PHLEGMONS OF SUBMANDIBULAR, SUBMENTAL AREAS, PTERYGOMANDIBULAR AREA. PHLEGMON OF THE ORBIT. PHLEGMONS OF ZYGOMATIC, CHEWING, PAROTID AREAS. PHLEGMONS OF PTERYGOPALATINAL SPACE, INFRATEMPORAL AND TEMPORAL FOSSAE.

 

Odontogenic Space Infection

Abstract:

Odontogenic infections are commonly the result of pericoronitis, carious teeth with pulp exposure, periodontitis, or complications of dental procedures.  Periapical and panoramic x-rays are reliable initial screening instruments and are used in determining etiology.  The mandibular molars are frequently one of the etiological factors.  The patients with multispace infections should be hospitalized.  Trismus and airway management are important considerations and may preclude the selection of other surgical approaches.
Introduction:

Dental infections are one of the most common diseases of the human body and can be a cause of death.  Not until the early twentieth century, however, was a casual relationship definitely established between dental infection and severe life- threatening conditions like Ludwig’s angina described over 100 years earlier.

Although the therapy has progressed, the scalpel, extraction forceps and endodontic reamer remain the keystone for the therapy for odontogenic infections as does the judicious use of antibiotics.

Prior to the antibiotic era, most serious odontogenic infections were known to be streptococcal but the problem of bacterial resistance to antibiotics soon became obvious in the oral cavity as elsewhere.  The streptococcus and mixed oral flora organism remain the most commonly identified in the majority of dental infections.  Considering the plethora of micro-organisms that grow luxuriantly in this wet, warm, dark and debris-strewn cavity one can only reflect with awe on the effectiveness of systemic and oral host defense mechanisms in preventing serious infection from commonplace minor trauma such as cheek biting or shedding of deciduous teeth.

There are several spaces in the head and neck region:  Buccal space, Buccinator space, Parapharyngeal space, Submandibular, Sublingual, lateral pharyngeal and Pterygoid space.⁷  The prototype of sublingual and submandibular infection is Ludwig’s angina.  Ludwig’s angina is caused by the extension of odontogenic infections in 70-80% of the patients.⁴   These conditions usually develop from an odontogenic infection especially from the 2nd and 3rd mandibular molars or as an extension of peritonsillar cellulites.  Contributing factors may include teeth extraction, poor oral hygiene and trauma.

These infections are potentially life-threatening due to the spread of bacteria into the perioral facial spaces.  Infection usually arises from the mandibular molars.  Affected tissues are swollen and have board-like hardness.  Glottis edema or spread into the mediastinum may be fatal.  The principal treatment remains surgical with drainage of pus augmented with antibiotic therapy.

 

Patient on the right is a 40 year old female with a submandibular and buccal space infection.

35 year old male with an infection involving the buccal and temporal space.

Axial CT

scan showing involvement of the temporal space with infection.

Coronal CT scan showing involvement of the buccal and temporal space with infection.

Discussion:

Odontogenic infections generally pass through three stages before they resolve during the first 1 to 3 days.  The swelling is soft, mildly tender and doughy in consistency.  Between two to five days, the swelling becomes hard, red and exquisitely tender.  Its borders are diffuse and spreading.  Between the fifth and seventh days, the center of the cellulites begins to soften and the underlying abscess undermines the skin and mucosa and makes it compressible and shiny.  At this stage, the infection is fluctuant.  The final stage of odontogenic infection is resolution which generally occurs after spontaneous or surgical drainage of an abscess cavity.  Trismus is an ominous sign in the patient with suspected odontogenic infection.⁵
Odontogenic infections rarely extend beyond the jawbone barrier into the deep space of the face and neck but once they occur they are often difficult to assess accurately by clinical and conventional radiographs and the outcome may be potentially life threatening.  CT scan has been used to assess and evaluate deep neck infections of odontogenic origin.  It is useful to depict the extent of infection and to plan treatment of extensive odontogenic infection.⁴

Maxillary space infection can originate from either the maxillary or mandibular teeth.  Temporal space can be divided into superficial and deep temporal space.  The superficial temporal space extends superiorly to the pericranium, lateral to the temporalis muscle and medial to the temporoparital fascia.  Inferiorly, this space is continuous with the masseteric space. The deep temporal space extends superiorly to the attachment of the temporalis muscle to the inferior temporal crest, lateral to the temporal bone and deep to the temporalis muscle.  Inferiorly, this space is continuous with the infratemporal space.  The temporal space along with the infratemporal, masseteric and pterigo mandibular space can be grouped together as masticator space.

The masticator space is defined by the superficial layer of the deep cervical fascia as it splits at the inferior border of the mandible.  The lateral portion covers the masseter as it connects to the zygomatic arch and continues on to cover the temporalis muscle.  The medial portion follows the medial pterygoid, superiorly, then continues with the levator veli palatine muscle.  The medial portion follows the medial pterygoid, superiorly, then continues with the levator palatine fascia to skull base.  Space adjacent to the masticator space are the parotid space, posteriorly, parapharyngeal space, medially, and submandibular and sublingual space, inferiorly.¹

Necrotizing fasciitis is occasionally found in the head and neck and is frequently due to odontogenic sources.  It is a rapidly spreading infection that follows the platysma muscle down the neck and to the anterior chest wall.  Diabetes and alcoholism have been shown to be significant predisposing factors, whereas, high-risk medical conditions, delay in surgery and mediastinitis are associated with increased mortality.

A suspicion of necrotizing fasciitis is a surgical emergency ,requiring broad spectrum antibiotics, repeated surgical dressing, drainage, intensive medical supportive care including fluid calcium and possibly blood transfusion.

Conclusion:

The diagnosis of odontogenic infections is usually obvious.  If not, a radiograph and a CT scan is performed.  Treatment of odontogenic infection is maintenance of airway patency, surgical incision, extraction of offending teeth, drainage and antibiotics.

 

Facial infections – an overview

PRACTICAL TIPS

Good oral examination requires:

• Bright light leaving both hands free – torch is unsatisfactory and fixed lights need too much adjustment. A head lamp such as a Petzel ($60-80) or preferably a simple halogen head lamp with transformer (about $400) is invaluable and may be used for multiple other uses and is also portable.
• Two tongue depressors or preferably two dental mirrors – these can be used to examine inaccessible spots, retract the cheeks and depress the tongue. The metalic handle is ideal for percussing teeth for tenderness.
• A square of gauze to dry oral secretions and check patency of salivary ducts. Also allows good grip on the tongue to inspect posterior 2/3 and the lateral
• border.
• A dental syringe with 27G long needles together with 2% Xylocaine with1: 80000 adrenaline – good for oral LA prior to aspiration, drainage etc. (very useful for other suture jobs – but remember high adrenaline concentration.)

Introduction
Facial infections are a relatively common presentation to both general medical and dental practice. Most originate in superficial structures (skin, subcutanous tissue etc.) and are often easily diagnosed and treated.

Infections originating in deeper structures can be severe, rapidly progressive and may cause prolonged morbidity, long term complications as well as potentially endanger life. Efficient treatment requires accurate diagnosis, early aggressive medical treatment and in most cases urgent decisive surgical management.

Severe buccal space infection

Complex and severe cases may require multidisciplinary approach including the GP, dental surgeon, radiologist, oral and maxillo-facial surgeon, ENT surgeon, a skilled anaesthetist as well as occasionally the infectious diseases specialist and possibly the intensivist. Ophthalmology and rarely neurosurgery may also be needed.

Submandibular space infection with external drains in situ

Ludwig’s angina – bilateral submandibular/sublingual space infection

Good nursing, speech pathology as well as a dietician can speed up the recovery phase.

Presentation
The patient presents with a swollen face and occasionally swolleeck. Toothache or facial pain may or may not be a feature. There is often general malaise and possibly rigors with fever. Patients may complain of trismus (inability to open the mouth fully), pain or difficulty in swallowing, drooling, sore throat and a hoarse voice.

History
One should document the usual historical features of the current complaint with additional attention to:

• Increased pain and swelling on exposure to food (salivary gland obstruction?).
• Recent dental treatment, especially root canal treatment and extractions.
• Any trauma to the face or teeth (either bony fractures or devitalized teeth).
• Recent oral surgery (surgical removal of wisdom teeth, cysts etc.).
• Past facial fractures fixation (infected plates, wires, etc?).
• Past salivary gland surgery.
• History of head and neck cancer with possible radiotherapy to the region (possible osteoradionecrosis of the jaw bones?).
• Upper respiratory tract viral infections, nasal discharge, etc.

Examination
Specific attention should be paid to the location of swelling, size, flactuance, any possible pointing and coexistent lymph node enlargement.

Good oral examination should include:

• presence of halitosis,
• evidence of intraoral pus draining and where, any tongue elevation, any sublingual or submandibular swelling,
• swelling in the mandibular or maxillary sulci,
• palatal swelling especially of the soft palate or uvula,
• general dental state, patency of salivary outlets (parotid, submandibular and sublingual),
• nature of saliva produced (clear, thick, pus?).

Suspect teeth should be tapped with a metallic object to elicit any tenderness to percussion.

Swelling should be palpated bimanually if possible with a finger of one hand intraorally and and the second hand extraorally (pushing towards the oral site). The neck should be evaluated for swelling, lymphadenopathy and possible tracheal deviation.

Aetiology of major facial infections
Most originate in the jaws, teeth, surrounding periodontal soft tissues as well as the paranasal sinuses and the major salivary glands.

Teeth can contribute by:

(1) Decay (caries) reaching the dental pulp=pulpitis, this in turn spreads to supporting bone resulting in (2) periapical abscess which in turn may spread subperiosteally.
(2) Periapical abscess may occur in seemingly intact but devitalised teeth (trauma, cracks or decay under fillings).
(3) Periapical and periodontal abscess may form as a result of chronic gingivitis and supporting bone and soft tissue loss (periodontal disease) – note again the tooth may be entirely intact clinically and radiographically.
(4) Erupting teeth (especially partially impacted lower third molars) can result in inflammation and infection of the gum flap preventing eruption (operculum) with swelling pus etc. around the crown (pericoronitis).
(5) Retained roots supragingival or subgingival.

The jaws:
(1) Can develop cysts or tumours that can range from odontogenic (=dental origin) to either primary or secondary malignancy. Most are derived from the dental apparatus and although benign caevertheless continuously grow and become secondarily infected on breaching the surrounding bone.
(2) Osteomyelitis although rare can be the result of chronic infection as mentioned before.
(3) Osteoradionecrosis occurs readily in irradiated jaws subjected to further trauma (such as extractions).
(4) Rarer are tuberculosis, Actinomycosis and syphilitic osteomyelitis.
(5) Most jaw fractures in the tooth bearing segments are by definition compound to the oral cavity and can easily be infected by the oral microbes.
(6) Extraction sites again are comparable to compound fractures and it is surprising that infection is so relatively rare.

Major salivary glands:
(1) May be the subject of either viral or bacterial infections often superimposed on obstruction of ducts (stone, stricture, etc).
(2) Tumours rarely also become secondarily infected.

Paranasal sinuses
(1) May be primarily infected, obstruct and result in facial swelling.
(2) May become infected secondary to infected teeth protruding into the maxillary sinus (upper premolar and molar teeth often do).
(3) Tumours or cysts may become infected.
(4) Fractures such as the orbital floor are by definition compound to the “outside” and may result in orbital cellulitis.

Microbiology
Facial infections tend to be polymicrobial with a predominance of anaerobic organisms. In severe cases Gram-ve organism tend to be involved as well.

Investigations
In many cases careful history and examination will make diagnosis clear, however certain investigation will still be necessary.

Plain X rays:
(1) The OPG (orthopantomogram) is invaluable in displaying the teeth, whole of mandible, tooth bearing segment of the maxilla as well as parts of the maxillary sinuses. Use for any suspected fractures of the mandible, periapical abscesses and bony cysts and tumours. Will show impacted third molars (‘wisdom teeth’).
(2) Occipito-mental 15 and 30 degrees (“Water’s view”) will show both maxillary sinuses (effusion?), orbital floor and most fractures of the maxilla.
(3) Mandibular occlusal views and lateral oblique views may demonstrate stones in the submandibular gland.
(4) ‘Puffed cheek’ view may demonstrate stones in the parotid duct.
Sialography:
Can be used for suspected gland obstruction however CT sialogram is the gold standard.

Ultrasound:
Useful in confirming collections as well as a guide to aspiration. Will also show stones in salivary ducts and glands.

CT scan:
With axial and coronal views will demonstrate exact extent of the swelling, potential airway compromise and is invaluable to both the surgeon and anaesthetist. However patients unwell enough to potentially obstruct their airway should be taken straight to theatre rather than risk an emergency in the radiology dept.

Microbiology of any pus or discharge.

The usual blood tests.

