Complications of Sinusitis ( Orbital and Intracranial )

Sinusitis can lead to local and systemic complications. Anatomically, most local complications are linked directly to the paranasal sinuses and other structures of the head, neck, and chest. The structures involved most often are those of the orbit, cranium, chest, and nose. Sinusitis can lead to the development of local complications, such as orbital cellulitis, subperiosteal abscess, and orbital abscess, intracranial disorders (brain abscess [BA], subdural empyema [SE] and meningitis, facial osteomyelitis, and thrombosis of the cavernous sinus and cortical vein (1,2). The precise rates of these complications are not known, but they occur in about 5% of patients hospitalized for sinusitis.

This page describes the microbiology, and antimicrobial management of orbital and intracranial complications of sinusitis. It is imperative to consider also the use of surgical treatment in these conditions. However, this review is not describing these issues.

Orbital complications 
The orbit is susceptible to contiguous spread of infection from the sinuses as it is surrounded by sinuses on three sides. This is more accentuated in children, because of their thinner bony septa and sinus wall, greater porosity of bones, open suture lines, and larger vascular foramina. Differential diagnosis of orbital involvement should include bacteremia (caused by Haemophilus influenzae or Streptococcus pneumoniae), facial infections, trauma, iatrogenic causes, tumors, and dacryocystitis. However, sinusitis is responsible for a least 75% of cases (3), and orbital complication may be the first and only presenting sign of sinusitis (1).
The orbit is separated from the ethmoid cells and maxillary sinus by thin bony plates (called the lamina papyracea) only, which have naturally congenital bony dehiscences. Infections can spread directly by penetration of the thin bones or through the small bony dehiscence.

Orbital anatomy 

 Infection can also extend directly by traversing through the anterior and posterior ethmoid foraminas. Since the ophthalmic venous system has no valves, the extensive venous and lymphatic communication between the sinuses and the surrounding structures allows flow in either direction, which enables retrograde thrombophlebitis and spread of the infection. 

Intra-cranial spread of infection from the periorbital area through retrograde thrombophlebitis.

Orbital complications have been categorized by Chandler et al. (4) into five separate stages according to severity.

Table: Orbital complications of sinusitis (4).

Class 1: Inflamatory edema and preseptal cellulites.
Class 2: Orbital cellulitis.
Class 3: Subperiostal abscess.
Class 4: Orbital abscess.
Class 5: Cavernous sinus thrombosis.

 Establishing the severity of the infection helps to make the appropriate decision with regard to medical and surgical therapy. The first class is an inflammatory eyelid edema or preseptal cellulitis, which results from venous obstruction caused by infection-induced inflammatory pressure on the ethmoid vessels. The patients present generally with signs and symptoms of sinusitis associated with edema and erythema of the eyelids, which can progress causing the eye to become swollen shut. However, no associated proptosis, visual impairment, or limitation of extraocular muscle mobility occurs. Barriers that limit the progression and spread of the infection to the orbit are the orbital septum and the tarsal plate.

Orbital cellulitis

The second class of orbital complications is orbital cellulitis, which represents an inflammation and cellulitis of the orbital contents with varying degrees of proptosis, chemosis, limitation of extraocular movement, and/or visual loss that depend on the severity of the process. Orbital involvement causes diffuse edema and bacterial infiltration of the adipose tissue, but no abscess.

The third class is subperiosteal abscess, which is often a progression of orbital cellulitis, and forms beneath the periosteum of the ethmoid, frontal, and maxillary bone. The abscess can cause limited or extended lateral (if it originated from the ethmoids) and downward (if it originated from the frontal sinus) displacements of the globe. As long as the infection is confined to the subperiosteal plane, no impairment of vision, ophthalmoplegia, or conjunctival signs occur. Vision is generally normal in the early stages, but can become impaired.

Subperiostal abscess

                  Axial enhanced CT- left medial orbital subperiosteal abscess secondary to left ethmoid sinusitis

The fourth class is orbital abscess, which represents pus accumulation in the orbital soft tissues behind the globe. The abscess develops because of an extended infection into the orbital fat and is associated with inflammatory edema, purulence, and fat necrosis. Severe chemosis, ptosis and complete ophthalmoplegia (cranial nerves II, III, IV, V, and VI are involved) and moderate-to-severe visual loss are present. The visual impairment is attributed to an increase in orbital pressure that causes retinal artery occlusion or optic neuritis. If prompt surgical and medical therapy is not provided, permanent blindness can result40. Generally, a displacement of the globe forward, or downward and outward, occurs.

Orbital abscess

Supper-perosteal  orbital abscess

CT of Orbital cellulitis with subperiosteal abscess

The fifth class is cavernous sinus thrombosis (CST), which is retro-orbital and occurs as an extension of the orbital infection. 

