ABSCESSES

ABSCESSES OF THE PALATE AND INFRAORBITAL AREAS: ETIOLOGY, ESPECIALLY OF THE TREATMENT, PREVENTION.

PHLEGMON OF THE ORBIT: CHARACTERISTICS OF ORIGIN, LOCALIZATION, CLINICAL COURSE, DIFFERENTIAL DIAGNOSIS, SURGICAL TREATMENT.

Normal Palate Anatomy

• Mucosa: The mucosa is moist, pink tissue that lines the inside of certain body parts. It lines the nose, mouth, lungs, and the urinary and digestive tracts.
• Hard Palate: The hard palate is the bony part of the roof of the mouth. It makes up the front part of the palate. It is in front of the soft palate. You don’t see the bone when you open your mouth because it is covered by the mucosa. With either your tongue or your finger, you can feel when the palate changes from hard to soft.

The hard palate separates the mouth from the nose. Without the hard palate, there is communication between the nasal cavity and the oral cavity. This communication between the two makes speech, eating and drinking difficult. The hard palate keeps food from going up the nose. The hard palate is also important for speaking as it keeps air from going out of the nose instead of the mouth.

• Soft Palate: The soft palate is the posterior fleshy part of the palate. If you run your tongue from the front of the roof of your mouth to the back, you can feel when the hard palate becomes the soft palate. If you open your mouth and take a deep breath in, you’ll see your soft palate lift. The soft palate moves up and down because of the action of the muscles in the palate.

When there is a cleft in the palate muscle, it does not function and speech is impaired. Specifically, speech becomes difficult to understand because air is going out of the nose instead of the mouth. Additionally, because the soft palate pushes food to the back of the throat when a person is swallowing, eating is more difficult in patients with a cleft of the soft palate.

• Uvula: The uvula is the part of the soft palate that hangs down the middle in the back of the mouth. In some people, it is very well-defined. Others may have a small one or may not have one at all.
• Alveolar Ridge: The alveolar ridge is also known as the “dental arch” or “gums.” The alveolar ridge is where the teeth emerge from. There is an upper alveolar ridge and a lower alveolar ridge.
• Primary Palate: The primary palate is the portion of the palate in front of the incisive foramen. It includes the front portion of the hard palate and is triangular in shape. It also includes the four central front teeth and the alveolar ridge.
• Secondary Palate: The secondary palate is the back portion of the hard palate (the portion behind the incisive foramen), including the posterior alveolar ridge, and all of the soft palate and uvula.
• Incisive Foramen: The incisive foramen is a structure that separates the primary palate from the secondary palate. It is an opening in the bony palate through which the blood vessels and nerves for the palate pass. It is directly behind the two front teeth. In a palate without a cleft, the incisive foramen cannot be seen as it is covered by the mucosa of the palate.

 

Palatal abscesses

 

Hard palate is the partition between the nose and floor of the mouth. Embryologically, hard palate is formed by the palatine process of maxilla and the horizontal plate of the palatine bone. Anterior portion of the hard palate contains irregular ridges which help during feeding. Hard palate continues posteriorly in a soft portion called soft palate.

 

Abscesses of hard palate are known. The etiology may be trauma, ulceration, secondarily infected nasopalatine cyst or infected tooth. The line of treatment will be antibiotics and anti-inflammatory followed by incision and drainage.

Dental abscesses

If a patient comes to you with a painful, throbbing, swollen, red face (a ”fat face’), perhaps with fever, trismus and lymphadenitis, he is probably suffering from an acute dental or oral infection, most probably an alveolar abscess. He may have:

(1) An alveolar abscess begins as an infection in the bone around a non-vital infected tooth. He has severe pain, which becomes less as pus is released into more superficial tissues and his face starts to swell. After 36 hours of cellulitis he usually has a fluctuant abscess which needs draining. If drainage is delayed, the pus in his abscess discharges spontaneously through a sinus (26-8) in his gum or face, which may become chronic.

First, control infection with antibiotics, and then drain the abscess, either by incising it where it is pointing, or by removing the infected tooth, which acts as a cork to prevent the pus escaping, or by doing both these things. If you remove a tooth before you have controlled the infection with antibiotics, and while his face is still severely swollen, you may spread the infection; your task will also be more difficult.