Spread of infections
Bony infection tends to perforate the cortical plates along path of least resistance. Subsequent subperiosteal spread tends to be directed by muscle and facial attachments. Thus infections of mandibular molar teeth for example tend to spread to the submandibular space.

A number of potential tissue spaces exist, the most important being: buccal space, sublingual space, submandibular space, parapharyngeal space and retropharyngeal space. Spread can occur throughout these with airway compression once the parapharyngeal and retropharyngeal spaces are filled.

Orbital floor can be perforated by pus from the sinus resulting in subperiosteal abscess or even orbital abscess. Preseptal cellulitis may result from buccal space infections and may progress to orbital cellulitis.

Lymphatic spread to the deep cervical lymphatics occurs commonly.

Occasionally haematogenous spread may result in bacteraemia, distant septic foci and cavernous sinus thrombosis.

Treatment
Antibiotics alone will not cure most deep facial infections.
Most infections have a distinct cause and only surgical treatment (removal of the cause and drainage of accumulated pus) will prevent worsening and recurrence.

In early cases the surgical treatment may be as simple as root canal treatment of the tooth suspected or alternatively simple tooth extraction by the patient’s dentist followed by oral antibiotics.

More advanced cases need urgent admission for intravenous antibiotics followed by urgent surgery to remove the cause as well as achieve incision and drainage of tissue spaces involved.

These cases may need expert fiberoptic endotracheal intubation with prolonged (few days) intubation and occasionally emergency surgical airway access such as cricothyrotomy or tracheostomy may be needed.

These cases will need ICU postoperatively until the safety of airway is assured.

Surgically most cases can be approached transorally. Removal of the cause (tooth, stone, etc) is followed by incision and drainage and drain insertion. One should avoid the temptation to cut through facial skin for reasons of facial nerve preservation as well as to avoid the ugly puckered scar that invariably results.

Submandibular and sublingual spaces full of pus need to be drained trancutanously via neck incisions with drains insertion. The patient should be on triple IV antibiotics covering aerobic Strep species as well as anaerobes as well as Gram-ve organisms. Eg: Amoxycillin 1g tds-qid+Metronidazole 500mg tds+Gentamicin 5mg/kg/day in single dose.

Early diagnosis, prompt antibiotic treatment (Amoxycillin and Flagyl), together with early removal of the cause should prevent most complications and result in early recovery.

Submandibular space infection is acute cellulitis of the soft tissues below the mouth. Symptoms include pain, dysphagia, and potentially fatal airway obstruction. Diagnosis usually is clinical. Treatment includes airway management, surgical drainage, and IV antibiotics.

Submandibular space infection is a rapidly spreading, bilateral, indurated cellulitis occurring in the suprahyoid soft tissues, the floor of the mouth, and both sublingual and submaxillary spaces without abscess formation. Although not a true abscess, it resembles one clinically and is treated similarly.

The condition usually develops from an odontogenic infection, especially of the 2nd and 3rd mandibular molars, or as an extension of peritonsillar cellulitis. Contributing factors may include poor dental hygiene, tooth extractions, and trauma (eg, fractures of the mandible, lacerations of the floor of the mouth).

Symptoms and Signs

Early manifestations are pain in any involved teeth, with severe, tender, localized submental and sublingual induration. Boardlike firmness of the floor of the mouth and brawny induration of the suprahyoid soft tissues may develop rapidly. Drooling, trismus, dysphagia, stridor caused by laryngeal edema, and elevation of the posterior tongue against the palate may be present. Fever, chills, and tachycardia are usually present as well. The condition can cause airway obstruction within hours and does so more often than do other neck infections.

Diagnosis

The diagnosis usually is obvious. If not, CT is done.

Treatment

• Maintenance of airway patency
• Surgical incision and drainage
• Antibiotics active against oral flora

Maintaining airway patency is of the highest priority. Because swelling makes oral endotracheal intubation difficult, fiberoptic nasotracheal intubation done with topical anesthesia in the operating room or ICU with the patient awake is preferable. Some patients require a tracheotomy. Patients without immediate need for intubation require intense observation and may benefit temporarily from a nasal trumpet.

Incision and drainage with placement of drains deep into the mylohyoid muscles relieve the pressure. Antibiotics should be chosen to cover both oral anaerobes and aerobes (eg, clindamycin, ampicillin/sulbactam, high-dose penicillin).

Submandibular space infections (Ludwig’s angina)

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.

Submandibular Space Infection

Anatomy-Space below the mandible and mylohyoid muscle, bordered medially by the anterior belly of the digastric muscle, posteriorly by the posterior border of the submandibular gland, and reaching inferiorly to the level of the hyoid bone. The submandibular space consists mainly of fat, the submandibular gland and lymph nodes.

   Spread of infection: (according to)

 

(I)      

 

1- The position of the myelohyoid ridge

 

The myelohyoid ridge runs obliquely, higher posteriorly than anteriorly

In the lower posterior aspect, the apices of teeth related to the area below the myelohyoid ridge will spread infection into the submandibular space.

2- Level of the apices of the lower arch (Direct penetration of the lingual plate).

(II)              Secondary to involvement of submandibular lymph nodes.

Sublingual space, superior to mylohyoid muscle. The submandibular space is inferior to the mylohyoid muscle

Spread of process superiorly and posteriorly elevates floor of mouth and tongue. In anterior spread, the hyoid bone limits spread inferiorly, causing a “bull neck” appearance.

    Signs & symptoms

–         Usual systemic signs & symptoms.

–         Massive browny swelling along the lower border of the mandible extending posteriorly to the angle.

–         Moderate mandibular limitation.

–         The swelling is board-like, tender, indurated, inflammatory red & hot.

¥    The moderate limitation of the mandible arise from the involvement of the medial pterygoid muscle which extend posteriorly in the space not within the infection.

¥    The difficulty with swallowing arise from the large surface area of myelohyoid muscle that is involved.

 

Treatment: Extra-oral Incision & Drainage

The incision should be done at the deepest area of infection to help the drainage rapidly & completely with the aid of gravity.

Incision in the stage of pitted on edema or localized swelling…

This incision should be:

1-     Anatomically should be away from any important anatomical structures (mandibular branch of facial nerve).

2-     At minimally scanning or disfiguring area “Cosmotic consideration” e.g along  skin creases

The incision should pass through the (skin, superficial fascia, platysma, deep fascia) layer by layer with blunt dissection.

Further more, a blunt instrument should be inserted within the infected space to completely damage any septi & partition to ensure complete drainage of pus.

The ideal blunt instrument is an index finger.

Finally, the space should be filled with gauze by a mosquito forceps & left there for 24 hours. This drain will allow pus evacuation from un-reached areas & the newly formed pus.

This drainage should be left in place to keep the incision line patent until the entire induration is relieved.

Finally, dressing is placed externally to allow healing.

 

Ludwig’s AnginaLudwig’s Angina is a severe form of cervico-fascial infection / cellulitis which
usually arises from the lower second or third molars (wisdom teeth).Deep fascial space infections cause gross inflammatory exudates (a fluid with a
high content of protein and cellular debris which has escaped from blood vessels
and has been deposited in tissues or on tissue surfaces, usually as a result of
inflammation. It may be septic or non-septic) and tissue œdema (swelling),
associated with fever and toxæmia (blood poisoning).  Before the advent of
antibiotics, the mortality was high and the disease is still life-threatening if
treatment is delayed.

The main fascial spaces involved in Ludwig’s Angina are the sublingual, submandibular and para-pharyngeal.  Normally, the spaces both side of the
midline (ie bilateral) are effected.

The characteristic features are:

•        diffuse swelling, pain, fever and malaise.
•        The swelling is tense and tender, with a characteristic ‘board-like’ firmness.
•        The overlying skin is taut and shiny.
•        Pain and œdema (swelling) that limit opening the mouth and often cause dysphagia (difficulties in swallowing)
•        Systemic upset is severe, with worsening fever, toxæmia (blood poisoning)
and leucocytosis.
•        The regional lymph nodes are swollen and tender.
•        In Ludwig’s Angina particularly, airway obstruction can quickly result in asphyxia.
Pathology Anærobic bacteria are primarily responsible and infection mainly spreads from mandibular third molars (lower jaw wisdom teeth) whose apices (root tips) are closely related to several fascial spaces.  Fasciæ, covering muscles and other
structures are normally adherent but can be spread apart by inflammatory exudate.

Spaces created in this way are almost avascular (do not have a blood supply) and
inflammatory exudate carries bacteria widely through them. It involves the sub-lingual and sub-mandibular spaces bilaterally (on both sides) almost
simultaneously; it readily spreads into the lateral pharyngeal and pterygoid spaces  
and can extend into the mediastinum. The main features are rapidly spreading sub-
lingual and sub-maxillary cellulitis with painful, brawny swelling of the upper part
of the neck and the floor of the mouth on both sides.  With involvement of the para-
pharyngeal space, the swelling tracks down the neck and œdema can quickly
spread to the glottis.

Swallowing and opening the mouth become difficult and the tongue may be pushed
up against the soft palate.  The latter or œdema of the glottis causes worsening respiratory obstruction. The patient soon becomes desperately ill, with fever, respiratory distress, headache and malaise.
Management The main requirements are:

•        immediate admission to hospital
•        procurement of a sample for culture and sensitivity testing
•        aggressive antibiotic treatment
•        securement of the airway by tracheostomy if necessary, and
•        drainage of the swelling to reduce pressure.

Submandibular space infection

 [Introduction]

Overview: submandibular space infection is acute suppurative submandibular space infection, the main clinical manifestations of submandibular District plump, swollen lymph nodes, tenderness.

[Cause]

submandibular space infection is caused by what the?

submandibular space (submandibular space) in the submandibular triangle, the space contains the submandibular gland, submandibular lymph nodes, and facial artery, vein before, lingual nerve, tongue under the nerve. The gap up by the posterior edge of mylohyoid muscle and the sublingual space with continued; back within the adjacent wing of the mandibular space, parapharyngeal space; forward through the submental space; down by loose connective tissue and the carotid artery and anterior triangular space connected to the . Therefore, infection can spread into the submandibular space and more space infection floor of the mouth (Figure 1).

Figure 1 submandibular space of anatomical location

prevalent in the lower jaw wisdom tooth pericoronitis, periapical mandibular teeth , alveolar abscess, odontogenic inflammation spread. Followed by the proliferation of submandibular lymphadenitis. Suppurative submandibular gland inflammation can sometimes secondary submandibular space infection.
[Symptoms]

submandibular space infection early symptoms?

1. there is a history of adult mandibular molars suppurative apical periodontitis, mandibular wisdom tooth pericoronitis history, infants, children and more able to ask the upper respiratory tract infection secondary to a history of submandibular lymphadenitis .

2. submandibular triangle clinical manifestations of inflammatory swelling, tenderness, early disease showed inflammatory infiltration block, there is tenderness; into the purulent stage with tenderness, a sense of volatility, skin flushing; easy to puncture pus. Patients with varying degrees of fever, leukocytosis and other systemic manifestations.

3. differential diagnosis of acute suppurative submandibular gland inflammation, often in chronic submandibular gland on the basis of acute inflammation, which the manifestations of tenderness and swelling of submandibular triangle body temperature, signs of acute inflammation of the increase in white blood cells, but not more than submandibular Abscess formation, and ipsilateral sublingual caruncle area, submandibular duct mouth swelling, purulent discharge from the oppression of the submandibular duct mouth out. Floor of the mouth bite taken X-ray film and more can be found in the submandibular gland duct stones.

most of the submandibular space infection is an early manifestation of their submandibular lymphadenitis, submandibular area for the full clinical manifestations, examination of the lymph nodes have a clear boundary, tenderness. Suppurative submandibular lymphadenitis extranodal spread to the formation of cellulitis. Clinical manifestations of submandibular space cellulitis swelling of submandibular triangle, the lower edge of the mandible contours disappear, skin tension, tenderness, pressing with pitting edema. Abscess formation, the central area of ​​the skin congestion, can reach significant fluctuations. Submandibular and sublingual space phase space due to continued infection can easily spread to the sublingual space (Figure 2), after the end of this time may be associated with the mouth were swollen tongue transported pain, dysphagia and other symptoms.

2 submandibular space Abscess caused by sublingual space Abscess of the anatomical relationship
[Diet]

submandibular space infection ate?

submandibular space infection diet (The following information is for reference only, details need to consult a doctor)

1, steamed lily : fresh lily washed, steamed food, continuous take.

2, Chine sugar water: sugar 500 grams (sliced), Rhizoma Imperatae 150 grams of tea decoction behalf.

3, wolfberry jujube meatballs meat porridge: date 15 grams of meat, round meat, 20 grams, 20 grams of wolfberry, 100 grams of rice, porridge, porridge cooked, add appropriate amount white sugar take. 2 times a day.

