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=== Post-operative care ===
=== Post-operative care ===
[[File:Endotracheal Tube.png|thumb|246x246px|Placement of an endotracheal tube to aid breathing.]]
[[Extubation]], which is the removal of endotracheal tube to liberate the patient from mechanical ventilation, should only be done when the patient’s airway is proved to be patent, allowing adequate breathing. This is indicated by a decrease in swelling and patient’s capability of breathing adequately around a uncuffed [[endotracheal tube]] with the lumen blocked.<ref>{{Cite book|url=https://www.worldcat.org/oclc/757994410|title=Current therapy in oral and maxillofacial surgery|date=2012|publisher=Elsevier Saunders|others=Bagheri, Shahrokh C., Bell, R. Bryan., Khan, Husain Ali.|isbn=9781416025276|location=Philadelphia|oclc=757994410}}</ref>
[[Extubation]], which is the removal of endotracheal tube to liberate the patient from mechanical ventilation, should only be done when the patient’s airway is proved to be patent, allowing adequate breathing. This is indicated by a decrease in swelling and patient’s capability of breathing adequately around a uncuffed [[endotracheal tube]] with the lumen blocked.<ref>{{Cite book|url=https://www.worldcat.org/oclc/757994410|title=Current therapy in oral and maxillofacial surgery|date=2012|publisher=Elsevier Saunders|others=Bagheri, Shahrokh C., Bell, R. Bryan., Khan, Husain Ali.|isbn=9781416025276|location=Philadelphia|oclc=757994410}}</ref>


Revision as of 11:47, 20 January 2018

Ludwig's angina
SpecialtyOtorhinolaryngology, oral and maxillofacial surgery Edit this on Wikidata

Ludwig’s angina, also known as Angina Ludovici, is named after a German physician, Wilhelm Frederick von Ludwig, who first described this condition in 1836.[1]

Ludwig’s angina is a type of severe, diffuse cellulitis, involving the bilateral tissue spaces on the floor of the mouth, namely the submandibular, submental, and sublingual spaces.[2] Cellulitis is a spreading infection of connective tissue through tissue spaces, normally with virulent and invasive organisms being the causative agents. This condition has an acute onset and develops rapidly, over a short course of hours, and majority of cases follow an inadequately managed or neglected odontogenic infection.[3]  Other causes include parapharyngeal abscesses, mandibular fracture, oral lacerations or piercing, or submandibular sialodentitis.[4]

The term “angina”, is derived from the Latin word “angere”, which means “choke”; and the Greek word “ankhone”, which means “strangle”. Placing it into context, Ludwig’s angina refers to the feeling of strangling and choking, secondary to obstruction of the airway, which is the most serious potential complication of this condition.[5]  At the initial stage, the floor of the mouth will be elevated and the patient will experience difficulty in swallowing saliva, which will pool and may be observed running from the patient’s mouth.[3] As the condition progresses, the airway is potentially compromised, due to the spread of infection to involve the floor of the mouth and pharyngeal spaces, resulting in a characteristic hardened induration of these spaces bilaterally and an elevation of the tongue.[6]

With the advent of antibiotics in 1940s, improved oral and dental hygiene, and more aggressive surgical approach, the incidence and mortality rate of this condition has significantly reduced. The treatment of any suspected dental infections without delay, and receiving of regular dental check-ups help to catch any impending problems early, before its progression to Ludwig’s angina. If the infection does occur, there will be an individualised treatment plan for each patient, which will be based on factors including the stage of disease and co-morbid conditions at the time of presentation, physician experience, and available resources.[7] The treatment and management strategies of this condition is further explored below.

Signs and symptoms

Ludwig's angina is a fascial space infection with bilateral involvement of the submandibular, sublingual and submental spaces. The external signs may include bilateral lower facial edema around the mandible and upper neck. Intraoral signs may include a raised floor of mouth due to sublingual space involvement and posterior displacement of the tongue. Symptoms may include dysphagia, pain with swallowing, difficulty breathing, and pain.

