The patient was a young man in his early 20s. He presented to the Emergency Department with pain in his neck and difficulty swallowing. He managed to tell the ED Doctor that he had had a bad toothache for over a week but had been putting off seeing a Dentist because “he had too many other things to do”.
On examination he was febrile and tachycardic and his respiratory rate was high. The ED Doctor could see that his neck was swollen even by looking from the end of the bed.
On examination he was febrile and tachycardic and his respiratory rate was high. The ED Doctor could see that his neck was swollen even by looking from the end of the bed.
Leaving the patient under the watchful eye of a senior nurse the ED Doctor went to make some phone calls.
First port of call was an Anaesthetist; second the ENT (Ear, Nose and Throat) Surgeon and finally the Microbiologist.
The first question from the Microbiologist was “have you called an Anaesthetist and an ENT Surgeon?”
Having established that help was on the way the Microbiologist got down to business.
“This sounds like Ludwig’s Angina. You need to secure the patients airway and then the ENT Surgeons need to consider going into the patient’s neck to relieve the pressure by resecting any infected material. Start IV Co-amoxiclav and IV Metronidazole and make sure we are sent some tissue from the operation.”
“But you always tell us we don’t need to use Metronidazole when we are using Co-amoxiclav” answered the ED Doctor.
“That’s true most of the time” replied the Microbiologist “but this is one of the few occasions when having two anti-anaerobic antibiotics is a good thing.”
At that point the Anaesthetist arrived and things started to move quickly in the ED Department. Not wanting to miss out on what was going on the ED Doctor rang off and went to write up the antibiotics and see what was happening.
What is Ludwig’s angina?
Ludwig’s angina was first described by a German Doctor called Wilhelm Frederick von Ludwig back in 1836. It is a severe bilateral infection of the soft tissue below the jaw (submandibular space) and tongue (sublingual space) as well as the upper part of the neck. Infection usually starts from an infected 2nd or 3rd molar tooth in the mandible leading to a rapidly progressive cellulitis; this has the potential to cause sufficient swelling to squash the patient’s trachea causing asphyxiation.
How does Ludwig’s angina present?
Patients are usually febrile with mouth pain, neck stiffness, drooling and difficulty swallowing (dysphagia). They often lean forward with the neck slightly extended to maximise the size of the airway. Many are unable to speak.
Over two thirds of patients with Ludwig’s angina have an infected 2nd or 3rd molar tooth, although it can also be secondary to peritonsilar abscess (quinsy) and parotitis (infection of the parotid gland).
The cellulitis of the neck feels as hard as wood, is very tender, symmetrical, and spreads rapidly. Cervical and post auricular (behind the ear) lymphadenopathy is absent. The tongue is often swollen (up to 3 times its normal size!) making it difficult for the patient to close their mouth.
Complications of Ludwig’s angina
Not only does Ludwig’s angina cause compression of the airway but it can also spread to the epiglottis and mediastinum.
Epiglottitis is an infection of the epiglottis causing it to swell and block the airway; urgent intubation or tracheostomy is often required to prevent the patient asphyxiating. Mediastinitis, infection of the mediastinum, is a severe infection of the structures in the centre of the chest including the aorta, trachea, oesophagus, heart and lungs… needless to say this is another severe life-threatening infection which may require extensive surgery and prolong antibiotics; even with treatment it still carries a high mortality. In the pre-antibiotic era the incidence of mediastinitis after Ludwig’s angina was 3.5% but it is now rare; however the mortality is 25% even with treatment so it is important to watch out for this serious complication.
What bacterium causes Ludwig’s angina?
Ludwig’s angina is caused by a real “zoo” of micro-organisms! It isn’t a single bacterium but in fact a mixture of mouth flora. The most common bacteria present include Viridans streptococci, and the oral anaerobes such as Peptostreptococcus spp., Fusobacterium spp., Bacteroides spp., Prevotella spp., Porphyromonas spp., and Actinomyces spp. Occasionally Gram-negative bacteria (e.g. Klebsiella spp.) and Staphylococcus aureus can be present, especially in diabetics and immunocompromised patients.
