clinical manifestations, imaging, and treatment of submandibular space infections (Ludwig's angina) will be reviewed here. Other deep neck space infections are discussed separately. (See "Deep neck space infections".)

DEFINITION — Although the term Ludwig's angina has been loosely applied to a heterogeneous array of infections involving the sublingual and submylohyoid (submaxillary) spaces, this diagnosis should be restricted to the following classical description:

●The infection begins in the floor of the mouth. It is characteristically an aggressive, rapidly spreading "woody" or brawny cellulitis involving the submandibular space.


●The infection is a rapidly spreading cellulitis without lymphatic involvement and generally without abscess formation.


●Both the submylohyoid and sublingual spaces are involved.


●The infection is bilateral.


ANATOMIC CONSIDERATIONS — The submandibular space lies within the submental and submandibular triangles between the mucosa of the floor of the mouth and the superficial layer of the deep cervical fascia. It is subdivided by the mylohyoid muscle into the sublingual space (which contains the sublingual gland, hypoglossal nerve, part of the submandibular gland, and loose connective tissue) and the submylohyoid space (which contains the submandibular salivary gland and lymph nodes) (figure 1). The two divisions communicate posteriorly around the mylohyoid muscle. This accounts for the bilateral involvement by contiguous spread of infection within the submandibular space in Ludwig’s angina.

An overview of the anatomy of the deep neck spaces and anatomical considerations for other deep neck space infections are discussed separately. (See "Deep neck space infections", section on 'Anatomic considerations'.)

MECHANISMS OF SPREAD — Although the submandibular space is divided by the mylohyoid muscle into the sublingual space above and the submylohyoid space below, it can be considered as a single unit due to a direct communication around the posterior aspect of the mylohyoid muscle (figure 1). Over two-thirds of patients with Ludwig’s angina have a dental source of infection, usually involving the second or third mandibular molar teeth [1]. The submylohyoid space is initially involved, since the roots of these teeth are located below the attachments of the mylohyoid muscle to the mandible (see "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections"). Other sources of infection include contiguous spread from peritonsillar abscess or suppurative parotitis [1].

Medial spread of infection is facilitated because the lingual aspects of periodontal bone around these teeth are thin. Infection extends contiguously to involve the sublingual and thus the entire submandibular space in a symmetrical manner. If infection were instead spread via the lymphatics, involvement would be unilateral instead of bilateral as is observed. An identical process, initially involving the sublingual space, can arise less commonly from infection of the premolars and other teeth or from trauma to the floor of the mouth.

Once established, infection evolves rapidly. The tongue may enlarge to two or three times its normal size and distend posteriorly into the hypopharynx, superiorly against the palate, and anteriorly protruding out of the mouth. Immediate posterior extension of the process will directly involve the epiglottis. There exists a little known dangerous connection between the submandibular and parapharyngeal spaces known as the buccopharyngeal gap. This is created by the styloglossus muscle as it leaves the tongue and passes between the middle and superior constrictor muscles to attach on the styloid process. Thus, cellulitis of the submandibular space may spread directly along the styloglossus muscle into the parapharyngeal space and from there to the retropharyngeal space and the superior mediastinum [2]. (See "Deep neck space infections".)

MICROBIOLOGY — Ludwig's angina is typically a polymicrobial infection involving the flora of the oral cavity (table 1) [3]. (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections".)

The most common organism isolated from deep neck space infections is Streptococcus viridans. Most abscesses originating from the teeth also harbor oral anaerobes, including Peptostreptococcus species, Fusobacterium nucleatum, pigmented Bacteroides (eg, Prevotella melaninogenica [formerly Bacteroides melaninogenicus] and Porphyromonas spp), and Actinomyces species.

In immunocompromised patients, gram-negative aerobes may also be present. Furthermore, Staphylococcus aureus, including methicillin-resistant S. aureus, may contribute to deep neck space infections in immunocompromised patients and others with specific risk factors [1,4]. This is discussed in detail separately. (See "Deep neck space infections", section on 'Microbiology'.)