Ludwig's angina should be treated urgently due to the airway being compromised. The infection may rapidly spread to other fascial spaces of the head and neck, further compromising the airway.

Causes

Dental infections account for approximately 80% of cases of Ludwig's angina.[8] Mixed infections, due to both aerobes and anaerobes, are of the cellulitis associated with Ludwig's angina. Typically, these include alpha-hemolytic streptococci, staphylococci and bacteroides groups.[8]

The route of infection in most cases is from infected lower molars or from pericoronitis, which is an infection of the gums surrounding the partially erupted lower (usually third) molars. Although the widespread involvement seen in Ludwig's usually develops in immunocompromised persons, it can also develop in otherwise healthy individuals. Thus, it is very important to obtain dental consultation for lower-third molars at the first sign of any pain, bleeding from the gums, sensitivity to heat/cold or swelling at the angle of the jaw.

There has been a single case reported where Ludwig's angina was thought to be caused by a recent Tongue piercing.[9][10][11] In addition, Filipino boxer Pancho Villa (1901–1925) died after contracting Ludwig's Angina following a bout with Jimmy McLarnin.[12]

Microbiology

There are a few methods that can be used for determining the microbiology of Ludwig’s angina. One of the traditionally used methods is taking culture samples although it has some limitations.[13] By taking pus samples from a patient with Ludwig’s angina, the microbiology were found to be commonly polymicrobial and anaerobic.[14][15] Some of the commonly found microbes are Viridans Streptococci, Staphylococci, Peptostreptococci, Prevotella, Porphyromonas and Fusobacterium.[14][15] Staphylococcus aureus and black-pigmented bacteroides (Prevotella & Porphyromonas) are highly virulent which can cause infection to spread rapidly.[16] It was also found in a study that Viridans Streptococci were found to be the main microbe found in deep neck infections followed by Staphylococcus aureus and Staphylococcus epidermidis.[14] Another study also compared the microbial content of pus obtained from patients with Ludwig’s angina and from patients without Ludwig’s angina.[16] Both anaerobic and aerobic microbes were isolated which can be found via the referenced link.[16]

Pathological anatomy

A diagram showing some of the fascia of the neck green line - superficial fascia pink line - superficial layer of the deep cervical fascia red line - carotid sheath yellow line - prevertebral layer of the deep layer of the deep cervical fascia

The knowledge and understanding of the anatomy of the fascial spaces where infection may spread and be contained is essential for the treatment of Ludwig’s angina.[17] Bands of connective tissues known as fascia surrounds structures such as muscles introduces potential spaces which allows infections to spread due to the nature of the fascia layering.[18][19] The fascia can be divided into two; superficial fascia and deep cervical fascia;

Superficial Fascia

The superficial fascia which is located just deep to the skin contains fat and goes from the base of the neck into the face and infections that occur in this space are noticeable early as they are superficial.

Deep Fascia

Deep to this superficial fascia is the deep cervical fascia under the platysma muscle and the deep cervical fascia helps in the movement of muscle as it restricts the volume of muscle contained within the fascia. Some muscles are also attached to it and it also has nerves and blood vessels enclosed within it.

The deep cervical fascia can be subdivided into four layers in the neck in which knowledge of the layers is required for an effective treatment of infection;

Superficial layer of the deep cervical fascia

This layer lies just deep to the superficial fascia and the platysma muscle. The fascia goes around the neck completely and splits when approaching the sternocleidomastoid muscle and the trapezius muscle causing it to lie on the outer and deeper surfaces of the said muscles.

The anterior attachment of the fascia is to the chin, hyoid bone and sternum and posteriorly is to the spinous process of the cervical vertebrae. The attachments superiorly are the occipital protuberance, the mastoid process, the inferior border of the mandible from the angle to the midline, the superior nuchal line, the inferior border of the zygomatic arch. Inferiorly, the fascia is attached to the clavicle and the acromion of the scapula, and the sternum where it divides to form an anterior and posterior part.