How is Ludwig’s angina diagnosed?
The main way to diagnose Ludwig’s angina is clinically. The presentation is pretty obvious. Occasionally patients may require a CT scan to show how extensive the infection is and guide whether surgery is required BUT this should only be done once the patient’s airway is secure.
How is Ludwig’s angina treated?
The most important part of the treatment of Ludwig’s angina is to protect the patient’s airway to prevent them asphyxiating. Not all patients need intubating but if not then close observation is required in case the patient deteriorates. If intubation is required but isn’t possible then a tracheostomy should be performed.
Surgery isn’t usually required unless there are abscesses present. These can take a few days to form. If abscesses are drained, pus should be sent for culture to confirm the presence of typical oral bacteria (not just a swab!).
Antibiotic treatment involves broad-spectrum cover with particular attention to anaerobic bacteria for 2-3 weeks depending on clinical response.
First port of call was an Anaesthetist; second the ENT (Ear, Nose and Throat) Surgeon and finally the Microbiologist.
The first question from the Microbiologist was “have you called an Anaesthetist and an ENT Surgeon?”
Having established that help was on the way the Microbiologist got down to business.
“This sounds like Ludwig’s Angina. You need to secure the patients airway and then the ENT Surgeons need to consider going into the patient’s neck to relieve the pressure by resecting any infected material. Start IV Co-amoxiclav and IV Metronidazole and make sure we are sent some tissue from the operation.”
“But you always tell us we don’t need to use Metronidazole when we are using Co-amoxiclav” answered the ED Doctor.
“That’s true most of the time” replied the Microbiologist “but this is one of the few occasions when having two anti-anaerobic antibiotics is a good thing.”
At that point the Anaesthetist arrived and things started to move quickly in the ED Department. Not wanting to miss out on what was going on the ED Doctor rang off and went to write up the antibiotics and see what was happening.
What is Ludwig’s angina?
Ludwig’s angina was first described by a German Doctor called Wilhelm Frederick von Ludwig back in 1836. It is a severe bilateral infection of the soft tissue below the jaw (submandibular space) and tongue (sublingual space) as well as the upper part of the neck. Infection usually starts from an infected 2nd or 3rd molar tooth in the mandible leading to a rapidly progressive cellulitis; this has the potential to cause sufficient swelling to squash the patient’s trachea causing asphyxiation.
How does Ludwig’s angina present?
Patients are usually febrile with mouth pain, neck stiffness, drooling and difficulty swallowing (dysphagia). They often lean forward with the neck slightly extended to maximise the size of the airway. Many are unable to speak.
Over two thirds of patients with Ludwig’s angina have an infected 2nd or 3rd molar tooth, although it can also be secondary to peritonsilar abscess (quinsy) and parotitis (infection of the parotid gland).
The cellulitis of the neck feels as hard as wood, is very tender, symmetrical, and spreads rapidly. Cervical and post auricular (behind the ear) lymphadenopathy is absent. The tongue is often swollen (up to 3 times its normal size!) making it difficult for the patient to close their mouth.
Complications of Ludwig’s angina
Not only does Ludwig’s angina cause compression of the airway but it can also spread to the epiglottis and mediastinum.
Epiglottitis is an infection of the epiglottis causing it to swell and block the airway; urgent intubation or tracheostomy is often required to prevent the patient asphyxiating. Mediastinitis, infection of the mediastinum, is a severe infection of the structures in the centre of the chest including the aorta, trachea, oesophagus, heart and lungs… needless to say this is another severe life-threatening infection which may require extensive surgery and prolong antibiotics; even with treatment it still carries a high mortality. In the pre-antibiotic era the incidence of mediastinitis after Ludwig’s angina was 3.5% but it is now rare; however the mortality is 25% even with treatment so it is important to watch out for this serious complication.