4, Sea Ginseng Rehmannia: Rehmannia 30 grams of sea cucumber 60 grams, the same into the steaming pot, add water, simmer for 2 hours to taste food.

submandibular space infection what to eat for good health?

diet should be light, should eat the cool of the goods, such as fresh vegetables, and Sydney, including mustard, celery, spinach, shepherd’s purse and so on.

submandibular space infection what to eat is unhealthy?

1, avoid alcohol and tobacco.

2, hot and spicy food.

3, not eat onions, garlic, shrimp, crab, eggs, and other deprivation of food caused by toxin.
[Prevention]

submandibular space infection should be how to prevent?
[Treatment]

submandibular space infection precautions before treatment?

prevention

prevent mandibular wisdom tooth pericoronitis, periapical mandibular teeth, alveolar abscess, odontogenic the spread of inflammation, followed by the proliferation of submandibular lymphadenitis, aggressive treatment of purulent inflammation of the submandibular gland submandibular space to avoid secondary infection.

submandibular space infection in Chinese medicine treatment methods

No information

Western submandibular space infection treatment

submandibular space abscess formation broader, abscess larger, but if the lymphadenitis caused by cellulitis, abscess may be confined to one or more lymph nodes, the formation of abscess incision and drainage must be separated before they can reach the lymph node capsule caused purposes.

submandibular space incision and drainage of the incision site, length, should refer to the abscess site, determine the area of ​​skin thinning. Edge of the mandibular body of men generally 2cm to do the following in parallel with the lower edge of the incision jaw; cut the skin, platysma, the blunt dissection forceps into the abscess. In the case of lymph node abscess lymph node capsule should be separated, while paying attention to the possibility of multiple lymph node abscess, surgery should be carefully examined, to be separately drainage.
[Check]

submandibular space infection should be how?

visual examination: visual examination found that the contours of the lower edge of the mandible due to swelling often disappear.

palpation: palpation sense of volatility.

puncture: puncture pus.
[Confused]

submandibular space infection and the diseases easily confused?

acute suppurative submandibular gland inflammation, often in chronic submandibular gland on the basis of acute inflammation, which the manifestations of tenderness and swelling of the submandibular triangle fever, increased white blood cells of acute inflammatory signs, but many are not formed submandibular abscess and ipsilateral sublingual caruncle area, submandibular duct mouth swelling, purulent discharge from the oppression of the submandibular duct mouth out. Floor of the mouth bite taken X-ray film and more can be found in the submandibular gland duct stones.

[Similar diseases]
no related data

Submental space infection

 [Introduction]

Overview: submental submental space infection is acute purulent infection clearance The main clinical manifestations of lymph nodes, submental triangle of skin congestion, pain there and so on.
[Cause]

submental space infection is caused by what the?

space under the chin (submental space) located in the suprahyoid region, the submental triangle within a single space. A small amount of adipose tissue within the gap and lymph nodes, this gap for the mylohyoid muscle, the submental hyoid muscle and the sublingual space apart. Connected with the submandibular space on both sides, the infection spread easily with each other (Figure 1).

Figure 1 submental space anatomy

submental space infections come from the lymph node inflammation. Lower lip, tongue, floor of mouth, sublingual caruncle, mandibular anterior teeth and periodontal tissues of the lymphatic flow can be remitted directly to the submental lymph nodes, it is more than one region of inflammation, mouth ulcers, mouth under the chin can cause go far lymphadenitis and cellulitis secondary to the submental space.
[Symptoms]

submental space infection early symptoms?

submental space as much as the lymph nodes caused by infection, it is generally slow progression, early limited lymph node enlargement, obvious clinical symptoms. When extranodal spread to the lymph node inflammation, the gap was caused by cellulitis tissue inflammation, swelling extended to cover different time to the submental triangle development area, skin redness, pain. Abscess formation after local skin purple, palpable pressure fluctuations have pitting edema, and infection. Back when the infection spread to submandibular space, and can demonstrate the appropriate symptoms.
[Diet]

submental space infection ate?
[Prevention]

submental space infection should be how to prevent?

prevention

lower lip, tongue, floor of mouth, sublingual caruncle, mandibular anterior teeth and periodontal tissue lymphatic drainage can be remitted directly to the submental lymph nodes, so the need to actively treat more than one region of inflammation, oral ulcers, mouth go far, avoid submental lymphadenitis, cellulitis and secondary to the submental space.
[Treatment]

submental space infection precautions before treatment?

abscess formation, swelling in the submental area to do the most prominent transverse skin incision, separated from the submental platysma of the gap and establish drainage.

submental space infection medicine treatment

No information

Western submental space infection treatment

No information
[Check]

submental space infection should be how?

oral examination.

obvious sense of deep abscess fluctuations, sometimes required by the puncture diagnosis.
[Confused]

submental space infection and the diseases easily confused?

detailed analysis of the history, combined with clinical and anatomical features, coupled with the biopsy, etc., is not difficult to make a correct diagnosis.
[Similar diseases]
no related data

Orbital Cellulitis

Background

Orbital cellulitis and preseptal cellulitis are the major infections of the ocular adnexal and orbital tissues. Orbital cellulitis is an infection of the soft tissues of the orbit posterior to the orbital septum, differentiating it from preseptal cellulitis, which is an infection of the soft tissue of the eyelids and periocular region anterior to the orbital septum. (See Presentation.)

Orbital cellulitis has various causes and may be associated with serious complications. As many as 11% of cases of orbital cellulitis result in visual loss. Prompt diagnosis and proper management are essential for curing the patient with orbital cellulitis (see the images below). (See Etiology, Prognosis, Presentation, Workup, Treatment, and Medication.)

A male patient with orbital cellulitis with proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited pain on eye movement, fever, headache, and malaise.

A male patient with orbital cellulitis who demonstrated proptosis, ophthalmoplegia, and edema and erythema of the eyelids. The patient also exhibited chemosis and resistance to retropulsion of the globe.

Anatomy

The orbital septum is a layer of fascia extending vertically from the periosteum of the orbital rim to the levator aponeurosis in the upper eyelid and to the inferior border of the tarsal plate in the lower eyelid.

Etiology

Orbital cellulitis occurs in the following 3 situations^[1] :

• Extension of an infection from the periorbital structures – Most commonly from the paranasal sinuses, but also from the face, the globe, and the lacrimal sac
• Direct inoculation of the orbit from trauma or surgery
• Hematogenous spread from bacteremia

Extension of infection

Orbital cellulitis can be caused by direct extension of infection from the globe, eyelids, ocular adnexum, and other periocular tissues, as well as from the sinuses. Orbital cellulitis may follow dacryocystitis, osteomyelitis of the orbital bones, phlebitis of the facial veins, and dental infections.

Orbital cellulitis is caused most commonly in all age groups by ethmoid sinusitis, accounting for more than 90% of all cases; aerobic, non-spore–forming bacteria are the organisms that are most frequently responsible. The process involves edema of the sinus mucosa, which leads to narrowing of the ostia and subsequent reduction or cessation of normal sinus drainage. Microflora indigenous to the sinuses and upper respiratory tract proliferate and invade the edematous mucosa, resulting in suppuration. It is enhanced by the reduced oxygen tension within the obstructed sinus cavity.

The organisms gain access to the orbit through thin bones of the orbital walls, venous channels, foramina, and dehiscences. Then, subperiorbital and intraorbital abscesses may occur. The resulting elevation of intraorbital pressure results in the typical signs of proptosis, ophthalmoplegia, and chemosis.

Orbital cellulitis resulting from infection of the maxillary sinus secondary to dental infections can be caused by microorganisms indigenous to the mouth, including anaerobes, commonly Bacteroides species.

Those cases stemming from dacryocystitis most commonly are caused by S aureus, S pneumoniae, Streptococcus pyogenes, and nontypeable H influenzae. Infections spreading from the soft tissues of the eyelids and face are due most commonly to staphylococci and S pyogenes. The initial antibiotic regimen can be modified if the response is inadequate or if the cultures dictate otherwise.

Traumatic causes

Infectious material may be introduced into the orbit directly through accidental (eg, orbital fracture) or surgical trauma. Indeed, orbital cellulitis may be caused by any injury perforating the orbital septum. Orbital inflammation^[2] may be noted within 48-72 hours after injury, or, in the case of a retained orbital foreign body, it may be delayed for several months.

Surgical procedures, including orbital decompression, dacryocystorhinostomy, eyelid surgery,^[3] strabismus surgery, retinal surgery, and intraocular surgery, have been reported as the precipitating cause of orbital cellulitis. Postoperative endophthalmitis can extend to the orbital soft tissues.

Bacterial causes

Streptococcus species, Staphylococcus aureus, and Haemophilus influenzae type B are the most common bacterial causes of orbital cellulitis. Pseudomonas, Klebsiella, Eikenella, and Enterococcus are less common culprits. Polymicrobial infections with aerobic and anaerobic bacteria are more common in patients aged 16 years or older.

Fungal causes

Fungal causes of orbital cellulitis are most commonly Mucor and Aspergillus species. Fungi can enter the orbit. Orbital cellulitis due to fungal infections carries a high mortality rate in patients who are immunosuppressed.

Mucormycosis^{[4, 5, 6]} has a wide distribution, while aspergillosis more commonly is seen in warm, humid climates. Mucormycosis has a rapid onset (1-7 days), while aspergillosis is much slower (months to years).

Aspergillosis initially results in chronic proptosis and decreased vision, while mucormycosis gives rise to the orbital apex syndrome (involving cranial nerves II, III, IV, V-1, and VI, and orbital sympathetics). More commonly, mucormycosis presents with pain, lid edema, proptosis, and visual loss. While aspergillosis and mucormycosis may each result iasal and palatal necrosis, mucormycosis also may lead to thrombosing arteritis and ischemic necrosis, while aspergillosis gives rise to chronic fibrosis and a nonnecrotizing granulomatous process.

Path of infection

The medial orbital wall is thin and is perforated not only by numerous valveless blood vessels and nerves but also by numerous defects (Zuckerkandl dehiscences). This combination of thin bone, foramina for neurovascular passage, and naturally occurring defects in the bone allows for easy communication of infectious material between the ethmoidal air cells and the subperiorbital space in the medial aspect of the orbit. The most common location of a subperiorbital abscess is along the medial orbital wall. The periorbita is adherent relatively loosely to the bone of the medial orbital wall, which allows abscess material to easily move laterally, superiorly, and inferiorly within the subperiorbital space.

In addition, the lateral extensions of the sheaths of the extraocular muscles, the intermuscular septa, extend from one rectus muscle to the next and from the insertions of the muscles to their origins at the annulus of Zinn, posteriorly. Posteriorly in the orbit, the fascia between the rectus muscles is thin and often incomplete, allowing easy extension between the extraconal and intraconal orbital spaces.

Venous drainage from the middle third of the face, including the paranasal sinuses, is mainly via the orbital veins, which are without valves, allowing the passage of infection anterograde and retrograde.

Epidemiology

An increased incidence of orbital cellulitis occurs in the winter nationally and internationally, because of the increased incidence of sinusitis in cold weather.

In the United States, an increase has beeoted in the frequency of orbital cellulitis due to community-acquired methicillin-resistant S aureus infections.^{[7, 8, 9, 10, 11, 12, 13]}

Sex- and age-related demographics

In children, orbital cellulitis has been reported as twice as common in males as in females. In adults, however, no difference in the frequency of orbital cellulitis exists between the sexes, except for cases caused by methicillin-resistant Saureus, which are more common in females than in males by a ratio of 4:1.

Orbital cellulitis, in general, is more common in children than in adults.^[14] The median age range of children hospitalized with orbital cellulitis is 7-12 years.

Prognosis

Prior to the availability of antibiotics, patients with orbital cellulitis had a mortality rate of 17%, and 20% of survivors were blind in the affected eye. As a result of prompt diagnosis and the appropriate use of antibiotics, however, this rate has been reduced significantly, although blindness still occurs in up to 11% of cases. Orbital cellulitis due to methicillin-resistant S aureus can lead to blindness despite antibiotic treatment.

Morbidity and mortality

Orbital cellulitis can result in orbital and intracranial complications. Subperiorbital or orbital abscess formation may occur (7-9%), while permanent vision loss may result from corneal damage secondary to exposure or neurotrophic keratitis, destruction of intraocular tissues, secondary glaucoma, optic neuritis, or central retinal artery occlusion. Blindness also may occur secondary to elevated intraorbital pressure or the direct extension of infection to the optic nerve from the sphenoid sinus.

Direct involvement of the ocular motor nerves or the extraocular muscles may lead to decreased ocular motility.

Intracranial complications include meningitis (2%), cavernous sinus thrombosis (1%), and intracranial, epidural, or subdural abscess formation. Cavernous sinus thrombosis has a mortality rate of 50% or higher, but it has become relatively rare in industrialized countries with proper treatment. Cavernous sinus thrombosis should be considered in any patient with orbital cellulitis and should be suspected in the presence of rapid progression of the clinical signs (eg, increasing proptosis, mydriasis, dilation of retinal veins, decreasing visual acuity, development of an afferent pupillary defect).