Middle layer of the deep cervical fascia

The middle layer can be further subdivided into three portions;

Muscular portion, which encircles the strap muscle.

  • The attachment superiorly is at the hyoid bone and the thyroid cartilage and attaches inferiorly at the medial sternum.

Visceral portion/buccopharyngeal portion, which is located deep to the superficial layer of the deep cervical fascia posterior to the pharynx

  • The muscular layer of the pharynx is covered by this portion and is continued forward onto the buccinator muscle. Its location is posterior to the pharynx and attaches to the base of the skull superiorly, then goes down into the mediastinum where it combines with the alar fascia.

Pre-tracheal layer, which encloses the thyroid gland, oesophagus, and the trachea.

  • The attachment of this portion is the larynx superiorly and the fibrous pericardium in the superior mediastinum inferiorly and encloses the thyroid gland.

Deep layer of the deep cervical fascia

The deep layer of the deep cervical fascia is made up of the prevertebral layer and the alar fascia.

Prevertebral layer

  • The prevertebral layer fully surrounds the cervical portions of the prevertebral and the postvertebral muscles completely. Its attachment is at the skull base superiorly and coccyx inferiorly.

Alar fascia

  • The alar fascia is located between the middle layer of the deep cervical fascia and the deep layer of the deep cervical fascia and is a portion of the prevertebral fascia. The alar fascia attaches superiorly to the base of the skull and combines with the visceral portion of the middle layer of the deep cervical fascia at the level of T2.
  • The alar fascia separates the retropharyngeal space from the “danger space”, which is a subdivision of the retropharyngeal space. The danger space goes from the base of the skull to the level of the diaphragm and can give rise to a pathway for the spreading of infection from the pharynx to the mediastinum.

Carotid sheath

The superficial, middle, and deep layer of the deep cervical fascia contribute to compose the carotid sheath which is sheath enclosing the carotid artery, internal jugular vein and the vagus nerve. It is attached superiorly to the base of the skull and merges inferiorly with the tissues surrounding the aortic arch.

The submandibular space

The submandibular space is made up of two potential spaces that goes from the oral cavity mucosa to the superficial layer of the deep cervical fascia. The space encircles the area between the mandible and the hyoid bone. The submandibular space is divided horizontally into the sublingual space above (supramylohyoid compartment) and the submaxillary/submandibular space below (inframylohyoid compartment). This division is due to the mylohyoid muscle which originates on the mylohyoid line located on the lingual surface of the mandible and the insertion of the muscle is at the symphysis menti, the mylohyoid raphe, and the body of the hyoid bone posteriorly.

The combination of these two spaces is commonly referred to as the submandibular space, where the compartments can communicate freely along the mylohyoid muscle posteriorly. The supramylohyoid compartment consists of loose areolar tissue, sublingual glands, submandibular glands, Wharton duct, lingual artery and vein, lingual nerve, hypoglossal nerve and the geniohyoid muscle. What can be found in the inframylohyoid compartments are the anterior bellies of the digastric muscles, submandibular glands, lymph nodes, and facial artery and vein. The submental space is in the inframylohyoid compartment where the space is confined between the anterior bellies of the digastric muscle.

In an event where there is an infection affecting the submental and sublingual spaces can cause an elevation and protrusion of the tongue which will compromise the airway. The submandibular space, the lateral pharyngeal space to an extent the retropharyngeal space can freely communicate with each other. Potential neck infections originating from the retropharyngeal space, located between the buccopharyngeal layer of the middle layer of the deep cervical fascia enclosing the pharynx and the anterior alar fascia can spread via perforation into the danger space which can affect the mediastinum and lungs. Another path of infection spread to the mediastinum from the submandibular space is via the carotid sheath.

Diagnosis

As documented above, the signs and symptoms associated with Ludwig’s angina are characteristic of a life-threatening condition associated with the potential for respiratory obstruction and sepsis. Understanding head and neck surgical anatomy and the paths of spreading infection is fundamental for accurate diagnosis and management.[20] Ludwig’s angina is no exception, and relies primarily upon clinical signs and symptoms for a provisional diagnosis. Further investigation includes imaging and blood sciences.