Location of the cavernous sinus 

This mode of spread is possible because of the absence of valves in the orbital veins that communicate with the cavernous sinus. This is a life-threatening complication that is diagnosed by ptosis, orbital pain, severe loss of visual acuity, prostration, hypoesthesia, dysesthesia, and paresthesia along cranial nerves VI or VII, rapid progression chemosis and limitation of extraocular muscle motility, severe retinal venous engorgement, spread of orbital cellulitis and visual loss to the contralateral eye, and clinical deterioration with the development of meningitis, toxicity, and sepsis. Temperature is high with septic emboli, which cause fever spikes. The rate of blindness and death is up to 20% (5-7).

Enhancement of the right cavernous sinus following gadolinium injection

The most common pathogens in cellulitis and abscesses are those seen in acute and chronic sinusitis, depending on the length and etiology of the primary sinusitis. These include Streptococcus pneumoniae, Haemophilus influenzae, S. aureus, anaerobic bacteria (Prevotella, Porphyromonas, Fusobacterium and Peptostreptococcus spp.) (1, 8).

We evaluated aspirates of 18 acutely infected maxillary sinuses that were associated with odontogenic infection in children who presented with periorbital cellulitis (9).  A total of 54 isolates were recovered (3.0/ The predominant aerobic and facultatives were a-hemolytic streptococci (4 isolates), microaerophilic streptococci (3), and Streptococcus pyogenes  and Staphylococcus aureus (2 each).  The predominant anaerobic bacteria were anaerobic Gram-negative bacilli ( 17), Peptostreptococcus  spp.), Fusobacterium spp. (8),  and Propionibacterium acnes (2).  

The organisms isolated in CST are S. aureus (50-70% of instances), Streptococcus spp. (20%) and Gram-negative anaerobic bacilli (pigmented Prevotella and Porphyromonas spp., and Fusobacterium spp.) (10,11). Similar organisms can be recovered from orbital abscesses and their corresponding maxillary sinusitis (12).

Medical treatment should be vigorous and aggressive from the early stages of periorbital cellulitis. If this is not done, the infection can progress to orbital cellulitis and abscess. The outcome of medical management depends to a large extent on the duration and stage of the orbital involvement. If orbital cellulitis or abscess is suspected, an ophthalmologist should be consulted. If rapidly advancing infection is suspected, time is crucial and imaging studies and therapeutic measures should be instituted without delay.

Patients with mild inflammatory eyelid edema or preseptal cellulitis (class 1) can be treated with oral antibiotics and decongestants, especially if they have not been treated with antimicrobial agents before. The most effective available oral ones are cefuroxime axetil amoxicillin-clavulanate. However, close supervision and follow-up is mandatory, and the initiation of parenteral antimicrobial agents in the hospital should be undertaken if postseptal involvement (classes 2 to 5) is suspected or has developed.
The parenteral agents include ceftriaxone or cefotaxime plus coverage for anaerobic bacteria (addition of metronidazole or clindamycin ). Drugs that have good brain-blood barrier penetration are preferred.

Antimicrobial agents that generally provide coverage for methicillin-sensitive S. aureus as well as aerobic and anaerobic bacteria include cefoxitin, carbapenems, and the combination of a penicillin (e.g. ticarcillin) and a beta-lactamase inhibitor (e.g. clavulanic acid). Metronidazole is administered in combination with an agent effective against aerobic or facultative streptococci and S. aureus. A glycopeptide (e.g. vancomycin) should be administered in cases where methicillin-resistant S. aureus (MRSA) is present or suspected.

Treatment of CST, includes high doses of parenteral wide-spectrum antimicrobial agents. The use of anticoagulants and corticosteroids is controversial (13). Anticoagulants are used to prevent further thrombosis, and the fibrinolytic activity of urokinase helps dissolve the clot.
Early diagnosis and vigorous treatment can yield a survival rate of 70-75%. However, permanent sequelae such as blindness and other cranial nerve palsies are common in survivors (14).

Intracranial complication

Intracranial extensions of sinusitis are infrequent in the antibiotic era, and occur in about 4% of patients hospitalized with acute or chronic sinusitis (15). However, they are the second most common complication of acute sinusitis. Even though the exact incidence of suppurative intracranial complications in sinusitis is unknown, paranasal sinusitis and dental infections are the origin of a third to two thirds of SE and BA (1,16).