Intracranial abscess formation is suggested by altered consciousness, signs of central nervous system disturbance, persistent fever despite adequate antibiotic therapy, and resolution of the sinusitis and orbital cellulitis components of the disease.

Orbital pseudotumor may cause rapidly developing orbital congestion, proptosis, and limitation of motility, but it typically occurs in older age groups. Orbital echography may be helpful in differentiation.

Usually, endocrine orbitopathy may be identified by its typical clinical features. Orbital myositis may produce mild vascular congestion and proptosis. A fast-growing, necrotic retinoblastoma may produce mild vascular congestion, proptosis, and rhabdomyosarcoma. A metastatic orbital tumor, especially breast carcinoma, may produce similar findings.

History

A thorough history and physical examination are critical in establishing a diagnosis of orbital cellulitis. Patients with orbital cellulitis frequently complain of fever, malaise, and a history of recent sinusitis or upper respiratory tract infection. Questioning the patient about any recent facial trauma or surgery, dental work,^[15] or infection elsewhere in the body is important.

Other common, but variable, signs that accompany orbital cellulitis include the following:

• Conjunctival chemosis
• Decreased vision
• Elevated intraocular pressure
• Pain on eye movement

The above signs may be accompanied by the following:

• Fever
• Headache
• Lid edema
• Rhinorrhea
• Increasing malaise

Physical Examination

Proptosis and ophthalmoplegia are the cardinal signs and symptoms of orbital cellulitis. The symptoms advance rapidly at an alarming rate and eventually lead to prostration.

Proptosis and ophthalmoplegia may be accompanied by the following:

• Conjunctival chemosis
• Decreased vision
• Elevated intraocular pressure
• Pain on eye movement
• Orbital pain and tenderness – Are present early
• Dark red discoloration of the eyelids, chemosis, hyperemia of the conjunctiva, and resistance to retropulsion of the globe may be present
• Purulent nasal discharge may be present

Vision may be normal early, but it may become difficult to evaluate in very ill children with marked edema.

Diagnostic Considerations

Orbital cellulitis should be suspected in any patient with adnexal, facial, or dental infection when orbital pain, proptosis, limitation of ocular motility, lid edema, or orbital congestion develops. A computed tomography (CT) scan should be obtained, and the patient should be hospitalized and placed on broad-spectrum, intravenous (IV) antibiotic therapy as deemed appropriate.

Conditions to consider in the differential diagnosis of orbital cellulitis include the following:

• Infection – Cavernous sinus thrombosis
• Endocrine dysfunction – Dysthyroid exophthalmos
• Idiopathic inflammation – Orbital myositis, orbital pseudotumor, Wegener granulomatosis
• Neoplasm with inflammation – Burkitt lymphoma, histiocytosis X (Letterer-Siwe), leukemia, metastatic carcinoma, retinoblastoma, rhabdomyosarcoma, sarcoidosis

Orbital cellulitis resulting from sinusitis usually can be distinguished easily from other causes of acute inflammatory proptosis by clinical signs, computed tomography (CT) scanning, and the assessment of risk factors.

Cavernous sinus thrombosis, a serious complication of paranasal sinusitis that most commonly results from the anterograde spread of infection involving the mid-third of the face (eg, orbit, mouth, paranasal sinuses), may be difficult to distinguish from simple orbital cellulitis. (It may also occur with and be caused by orbital cellulitis.)

A patient with cavernous sinus thrombosis without orbital cellulitis will show marked restriction of ocular motility out of proportion to the degree of proptosis. A patient also will have normal retropulsion of the globe, hypesthesia in the distribution of the first and second divisions of the trigeminal nerve, dilated retinal veins, orbital congestion, and possibly neurologic defects (eg, altered sensorium). A cranial magnetic resonance imaging (MRI) scan can help to confirm the diagnosis of cavernous sinus thrombosis.

Differential Diagnoses

• Exophthalmos
• Mucormycosis
• Retinoblastoma
• Sarcoidosis
• Spider Bites
• Thyroid Ophthalmopathy

Approach Considerations

Lab studies

Laboratory evaluation should include the following (needle aspiration of the orbit is contraindicated):

• Complete blood count (CBC) – Leukocytosis greater than 15,000 with a shift to the left commonly is seen.
• Blood cultures – Obtain blood cultures prior to the administration of any antibiotics, although they are unlikely to reveal the responsible organism
• Purulent material assessment – Collect purulent material from the nose with a cotton or calcium alginate swab, smear for Gram stain, and culture on aerobic and anaerobic media; assess any material obtained from the sinuses or directly from an orbital abscess in the same manner

Imaging studies

High-resolution CT scanning with contrast infusion, including axial and coronal views, is essential. Axial views should include low, narrow cuts of the frontal lobes to rule out peridural and parenchymal brain abscess formation.

Coronal views are helpful in determining the presence and extent of any subperiorbital abscesses. However, coronal views require hyperflexion or hyperextension of the neck and may be difficult to obtain in uncooperative children and in patients who are acutely ill.

MRI may be helpful in defining orbital abscesses and in evaluating the possibility of cavernous sinus disease.

Procedures

Lumbar puncture is advisable if cerebral or meningeal signs develop.

Approach Considerations

The patient with orbital cellulitis should be promptly hospitalized for treatment, with hospitalization continuing until the patient is afebrile and has clearly improved clinically. Historically, the presence of subperiosteal or intraorbital abscess was an indication for surgical drainage in addition to antibiotic therapy. However, medical management alone is successful in many cases.^{[16, 17]}

Surgery

Consider orbital surgery, with or without sinusotomy, in every case of subperiosteal or intraorbital abscess formation; the drains should be left in place for several days. In cases of fungal infection, surgical debridement of the orbit is indicated and may require exenteration of the orbit and the sinuses. Canthotomy and cantholysis should be performed on an emergency basis if an orbital compartment syndrome is diagnosed at any point in the course of the disease.

Consider surgical drainage if the response to appropriate antibiotic therapy has been poor within 48-72 hours or if the CT scan shows the sinuses to be completely opacified.

Consultations

Consult other specialties as indicated. Generally, obtain consultation with a pediatrician, an internist, or a family physician, as well as with an infectious disease specialist, in any case of orbital cellulitis.

Ear, nose, and throat (ENT) consultation is appropriate for cases of orbital cellulitis arising from sinus disease. Neurosurgical consultation is indicated if brain abscesses appear.

Transfer

If necessary, the patient may be transferred for further diagnostic evaluation or for surgical intervention.

Deterrence/prevention

No foolproof method for the prevention of orbital cellulitis exists; however, proper treatment of conditions that may precipitate orbital cellulitis (eg, preseptal cellulitis, sinusitis, dental disease) is the best deterrent.

Diet

No special dietary requirements are indicated other than adequate hydration of the patient.

Follow-up

The patient should be monitored by an infectious disease specialist, as well as by an ophthalmologist, until the infectious disease specialist believes that the medications can be discontinued.

Inpatient Care

Closely monitor the patient at least daily, with vision reevaluated by standardized vision testing, preferably by the same examiner, as appropriate. Evaluate the antibiotic coverage daily and change it as needed, depending on the results of cultures and the patient’s clinical course.^[18] Repeat CT scans if the patient’s condition worsens or does not respond to appropriate antibiotics.

Once the patient is clearly improving and has been afebrile for at least 48 hours, he or she can be changed from IV antibiotics to oral antibiotics (eg, ampicillin, cefpodoxime, cefuroxime, cefprozil) for aerobic infections or to metronidazole for anaerobic infections.

Pharmacologic Therapy

Medical care of orbital cellulitis consists of the proper use of the appropriate antibiotics. Broad-spectrum IV antibiotics should be started immediately and continued until the choice of antibiotics can be tailored for specifically identified pathogens identified on cultures. Typically, IV antibiotic therapy should be continued for 1-2 weeks and then followed by oral antibiotics for an additional 2-3 weeks. Fungal infection requires IV antifungal therapy along with surgical debridement.

Regarding pediatric care, a study by Emmett et al found that the length of IV therapy associated with successful nonsurgical management of children with subperiosteal abscess was considerably shorter than the length of time normally recommended in pediatric infectious disease literature. This result suggested that clinical judgment regarding each patient’s initial CT scan findings and evolving signs, symptoms, and laboratory profile should be taken into account when scheduling IV intervals.

Indications for Surgical Drainage

Surgical drainage of an orbital abscess is indicated in any of the following instances:

• A decrease in vision occurs
• An afferent pupillary defect develops
• Proptosis progresses despite appropriate antibiotic therapy
• The size of the abscess does not reduce on CT scan within 48-72 hours after appropriate antibiotics have been administered; if brain abscesses develop and do not respond to antibiotic therapy, craniotomy is indicated.
• The presence of a drainable fluid collection is evident on CT scan in patients older than 16 years

Medication Summary

Prompt administration of appropriate antibiotics is key to successful treatment of orbital cellulitis. Most cases of orbital cellulitis result from ethmoid sinusitis; in such cases, the initial antibiotics are chosen based on the most likely sinus pathogens, primarily Streptococcus pneumoniae and other streptococci, S aureus, H influenzae, and non-spore–forming anaerobes.

The occurrence of methicillin-resistant S aureus in orbital cellulitis is increasing, and empiric antimicrobial therapy should be directed against this organism if it is prevalent in the community. Infection due to methicillin-resistant S aureus is best treated with vancomycin, cefotaxime, and clindamycin.

Fungal orbital cellulitis also occurs and is primarily due to Mucor and Aspergillus species. Fungal infection requires antifungals, such as amphotericin.

Corticosteroids may be helpful, but they should not be started until after any surgery is performed and until the patient has been on appropriate antibiotics for 2-3 days.

If glaucoma develops secondary to orbital cellulitis, ocular antihypertensives should be administered promptly. In cases of posttraumatic orbital cellulitis, tetanus prophylaxis should be given according to standard protocol.

Antibiotics, Other

Class Summary

Appropriate antibiotics may include nafcillin (for Staphylococcus and Streptococcus species), cefotaxime (for gram-negative organisms, nontypeable H influenzae, Moraxella, and resistant pneumococci), and metronidazole (for anaerobes).

Ticarcillin-clavulanate would cover most gram-positive and gram-negative organisms and most anaerobes. Nafcillin in combination with ceftazidime is also appropriate, although chloramphenicol may be substituted for ceftazidime. Cefazolin can be used in place of nafcillin in cases of mild allergy to penicillin and vancomycin can be used in cases of severe penicillin allergy.

Vancomycin, cefotaxime, clindamycin, and trimethoprim/sulfamethoxazole double-strength would be appropriate for susceptible penicillinase- and non-penicillinase-producing strains of methicillin-resistant S aureus.

Vancomycin

 

Vancomycin is a tricyclic glycopeptide antibiotic for IV administration. It is indicated for the treatment of susceptible strains of methicillin-resistant (beta-lactam resistant) staphylococci in penicillin-allergic patients.

Clindamycin (Cleocin)

 

Clindamycin inhibits bacterial protein synthesis at the bacterial ribosomal lever, binding with preference to the 50S ribosomal subunit and affecting the peptide chain initiation process.

Cefotaxime (Claforan)

 

Cefotaxime is a semisynthetic, broad-spectrum antibiotic for parenteral use. It is effective against gram-positive aerobes, such as S aureus, including penicillinase- and non-penicillinase-producing strains (but it does not cover methicillin-resistant strains) and S pyogenes; gram-negative aerobes (eg, H influenzae); and anaerobes (eg, Bacteroides species).

Nafcillin

 

Nafcillin is a semisynthetic penicillin that is effective against a wide gram-positive spectrum, including Staphylococcus, pneumococci, and group A beta-hemolytic streptococci.

Ceftazidime (Fortaz, Tazicef)

 

Ceftazidime is a semisynthetic, broad-spectrum, beta-lactam antibiotic for parenteral injection. It has a broad spectrum of effectiveness against gram-negative aerobes, such as H influenzae; gram-positive aerobes, such as S aureus (including penicillinase and non-penicillinase-producing strains) and S pyogenes; and anaerobes, including Bacteroides species.

Chloramphenicol

 

Chloramphenicol exerts a bacteriostatic effect on a wide range of gram-negative and gram-positive bacteria and is particularly effective against H influenzae.

Ticarcillin and clavulanate potassium (Timentin)

 

Ticarcillin is a semisynthetic, injectable penicillin that is bactericidal against gram-positive and gram-negative organisms, including H influenzae, S aureus (non-penicillinase producing), beta-hemolytic streptococci (group A), S pneumoniae, and anaerobic organisms, such as Bacteroides and Clostridium species. Clavulanate potassium is a beta-lactamase inhibitor that protects against resistance by beta-lactamase producing enzymes.