Prior to undertaking any further investigation, the surgeons and anaesthetists involved with the patient’s care must decide whether the infection spread allows time for initial imaging or whether to prioritise immediate acute airway management.

Odontogenic infection associated with lower second and third molars is the most common origin of Ludwig’s angina.[21] Taking an OPT (orthopantomogram) radiograph will screen and identify any carious teeth if the infection source is of odontogenic origin. An urgent CT scan of the neck with contrast material is indicated for deep neck space infections.[22] If there is suspicion of descending mediastinitis, inclusion of the thorax for CT imaging might be indicated,[20] or plain chest imaging could be an adequate pre-requisite.

Given the high risk of sepsis, patient management should follow local trust policies. NICE guidelines for the diagnosis of sepsis in patients 18 years old and over that fall into the high-risk criteria are based on clinical signs (e.g. behaviour, cyanosis of skin, lips or tongue), observations (e.g. increased heart rate, respiratory rate, systolic blood pressure) and urine output.[23] Their algorithm tool identifies a battery of venous bloods tests to take which includes: a blood gas for glucose and lactate, blood cultures, FBC, U&E (including creatinine), coagulation screen and CRP.[23]

Obtaining a sample or aspirate from any developing localised abscess formation should be performed preferably prior to initiation of empirical antibiotic therapy.[24] Sending the sample for M, C & S (microscopy, culture and sensitivity) to the laboratory for analysis will help to determine the best course of antibiotics to treat the patient.

It is important to consider a differential diagnosis in any case, and Ludwig’s angina is no different. There are non-infectious causes of acute upper airway obstruction confused with Ludwig’s angina which include angioneurotic oedema, lingual carcinoma and sublingual haematoma formation following anticoagulation.[22]

Treatment

For each patient, the treatment plan should be done with consideration of each of the individual patient’s differing factors. They are namely the stage of the disease and co-morbid conditions at the time of presentation, physician experience, available resources, and personnel are critical factors in formulation of a treatment plan.[25] There are four principles that guide the treatment of Ludwig’s Angina[26]: Sufficient airway management, early and aggressive antibiotic therapy, incision and drainage for any who fail medical management or form localized abscesses, and adequate nutrition and hydration support. Each will be explained in detail below.

Sufficient airway management

  • Airway management has been found to be the most important factor in treating patients with Ludwig’s Angina,[24] i.e. it is the “primary therapeutic concern”.[27] Airway compromise is known to be the leading cause of death from Ludwig’s Angina.[4]
  • The basic method to achieve this is to allow the patient to sit in an upright position, with supplemental oxygen provided by masks or nasal prongs.[24] Patients should never be left unattended, particularly if there is an absence of intubation or a surgical airway in place.[24]
  • Methods of airway management range from conservative airway management – consisting of close observation and intravenous antibiotics, to airway intervention with endotracheal intubation or tracheostomy.[24]
  • If the oxygen saturation levels are adequate and antimicrobials have been given, simple airway observation can be done.[24] This is a suitable method to adopt in the management of children, as a retrospective study described that only 10% of children required airway control. However, a tracheostomy was performed on 52% of those affected with Ludwig’s Angina over 15 years old.[28]
  • Airway control is compulsory if a surgical procedure is required.[4]
    • Flexible nasotracheal intubation require skills and experience.[4]
    • If nasotracheal intubation is not possible, cricothyrotomy and tracheostomy under local anaesthetic can be done. This procedure is carried out on patients with advanced stage of Ludwig’s Angina.[4]
    • Endotracheal intubation has been found to be in association with high failure rate with acute deterioration in respiratory status.[4]
    • Elective tracheostomy is described as a safer and more logical method of airway management in patients with fully developed Ludwig’s Angina.[29]
    • Fibre-optic nasoendoscopy can also be used, especially for patients with floor of mouth swellings.[24]
  • It is important that incision and drainage are preceded by consulting the anaesthesiologist about possible airway problems at intubation.[24] A tracheostomy set should always be present in the operating room in case there is requirement for local tracheostomy or an emergency cricothyrotomy.[24]