(2) A periodontal abscess at the side of a tooth, caused by spread from an infected gum.

(3) A pericoronal abscess caused by infection of the gum over the crown of an unerupted and impacted tooth, usually a lower third molar (”an infected wisdom tooth’). Often, an abscess does not form, and the gum round the tooth is merely inflamed.

Pus from all three of these foci of infection, and particularly from an alveolar abscess, can track in various directions, towards his cheek, his tongue, or his palate, or downwards into his neck. It can discharge inside his mouth or outside. It can collect: (1) On any of the surfaces of his gum (”gumboils’). (2) In the buccal sulcus of either jaw on the oral or deeper side of the attachment of his buccinator muscle (common). (3) On the surface of his face superficial to the buccinator attachment. (4) On his palate (less common). (5) In his submasseteric space between his masseter and the ascending ramus of his mandible. (6) In his pterygomandibular space between his medial pterygoid and the ascending ramus of his mandible. (7) In his sublingual space above or below his mylohyoid muscle. (8) In his submandibular space superficial to his mylohyoid. (9) In his submental space in the midline under his jaw. (10) Anywhere down the side of his neck. Don’t be daunted by the complexity of this anatomy. Some of these spaces communicate with one another and more than one space may be involved[md]incise the abscess where it points, having due regard, where you can, for the skin lines on his face (61- 3).

Infection can spread in some particularly dangerous directions: (1) From his upper jaw (or upper lip or nose) to his cavernous sinus, which may thrombose, perhaps fatally (5.5). (2) From his lateral pharyngeal space up towards the base of his skull, down to his glottis or into his mediastinum. Infection of this space is one of the most dangerous conditions in dentistry. He has difficulty swallowing and speaking. (3) From his lower jaw, via his sublingual and submandibular spaces, to the tissues of his neck, where it may cause oedema of his glottis, respiratory obstruction and death. This is Ludwig’s angina (5.10).

The attachments of a patient’s mylohyoid and buccinator muscles determine whether pus, orginating in his lower jaw, points inside or outside his mouth. A, shows pus from his lower third molar spreading into his buccal space, his submasseteric space, and his lateral pharyngeal space. B, shows the attachments of his mylolyoid and buccinator muscles. The attachments of these muscles determine whether pus spreads into his sublingual space, his submandibular space, his buccal sulcus, or on to the surface of his face. C, shows the incision of an abscess in his buccal sulcus.

HISTORY AND EXAMINATION. A patient of any age over 5 years walks into casualty with a fat face looking ill and distressed. He has usually had toothache in the past, but the pain has gone. Now he tells you that he has had pain for a week. He has fever, trismus, and a unilateral, tender, shiny, warm, indurated swelling. Looking at him will tell you which side of his face and which jaw is involved. Feel for warmth with the back of your index finger and test for fluctuation. A tooth with large holes in it probably has an apical abscess under it. It may be firm, but is usually loose. If he has obvious periodontal disease, or several loose teeth, suspect a periodontal abscess.

If you are in doubt as to which of his teeth is the site of infection, tap them with some metal object or press them with your gloved index finger. A tooth which is much more painful than the others is probably the source of an alveolar infection. It may also be slightly raised in its socket. A tooth with a periodontal abscess is much less tender to percussion.

X-RAYS. If possible, X-ray the offending tooth. You may see: (1) A a radiolucent area at its apex when an apical abscess has been present for 2 or 3 weeks. (2) Caries between two adjacent teeth which may not be visible from his mouth. (3) The impacted tooth which is responsible for a pericoronal abscess. (4) Some other source for the infection, such as an infected cyst, or a fracture.

THE DIFFERENTIAL DIAGNOSIS includes acute inflammation of the salivary glands (5.9), mumps, Burkitt’s lymphoma (32.3), lymph node swellings and glandular fever.

GENERAL MEASURES. Admit him and make sure that his fluid intake is adequate; he may find drinking difficult.

CAUTION ! Don’t apply poultices or any kind of local heat to his face[md]they may spread the infection. If an abscess is pointing inside his mouth, hot saline mouth washes may ease his pain.