Cefazolin

 

Cefazolin is a semisynthetic cephalosporin for intramuscular (IM) or IV administration. It has a bactericidal effect against S aureus (including penicillinase-producing strains), group A beta-hemolytic streptococci, and H influenzae.

Trimethoprim and sulfamethoxazole (Bactrim, Bactrim DS, Septra DS)

 

Trimethoprim/sulfamethoxazole inhibits bacterial growth by inhibiting the synthesis of dihydrofolic acid. The antibacterial activity of trimethoprim/sulfamethoxazole includes common urinary tract pathogens, except Pseudomonas aeruginosa.

Antifungals, Systemic

Class Summary

Fungal orbital cellulitis is a potentially lethal condition, and the principal organisms involved, Mucor and Aspergillus, require the use of antifungals.

Amphotericin B deoxycholate (AmBisome)

 

This is a lipid preparation consisting of amphotericin B within unilamellar liposomes. It delivers higher concentrations of the drug, with a theoretical increase in therapeutic potential and decreased nephrotoxicity.

Amphotericin is the antifungal medication of choice in the treatment of fungal orbital cellulitis. It is administered intravenously and, in cases of severe infection, may be appropriately provided before laboratory confirmation of fungal infection.

Decongestants, Intranasal

Class Summary

Nasal decongestants may help to open the sinus ostia and aid with drainage in cases of orbital cellulitis secondary to sinusitis.

Phenylephrine nasal (Neo-Synephrine)

 

This agent is beneficial in the treatment of nasal congestion that may cause blockage of the ostia of the sinus, interfering with sinus drainage.

Oxymetazoline (Afrin, Dristan, Duramist Plus)

 

Oxymetazoline is applied directly to mucous membranes, where it stimulates alpha-adrenergic receptors and causes vasoconstriction. Decongestion occurs without drastic changes in blood pressure, vascular redistribution, or cardiac stimulation.

Antiglaucoma, Carbonic Anhydrase Inhibitors

Class Summary

These agents reduce intraocular pressure (IOP).

Acetazolamide (Diamox Sequels)

 

Acetazolamide inhibits the enzyme carbonic anhydrase, reducing IOP by reducing the rate of aqueous humor formation. It is used for the adjunctive treatment of chronic simple (open-angle) glaucoma and secondary glaucoma and is employed preoperatively in acute angle-closure glaucoma when there is a desire to delay surgery in order to lower IOP.

Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. These agents modify the body’s immune response to diverse stimuli. Corticosteroids may be helpful, but they should not be started until after any surgery is performed and until the patient has been on appropriate antibiotics for 2-3 days.

Prednisone

 

Prednisone inhibits phagocytosis of platelets and may improve RBC survival.

Prednisolone (Orapred ODT, Prelone, Millipred)

 

Prednisolone decreases autoimmune reactions, possibly by suppressing key components of the immune system. This agent does not need to undergo hepatic metabolism.

 

Buccal mucosa and Masticator space anatomy

Anatomy of the buccal mucosa:The buccal mucosa is bordered vertically by the maxillary and mandibular vestibular folds, whereas its anterior and posterior borders are formed by the outer commissure of the lips and the anterior tonsillar pillar, respectively. The buccal mucosa is primarily innervated by the long buccal nerve (CN V3), and by the anterior, middle, and posterior superior alveolar nerves of the second division of the trigeminal nerve (CN V2). Additionally there is limited sensory innervation from the facial nerve. The blood supply of the buccal mucosa originates primarily from: 

1) The buccal artery—a branch of the maxillary artery
2) The anterior superior alveolar artery of the infraorbital artery—a branch of the third part of the maxillary artery
3) The middle and posterior superior alveolar arteries—branches of the maxillary artery
4) Accessory vessels from the transverse facial artery—a branch of the superficial temporal artery 
The harvesting surgeon must continually be aware of the parotid (Stensen) duct. This duct originates from the parotid gland, travels across the body of the masseter muscle, turns medially at the anterior border of the masseter, crosses the buccal fat pad, pierces the buccinator muscle, and finally terminates at its orifice. This orifice is clinically visible by a papilla located on the mucosa of the inner aspect of the cheek adjacent to the maxillary second molar.

The anatomic buccal space located lateral to the buccinator muscle consists of: adipose tissue (buccal fat pad) , Stensen’s duct, the facial artery and vein, lymphatic vessels, minor salivary glands. and branches of CN 7 and CN 9. The surgeon must be aware of these structures underlying buccinator muscle. However, they should not be exposed in the process of harvesting the buccal mucosal graft which is dissected lateral to the buccinator muscle.  Failure to leave the buccinator muscle intact could result in poor wound closure at the donor site and dysfunction of the buccinator muscle, which serves as a muscle of facial expression.
The mucous membrane lining the cheek is reflected above and below upon the gums is continuous behind with the lining membrane of the soft palate. Opposite the second molar tooth of the maxilla is a papilla, on the summit of which is the aperture of the parotid duct. (Gray’s anatomy)

Masticator Space
Located:
                 -inferior to the temporal space
                 -anterolateral to the parapharyngeal space
                 -the masticator space lies lateral to the infratemporal fossa
Contains:                
                 -masseter muscle
                 -the external (lateral) and internal (medial) pterygoid muscles
                 -the posterior body and the ramus of the mandible
                 -the inferior alveolar vessels and nerves
                 -the insertion of the temporalis muscles

The space is traversed by the mandibular nerve and internal maxillary vessels. 

Masticator space is formed superficial layer of the deep fascial surrounding loose connective tissue and fat pad along with the above structures.

The masticator space is further subdivided into the following compartments:
                -Masseteric
                -Pterygoid
                -Superfical temporal
                -Deep temporal

Each of these subdivisions of the masticator space require directed approach to address masses or infection
                -The most common source of infection is dental in origin, most commonly the third molar.
Due to close proximity of the muscules of mastication, patients with infections often have severe trismus as well as tenderness along the mandible
                -Suspicion of metastasis/malignancy should lead to clinical evaluation of V3, which exits through foramen ovale into the masticator space. 

Surgical approaches may be made either via an intraoral incision along retromolar trigone area or via an extraoral approach along the inferior mandible.

Infectious lesions of the masticator space

Odontogenic abscess (Figure 15) is the most common lesion of the masticator space. Infection of the space arises from a dental cause in 80% of cases, and other causes are facial infection, post-trauma from foreign bodies and iatrogenic (maxillary sinus puncture) [4]. Trismus is the initial symptom and may prevent adequate clinic examination, which explains why imaging is so important in this pathology. Infectious lesions often involve several deep spaces with no respect for anatomical boundaries. CT is particularly useful for guiding treatment in emergency cases: if it reveals only inflammatory changes (cellulitis) (Figure 16), then antibiotic therapy should be started. Fluid collections must be treated surgically by intra- or extraoral drainage. CT can also reveal signs of osteomyelitis (lytic changes with mandible cortical disruption, thickening and abnormal enhancement of the muscles of mastication), which require subperiosteal drainage. Sometimes, CT is not able to diagnose osteomyelitis (Figure 17), in which case, MRI may show loss of the normal signal void of cortical bone with obliteration of the normal signal from medullary fat on T1-weighted images, and hyperintense signals from within the medullary part of the mandible on T2-weighted images. The masticator muscles are hyperintense on T2 with significant enhancement after contrast administration. Osteoradionecrosis can mimic osteomyelitis on radiology [10]. CT in these patients reveals cortical disruption while MRI will show abnormal T1 hypointense signals and T2 hyperintense signals, with strong enhancement of the mandible bone marrow. The masticator muscles also show abnormal T2 hyperintense signals and strong enhancement that is often difficult to distinguish from a recurrent tumor.

Figure 15.

Abscess on axial CT with contrast is seen as a heterogeneous lesion with a hypoattenuating center in the right masticator space.

Figure 16.

Cervicofacial cellulitis on axial CT after contrast injection (A, B) is seen as an odontogenic cellulitis involving the right masticator space with no fluid collections.

Figure 17.

Osteitis on axial CT (A) and MRI T1-weighted (B) images is seen as a mass centered on the right mandible with lysis and loss of the bone marrow T1 hyperintense signals. The right masticatory muscles are also involved.

 

Infratemporal fossa

The infratemporal fossa is an irregularly shaped cavity, situated below and medial to the zygomatic arch. Boundaries defined by:

• anteriorly, by the infratemporal surface of the maxilla and the ridge which descends from its zygomatic process

• posteriorly, by the articular tubercle of the temporal and the spinal angularis of the sphenoid

• superiorly, by the greater wing of the sphenoid below the infratemporal crest, and by the under surface of the temporal squama, containing the foramen ovale, which transmits the mandibular branch of the trigeminal nerve, and the foramen spinosum, which transmits the middle meningeal artery

• inferiorly, by the medial pterygoid muscle attaching to the mandible

• medially, by the lateral pterygoid plate

• laterally, by the ramus of mandible, which contains the mandibular foramen, leading to the mandibular canal through which the inferior alveolar nerve passes. This also contains the lingula, a triangular piece of bone that overlies the mandibular foramen antero-medially. Finally, the mylohyoid groove descends obliquely transmitting the mylohyoid nerve the only motor branch of the posterior division of the trigeminal nerve.

Infratemporal fossa

Left infratemporal fossa.

Infratemporal fossa

Contents of the infratemporal fossa

Muscles

• Lower part of the Temporalis muscle
• Lateral and medial pterygoid muscles

Vessels

The internal maxillary vessels, consisting of the maxillary artery originating from the external carotid artery and its branches.

Internal maxillary branches found within the infratemporal fossa including the

• middle meningeal artery
• inferior alveolar artery
• deep temporal artery
• buccal artery

Veins

• pterygoid venous plexus

Nerves

Mandibular nerve, inferior alveolar nerve, lingual nerve, buccal nerve, chorda tympani nerve, and otic ganglion.^[1]

Mandibular nerve

• Mandibular nerve which is the third branch of the trigeminal nerve (CN V₃), also known as the “inferior maxillary nerve” or nervus mandibularis, enters infratemporal fossa from middle cranial fossa through foramen ovale.

Motor branches:

• masseteric nerve
• deep temporal nerve
• lateral pterygoid nerve and medial pterygoid nerve

Its motor fibers innervate all the muscles of mastication plus the mylohyoid, anterior belly of the digastric, and the tensores veli palati and tympani

Sensory innervation:

• meningeal nerve
• buccal nerve
• auriculotemporal nerve
• lingual nerve
• inferior alveolar nerve
• auricle
• external acoustic meatus
• tympanic membrane
• temporal region
• cheek
• skin overlying the mandible (except at the angle of the mandible)
• floor of mouth
• lower teeth
• gingiva

Infratemporal fossa

Osteology

The foramen ovale and foramen spinosum open on its roof, and the alveolar canals on its anterior wall.

At its upper and medial part are two fissures, which together form a T-shaped fissure, the horizontal limb being named the inferior orbital, and the vertical one the pterygomaxillary.

Temporal fossa

The temporal fossa is a shallow depression on the side of the skull bounded by the temporal lines and terminating below the level of the zygomatic arch.

Boundaries

• Medial: Os frontale, os parietale, os temporale, os sphenoidale, os occipitale (bones of neurocranium).
• Lateral: Temporal fascia
• Anterior: Posterior surface of the frontal process of the zygomatic bone and the posterior surface of the zygomatic process of the frontal bone.
• Superior: Pair of temporal lines (superior and inferior temporal lines) that arch across the skull from the zygomatic process of the frontal bone to the supramastoid crest of the temporal bone
• Inferior: Zygomatic arch laterally and by the infratemporal crest of the greater wing of the sphenoid medially.

Contents

• Temporalis muscle
• Deep temporal arteries
• Deep temporal nerves
• Superficial temporal artery (from external carotid)
• Zygomaticotemporal nerve

Temporal fossa

The temporal fossa is clearly visible in this picture

Temporal fossa

ANATOMY OF THE CERVICAL FASCIA

 

The fibrous connective tissue that constitutes the cervical fascia varies from loose areolar tissue to dense fibrous bands.  This fascia serves to envelope the muscles, nerves, vessels and viscera of the neck, thereby forming planes and potential spaces that serve to divide the neck into functional units.  The cervical fascia functions to both direct and limit the spread of disease processes in the neck and therefore a sound knowledge of the fascial layers is essential to understanding the presentation, treatment and potential complications of infections in the neck.

 

The cervical fascia was first described by Burns in 1811 and in the ensuing years was the subject of much controversy.  As summarized by Malgaine, a French anatomist, “the cervical fascias appear in a new form under the pen of each author who attempts to describe them.”  In reality, for the past several thousand years, head and neck anatomy has not significantly changed, so that it is not so much the anatomy that is confusing as it is the various terminology used to describe the anatomy.  It is now generally agreed upon that the cervical fascia can be divided into a simpler superficial layer and a more complex deep layer that is further subdivided into superficial, middle and deep layers.