• Epidural empyema
• Subdural empyema
• Sagittal sinus and cortical vein thrombosis
• Meningitis
• Facial osteomyelitis
• Mucocele

Epidural empyema

Subdural empyema

MRV of superior sagittal sinus thrombosis with some visible collateral veins

CT of brain abscess


Intracranial complications are potentially life threatening and include meningitis, epidural empyema and abscess, venous sinus thrombosis (cavernous and sagittal), and intraparenchymal BA. Usually, BAs are single, but they are multiple in 13% of cases. These complications, even though rare, should always be watched for in patients with sinusitis.

Intracranial extension can occur directly or by retrograde thrombophlebitis. Direct extension can progress through necrotic areas of osteomyelitis in the posterior wall of the frontal sinus. Bacteria penetrate the dura along the course of transversing small vessels, dural thickening with inflammatory exudates and granulation tissue forms, and SE develops, which generates an arachnoidal inflammatory reaction. Direct extension is more commonly seen in chronic media otitis than in sinusitis (17).

The other route of extension is through the valveless venous system that interconnects the intracranial venous system with the sinus mucosal vasculature (18). Thrombophlebitis that originates in the sinus mucosal veins can progress through this network to the emissary skull veins, dural venous sinuses, subdural veins, and cerebral veins. It is common in acute sinusitis and in acute exacerbations of chronic sinusitis. Intraparenchymal BA is seeded by the hematogenous route and therefore can be found in all regions of the brain, but predominantly the frontal lobes.

In infants the infection can spread through the immature arachnoid and cause meningitis, which occurred in 75% of cases in one series of SE. In adults, however, the arachnoid forms a better barrier and bacterial meningitis rarely complicates SE (19).
Extensive cortical thrombophlebitis is also a common complication (19). The hyperemia, edema, and small foci of infarction are common in the involved gyri (20). Septic thrombosis of a dural sinus can also occur and induces bilateral cerebral edema and hemorrhagic infarction (19,20), which generate local neurological deficits, seizures, and increased intracrancial pressure.

The exact mechanism of brain infection is unclear. It may be secondary to an initial focus of ischemia or necrosis caused by cortical venous obstruction that enables the growth of microaerophilic and anaerobic bacteria (21). The infection may thereafter progress deeper through the cerebral vessels into the white matter - causing cerebritis - which gradually liquefies as the perimeter is surrounded by a capsule made of an inner granulation tissue layer, middle layer of collagen, and an outermost glial cell shell. The process of abscess maturation takes 2-3 weeks. Abscesses in the deeper white matter are less vascular than those in the cortex, their walls are thinnest when they are near the ventricle, and they often rupture into the ventricular system.

                                      Sites of intracranial abscesses complicating sinusitis

Accumulation of SE occurs at four distinct sites (17-20). The pus can form over the frontal parietal convexity, and can be located focally anywhere, but mostly over the frontal pole and occipital complex, or under the posterior fossa tentorium.

The organisms recovered from BA as a complication of sinusitis are anaerobic, aerobic, and microaerophilic bacteria. Anaerobes can be isolated in over two thirds of the patients, and include pigmented Prevotella and Porphyromonas spp., Fusobacterium spp. and Peptostreptococcus spp. (16) Microaerophilic streptococci are also very common, and can be isolated from abscesses caused by maxillary sinusitis that originates from dental infection of the upper jaw (18). The most common aerobe is S. aureus, and H. influenzae is rarely isolated.

Cerebrospinal fluid in meningitis caused by  Streptococcus pneumoniae 

We studied the microbiology of pus from 10 infected sinuses and their corresponding intracranial abscess (IA) (22).BA and SE was present in 5 patients, and both BA and SE were present in one. Four of the patients were children and all had SE. Five had Polymicrobial flora was found in 9 sinuses and 8 IA.  A total of 26 isolates (2.6 isolates per specimen, 19 anaerobic, 7 aerobic or facultative and 1 microaerophilic) were recovered from the sinuses, and 17 isolates (1.7 isolates per site, 13 anaerobic, 2 aerobic or facultative and 2 microaerophilic) were found in the IA.  Concordance in the microbiological findings between the sinus and the IA was found in all instances The predominant anaerobes were Fusobacterium spp.  Prevotella spp., Peptostreptococcus spp. , S. aureus , H. influenzae type-b, micoaerophilic streptococci , Bacteroides ureolyticus , and S. pneumoniae . These data illustrate the concordance in the recovery of organisms from infected sinuses and their associated IA and confirm the importance of anaerobic bacteria in sinusitis and IA.

We described two children with periapical abscess in the upper incisors, ethmoid and maxillary sinusitis, and intracranial abscess (23).SE occurred in both, and one of the children had also cerebritis and brain abscess. Anaerobic bacteria were isolated from the infected subdural empyemas. Peptostreptococcus intermedius and microaerophilic streptococci were recovered in one patient and Fusobacterium spp. in the other.