ANTIBIOTICS are often unnecessary, because many dental infections can be treated by local drainage only. If there is spreading cellulitis he needs an antibiotic. Procaine penicillin 600,000 units (2 ml) intramuscularly is adequate in most cases. But if his condition is serious give him a megaunit of benzyl penicillin 4 to 6-hourly.

When you have drained an abscess, culture the pus and change the antibiotic if necessary.

CAUTION ! Make sure that he understands that a course of antibiotics is not sufficient treatment for his abscess, and that he must return, even if his swelling improves.

ANAESTHESIA. (1) 2% or 4% lignocaine spray or a swab soaked in lignocaine solution. (2) Inject a local anaesthetic solution into the outer wall of the abscess over the proposed site of the incision. (3) Ethyl chloride local spray is suitable for an abscess which presents on his face or in his labial or buccal sulci. Isolate the infected area with gauze packs, and then spray on ethyl chloride until crusting occurs. Then open the abscess with a No. 11 blade.

CAUTION! Avoid general anaesthesia, if you can, unless it is expert (especially if he is in danger of respiratory obstruction[md]see A 13.2), and you can intubate him and pack off his throat.

ALVEOLAR ABSCESSES If you can refer him, a dentist may be able to save his tooth by draining the abscess through it, and later filling its root. If you cannot refer him, remove it. Many abscessed teeth are loose, and you can easily pick them out of their sockets. Removing his tooth to allow pus to drain through the socket, combined with antibiotic treatment may be sufficient. Don’t incise a non-fluctuant swelling. If it is not yet fluctuant and ripe for incision, ask him to use hot saline mouth washes, as hot as he can bear without the risk of being scalded, several times a day. Give him an antibiotic and wait. This may control his infection and arrest pus formation.

CAUTION ! (1) Don’t pull out his tooth (26.3) before you have controlled his cellulitis. (2) If he has a tense inflammatory swelling of the upper part of his neck, suspect Ludwig’s angina and treat him urgently (5.10).

PUS POINTING INSIDE HIS MOUTH can point in several places:

If an abscess is pointing on his alveolus, open it into his mouth.

If it is pointing in his labial sulcus (C, 5-7), make a 1.5 cm incision through his mucous membrane parallel to his alveolar ridge. Push a fine haemostat into it and open the jaws.

If it is pointing in his palate, make an anteroposterior incision, parallel to its nerves and vessels, remove an ellipse of tissue and let the pus flow out.

If he has pus in his pterygomandibular, lateral pharyngeal, or submasseteric spaces, drain it through a vertical incision inside his mouth parallel to the ascending ramus of his mandible, taking care to avoid his parotid duct (61-5). This runs in his cheek under the middle third of a line between the tragus of his ear and the commissure of his lips, and opens in line with his first molar tooth. Push forceps to the lingual or buccal side of his ramus, wherever the pus seems to be pointing. If it is under his masseter, insert a drain deep to this muscle down to his mandible from outside his face. Insert the drain through an incision just below the inferior border of his mandible.

PUS POINTING OUTSIDE HIS MOUTH. Drain it through one of the incisions below, as soon as any cellulitis he may have has stopped spreading. Removing his tooth to let the pus drain is not enough, even if it does drip from his root canal. If his abscess is fluctuant, it needs draining too. If you are not sure if it is ready for drainage or not, insert a wide bore needle under local anaesthesia. If you aspirate pus, incise it by Hilton’s method (5.2) where it points at the softest and most tender spot. To minimize scarring, make an incision below the inferior border of his mandible, where possible. If you have to make it on his face, make it in line with the creases in his skin (61-3). These may not always be over the most fluctuant part of the abscess.

CAUTION ! When you plan your incision, consult Figures 5-7a and 61-3 and remember: (1) The extension of the lower pole of his parotid gland into the side of his neck (61-5). (2) The mandibular branches of his facial nerve. These run horizontally and cross the lower border of his mandible, just anterior to his masseter, deep to his platysma muscle in his anterior mandibular region and deep to the fascia posteriorly. (3) His facial artery and vein. These enter his face from between his submandibular salivary gland and the lower border of his mandible; they cross the ramus of his mandible 3 cm from the angle of his jaw and then run obliquely across the lower third of his face superficially on his buccinator muscle. You may have to compromise between chosing the best site for dependent drainage and an inconspicuous scar in the crease lines of his face. Here are some likely sites:

If he has a submental abscess, drain it through a small midline transverse incision under his chin.