 

The superficial layer of cervical fascia ensheaths the platysma in the neck and extends superiorly in the face to cover the mimetic muscles.  It is the equivalent of subcutaneous tissue elsewhere in the body and forms a continuous sheet from the head and neck to the chest, shoulders and axilla.

 

The superficial layer of the deep cervical fascia is also known as the investing layer, the enveloping layer, the external layer and the anterior layer of the deep fascia.  It has been described using the “rule of twos”—it envelops two muscles, two glands and forms two spaces.  This layer originates from the spinous processes of the vertebral column and spreads circumferentially around the neck, covering the sternocleidomastoid and trapezius muscles.  In the midline, it attaches to the hyoid and continues superiorly to enclose the submandibular and parotid glands.  Here it also covers the anterior bellies of the digastrics and the mylohyoid, thereby forming the floor of the submandibular space.  At the mandible, the fascia splits into an internal layer, which covers the medial surface of the medial pterygoid to the skull base and an outer layer that covers the masseter and inserts on the zygomatic arch.  The two spaces it forms are the space of the posterior triangle on either side of the neck and the suprasternal space of Burns in the midline.

 

The middle layer of the deep cervical fascia is also known as the visceral fascia, the prethyroid fascia and the pretracheal fascia.  It can be thought of in two subdivisions, the muscular division, which surrounds the infrahyoid strap muscles, and the visceral division, which envelops the pharynx, larynx, esophagus, trachea, and thyroid gland.  The superior extent of the muscular division is the hyoid and thyroid cartilage, inferiorly it inserts on the sternum and clavicle.  The visceral division passes inferiorly into the upper mediastinum where it is continuous with the fibrous pericardium and covers the thoracic trachea and esophagus.  The antero-superior extent of the visceral division is the hyoid and thyroid cartilage, while posteriorly this fascia covers the buccinator and the pharyngeal constrictors to the skull base—this portion is also called the buccopharyngeal fascia.

 

The deep layer of the deep cervical fascia originates from the spinous processes of the cervical vertebra and the ligamentum nuchae.  At the transverse processes of the cervical vertebra, it divides into an anterior alar layer and a posterior prevertebral layer.  The alar fascia extends from the base of the skull to the second thoracic vertebra, where it joins the visceral fascia.  It lies between the visceral layer of the middle fascia and the prevertebral layer.  The prevertebral fascia lies just anterior to the vertebral bodies and extends the entire length of the vertebral column.  It travels circumferentially around the neck and covers the vertebral muscles, the deep muscles of the posterior triangle of the neck and the scalene muscles.  This layer of fascia surrounds the brachial plexus and subclavian vessels and continues laterally as the axillary sheath.

 

The carotid sheath is a fascial layer that is associated with but is anatomically separate from the previously described layers.  It receives contributions from all three layers of deep cervical fascia and contains the carotid artery, internal jugular vein and vagus nerve.  It continues from the skull base through the neck along the anterior surface of the prevertebral fascia, and enters the chest behind the clavicle (1,2,3).

 

ANATOMY OF THE DEEP NECK SPACES

 

The various layers of cervical fascia, as they pass around and attach to structures in the neck, form several potential spaces.  The hyoid is the most important structure that limits the spread of infection in the neck and is the most reliable landmark when performing surgery for deep neck abscesses.  Therefore, when studying these spaces, it is reasonable to group them according to their relationship to the hyoid into three categories—spaces involving the entire length of the neck, suprahyoid spaces and infrahyoid spaces.

 

Spaces Spanning the Entire Length of the Neck

 

The superficial space is located between the superficial fascia and the superficial layer of the deep fascia.  This potential space lies superficial and deep to the platysma and contains loose areolar tissue, lymph nodes, nerves and vessels—the most significant of which is the external jugular vein.  The loose areolar tissue provides the dissection plane for raising subplatysmal skin flaps.  This space is most commonly involved with superficial cellulitis of the neck, but if abscess formation does occur, diagnosis is not difficult as this will present with obvious fluctuance, erythema, warmth and tenderness.  A superficial space abscess can be approached with a transverse incision within Langers lines in the area of prominence, followed by evacuation of purulent material, local wound care and appropriate antibiotic therapy.

 

The deep neck spaces that run the entire length of the neck include the retropharyngeal space, the danger space, the prevertebral space and the visceral vascular space.  The retropharyngeal space is also known as the posterior visceral space, the retrovisceral space and the retroesophageal space.  It occupies the space posterior to the pharynx and esophagus.  Its anterior wall is made up of the buccopharyngeal fascia superiorly and the visceral division of the middle fascia inferiorly, the posterior wall is the alar layer of the deep fascia, and the lateral boundary is the carotid sheath.  This space extends from the base of the skull to the level of the first and second thoracic vertebra, where the fascial layers making up its walls join together.

 

Posterior to the retropharyngeal space lies the danger space, so named because it contains loose areolar tissue and offers little resistance to the spread of infection.  It is the space between the alar layer and prevertebral layer of the deep fascia and runs from the skull base to the diaphragm.

 

The prevertebral space is limited anteriorly by the prevertebral fascia, laterally by the attachment of this fascia to the transverse processes and posteriorly by the anterior longitudinal ligament, the vertebral bodies and the deep musculature.  It extends the entire length of the vertebral column.  Infection in this space tends to stay somewhat localized due to the dense fibrous attachments between the fascia and the deep muscles.

 

The visceral vascular space is the potential space within the carotid sheath.  Like the prevertebral space the visceral vascular space is quite compact, contains little areolar tissue and is resistant to the spread of infection.  However, it was not termed the “Lincoln’s highway” of the neck for no reason.  It extends from the base of skull into the mediastinum and because it receives contributions from all three layers of deep fascia it can become secondarily involved by infection in any other deep neck space by direct spread.

 

Suprahyoid Spaces

 

The spaces limited to above the hyoid include the submandibular space, the parapharyngeal space, the peritonsillar space, the masticator space, the temporal space and the parotid space.  The submandibular space is bounded by the mandible anteriorly and laterally, the lingual mucosa superiorly, the hyoid postero-inferiorly and the superficial layer of the deep cervical fascia inferiorly.  The mylohyoid muscle divides this space into a superior sublingual space and an inferior submaxillary (perhaps better called submylohyoid) space.  The sublingual space contains loose areolar tissue, the hypoglossal and lingual nerves, the sublingual gland and Wharton’s duct.  The submylohyoid space contains the anterior bellies of the digastrics and the submandibular glands.  These two subdivisions freely communicate around the posterior border of the mylohyoid.

 

The parapharyngeal space is also called the pharyngomaxillary space, the lateral pharyngeal space and the peripharyngeal space.  It has been described as having the shape of an inverted cone, with the base at the base of the skull and the apex at the hyoid.  The boundaries of this space are the skull base superiorly (petrous portion of temporal bone vs. sphenoid), the hyoid inferiorly, the pterygomandibular raphe anteriorly, the prevertebral fascia posteriorly, the buccopharyngeal fascia medially and the superficial layer of the deep fascia over the mandible, medial pterygoid and parotid laterally.  The parapharyngeal space communicates with several other deep neck spaces, including the submandibular space, the retropharyngeal space, the parotid space and the masticator space.  This has important implications in the spread of infection in the neck.

 

The parapharyngeal space is subdivided by the styloid process into an anterior, muscular or prestyloid compartment and a posterior, neurovascular or poststyloid compartment.  The prestyloid space contains fat, muscle, lymph nodes and connective tissue and is bounded by the tonsillar fossa medially and the medial pterygoid laterally.  The poststyloid space contains the carotid sheath and cranial nerves IX, X and XII.  The stylopharyngeal aponeurosis of Zuckerkandel and Testus is formed by the intersection of the alar, buccopharyngeal and stylomuscular fascia and acts as a barrier to the spread of infection from the prestyloid compartment to the poststyloid compartment.

 

The peritonsillar space is formed by the capsule of the palatine tonsil medially, the superior constrictor laterally, the anterior tonsillar pillar superiorly and the posterior tonsillar pillar inferiorly.  This space contains loose areolar tissue, primarily in the area adjacent to the soft palate, which explains why the majority of peritonsillar abscesses will localize to the superior pole of the tonsil.

 

The masticator space is formed by the superficial layer of the deep cervical fascia as it surrounds the masseter laterally and the pterygoid muscles medially.  This space contains these muscles as well as the body and ramus of the mandible, the inferior alveolar nerves and vessels and the tendon of the temporalis muscle.  The masticator space is in direct communication with the temporal space superiorly deep to the zygoma.  The temporal space has as its lateral boundary the superficial layer of deep fascia as it attaches to the zygoma and temporal ridge and its medial boundary the periosteum of the temporal bone.  It is subdivided into superficial and deep spaces by the body of the temporalis muscle.  This space contains the internal maxillary artery and the mandibular nerve.

 

The parotid space is surrounded by the superficial layer of the deep fascia that sends dense connective tissue septa from the capsule into the gland.  In addition to the parotid gland, this space contains the parotid lymph nodes, the facial nerve and posterior facial vein.  The fascial envelope is deficient on the supero-medial surface of the gland, facilitating direct communication between this space and the parapharyngeal space. 

 

Infrahyoid Spaces

 

The only potential space limited to below the hyoid is the anterior visceral space.  This area is enclosed by the middle layer of the deep cervical fascia and contains the thyroid gland, esophagus and trachea.  This potential space runs from the thyroid cartilage into the anterior superior mediastinum to the arch of the aorta.  Below the level of the thyroid gland this space communicates laterally with the retropharyngeal space (1,2,3).

 

DEEP NECK SPACE INFECTIONS

 

The incidence and morbidity of deep neck space infections has been significantly reduced with the introduction of antibiotic therapy.  However, these potentially life-threatening infections continue to occur and can often present diagnostic and therapeutic dilemmas to the physician.  In the following text, the presentation, origin of infection, microbiology, imaging, treatment and complications of deep neck infections will be reviewed.

 

Presentation/Origin of Infection

 

The presenting symptoms and signs of the patient with a deep neck space infection, as well as the source of infection, will vary somewhat depending upon which of the previously described spaces is involved.  Retropharyngeal abscesses are the most common deep neck abscesses in the pediatric population.  Nearly one-half of these abscesses affect patients between 6 and 12 months of age and 96% occur prior to 6 years of age.  This is explained by the fact that the retropharyngeal space contains lymph node chains that tend to involute with age.  The source of infection in children is most often a suppurative process in these nodes that drain the nose, adenoids, nasopharynx and paranasal sinuses.  The more rare retropharyngeal abscess in the adult is typically caused by penetrating or blunt trauma, instrumentation such as endoscopy, intubation or NG tube placement or extension of infection from an adjoining deep neck space.  The child with a retropharyngeal abscess will typically present with fever, irritability, enlarged cervical nodes and neck stiffness or torticollis.  Trismus is uncommon and if the posterior pharynx can be visualized, a lateralized bulging of the posterior pharyngeal wall may be noted.  A history of poor oral intake, complaint of sore throat or dysphagia and drooling may also be found.  Laryngeal edema with resultant respiratory distress is not uncommon.  The presentation in the adult population is slightly different in that pain, dysphagia, anorexia, snoring, nasal obstruction and regurgitation are more commonly reported.

 

Infection of the danger space presents in much the same manner as the retropharyngeal space.  The source of infection is most often extension from the neighboring retropharyngeal, parapharyngeal or prevertebral spaces.

 

Historically, the most common cause of a prevertebral abscess was the extension of a tuberculous infection of a vertebral body, a Pott’s abscess.  The incidence of this has declined as tuberculosis has become less prevalent.  Other sources of prevertebral abscess include trauma, postoperative infection, anterior spread of cervical osteomyelitis or posterior spread from the retropharyngeal space.  Complaints of these patients can be nonspecific and may include neck, back or shoulder pain that worsens with swallowing, dysphagia and rarely, dyspnea.  Physical examination can be unremarkable but may include a midline bulge in the oropharynx.

 

 It would be quite unusual to have an isolated infection of the visceral vascular space, although among intravenous drug abusers, this space may be the origin of infection.  Signs of carotid sheath involvement would include pain and induration of the sternocleidomastoid, torticollis away from the affected side and spiking fevers along with evidence of sepsis.

