**13. Intracranial extension of orbital abscess**

permanent vision loss one of which progressed to no light perception vision. Loss of vision with orbital inflammation may result from optic neuritis as a reaction to adjacent or nearby in‐ fection, ischemia due to thrombophlebitis along valveless orbital veins, or compressive/pres‐ sure ischemia possibly resulting in central artery/occlusion, (Figure 12). [22], [26] Permanent irreversible visual loss may occur in cases with orbital and subperiosteal abscess despite early intervention. In a survey of 46 cases with confirmed diagnosis of orbital and subperiosteal ab‐ scess in which visual results were reported, permanent loss of vision occurred in 15% of the cases. [48] Blindness was attributed to the central retinal artery occlusion in 4, optic atrophy in 2 of hese patients. Permanent visual loss in orbital cellulitis probably has a vascular cause, whereas partial vision loss that respond to antibiotic therapy and drainage procedures may be due to inflammatory infiltrates or presence of compressive optic neuropathy. [21] It is be‐ lieved that the confinement of the optic nerve in the orbital apex area and within its bony ca‐ nal along with its proximity to the posterior ethmoid and sphenoid sinuses may further highlight the importance of the these factors in the exacerbation of posterior orbital celluliltis. Physcians need to be aware that patients with sinusitis and associated orbital cellulitis may be at risk for developing severe vision deficit requiring timely intervention. In a review of 148 pa‐ tients with orbital abscess from 13 series reported by Hornblass [15], 3 patients had evidence of

Clinical examination by itself may not exactly delineate the nature of orbital inflammatory processes, clinicians may have to rely on imaging studies to select potential surgical candi‐ dates. Despite availability of modern CT-Scan and MRI studies, the physician stil needs to re‐ ly on the clinical progression of the inflammation based on vision, pupillary fuction, and assessment of ocular motility. Patt and Manning [26], reported 4 patients with vision loss due to orbital cellulitis and in each of these cases had CT-scan readings of "no definite abscess" contributing to the delay in diagnosis of orbital abscess, with a resultant delay in surgical

Ethmoidal sinuses are separated from the orbital cavity by the lamina papyracea and anterior and posterior ethmoidal foramina serve as additional connections that may allow infection to gain access from ethmoidal air cells to the orbital cavity, (Figure 5). Periorbita in this area is loosely attached to bone and may be elevated by a purulent collection, resulting in subperios‐ teal abscess. Acute visual loss due to sinusitis may either be secondary to complications of or‐ bital cellulitis or may be seen as a part of orbital apex syndrome. orbital cellulitis or as a part of the orbital apex syndrome. [27] Two cases of acute visual loss have been reported by El-Sayed and Muhaimeid [49], as a complication of orbital cellulitis due to sinusitis. One of these pa‐ tients had dramatic improvement in vision from hand motion to normal vision after systemic antibiotic treatment of pansinusitis and associated orbital cellulitis. The second patient, (a 10 year old girl), achieved normal visual acuity from no light perception after only surgical inter‐ vention by exploration of sphenoid and ethmoid sinuses along-with intravenous antibiotic administration. Three cases of sphenoethmoiditis with minimal signs of orbital inflammation causing permanent loss of vision have been reported by Slavin and Glaser. [48] These authors suggested the use of term "posterior orbital cellulitis" for such cases and defined it as a clini‐ cal syndrome in which early severe visual loss overshadows or precedes accompanying in‐ flammatory orbital signs. Acute blindness may also result from orbital infarction syndrome.

no light perception vision.

138 Common Eye Infections

drainage.

In the pre-antibiotic era, Birch-Hirschfeld reported that 19% of 275 cases of orbital cellultis reported in the studies from 1907-1930 died mostly due to the intracranial complications of orbital cellulitis. [2] More recently, Hartstein et al, [51], reported case-studies of 3 patients who were found to have pansinusitis which progressed to subperiosteal abscess of the orbit and subsequent intracranial extension. All 3 patients had been treated with systemic antibiotics and surgical drainage of the orbital abscesses as well as sinuses. Two of the 3 patients required surgical drainage of their intracranial abscesses.

In our series of 218 patients with orbital cellulitis, there were 9 cases of intracranial extension of orbital abscesses that required either extended treatment with systemic antibiotics alone or in combination with neurosurgical intervention. [8] Nineteen cases of intracranial abscesses due to mid-face infection had been reported by Maniglia et al, [7] anaerobic organisms were the most common cause of their abscesses. Most of these intracranial complications were due to the nasal, sinus and orbital disease while cavernous sinus thrombosis occurred in only one of these patients. Intracranial abscesses were mostly located in frontal lobe, epidural or subdural. Handler et al [52], recommend surgical drainage for those with deterioration of ocular motility and vision. Ethmoidal sinusitis was overwhelming predisposing cause in their study of orbital cellulitis and intracranial spread occurred in 6 of their 65 patients with orbital cellulitis. Sinus infections appear to be more common cause of intracranial abscess, the most common being frontal sinus, followed by ethmoid and maxillary sinuses. While the superior ophthalmic vein drains into the cavernous sinus, the inferior ophthalmic vein may drain either into the cavernous sinus through the superior orbital fissure or into the pterigoid plexus through the inferior orbital fissure (Figure 13). [15]