If the abscess is under the body of his mandible, drain it through a horizontal incision 1 to 2 cm below the lower border of his mandible, taking care to avoid the mandibular branch of his facial nerve and his facial vessels. Push sinus forceps towards the lingual side of his mandible to drain the pus there.

If the abscess points external to his buccinator, drain it through a small incision over the swelling.

DRAINS. Stitch a corrugated or tubular rubber or plastic drain into the wound for 2 to 5 days, or leave it open with its edges separated by gauze.

PERIODONTAL ABSCESS. If you cannot refer him for a conservative operation, pull out his tooth (26.3).

PERICORONAL INFECTION (infected ”wisdom tooth’). See Section 26.4.

POSTOPERATIVELY, after you have incised any intraoral abscess, give him hot mouth washes to help the incision stay open as long as is necessary.

DIFFICULTIES. If  he CANNOT OPEN HIS MOUTH to let you get at the abscess, he probably still has cellulitis, and his abscess is not yet fit for incision. So continue antibiotics and try again later.

Picture of  Palatal Abscess

(Dentoalveolar abscess extending to the palate)

 

This palatal abscess started as a dentoalveolar abscess of the adjacent lateral incisor and spread posteriorly to the hard palate.

ABSCESS INCISION AND DRAINAGE

Abscesses are localized infections of tissue marked by a collection of pus surrounded by inflamed tissue. Abscesses may be found in any area of the body, but most abscesses presenting for urgent attention are found on the extremities, buttocks, breast, perianal area, or from a hair follicle. Abscesses begin when the normal skin barrier is breached, and microorganisms invade the underlying tissues. Causative organisms commonly include Streptococcus, Staphylococcus, enteric bacteria (perianal abscesses), or a combination of anaerobic and gram-negative organisms.

            Abscess resolve by drainage. Smaller (<5mm in diameter) abscesses may resolve to conservative measures (warm soaks) to promote drainage. Larger abscesses will require incision to drain them, as the increased inflammation, pus collection, and walling off of the abscess cavity diminish the effectiveness of conservative measures.

Indications

1.                  Abscess on the skin which is palpable

Contraindications

1.                  Extremely large abscesses which require extensive incision, debridement, or irrigation (best done in OR)

2.                  Deep abscesses in very sensitive areas (supralevator, ischiorectal, perirectal) which require a general anesthetic to obtain proper exposure

3.                  Palmar space abscesses, or abscesses in the deep plantar spaces

4.                  Abscesses in the nasolabial folds (may drain to sphenoid sinus, causing a septic phlebitis)

Materials

1.                  Universal precautions materials

2.                  1% or 2% lidocaine WITH epinephrine for local anesthesia, 10 cc syringe and 25 gauge needle for infiltration

3.                  Skin prep solution

4.                  #11 scalpel blade with handle

5.                  Draping

6.                  Gauze

7.                  Hemostat, scissors, packing (plain or iodoform, 1/2”)

8.                  Tape

9.                  Culture swab

Preprocedure education

1.                  Obtain informed consent

2.                  Inform the patient of potential severe complications and their treatment

3.                  Explain the steps of the procedure, including the not insignificant pain associated with anesthetic infiltration

4.                  Explaiecessity for follow-up, including packing change or removal

Procedure

1.                  Use universal precautions

2.                  Cleanse site over abscess with skin prep

3.                  Drape to create a sterile field

4.                  Infiltrate local anesthetic, allow 2-3 minutes for anesthetic to take effect

5.                  Incise widely over abscess with the #11 blade, cutting through the skin (Figure 1) into the abscess cavity. Follow skin fold lines whenever able while making the incision

Figure 1: Making the incision

6.                  Allow the pus to drain, using the gauzes to soak up drainage and blood. Use culture swab to take culture of abscess contents, swabbing inside the abscess cavity

7.                  Use the hemostat to gently explore the abscess cavity to break up any loculations within the abscess

8.                  Using the packing strip, pack the abscess cavity (Figure 2 )

Figure 2: Packing the abscess

9.                  Place gauze dressing over wound, and tape in place

 