 

In recent years, submandibular space abscess has become the most common of the deep neck space infections.  Seventy to 85% of these cases are odontogenic in origin, the rest are caused by sialadenitis, lymphadenitis, floor of mouth lacerations or mandible fractures.  The insertion of the mylohyoid along the mandible dictates which subspace is initially affected by an odontogenic infection.  The apex of the first molar is above the mylohyoid, so involvement of this tooth, or teeth anterior to this, will first involve the sublingual space.  In contrast, the apices of the second and third molars are below the mylohyoid and infection here will first spread to the submylohyoid space.  However, as previously mentioned, these spaces freely communicate around the posterior border of the mylohyoid, and both subspaces are typically involved.  These patients will present with pain in the oral cavity, drooling, dysphagia and neck stiffness but trismus is uncommon.  With continued progression, the floor of mouth becomes remarkably indurated and edematous.  The superficial layer of deep fascia serves as the floor of the submandibular space.  It is somewhat rigid and nondistendible and limits inferior swelling.  The mucosa of the floor of mouth, on the other hand, is distensible and accommodates edema but this subsequently causes superior and posterior displacement of the tongue with the potential for airway obstruction.

 

Ludwig’s angina is the prototypical submandibular space infection, however this term should not be applied to all submandibular abscesses.  In his original description in 1836, Ludwig noted the absence of concomitant pharyngeal inflammation, the “woody” induration of the neck and floor of mouth, the limitation of involvement in the neck to the submental and submandibular triangles and the lack of cervical lymphadenopathy.  Some authors now recommend that the term “Ludwig’s angina” be reserved for those infections that meet the following five criteria:  1.  a cellulitic process of the submandibular space, not an abscess; 2.  involvement of only the submandibular space, although this could be bilateral; 3.  the finding of gangrene with foul serosanguinous fluid on incision, but no frank purulence; 4.  involvement of the fascia, muscle and connective tissue, with sparing of the glandular tissue; and 5.  direct spread of infection rather than spread by lymphatics.  Patients with a true Ludwig’s angina present with tender, firm swelling in the anterior neck without fluctuance, a muffled or “hot potato” voice and sialorrhea.   Tachypnea, dyspnea and stridor signal impending airway compromise and warrant immediate treatment.

 

Parapharyngeal space abscess may follow infection in the pharynx, tonsils, adenoids, teeth, parotid or lymph node chains.  Middle ear infections or mastoiditis may involve the parapharyngeal space after rupture of a Bezold’s abscess on the inner aspect of the mastoid tip along the digastric ridge.  Perhaps more commonly, the parapharyngeal space becomes involved from extension of infection from the nearby peritonsillar space, submandibular space, retropharyngeal space or masticator space.  Despite the multitude of potential sources, in nearly half of these cases, the etiology cannot be defined.  Signs and symptoms of parapharyngeal abscess differ depending on whether the prestyloid or poststyloid compartment is involved.  In addition to fever, chills and malaise, anterior infection will often cause pain, dysphagia and significant trismus due to medial pterygoid irritation.  Edema in this area will cause a medial bulging of the lateral pharyngeal wall and tonsil and there will be swelling at the angle of the mandible.  Posterior compartment infection does not tend to be associated with trismus or tonsillar displacement and may have no localizing signs on examination.  Despite this, these patients do appear toxic and may receive the diagnosis “fever of unknown origin.”  Involvement of the neurovascular structures found in this area may lead to cranial neuropathies, Horner’s syndrome, septic internal jugular thrombosis or carotid artery rupture.  Any bleeding from the nose, mouth or ear in a patient with suspected deep neck abscess could be a sentinel event and should be taken very seriously.

 

Peritonsillar abscesses develop by direct extension of infection from a suppurative tonsillitis.  These infections are uncommon in the pediatric population, but instead tend to effect post-pubescent individuals.  Patients present with complaints of gradually worsening dysphagia and odynophagia, often associated with low-grade fever and malaise.  They may have previously been diagnosed with pharyngitis and received antibiotic therapy, with some improvement of symptoms only to then have an abrupt recurrence of symptoms.  Classic findings on examination include “hot potato” voice, trismus, bulging of the superior tonsillar pole and adjacent soft palate and deviation of the uvula to the opposite side.

 

Masticator and temporal space infection most often arise from infections of the third molars.  Inflammation of the pterygoid muscles leads to marked trismus and pain.  The posterior floor of mouth may become edematous and indurated.  Externally, swelling occurs over the ramus of the mandible.

 

Patients with a history of chronic sialadenitis, sialolithiasis or Sjogren’s syndrome are more prone to parotid space infections.  Signs of abscess formation include severe trismus, bulging of the postero-lateral pharyngeal wall and swelling over the angle of the mandible. 

 

Anterior visceral space infections are most commonly caused by hypopharyngeal or esophageal trauma by foreign bodies or instrumentation.  Much less frequently, this space may become secondarily involved by an infectious process in the thyroid.  Symptoms include hoarseness, dyspnea, dysphagia or odynophagia.  Examination may reveal erythema or edema of the hypopharynx, anterior neck edema, induration or crepitus.  Progression of the infection may cause glottic or supraglottic edema with resultant airway compromise (1,3,4,5).

 

Microbiology

 

The vast majority of deep neck abscesses will be caused by a polymicrobial infection, and can grow as many as six different bacteria on culture.  Staphylococcus aureus was the most commonly cultured organism in the preantibiotic era.  Currently, aerobic Streptococcal species and non-streptococcal anaerobes are found most frequently.  Other aerobes that can be involved include H. influenza, S. pneumonia, M. catarrhalis, Klebsiella, Neisseria species and Borrelia vincentii.  Commonly isolated anaerobes include Peptostreptococcus, Fusobacterium and Bacteroides.  Eikenella corrodens is becoming a more frequently cultured participant in these infections, this is of clinical importance because this organism is often resistant to clindamycin.  One must also remember when choosing an antibiotic, that it is not unusual for these organisms, both aerobes and anaerobes, to produce beta-lactamase.  The presence of gram-negative rods in deep neck abscess is unusual although this may be seen in the elderly, debilitated, diabetic or immunocompromised patient (4,6,7).

 

Imaging

 

The diagnosis of deep neck space infection may be difficult to make based on historical and physical findings alone.  Several radiographic studies are available to aid in making the diagnosis, distinguishing between cellulitis and abscess and delineating the extent of infection.  The lateral neck plain film has been used in the past as a screening x-ray to look primarily at the retropharyngeal and prevertebral spaces.  The quality of these x-rays is highly technique dependent–they need to be taken during inspiration with the neck in extension. The thickness of the prevertebral soft tissue can be effected not only by positioning and breathing, but also by crying and swallowing.  The normal width of this soft tissue at C-2 is 7mm, at C-6 it is 14mm in children and 22mm in adults (5,8).  Nagy and Backstrom, in a study of 57 pediatric patients, found that in 25% of cases, lateral x-ray was unable to definitively demonstrate the presence of deep neck infection.  They demonstrated a sensitivity of 83% for lateral radiograph, compared to 100% for CT scan with contrast and concluded that despite the difference in cost, (x-ray $39.14 vs. CT $487.19) CT scan is the definitive study and lateral neck films do not contribute to the evaluation of patients with suspected deep neck abscess (8).

 

High-resolution ultrasound, although advocated by some authors, has not been widely accepted for the imaging of deep neck infection.  In the hands of an experienced ultrasonographer this study can provide much useful information.  It has the advantages of being portable and involving no radiation.  However, even in the best of circumstances, ultrasound does not provide the kind of anatomic detail that CT with contrast is capable of producing.  Ultrasound may have a role in following infection during therapy to verify improvement, or, as will be discussed later, in the use of image guided aspiration of abscesses (11).

 

Contrast-enhanced CT scan has become the imaging modality of choice in the evaluation of the patient with a deep neck abscess.  The advantages of CT scanning are that it is a quick and easy study to obtain, it is widely available and most head and neck surgeons are very comfortable reading the images.  CT is capable of providing superior anatomic detail, which delineates the extent of infection and can differentiate between cellulitis and abscess.  This information is crucial for operative planning.  The disadvantages of CT scan include the use of potentially allergenic injectable contrast material, the dose of ionizing radiation, the difficulty differentiating adjacent soft tissues of similar radiodensity but different composition and the production of artifact from dental amalgam (9).  A study by Miller, et al compared the accuracy of diagnosing deep neck infection by physical examination (PE) versus CT scan.  They found that PE was accurate in determining the presence or absence of a drainable abscess in 63% of cases, while CT scan was 77% accurate.  The sensitivity and specificity for PE was 55% and 73%, compared to 95% and 53% for CT scan.  They concluded that the most accurate method for diagnosis was the combination of PE and CT, and although CT demonstrated a high false positive rate, it provided the correct diagnosis in 8/20 cases of abscess missed by PE and significantly influenced the choice of surgical approach in 25% of cases (10).

 

Magnetic resonance imaging (MRI) of the neck, like CT scan, can provide excellent anatomic detail.  Advantages of MRI over CT include absence of ionizing radiation, a safer injectable contrast material, increased soft tissue sensitivity and contrast, multiplanar images and less artifact produced by amalgam.  Disadvantages are the increased cost, increased examination time, increased dependence on patient cooperation, difficulty in performing MRI emergently and frequent distant location of the scanner, requiring transport of the patient.  The utility of CT and MRI was compared in a study by Munoz, et al looking at 47 patients with neck infections.  MRI was found to be better than CT in delineating anatomy, recognizing abnormality, determining extent of infection and identifying the effected spaces in the neck.  Based upon these findings, they concluded that MRI may be a reasonable first choice for imaging neck abscesses (9).  

 

Treatment

 

The three keys to successful management of deep neck infections are protection and control of the airway, antibiotic therapy and surgical drainage.  The age-old dictum that all abscesses must be surgically drained has recently been tested in studies looking at the medical management of neck abscesses and the use of image guided aspiration of abscesses.  However, many still practice by Levitt’s thinking that “antibiotics are not a substitute for surgery, they should be used in conjunction with proper surgical drainage” (12).

 

Management of the airway in the patient with a deep neck infection is dependent upon the stability of the patient, the extent of disease and the plan of therapy.  The patient who presents with dyspnea and stridor obviously necessitates immediate steps to evaluate and secure the airway.  The patient who does not have signs or symptoms of airway compromise, and who does not require surgical intervention, may be closely observed, typically in an intensive care unit or monitored bed setting.  For the stridorous patient or those patients going to the operating room, the airway can be secured by endotracheal intubation or tracheostomy.  Oral intubation can be quite challenging if the abscess causes obstruction of the upper airway.  Direct laryngoscopy, if not performed with extreme care, runs the risk of rupture of the abscess with subsequent aspiration of abscess contents and pneumonia.  If the anesthesiologist has experience and is comfortable with fiberoptic intubation, this is a viable option for securing the difficult airway and avoiding a tracheostomy.  If a surgical airway is necessary, it is preferable to be done in a planned and controlled manner.  Although it is less than ideal, some situations may require a cricothyroidotomy or “slash” tracheostomy to secure the airway.  Ideally, tracheostomy is performed with the patient awake under local anesthesia, and this is a safe and reliable method to stabilize the airway.  However, the surgeon must keep in mind that tissue planes are likely to be distorted and the trachea may be deviated (6,5,11).  In a review of 210 patients with deep neck abscess, Parhiscar and Har-El found that 43/210 or 20.5% of patients required tracheostomy.  Seventy-five percent of patients that presented with Ludwig’s angina eventually required a tracheostomy.  In fact, out of 20 patients with Ludwig’s angina in which endotracheal intubation was attempted, 11 failed and required “slash” tracheostomy (13).

 

The idea that a select group of patients with deep neck space infection can be treated with antibiotic therapy alone is gaining popularity.  Obviously, those patients with CT evidence of cellulitis rather than abscess can be managed with intravenous antibiotic therapy, and the majority will improve.  Most authors agree that if clinical improvement does not occur within 24 to 48 hours of medical therapy, re-imaging and possibly surgery are indicated (6,7).  Currently, there are an increasing number of reports in the literature on patients with deep neck abscesses being treated successfully with medical management alone.  Mayor, et al prospectively studied 31 patients with parapharyngeal, retropharyngeal or mixed deep neck infections.  Based on CT findings, 19 patients were diagnosed with abscessed, while 12 patients had cellulitis.  The majority of patients were treated with the combination of cefotaxime and metronidazole, several received clindamycin and a few were given amoxicillin/clavulanic acid.  All patients received methylprednisolone and intravenous fluid hydration.  They found that 90% of their patients responded to this regimen and only 3 patients required surgical drainage, although another 4 patients had their parapharyngeal abscesses rupture spontaneously.  The average length of hospital stay for their patients was 8 days, which compares favorably with other series looking at length of stay after surgery (14).  Nagy et al, evaluated similar points in a review of 47 pediatric patients.  In this study, 51% of patients responded to medical therapy alone, however only 7/24 had CT evidence of abscess, the remainder had cellulitis.  The antibiotics used in this study were either intravenous clindamycin, ceftriaxone, ampicillin/sulbactam or a combination.  In the group treated with antibiotics, they found an average length of stay of 4.8 days, compared to 3.6 days for patients that had incision and drainage (15). 