Early and aggressive antibiotic therapy

Incision and drainage for any who fail medical management or form localized abscesses

  • Surgical incision and drainage are the main methods in managing severe and complicated deep neck infections that fail to respond to medical management within 48 hours.[24]
  • It is indicated in cases of:[24]
  • Bilateral submandibular incisions should be carried out in addition to a midline submental incision. Access to the supramylohyoid spaces can be gained by blunt dissection through the mylohyoid muscle from below.[24]
  • Penrose drains are recommended in both supramylohyoid and inframylohyoid spaces bilaterally. In addition, through and through drains from the submandibular space to the submental space on both sides should be placed as well.[24]
  • The incision and drainage process is completed with the debridement of necrotic tissue and thorough irrigation.[24]
  • It is necessary to mark drains in order to identify their location. They should be sutured with loops as well so it will be possible to advance them without re-anaesthetizing the patient while drains are re-sutured to the skin.[24]
  • An absorbent dressing is then applied. A bandnet dressing retainer can be constructed so as to prevent the use of tape.[24]

Nutritional support

Adequate nutrition and hydration support is essential in deciding the outcomes in any patient following surgery, particularly young children.[30] In this case, pain and swelling in the neck region would usually cause difficulties in eating or swallowing, hence reducing patient’s food and fluid intake. As a result, patients suffer from weight loss due to loss of fat, muscle and skin initially, followed by bone and internal organs in the late phase. Meanwhile, at the cellular level, the cells would be less able to maintain homeostasis in the presence of stressors such as infection and surgery. Patients must therefore be well-nourished and hydrated to promote wound healing and to fight off infection.[31]

Post-operative care

Placement of an endotracheal tube to aid breathing.

Extubation, which is the removal of endotracheal tube to liberate the patient from mechanical ventilation, should only be done when the patient’s airway is proved to be patent, allowing adequate breathing. This is indicated by a decrease in swelling and patient’s capability of breathing adequately around a uncuffed endotracheal tube with the lumen blocked.[32]

During the hospital stay, patient’s condition will be closely monitored by:

  • carrying out cultures and sensitivity tests to decide if any changes need to be made to patient’s antibiotic course
  • observing patient’s body temperature - a rise implies further infection
  • monitoring patient’s white blood cell count - a decrease implies effective and sufficient drainage
  • repeating CT scans to prove patient’s restored health status or if infection extends, the anatomical areas that are affected[33]

Moreover, it is advised to never left young children with significant neck swelling unattended and they should always be seated to prevent suffocation.[34]