CLINICAL FEATURES — Patients typically present with fever, chills, and malaise, as well as mouth pain, stiff neck, drooling, and dysphagia, and may lean forward to maximize the airway diameter [5]. They may have a muffled voice or be unable to speak at all. Trismus is usually absent unless there is spread into the parapharyngeal space. As the illness progresses, breathing may become difficult; stridor and cyanosis are considered ominous signs. (See 'Airway management' below.)

On physical examination, patients have tender, symmetric, and "woody" induration, sometimes with palpable crepitus, in the submandibular area [5]. The mouth is held open by lingual swelling. There is typically no lymphadenopathy. The floor of the oropharynx is usually elevated and erythematous, and is tender to palpation. Occasionally, the inflammation extends to the epiglottis.

IMAGING — Computed tomography (CT) is the imaging modality of choice for the diagnosis of Ludwig's angina and other deep neck space infections [6]. This is discussed in detail separately. (See "Deep neck space infections", section on 'Imaging'.)

DIAGNOSIS — The diagnosis of Ludwig's angina is established based on the presence of suggestive clinical findings, usually with the support of imaging studies. When needle aspiration or incision and drainage is indicated, samples should be obtained for Gram stain and culture [7]. (See 'Surgery' below.)

Since Ludwig's angina does not usually involve abscess formation, a microbiologic diagnosis from the site of infection is often not possible. Needle aspiration of the submandibular space may be attempted and specimens should be transported for culture of both facultative and anaerobic organisms. Blood cultures should be obtained from patients with Ludwig's angina. (See "Blood cultures for the detection of bacteremia".)

TREATMENT — The treatment of Ludwig's angina involves timely assessment and management of the airway, and empiric broad-spectrum antibiotics [5,8]. Surgery is not usually necessary since it is uncommon to have a drainable collection in the early stages of infection. Surgical drainage is important once abscesses are identified by CT or MRI.

Airway management — While maintenance of an adequate airway is the primary concern and may necessitate urgent tracheostomy [9,10], most cases can be managed initially by close observation and intravenous antibiotics. If cellulitis and swelling continue to advance or if dyspnea occurs, artificial airway control should be gained immediately, before the onset of stridor, cyanosis, and asphyxia. Tracheostomy under emergency conditions may be required in more severe cases.

If airway compromise is suspected, a recommended approach is to perform fiberoptic intubation via the nasal route. Fibroscopic laryngoscopy is carried out to assess the airway and to aid in nasal intubation of an endotracheal tube under direct observation [11]. Blind oral or nasotracheal intubation is both traumatic and unsafe in advanced Ludwig's angina because of the potential for inducing severe laryngospasm.

If intubation is not possible, tracheostomy is the most widely recommended means of surgical airway control, although cricothyroidotomy is advocated by some experts because of a lower complication rate. (See "Emergent surgical cricothyrotomy (cricothyroidotomy)".)

Antibiotics — The treatment of Ludwig's angina has not been evaluated in clinical trials. Empiric antimicrobial regimens are based on the expected microbiology, and should be tailored if microbiologic data become available. (See 'Microbiology' above.)

The antibiotic doses recommended below are intended for patients with normal renal function; dosing of some of these agents must be reduced in patients with renal dysfunction.

Immunocompetent hosts — Empiric antibiotic treatment of immunocompetent patients requires broad-spectrum antibiotics with activity against beta-lactamase-producing aerobes and anaerobes, and Staphylococcus aureus, including in some cases, methicillin-resistant S. aureus (MRSA) (table 2).

For immunocompetent hosts, we suggest one of the following regimens:

●Ampicillin-sulbactam (3 g IV every six hours) or

●Penicillin G (2 to 4 MU IV every four to six hours) plus metronidazole (500 mg IV every six to eight hours) or

●Clindamycin (600 mg IV every six to eight hours)


Clindamycin is the drug of choice in penicillin-allergic patients (table 2).