 

Complication	Prevention	Management
Insufficient anesthesia	Remember that the tissue around an abscess is acidotic, and local anesthetic loses effectiveness in acidotic tissues	Do a field block; use sufficient quantity of anesthetic; allow time for anesthetic effect
No drainage	Localize site of incision by palpation	Extend incision deeper or wider as needed
Drainage is sebaceous material	Abscess was an inflamed sebaceous cyst	Express all material, break up sac with hemostat, pack open as with an abscess

 

Complications, Prevention, and Management Documentation on the medical record 1.                  Consent 2.                  Procedure used, prep, anesthetic (and quantity), success of drainage, culture if made 3.                  Any complications (or “none) 4.                  Who was notified of any complication (family, attending MD) 5.                  Follow-up arrangements  Items for evaluation of person learning this procedure 1.                  Anatomy of skin and subcutaneous tissues 2.                  Indications and contraindications for this procedure 3.                  Interaction between MD, patient, and family 4.                  Use of sterile technique and Universal Precautions 5.                  Technical ability 6.                  Appropriate documentation 7.                  Understanding of potential complications and their correction

 

Fundamental Principles of Treatment of Infection-Oral Surgery Lecture Note

In order to treat an acute dent alveolar infection as well as a fascial space abscess correctly, the following are considered absolutely necessary:

         Take a detailed medical history from the patient.

         Drainage of pus, when its presence in tissues is established.

This is achieved (1) by way of the root canal, (2) with an intraoral incision, (3) with an extraoral incision, and (4) through the alveolus of the extraction. Without evacuation of pus, that is with administration of antibiotics alone, the infection will not resolve.

      Drilling of the responsible tooth during the initial phase of inflammation, to drain exudate through the root canal, together with heat therapy. In this way, spread of inflammation is avoided and the patient is relieved of the pain. Drainage may also be performed with trephination of the buccal bone, when the root canal is inaccessible.

         Antisepsis of the area with an antiseptic solution before the incision.

     Anesthesia of the area where incision and drainage of the abscess are to be performed, with the block technique together with peripheral infiltration anesthesia at some distance from the inflamed area, in order to avoid the risk of existing microbes spreading into deep tissues.

         Planning of the incision so that:

– Injury of ducts (Wharton, Stensen) and large vessels and nerves is avoided.

– Sufficient drainage is allowed. The incision is performed superficially, at the lowest point of the accumulation, to avoid pain and facilitate evacuation of pus under gravity.

– The incision is not performed in areas that are noticeable, for esthetic reasons; if possible, it is performed intraorally.

       Incision and drainage of the abscess should be performed at the appropriate time. This is when the pus has accumulated in the soft tissues and fluctuates during palpation, that is when pressed between the thumb and middle finger, there is a wave-like movement of the fluid inside the abscess. If the incision is premature, there is usually a small amountof bleeding, no pain relief for the patient and the edema does not subside.

 

Incision for drainage of a sublingual abscess. The incision is performed parallel to the submandibular duct and the lingual nerve

Incision for drainage of a palatal abscess, parallel to the greater palatine vessels

Incisions for drainage of a submandibular or parotid (a), and a submasseteric (b) abscess. During cutaneous incisions, the course of the facial artery and vein must be taken into consideration (a), as well as that of the facial nerve (b)

·       The exact localization of pus in the soft tissues (if there is no fluctuation present) and the incision for drainage must be performed after interpretation of certain data; for example, ascertaining the softest point of swelling during palpation, redness of the skin or mucosa, and the most painful point to pressure. This area indicates where the superficial incision with a scalpel is to be made. If there is no indication of accumulation of pus to begin with, hot intraoral rinses with chamomile are recommended to speed up development of the abscess and toensure that the abscess is mature.

·       Avoid the application of hot compresses extraorally, because this entails an increased risk of evacuation of pus towards the skin (spontaneous drainage)

Superficial incisions on the skin (a) and on the mucosa of the oral cavity (b)

 

Spontaneous extraoral (undesirable) drainage of an abscess, after the erroneous placement of hot compresses on the skin

 

·     Drainage of the abscess is initially performed with a hemostat, which, inserted into the cavity of the abscess with closed beaks, is used to gently explore the cavity with open beaks and is withdrawn again with open beaks. At the same time as the blunt dissection is being performed, the soft tissues of the region are gentlymassaged, to facilitate evacuation of pus.