See also

References

  1. ^ Murphy SC (October 1996). "The person behind the eponym: Wilhelm Frederick von Ludwig (1790-1865)". Journal of Oral Pathology & Medicine. 25 (9): 513–5. doi:10.1111/j.1600-0714.1996.tb00307.x. PMID 8959561.
  2. ^ Candamourty R, Venkatachalam S, Babu MR, Kumar GS (July 2012). "Ludwig's Angina - An emergency: A case report with literature review". Journal of Natural Science, Biology, and Medicine. 3 (2): 206–8. doi:10.4103/0976-9668.101932. PMID 23225990.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  3. ^ a b Coulthard, Paul; Horner, Keith; Sloan, Philip; Theaker, Elizabeth D. (2013-05-17). Master dentistry (3rd ed.). Edinburgh: Elsevier. ISBN 978-0-7020-4600-1. OCLC 786161764. {{cite book}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)CS1 maint: date and year (link)
  4. ^ a b c d e f Saifeldeen K, Evans R (March 2004). "Ludwig's angina". Emergency Medicine Journal. 21 (2): 242–3. doi:10.1136/emj.2003.012336. PMID 14988363.
  5. ^ Costain N, Marrie TJ (February 2011). "Ludwig's Angina". The American Journal of Medicine. 124 (2): 115–7. doi:10.1016/j.amjmed.2010.08.004. PMID 20961522.
  6. ^ Kremer MJ, Blair T (December 2006). "Ludwig angina: forewarned is forearmed". AANA Journal. 74 (6): 445–51. PMID 17236391.
  7. ^ Saifeldeen K, Evans R (March 2004). "Ludwig's angina". Emergency Medicine Journal. 21 (2): 242–3. doi:10.1136/emj.2003.012336. PMID 14988363.
  8. ^ a b Dhingra, PL; Dhingra, Shruti; Dhingra, Deeksha (2010) [1992]. Nasim, Shabina (ed.). Diseases of Ear, Nose and Throat (5 ed.). New Delhi: Elsevier. pp. 277–78. ISBN 978-81-312-2364-2. {{cite book}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  9. ^ Williams AM, Southern SJ (2005). "Body piercing: to what depths? An unusual case and review of associated problems". Plastic and Reconstructive Surgery. 115 (3): 50e–54e. PMID 15731662.
  10. ^ Koenig LM, Carnes M (June 1999). "Body piercing medical concerns with cutting-edge fashion". Journal of General Internal Medicine. 14 (6): 379–85. doi:10.1046/j.1525-1497.1999.00357.x. PMC 1496593. PMID 10354260. Archived from the original on 2011-07-14. {{cite journal}}: Unknown parameter |deadurl= ignored (|url-status= suggested) (help)
  11. ^ Zadik Y, Becker T, Levin L (January 2007). "[Intra-oral and peri-oral piercing]". Refu'at Ha-Peh Veha-Shinayim. 24 (1): 29–34, 83. PMID 17615989.
  12. ^ "Pancho Villa". International Boxing Hall of Fame.
  13. ^ Siqueira JF, Rôças IN (April 2013). "Microbiology and treatment of acute apical abscesses". Clinical Microbiology Reviews. 26 (2): 255–73. doi:10.1128/CMR.00082-12. PMID 23554416.
  14. ^ a b c Candamourty R, Venkatachalam S, Babu MR, Kumar GS (July 2012). "Ludwig's Angina - An emergency: A case report with literature review". Journal of Natural Science, Biology, and Medicine. 3 (2): 206–8. doi:10.4103/0976-9668.101932. PMC 3510922. PMID 23225990.{{cite journal}}: CS1 maint: unflagged free DOI (link)
  15. ^ a b Costain N, Marrie TJ (February 2011). "Ludwig's Angina". The American Journal of Medicine. 124 (2): 115–7. doi:10.1016/j.amjmed.2010.08.004. PMID 20961522.
  16. ^ a b c Patel M, Chettiar TP, Wadee AA (November 2009). "Isolation of Staphylococcus aureus and black-pigmented bacteroides indicate a high risk for the development of Ludwig's angina". Oral Surgery, Oral Medicine, Oral Pathology, Oral Radiology, and Endodontics. 108 (5): 667–72. doi:10.1016/j.tripleo.2009.06.033. PMID 19836722.
  17. ^ Bagheri, Shahrokh C.; Bell, R. Bryan; Khan, Husain Ali (2012). Current Therapy in Oral and Maxillofacial Surgery. Philadelphia: Elsevier Saunders. ISBN 978-1-4160-2527-6. OCLC 757994410. {{cite book}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  18. ^ Norton NS (2007). Netter's Head and Neck Anatomy for Dentistry. Philadelphia: Saunders Elsevier. p. 460. ISBN 978-0-323-46209-9.