 

The decision on which antibiotic therapy to empirically start for patients with deep neck space infections should be directed by the fact that the most commonly isolated organisms are Streptococcal species and anaerobes.  The majority of infections are polymicrobial so broad antibiotic coverage is desirable.  The percentage of beta-lactamase producing bacteria varies in different reports, 17 to 46%, but most authors consider it reasonable to begin therapy with a beta-lactamase resistant penicillin, likely in combination with metronidazole to improve anaerobe coverage.  Third generation cephalosporins are an alternative, as is clindamycin for the penicillin allergic patient.  One caveat would be to be careful when using clindamycin alone because of the resistance of Eikenella species to this antibiotic.  Improved gram-negative coverage should be considered in debilitated patients or immunocompromised patients.  Of course, antibiotic therapy should always be adjusted as directed by culture and sensitivity findings in those cases in which a specimen is obtained (11).

 

For those patients requiring surgical drainage, the approach will be dictated by the location of the abscess and its relationship to other structures in the neck.  First, one must decide if intraoral incision is an option, or if external drainage is required.  In the past, the use of transoral incision and drainage was essentially limited to isolated retropharyngeal abscesses.  It was thought that the use of this approach to the parapharyngeal space placed the neurovascular structures of the poststyloid compartment at undue risk.  However, with the reliable imaging produced by contrast-enhanced CT scanning, we are now capable of identifying the location of the great vessels in relation to the abscess cavity.  Using preoperative imaging, Nagy, et al found that 22/23 children were successfully treated by transoral drainage of their retropharyngeal, parapharyngeal or combined abscess.  Only one patient failed this treatment and required a second operation with external drainage.  The medial border of the parapharyngeal space is the buccopharyngeal fascia around the superior pharyngeal constrictor.  Transoral drainage involves a cruciate incision through the mucosa followed by blunt dissection through the constrictor muscle (15).  This approach is probably only safe if the great vessels can be definitively identified on preoperative CT and confirmed to be lateral to the abscess cavity.  Cases in which the vessels are located medial to or within the abscess should not be approached in this manner since if bleeding were to be encountered, getting proximal and distal control of the vessels would be difficult.

 

External drainage of deep neck abscesses can be accomplished in several ways.  When it comes to these procedures, the priorities of the patient and surgeon are likely to be different.  The patient is worried about where the incision will be and the cosmetic outcome.  The surgeon is worried about adequate exposure to eradicate the infection while avoiding damage to vital structures.  Therefore, the importance of preoperative counseling and informed consent cannot be over emphasized.  Again, the approach will be primarily dictated by the location of the abscess and what spaces in the neck are involved.  Levitt describes using either an anterior or a posterior approach to the retropharyngeal, danger, prevertebral and visceral vascular spaces.  The anterior approach involves an incision paralleling the anterior border of the sternocleidomastoid, dissection along the anterior border of the muscle, lateral retraction of the carotid sheath, medial retraction of the larynx, trachea and thyroid and exposure of the abscess cavity at the hypopharynx.  The posterior approach utilizes an incision behind the sternocleidomastoid, medial and anterior retraction of the muscle and carotid sheath, opening into the abscess from posterior to the great vessels.  This approach potentially places at risk the sympathetic chain and phrenic nerve.  The submandibular space can be drained via a transverse incision paralleling and 2 cm below the mandible, similar to that used for a submandibular gland excision.  In this case, the posterior belly of the digastric is identified under the gland, which is then retracted laterally.  The mylohyoid muscle is then bluntly divided perpendicular to it fibers, thereby opening into this space.  More limited infections here can be approached with a transverse submental incision and blunt spreading of the mylohyoid.  The parapharyngeal space can be approached using an incision along the anterior sternocleidomastoid, the above described submandibular incision or a T-shape incision that combines the two.  Dissection proceeds along the anterior aspect of the muscle until the digastric sling is encountered.  This is followed anteriorly and the muscle and overlying submaxillary gland are elevated.  Blunt finger dissection can then used in this space from the styloid process and skull base, inferiorly along the carotid sheath (12).

 

An alternative to open drainage of neck abscesses is the use of image guided aspiration or catheter insertion.  The successful use of these methods probably is most dependent upon proper patient selection.  Those patients with smaller, more isolated and uniloculated abscesses are more likely to respond favorably to this treatment.  The use of image guidance, whether CT or ultrasound, to perform aspiration helps to ensure that the needle or catheter is being placed appropriately in the affected space while vital structures are avoided.  Also, reexamination after aspiration can determine if the evacuation is complete.  Poe, et al described a small series of patients that were successfully treated with percutaneous CT guided aspiration of deep neck abscess along with antibiotic therapy.  They propose that CT guided aspiration has the benefits of early collection of a specimen to identify the infecting organisms, significantly reduced expense compared to a trip to the operating room and the avoidance of a scar on the neck (16).  Ultrasound guidance was used for needle aspiration or pigtail catheter insertion in a study by Yeow, et al.  This was a prospective study of 15 patients with uniloculated deep neck abscesses.  Ten patients had needle aspiration, six needed only one aspiration, two needed two aspirations and two eventually required open surgical drainage.  All five patients treated with pigtail catheter placement responded well and avoided surgery (17).  Both authors admit that while no complications were encountered in their series, the potential for damage to neurovascular structures does exist and must be discussed with the patients.  Also, the successful performance of these procedures is highly dependent upon the skill and experience of the interventional radiologist.

 

Complications

 

The incidence of complications from deep neck space infections has remarkably decreased since the advent of antibiotic therapy.  Despite this, the potentially devastating outcomes associated with these complications remind the physician to remain vigilant for their signs.  Airway obstruction and asphyxia is a potential complication of any deep neck infection, but has been most commonly associated with Ludwig’s angina.  Early evaluation and management of these patients is paramount.  Rupture of the abscess, either spontaneously or with manipulation such as intubation, with associated aspiration can result in severe pneumonia, lung abscess or empyema. 

 

   Vascular complications of deep neck infections can include jugular vein thrombosis or carotid artery rupture.  Lemierre’s syndrome is jugular vein thrombosis that occurs specifically in association with an oropharyngeal infection, however, any infection of the parapharyngeal or visceral vascular spaces can cause this complication.  Jugular vein thrombosis presents with fevers, chills and prostration as well as swelling and pain along the sternocleidomastoid.  It can lead to bacteremia or septic embolization with resultant distant infection.  Pulmonary embolism occurs in up to 5% of these patients.  Patients that develop deep neck infection secondary to intravenous drug abuse are particularly prone to have this complication.  The most common organism causing Lemierre’s syndrome is Fusobacterium necrophorum, while in IV drug abusers Staphylococcus is most common.  Imaging with either ultrasound, CT or MRI may assist in making the diagnosis.  Treatment involves intravenous antibiotic therapy, preferably directed by blood culture results.  The use of anticoagulation is controversial but may speed recovery and prevent pulmonary embolism.  If medical therapy fails, then ligation and excision of the infected vessel is indicated.

 

Carotid artery rupture, although rare, carries a mortality rate between 20% and 40%.  This can occur when infection involving the carotid sheath leads to arterial wall weakening, erosion and eventual hemorrhage.  Salinger and Pearlman, in a review of 227 cases of deep neck abscess complicated by hemorrhage, found that 62% of ruptures occur from the internal carotid artery, 25% involve the external carotid and 13% involve the common carotid.  In their series, of the 73 patients who were treated with artery ligation, 64% survived.  Artery rupture may be heralded by recurrent small bleeds from the ear, nose or mouth, the onset of shock, a protracted clinical course, hematoma in the nearby tissue, Horner’s syndrome or unexplained cranial neuropathies.  Treatment necessitates obtaining proximal and distal control, followed by ligation of the vessel.  Repair of the artery by patching or grafting is restricted by the infected environment.

 

Extension of infection from the anterior visceral, retropharyngeal, visceral vascular, danger or prevertebral spaces can lead to mediastinitis.  Patients will complain of increasing difficulty breathing and chest pain.  Chest x-ray may show a widened mediastinum or pneumomediastinum. 

A CT

scan of the chest can help to delineate the extent of involvement.  Treatment involves aggressive antibiotic therapy and immediate surgical drainage.  Disease limited above the tracheal bifurcation can often be managed through a transcervical approach.  More extensive disease will likely require chest tube placement or thoracotomy (3,4,6,7,11)

 

Special Consideration

 

The treatment of deep neck space infections with antibiotic therapy and drainage via aspiration or surgery is most often definitive and recurrence of these cases is rare.  The exception to this rule is the deep neck infection that occurs in association with a preexisting congenital abnormality.  So that, in the patient that presents with a prior history of a similar deep neck infection or abscess, the level of suspicion should be raised for an underlying lesion.  Imaging, particularly CT scan, can be extremely helpful in making the diagnosis in these cases.  In a review of 12 cases of recurrent deep neck infection, Nusbaum, et al, found the most common underlying congenital anomaly to be a second branchial cleft cyst.  Other causes included first, third and fourth branchial cleft cysts, lymphangiomas, thyroglossal duct cysts and a cervical thymic cyst (18).  

 

 

 

BIBLIOGRAPHY

 

1.      Levitt, GW.  Cervical fascia and deep neck infections.  Laryngoscope, 1970; 80 (3): 409-35.

2.      Panoessa, DF, Goldstein, JC.  Anatomy and physiology of head and neck infections (with emphasis on the fascia of the head and neck).  Otolaryngologic Clinics of North America, 1976; 9 (3): 561-80.

3.      Gidley, PW, Stiernberg, CM.  Deep Neck Space Infections.  In: Infectious Diseases and Antimicrobial Therapy of the Ears, Nose and Throat, Johnson, JT and Yu, VL eds.  Philadelphia, WB Saunders Company, 1997: 500-9.

4.      Hotaling, AJ.  Deep Neck Infections: Recognition, Evaluation, Therapy.  In: Practical Pediatric Otolaryngology, Cotton, RT and Myer, CM eds.  Philadelphia, Lippincott-Raven Publishers, 1999: 711-25.

5.      Marra, S, Hotaling, AJ.  Deep neck infections.  American Journal of Otolaryngology, 1996; 17 (5): 287-98.

6.      Scott, BA, Stiernberg, CM, Driscoll, BP.  Deep Neck Space Infections. In: Head and Neck Surgery—Otolaryngology, 2^nd ed., Bailey, BJ ed.  Philadelphia, Lippincott-Raven Publishers, 1998; 819-35. 

7.      Stiernberg, CM.  Deep-neck space infections.  Archive of Otolaryngology Head and Neck Surgery, 1986; 112: 1274-79.

8.      Nagy, M, Backstrom, J.  Comparison of the sensitivity of lateral neck radiographs and computed tomography scanning in pediatric deep-neck infections.  Laryngoscope, 1999; 109 (5): 775-779.

9.      Munoz, A, Castillo, M, Melchor, MA, Gutierrez, R.  Acute neck infections: Prospective comparison between CT and MRI in 47 patients.  Journal of Computer Assisted Tomography, 2001; 25 (5): 733-41.

10.  Miller, WD, Furst, IM, Sandor, GK, Keller, MA.  A prospective, blinded comparison of clinical examination and computed tomography in deep neck infections.  Laryngoscope, 1999; 109 (11): 1873-79.

11.  Gidley, PW, Ghorayed, BY, Stiernberg, CW.  Contemporary management of deep neck space infections.  Otolaryngology-Head and Neck Surgery, 1997; 116 (1): 16-22.

12.  Levitt, GW.  The surgical treatment of deep neck infections.  Laryngoscope, 1971; 81 (3): 403-11.

13.  Parhiscar, A, Har-El, G.  Deep neck abscess: A retrospective review of 210 cases.  Annals of Otology, Rhinology and Laryngology, 2001; 110 (11): 1051-54.

14.  Mayor, GP, Martinez-San Millan, J, Martinez-Vidal, A.  Is conservative treatment of deep neck space infections appropriate?  Head and Neck, 2001; 23 (2): 126-33.

15.  Nagy, M, Pizzuto, M, Backstrom, J, Brodsky, L.  Deep neck infections in children: A new approach to diagnosis and treatment.  Laryngoscope, 1997; 107 (12): 1627-34.

16.  Poe, LB, Petro, GR, Matta, I. 

Percutaneous CT

-guided aspiration of deep neck abscesses.  American Journal of Neuroradiology, 1996; 17: 1359-63.

17.  Yeow, KM, Liao, CT, Hao, SP.  US-guided needle aspiration and catheter drainage as an alternative to open surgical drainage for uniloculated neck abscesses.  Journal of Vascular and Interventional Radiology, 2001; 12 (5): 589-94.

18.  Nusbaum, AO, Som, PM, Rothschild, MA, Shugar, JM.  Recurrence of a deep neck infection. A clinical indication of an underlying congenital lesion.  Archives of Otolaryngology Head and Neck Surgery, 1999; 125: 1379-82.