·      Placement of a rubber drain inside the cavity and stabilization with a suture on one lip of the incision, aiming to keep the incision open for continuous drainage of newly accumulated pus.

·        Removal of the responsible tooth as soon as possible, to ensure immediate drainage of the inflammatory material, and elimination of the site of infection. Extraction is avoided if the tooth can be preserved, or if there is an increased risk of serious complications in cases where removal of the tooth is extremely difficult.

·   Administration of antibiotics, when swelling is generally diffuse and spreading, and especially if there is fever present, and infection spreads to the fascial spaces, regardless of whether there is an indication of the presence of pus. Antibiotic therapy is usually empiric, given the fact that it takes time to obtain the results from a culture sample. Because the microorganisms isolatedmost often in odontogenic infections are streptococci (aerobic and anaerobic), penicillin remains the antibiotic of choice for treatment.

Diagrammatic illustrations showing the incision of an intraoral abscess and the placement of a hemostat to facilitate the drainage of pus

Diagrammatic illustrations showing the placement of a rubber drain in the cavity and stabilization with a suture on one lip of the incision.

Treatment of Infection in Cellular Stage

In this stage, treatment of the infection depends on the location of existing pus. Localization, as already mentioned, may be intraalveolar, subperiosteal, submucosal or subcutaneous.

ORBITAL AND INTRACRANIAL COMPLICATIONS

Odontogenic infections that spread to involve the orbit and the brain are rare. Orbital and intracranial abscesses may have an odontogenic origin, however, and the dental condition of patients with these conditions should be evaluated by a dentist. Probably no more than 5 to 10 percent of orbital cellulitis is odontogenic in origin. This infection generally is unilateral and is characterized by proptosis, chemosis, lid edema, and restriction of extraocular motion secondary to edema.  No nerve palsies or visual changes are present. Treatment includes surgical drainage, antibiotics, and elimination of the dental infection.

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.

Specific Organisms and Therapeutic Regimens

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, or the lacrimal sac; (2) direct inoculation of the orbit from trauma or surgery; and (3) hematogenous spread from bacteremia.^{[1, 2]}

Organism-specific therapeutic regimens are provided below, including those for Staphylococcus aureus, Streptococcus pneumoniae and pyogenes, Zygomycetes, and Aspergillus.

Methicillin-sensitive Staphylococcus aureus (MSSA)

• Nafcillin 2 g IV q4h or
• Oxacillin 2 g IV q4h or
• Ampicillin-sulbactam 1.5-3 g IV q6h or
• Cefuroxime 1.5 g IV q8h or
• Ceftriaxone 1 g/day IV or
• Clindamycin 600 mg IV q8h

Methicillin-resistant S aureus (MRSA)

• Vancomycin 1 g (15 mg/kg) IV q12h or
• Daptomycin 6 mg/kg IV q24h^{[3, 4]}

Streptococcus pneumoniae

• Amoxicillin-clavulanate 875 mg/125 mg (20-40 mg/kg) PO q12h or
• Cefpodoxime 200 mg (5 mg/kg) PO q12h or
• Cefdinir 600 mg/day (14 mg/kg/day) PO

Streptococcus pyogenes

• Ampicillin-sulbactam 1.5-3 g IV q6h or
• Ceftriaxone 1 g/day IV or
• Clindamycin 600 mg IV q8h

Zygomycetes or Aspergillus

• Voriconazole 6 mg/kg IV q12h for 2 doses, then 4 mg/kg IV q12h or
• Voriconazole 200-300 mg PO q12h or
• Amphotericin B deoxycholate 1 mg/kg IV q24h or
• Liposomal amphotericin 3-5 mg/kg q24h

Special considerations

• Patients with orbital cellulitis frequently complain of fever, malaise, and a history of recent sinusitis or upper respiratory tract infection
• Consider surgical drainage if the response to appropriate antibiotic therapy is poor within 48-72h or if computed tomography (CT) shows the sinuses to be completely opacified
• If the presence of a drainable fluid collection is evident on CT scan, surgical drainage should be considered in patients > 16y
• Consider orbital surgery, with or without sinusotomy, in every case of subperiosteal or intraorbital abscess formation, leaving the drains in place for several days
• In cases of fungal infection, surgical debridement of the orbit is indicated and may necessitate 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