  19. ^ Grodinsky, Manuel; Holyoke, Edward A. (1938-11-01). "The fasciae and fascial spaces of the head, neck and adjacent regions". American Journal of Anatomy. 63 (3): 367–408. doi:10.1002/aja.1000630303. {{cite journal}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  20. ^ a b Bagheri, Shahrokh C (2014). Clinical Review of Oral and Maxillofacial Surgery: A Case-Based Approach (Second ed.). St. Louis: Mosby Elsevier. pp. 95–118. ISBN 978-0-323-17127-4. {{cite book}}: Unknown parameter |name-list-format= ignored (|name-list-style= suggested) (help)
  21. ^ Spitalnic SJ, Sucov A (July 1995). "Ludwig's angina: case report and review". The Journal of Emergency Medicine. 13 (4): 499–503. PMID 7594369.
  22. ^ a b Crespo AN, Chone CT, Fonseca AS, Montenegro MC, Pereira R, Milani JA (November 2004). "Clinical versus computed tomography evaluation in the diagnosis and management of deep neck infection". Sao Paulo Medical Journal = Revista Paulista De Medicina. 122 (6): 259–63. doi:10.1590/S1516-31802004000600006. PMID 15692720.
  23. ^ a b "Sepsis: recognition, diagnosis and early management | Guidance and guidelines | NICE". www.nice.org.uk. Retrieved 2018-01-18.
  24. ^ a b c d e f g h i j k l m n o p q r s t u v w Bagheri SC, Bell RB, Khan HA (2011). Current Therapy in Oral and Maxillofacial Surgery. Philadelphia: Elsevier. pp. 1092–1098. ISBN 978-1-4160-2527-6.
  25. ^ Shockley WW (May 1999). "Ludwig angina: a review of current airway management". Archives of Otolaryngology--Head & Neck Surgery. 125 (5): 600. PMID 10326825.
  26. ^ Chou YK, Lee CY, Chao HH (December 2007). "An upper airway obstruction emergency: Ludwig angina". Pediatric Emergency Care. 23 (12): 892–6. doi:10.1097/pec.0b013e31815c9d4a. PMID 18091599.
  27. ^ Moreland LW, Corey J, McKenzie R (February 1988). "Ludwig's angina. Report of a case and review of the literature". Archives of Internal Medicine. 148 (2): 461–6. PMID 3277567.
  28. ^ Kurien M, Mathew J, Job A, Zachariah N (June 1997). "Ludwig's angina". Clinical Otolaryngology and Allied Sciences. 22 (3): 263–5. PMID 9222634.
  29. ^ Parhiscar A, Har-El G (November 2001). "Deep neck abscess: a retrospective review of 210 cases". The Annals of Otology, Rhinology, and Laryngology. 110 (11): 1051–4. doi:10.1177/000348940111001111. PMID 11713917.
  30. ^ Chou, Yu-Kung; Lee, Chao-Yi; Chao, Hai-Hsuan (December 2007). "An upper airway obstruction emergency: Ludwig angina". Pediatric Emergency Care. 23 (12): 892–896. doi:10.1097/pec.0b013e31815c9d4a. ISSN 1535-1815. PMID 18091599.
  31. ^ Current therapy in oral and maxillofacial surgery. Bagheri, Shahrokh C., Bell, R. Bryan., Khan, Husain Ali. Philadelphia: Elsevier Saunders. 2012. ISBN 9781416025276. OCLC 757994410.{{cite book}}: CS1 maint: others (link)
  32. ^ Current therapy in oral and maxillofacial surgery. Bagheri, Shahrokh C., Bell, R. Bryan., Khan, Husain Ali. Philadelphia: Elsevier Saunders. 2012. ISBN 9781416025276. OCLC 757994410.{{cite book}}: CS1 maint: others (link)
  33. ^ Current therapy in oral and maxillofacial surgery. Bagheri, Shahrokh C., Bell, R. Bryan., Khan, Husain Ali. Philadelphia: Elsevier Saunders. 2012. ISBN 9781416025276. OCLC 757994410.{{cite book}}: CS1 maint: others (link)
  34. ^ Chou, Yu-Kung; Lee, Chao-Yi; Chao, Hai-Hsuan (December 2007). "An upper airway obstruction emergency: Ludwig angina". Pediatric Emergency Care. 23 (12): 892–896. doi:10.1097/pec.0b013e31815c9d4a. ISSN 1535-1815. PMID 18091599.
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