What bacterium causes Ludwig’s angina?
Ludwig’s angina is caused by a real “zoo” of micro-organisms! It isn’t a single bacterium but in fact a mixture of mouth flora. The most common bacteria present include Viridans streptococci, and the oral anaerobes such as Peptostreptococcus spp., Fusobacterium spp., Bacteroides spp., Prevotella spp., Porphyromonas spp., and Actinomyces spp. Occasionally Gram-negative bacteria (e.g. Klebsiella spp.) and Staphylococcus aureus can be present, especially in diabetics and immunocompromised patients.
How is Ludwig’s angina diagnosed?
The main way to diagnose Ludwig’s angina is clinically. The presentation is pretty obvious. Occasionally patients may require a CT scan to show how extensive the infection is and guide whether surgery is required BUT this should only be done once the patient’s airway is secure.
How is Ludwig’s angina treated?
The most important part of the treatment of Ludwig’s angina is to protect the patient’s airway to prevent them asphyxiating. Not all patients need intubating but if not then close observation is required in case the patient deteriorates. If intubation is required but isn’t possible then a tracheostomy should be performed.
Surgery isn’t usually required unless there are abscesses present. These can take a few days to form. If abscesses are drained, pus should be sent for culture to confirm the presence of typical oral bacteria (not just a swab!).
Antibiotic treatment involves broad-spectrum cover with particular attention to anaerobic bacteria for 2-3 weeks depending on clinical response.
1st line |
IV Co-amoxiclav PLUS IV Metronidazole |
2nd line (if 1st line contraindicated) |
IV Clindamycin PLUS IV Metronidazole |
If Immunocompromised |
IV Meropenem |
If MRSA positive |
ADD IV Teicoplanin OR IV Vancomycin |
Prognosis
Before the discovery of antibiotics the mortality from Ludwig’s angina was over 50%! At present it is <4% but with increasing antibiotic resistance this is likely to go up again over time.
So the Anaesthetist arrived, took one look at the increasing swelling in the patient’s neck and decided to anaesthetise them and protect the airway with an endotracheal tube. Shortly after the ENT Surgeon arrived and agreed that the diagnosis was likely to be Ludwig’s Angina and that the patient needed urgent surgical assessment in case any abscesses had developed.
The patient had to have quite a bit of soft tissue from the neck removed as multiple abscesses appeared over the next couple of days, which later required skin grafting by the Plastic Surgeons. The infected 3rd lower molar tooth was also extracted by the Maxillofacial Surgeons. The patient spent a few days intubated on the Intensive Care Unit until the swelling had sufficiently settled to make it safe to remove the endotracheal tube. After a week in hospital the patient was well enough to go home with very clear instruction never to ignore a dental infection again… though they had come to that conclusion themselves already.
Before the discovery of antibiotics the mortality from Ludwig’s angina was over 50%! At present it is <4% but with increasing antibiotic resistance this is likely to go up again over time.
So the Anaesthetist arrived, took one look at the increasing swelling in the patient’s neck and decided to anaesthetise them and protect the airway with an endotracheal tube. Shortly after the ENT Surgeon arrived and agreed that the diagnosis was likely to be Ludwig’s Angina and that the patient needed urgent surgical assessment in case any abscesses had developed.
The patient had to have quite a bit of soft tissue from the neck removed as multiple abscesses appeared over the next couple of days, which later required skin grafting by the Plastic Surgeons. The infected 3rd lower molar tooth was also extracted by the Maxillofacial Surgeons. The patient spent a few days intubated on the Intensive Care Unit until the swelling had sufficiently settled to make it safe to remove the endotracheal tube. After a week in hospital the patient was well enough to go home with very clear instruction never to ignore a dental infection again… though they had come to that conclusion themselves already.
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