 

Specific Organisms and Therapeutic Regimens

Organism-specific therapeutic regimens for periorbital cellulitis are provided below, including those for Haemophilus influenzae, methicillin-susceptible Staphylococcus aureus (MSSA), and methicillin-resistant S aureus (MRSA).^[1]

Haemophilus influenzae

• Amoxicillin-clavulanate 875 mg/125mg PO q12h for 10-14d or
• Cefpodoxime 200 mg PO q12h for 10-14d or
• Cefdinir 600 mg PO daily for 10-14d

Staphylococcus aureus, methicillin susceptible (MSSA)

• Ampicillin-sulbactam 1.5-3 g IV q6h for 10-14d or
• Cefuroxime 1.5 g IV q8h for 10-14d or
• Ceftriaxone 1 g IV daily for 10-14d or
• Clindamycin 600 mg IV q8h for 10-14d

Staphylococcus aureus, methicillin resistant (MRSA)

• Vancomycin 1 g (15 mg/kg) q12h for 10-14d or
• Daptomycin 4-6 mg/kg IV q24h^[2]

Special considerations

• Preseptal cellulitis is a common infection of the eyelid and periorbital soft tissues characterized by acute eyelid erythema and edema
• This bacterial infection usually results from the local spread of an adjacent upper respiratory tract infection or an external ocular infection or following trauma to the eyelids
• Clinical improvement should be seen within 24-48h
• If the patient worsens, then consider an underlying orbital process or resistant organisms
• Surgical drainage is indicated only for abscesses and usually is not needed for uncomplicated preseptal cellulitis

 

Preseptal and Orbital Cellulitis

Complications include vision loss (3 to 11%) due to ischemic retinopathy and optic neuropathy caused by increased intraorbital pressure; restricted ocular movements (ophthalmoplegia) caused by soft-tissue inflammation; and intracranial sequelae from central spread of infection, including cavernous sinus thrombosis, meningitis, and cerebral abscess.

Symptoms and Signs

Symptoms and signs of preseptal cellulitis include tenderness, swelling, warmth, redness or discoloration (violaceous in the case of H. influenzae) of the eyelid, and sometimes fever. Patients may be unable to open their eyes because of eyelid swelling. The swelling and discomfort can make it difficult to examine the eye, but when accomplished, examination shows that visual acuity is not affected, ocular movement is intact, and the globe is not pushed forward (proptosis).

 

Symptoms and signs of orbital cellulitis include swelling and redness of the eyelid and surrounding soft tissues, conjunctival hyperemia and chemosis, decreased ocular motility, pain with eye movements, decreased visual acuity, and proptosis caused by orbital swelling. Signs of the primary infection are also often present (eg, nasal discharge and bleeding with sinusitis, periodontal pain and swelling with abscess). Fever is usually present. Headache and lethargy should raise suspicion of associated meningitis. Some or all of these findings may be absent early in the course of the infection.

Preseptal Cellulitis

Orbital Cellulitis

Subperiosteal abscesses, if large enough, can contribute to symptoms of orbital cellulitis such as swelling and redness of the eyelid, decreased ocular motility, proptosis, and decreased visual acuity.

Diagnosis

• Mainly clinical evaluation
• CT or MRI if orbital cellulitis is possible

Diagnosis is suspected clinically. Other disorders to consider include trauma, insect or animal bites without cellulitis, retained foreign bodies, allergic reactions, tumors, and inflammatory orbital pseudotumor.

Eyelid swelling may require the use of lid retractors for evaluation of the globe, and initial signs of complicated infection may be subtle. An ophthalmologist should be consulted when orbital cellulitis is suspected.

Preseptal cellulitis and orbital cellulitis are often distinguishable clinically. Preseptal cellulitis is likely if eye findings are normal except for eyelid swelling. The presence of a local nidus of infection on the skin makes preseptal cellulitis even more likely.