In the past, intracranial abscess formation had a poor prognosis with a significant mortali‐ ty rate. The valveless veins interconnect the orbit with sinuses, eyelids and the cavernous sinus, (Figure 13). Since intracranial abscess may be a life-threatening complication of orbi‐ tal processes, it may require aggressive intervention by multidisciplinary team. Undesira‐ ble complications of intracranial abscess may result from cavernous sinus thrombosis as well as intracranial rupture of the abscess. Patient with intracranial abscess may be asymp‐ tomatic or present with nausea, vomiting, seizures and change of their mental status. [27] Among other signs, neurological signs of intracranial abscess may include fever or altered mental status. The classic neurological presentation of intracranial abscess seen in adults may be typical, while in children these symptoms may be minimal or even absent, (Figure 14). [27] Cavernous sinus thrombosis may represent the most severe form of orbital celluli‐ tis. The condition may be suspected clinically by the presence of bilateral orbital process along with ophthalmoplegia and loss of vision. [53], [54] Repeat imaging studies may be necessary when there is evidence of neurologic deficit, to rule out presence of epidural or subdural empyema, brain abscess, or cavernous sinus thrombosis. [55]- [57] In such cases, successful management of orbital and/or intracranial abscesses may require timely recogni‐ tion of the infectious process, administration of systemic antibiotics, serial head and orbital imaging studies, early surgical management of orbit disease and often the intracranial process, (Figure 14). Computed tomography scan of the orbit and sinuses with fine cuts is the recommended imaging study of choice. [8], [51], [57] Magnetic resonance imaging studies with fat suppression has been found to be useful for visualizing the intracranial ab‐ scesses in suspected cases. The cause of most of the intracranial infectious complications of sinusitis are polymicrobial organisms, with anaerobes being the most common pathogens. [38], [51]- [54] Although no specific species or combination of bacterial microorganisms is found to be predominant; Streptococcus, Staphylococcus, Bacteriodes, and Fusobacterium species are frequently encountered. Hartstein et al. reported 3 cases of intracranial abscess all of which had evidence of polymicrobial infection with no predominance of any one particular organism. [51] Initial treatment of such patients requires broad-spectrum antibi‐ otics including beta-lactamase resistant antibiotics that have good anaerobic coverage, as well as good central nervous system penetration. [20], [23], [27], [51] Routine follow-up imaging studies may be indicated based on the clinical examination. Proper management of these patients may require a multidisciplinary team that includes an orbital surgeon, otolaryngologists, neurosurgeon, and an infectious disease specialist.

subsequent intracranial extension. All 3 patients had been treated with systemic antibiotics and surgical drainage of the orbital abscesses as well as sinuses. Two of the 3 patients required

In our series of 218 patients with orbital cellulitis, there were 9 cases of intracranial extension of orbital abscesses that required either extended treatment with systemic antibiotics alone or in combination with neurosurgical intervention. [8] Nineteen cases of intracranial abscesses due to mid-face infection had been reported by Maniglia et al, [7] anaerobic organisms were the most common cause of their abscesses. Most of these intracranial complications were due to the nasal, sinus and orbital disease while cavernous sinus thrombosis occurred in only one of these patients. Intracranial abscesses were mostly located in frontal lobe, epidural or subdural. Handler et al [52], recommend surgical drainage for those with deterioration of ocular motility and vision. Ethmoidal sinusitis was overwhelming predisposing cause in their study of orbital cellulitis and intracranial spread occurred in 6 of their 65 patients with orbital cellulitis. Sinus infections appear to be more common cause of intracranial abscess, the most common being frontal sinus, followed by ethmoid and maxillary sinuses. While the superior ophthalmic vein drains into the cavernous sinus, the inferior ophthalmic vein may drain either into the cavernous sinus through the superior orbital fissure or into the pterigoid plexus

In the past, intracranial abscess formation had a poor prognosis with a significant mortali‐ ty rate. The valveless veins interconnect the orbit with sinuses, eyelids and the cavernous sinus, (Figure 13). Since intracranial abscess may be a life-threatening complication of orbi‐ tal processes, it may require aggressive intervention by multidisciplinary team. Undesira‐ ble complications of intracranial abscess may result from cavernous sinus thrombosis as well as intracranial rupture of the abscess. Patient with intracranial abscess may be asymp‐ tomatic or present with nausea, vomiting, seizures and change of their mental status. [27] Among other signs, neurological signs of intracranial abscess may include fever or altered mental status. The classic neurological presentation of intracranial abscess seen in adults may be typical, while in children these symptoms may be minimal or even absent, (Figure 14). [27] Cavernous sinus thrombosis may represent the most severe form of orbital celluli‐ tis. The condition may be suspected clinically by the presence of bilateral orbital process along with ophthalmoplegia and loss of vision. [53], [54] Repeat imaging studies may be necessary when there is evidence of neurologic deficit, to rule out presence of epidural or subdural empyema, brain abscess, or cavernous sinus thrombosis. [55]- [57] In such cases, successful management of orbital and/or intracranial abscesses may require timely recogni‐ tion of the infectious process, administration of systemic antibiotics, serial head and orbital imaging studies, early surgical management of orbit disease and often the intracranial process, (Figure 14). Computed tomography scan of the orbit and sinuses with fine cuts is the recommended imaging study of choice. [8], [51], [57] Magnetic resonance imaging studies with fat suppression has been found to be useful for visualizing the intracranial ab‐ scesses in suspected cases. The cause of most of the intracranial infectious complications of sinusitis are polymicrobial organisms, with anaerobes being the most common pathogens. [38], [51]- [54] Although no specific species or combination of bacterial microorganisms is

surgical drainage of their intracranial abscesses.

140 Common Eye Infections

through the inferior orbital fissure (Figure 13). [15]

**Figure 13.** Lateral view of the schematic drawing showing extensive venous drainage of the facial structures along with orbital veins and their direct connections with cavernous sinus.

**Figure 14.** External photograph and MRI (axial view) of the orbits and brain of an infant with bilateral orbital cellulitis/ abscesses and its extension to the brain requiring broad-spectrum systemic antibiotics along with drainage of right orbital abscess.