In addition, patients who are at increased risk of MRSA carriage or infection, who are septic or at risk of rapid deterioration, should be treated empirically for MRSA [5]. For MRSA coverage, in addition to one of the above regimens, we suggest vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or linezolid (600 mg orally or IV every 12 hours). Risk factors for MRSA include a history of intravenous drug use, comorbid disease (eg, diabetes mellitus), or residing in a community or hospital where there is a substantial incidence of MRSA.

If MRSA is not present on deep cultures, coverage for this organism can be discontinued. Dosing and monitoring of vancomycin is discussed in detail separately. (See "Vancomycin dosing and serum concentration monitoring in adults", section on 'Routine administration'.)

Immunocompromised hosts — Empiric antibiotic treatment of immunocompromised patients requires broad-spectrum antibiotics with activity against facultative gram-negative rods, and beta-lactamase-producing aerobes and anaerobes. A cephalosporin with activity against Pseudomonas aeruginosa, in combination with an agent with activity against oral anaerobes, are frequently given. Alternatively, a carbapenem (eg, imipenem or meropenem) or an extended-spectrum beta-lactamase-inhibitor combination (eg, piperacillin-tazobactam) may be used, particularly in the immunocompromised host with severe infection (table 2).

Treatment for immunocompromised patients may include one of the following regimens:

●Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV every six to eight hours) or

●Imipenem (500 mg IV every six hours) or

●Meropenem (1 g IV every eight hours) or

●Piperacillin-tazobactam (4.5 g IV every six hours)


In addition, patients with risk factors for MRSA infection should be treated empirically with vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or linezolid (600 mg orally or IV every 12 hours). Risk factors for MRSA include a history of intravenous drug use, comorbid disease (eg, diabetes mellitus), or residing in a community or hospital where there is a substantial incidence of MRSA.

Duration — In general, antimicrobial therapy should be continued for two to three weeks until clear evidence of clinical improvement is present, and fever and leucocytosis have subsided. Longer courses are required when complications are present. We favor intravenous antibiotics for the entire duration of treatment.

Surgery — Early surgical decompression is unlikely to locate pus and, at best, may only moderately improve the airway. Abscesses develop relatively late (not usually in the first 24 to 36 hours) and are sometimes difficult to detect clinically.

If the patient is not responding adequately to antibiotics alone after this initial period, or if fluctuance is detectable or a collection is observed on imaging, needle aspiration or a more formal incision and drainage procedure under general anesthesia should be performed. This should be done with a cuffed tracheostomy in place. Additionally, when a tooth is implicated as the source of infection, it should be extracted. (See "Complications, diagnosis, and treatment of odontogenic infections".)

When needle aspiration or incision and drainage is indicated, samples should be obtained for Gram stain and cultured for both aerobic and anaerobic microorganisms. (See 'Diagnosis' above.)

COMPLICATIONS — As noted above, airway compromise is a potential complication of Ludwig's angina, and requires careful monitoring and rapid intervention for prevention of asphyxia or aspiration pneumonia. (See 'Airway management' above.)

Mediastinitis is a rare complication resulting from spread into the parapharyngeal space and from there to the retropharyngeal space and the superior mediastinum [2]. (See 'Mechanisms of spread' above.)

PROGNOSIS — With the combined use of systemic antibiotics and aggressive surgical intervention in selected patients, the mortality rate for Ludwig's angina has declined dramatically from over 50 percent in the preantibiotic era to 0 to 4 percent [2].

SUMMARY AND RECOMMENDATIONS

●Ludwig's angina is a bilateral infection of the submandibular space that begins in the floor of the mouth, most commonly related to the second or third mandibular molar teeth. It is an aggressive, rapidly spreading "woody" or brawny cellulitis without lymphadenopathy. Airway compromise is a potential complication, and requires careful monitoring and rapid intervention for prevention of asphyxia and aspiration pneumonia. (See 'Definition' above and 'Mechanisms of spread' above and 'Complications' above.)


●The submandibular space lies within the submental and submandibular triangles between the mucosa of the floor of the mouth and the superficial layer of the deep cervical fascia. Although the submandibular space is further divided by the mylohyoid muscle into the sublingual space above and the submylohyoid space below, it can be considered as a single unit due to a direct communication around the posterior aspect of the mylohyoid muscle (figure 1). (See 'Anatomic considerations' above and 'Mechanisms of spread' above.)