If findings are equivocal, if the examination is difficult (as in young children), or if nasal discharge is present (suggesting sinusitis), CT or MRI should be done to exclude orbital cellulitis, tumor, and pseudotumor. MRI is better than CT if cavernous sinus thrombosis is being considered.

The direction of proptosis may be a clue to the site of infection; eg, extension from the frontal sinus pushes the globe down and out, and extension from the ethmoid sinus pushes the globe laterally and out.

Blood cultures are often done (ideally before beginning antibiotics) in patients with orbital cellulitis but are positive in less than one third. Lumbar puncture is done if meningitis is suspected. Cultures of the paranasal sinus fluid are done if sinusitis is the suspected source. Other laboratory tests are not particularly helpful.

Treatment

• Antibiotics

Preseptal cellulitis:

Initial therapy should be directed against sinusitis pathogens (S. pneumoniae, nontypeable H. influenzae, S. aureus, Moraxella catarrhalis); however, in areas where methicillin-resistant S. aureus is prevalent, clinicians should add appropriate antibiotics (eg, clindamycin

, trimethoprim/sulfamethoxazole

, or doxycycline

for oral treatment and vancomycin

for inpatient treatment). In patients with dirty wounds, gram-negative infection must be considered.

 

Outpatient treatment is an option if orbital cellulitis has been definitively excluded; children should have no signs of systemic infection and should be in the care of responsible parents or guardians. Patients should be closely followed by an ophthalmologist. Outpatient treatment options include amoxicillin/clavulanate

30 mg/kg po q 8 h (for children < 12 yr) or 500 mg po tid or 875 mg po bid (for adults) for 10 days.

For inpatients, ampicillin/sulbactam

50 mg/kg IV q 6 h (for children) or 1.5 to 3 g (for adults) IV q 6 h (maximum 8 g ampicillin

/day) for 7 days is an option.

Orbital cellulitis:

Patients with orbital cellulitis should be hospitalized and treated with meningitis-dose antibiotics. A 2nd- or 3rd-generation cephalosporin, such as cefotaxime

50 mg/kg IV q 6 h (for children < 12 yr) or 1 to 2 g IV q 6 h (for adults) for 14 days, is an option when sinusitis is present; imipenem, ceftriaxone , and piperacillin/tazobactam are other options. If cellulitis is related to trauma or foreign body, treatment should cover gram-positive (vancomycin

1 g IV q 12 h) and gram-negative (eg, ertapenem

100 mg IV once/day) pathogens and be taken for 7 to 10 days or until clinical improvement.

 

Surgery to decompress the orbit, drain an abscess, open infected sinuses, or a combination is indicated in any of the following circumstances:

• Vision is compromised.
• Suppuration or foreign body is suspected.
• Imaging shows orbital or large subperiosteal abscess.
• The infection does not resolve with antibiotics.

Key Points

• Preseptal and orbital cellulitis are differentiated by whether infection is anterior or posterior to the orbital septum.
• Orbital cellulitis is usually caused by contiguous spread of ethmoid or frontal sinusitis, whereas preseptal cellulitis is commonly caused by contiguous spread from local facial or eyelid injuries, insect or animal bites, conjunctivitis, and chalazion.
• Both disorders can cause tenderness, swelling, warmth, redness or discoloration of the eyelid, and fever.
• Orbital cellulitis is likely if there is decreased ocular motility, pain with eye movements, proptosis, or decreased visual acuity.
• Antibiotic therapy is indicated, with surgery reserved for complicated orbital cellulitis (eg, abscess, foreign body, impaired vision, antibiotic failure).

COMPLICATIONS OF ODONTOGENIC INFECTIONS

FASCIAL SPACE INFECTIONS

Spread of infection to the fascial spaces may result in dramatic facial swelling and high fever and, if untreated, respiratory embarrassment. The characteristics of the more common fascial space infections related to odontogenic infection are described here.

Infraorbital space infections generally are related to maxillary anterior teeth and are well localized to the infraorbital fossa by the levator labii superioris and levator anguli oris muscles. Facial swelling lateral to the nose is prominent, as is decreased mobility of the upper lip caused by inflammation of these muscles. If the area is fluctuant, intraoral incision and drainage with placement of a small Penrose drain for 1 to 2 days generally are sufficient treatment. Antibiotics are indicated for all infections of the fascial spaces.