Brook evaluated aspirates of pus from 8 infected sinuses associated with odontogenic infections and their corresponding IA (24.) Concordance in the microbiological findings between the sinus and the IA was found in all instances, and  polymicrobial flora was found in all 8 sinuses and 7 IA, and the number of isolates varied from one to 5.  A total of 27 isolates (3.4 isolates/site, 23 strict anaerobic, 2 aerobic or facultative and 2 microaerophilic) were recovered from the sinuses, and 20 isolates (2.5 isolates/site, 16 strict anaerobic, 1 aerobic or facultative and 3 microaerophilic) were found in the IA.  The predominate anaerobic isolates were Fusobacterium spp. (13 isolates), Prevotella spp. (11),  Peptostreptococcus spp. (13), microaerophilic streptococci and ( 4), Veillonella parvula (3), beta-hemolytic streptococci Group F ( 2), and alpha-hemolytic streptococci (1). These data illustrate the concordance in the recovery of organisms from sinusitis of dental origin and their associated IA and confirm the importance of anaerobic bacteria in sinusitis and IA of dental origin.

In the early stages of cerebritis (before abscess encapsulation) antimicrobial agents can prevent the formation of an abscess (25). Once a BA has formed, surgical excision or drainage combined with a long course of antibiotics (4-8 weeks) remains the treatment of choice. Increased intracranial pressure may necessitate the use of mannitol, hyperventilation, or dexamethasone preoperatively.

To establish a microbiological diagnosis is important in planning the appropriate antimicrobial therapy. Needle aspiration guided by CT may provide this important information and enable adjustment of empirical antimicrobial therapy when necessary. Frequent scans are essential to monitor treatment response. Although surgical intervention remains an essential treatment, selected patients may respond to high-dose antibiotics alone that are given for an extended period of time (26).

Corticosteroid use is controversial. Steroids can retard the encapsulation process, increase necrosis, reduce antibiotic penetration into the abscess, and alter CT scans. Steroid therapy can also produce a rebound effect when discontinued. If used to reduce cerebral edema, therapy should be of short duration. The appropriate dosage, the proper timing, and any effect of steroid therapy on the course of the disease are unknown.

Initial empirical antimicrobial therapy is based on the expected etiological agents according to the likely primary infection source. Penicillin penetrates well into the abscess cavity and is active against non-beta-lactamase-producing anaerobes and aerobic organisms. (27) Chloramphenicol and metronidazole penetrate well into the intracranial space; also, chloramphenicol is active against Haemophilus spp. and most obligate anaerobes, whereas metronidazole is only active against strict anaerobic bacteria (27,28). Third-generation cephalosporins (i.e. cefotaxime and ceftriaxone) are generally adequate for aerobic Gram-negative organisms and also provide some coverage for Streptococcus spp. For coverage of Pseudomonas aeruginosa, ceftazidime or cefipime is given. Aminoglycosides do not penetrate well into the CNS. Beta-lactamase-resistant penicillins (i.e. methicillin) and glycopeptides (e.g. vancomycin) provide good coverage against S. aureus and Staphylococcus epidermidis (29).Vanccomycin is effective against MRSA.

The agents effective against anaerobes include metronidazole, chloramphenicol, a penicillin plus beta-lactamase inhibitor, and a carbapenem (e.g. meropenem). ( Penicillin should be added to metronidazole to cover aerobic and microaerophilic streptococci.
Although appropriate selection of antimicrobial therapy is of primary importance in the management of intracranial infections, surgical drainage may be required. Delay in surgical drainage and decompression can be associated with high morbidity and mortality (25). Surgical drainage may be necessary in many patients to ensure adequate therapy and complete resolution of infection. Surgical drainage of the concomitant sinus infection and any orbital collection of pus should also be performed concomitantly. Periodontal abscess or any other dental lesion should also be drained and/or corrected.


Certain indications warrant the referral of a patient with bacterial sinusitis to an otolaryngologist, who may perform nasal endoscopy as well as antral puncture for culture and therapeutic irrigation. Some of these referrals are of urgent nature, especially when complications are present or suspected, and the patient should be examined and treated after only minimal delay.

The indications for referral are:
Urgent referrals:
1. Complications (septic)
2. Deterioration of clinical condition despite medical therapy.
3. Frontal or sphenoid sinusitis.
4. Failure to improve after 2 courses of antimicrobial therapy.
5. Nosocomial infection.

Non urgent referral:
1. Treatment failure of chronic infection (without urgent complication).
2. Persistent nasal polyps with nasal obstruction.
3. History of recurrent episodes of sinusitis 9more than 3 per year).


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