●Ludwig's angina is typically a polymicrobial infection. The most common organisms implicated in deep neck space infections of odontogenic origin are Streptococcus viridans and oral anaerobes. Gram-negative aerobes may also play a role in immunocompromised patients. Staphylococcus aureus, including methicillin-resistant S. aureus, may also be involved in immunocompromised patients and others with specific risk factors. (See 'Microbiology' above.)


●Patients typically present with fever, chills, and malaise, as well as mouth pain, stiff neck, drooling, and dysphagia, and may lean forward to maximize the airway diameter. They may have a muffled voice or be unable to speak at all. As the illness progresses, breathing may become difficult; stridor and cyanosis are considered ominous signs. (See 'Clinical features' above.)


●On physical examination, patients have tender, symmetric, and "woody" induration, sometimes with palpable crepitus, in the submandibular area. The mouth is held open by lingual swelling. The floor of the oropharynx is usually elevated and erythematous, and is tender to palpation. (See 'Clinical features' above.)


●Computed tomography (CT) is the imaging modality of choice for the diagnosis of Ludwig's angina (see 'Imaging' above). Magnetic resonance imaging (MRI) is useful for delineating soft tissue involvement particularly if septic jugular thrombophlebitis is suspected.


●The diagnosis of Ludwig's angina is established based on the presence of suggestive clinical findings, usually with the support of imaging studies. When needle aspiration or incision and drainage are indicated, samples should be obtained for Gram stain and both aerobic and anaerobic culture. Blood cultures should be obtained in patients with Ludwig's angina. (See 'Diagnosis' above.)


●While maintenance of an adequate airway is the primary concern and may necessitate urgent tracheostomy, most cases can be managed initially by close observation and intravenous antibiotics. (See 'Airway management' above.)


●Patients with Ludwig's angina should be treated empirically with broad-spectrum aerobic and anaerobic coverage, including in some cases, coverage for methicillin-resistant S. aureus (MRSA). The appropriate regimen depends on the immune status of the patient and risk factors for MRSA. Risk factors for MRSA include a history of intravenous drug use, comorbid disease (eg, diabetes mellitus), or residing in a community or hospital where there is a substantial incidence of MRSA.


●Immunocompetent hosts may receive one of the following regimens:


•Ampicillin-sulbactam (3 g IV every six hours) or


•Penicillin G (2 to 4 MU IV every four to six hours) plus metronidazole (500 mg IV every six to eight hours) or


•Clindamycin (600 mg IV every six to eight hours)

In addition to one of the above regimens, we suggest that immunocompetent patients who are at increased risk for MRSA infection be treated empirically with vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or linezolid (600 mg orally or IV every 12 hours). (See 'Immunocompetent hosts' above.)



●Immunocompromised hosts may receive one of the following regimens:


•Cefepime (2 g IV every 12 hours) plus metronidazole (500 mg IV every six to eight hours) or


•Imipenem (500 mg IV every six hours) or


•Meropenem (1 g IV every eight hours) or


•Piperacillin-tazobactam (4.5 g IV every six hours)

In addition to one of the above regimens, we suggest that immunocompromised patients who are at increased risk for MRSA infection be treated empirically with vancomycin (15 to 20 mg/kg IV every 8 to 12 hours, not to exceed 2 g per dose) or linezolid (600 mg orally or IV every 12 hours). (See 'Immunocompromised hosts' above.)


●In general, antimicrobial therapy should be continued for two to three weeks until clear evidence of clinical improvement is present, and fever and leucocytosis have subsided. Longer courses are required when complications are present. (See 'Duration' above.)


●If the patient is not responding adequately to antibiotics alone after this initial period, or if fluctuance is detectable or a collection is observed on imaging, needle aspiration or a more formal incision and drainage procedure under general anesthesia should be performed. (See 'Surgery' above.)



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[kemple]

Strong work Bahhur.

[Bjs04f]

she did well in the ICU, as she was my pt there. Multiple debridements with penrose drains left in. When I left things were improving