Rhinogenic ophthalmologic complications: causes, symptoms, diagnosis, treatment

The occurrence of rhinogenic ophthalmologic complications is facilitated by the close anatomical connections of the nose and paranasal sinuses with the orbit and its contents. The commonality of their bone walls is not a significant obstacle to the penetration of infection from the paranasal sinuses into the orbit; even the deep-lying sphenoid sinus is often a source of spreading infection to the base of the skull and to the meninges through which the cranial nerves pass. The transition of infection from the maxillary sinus to the orbit is facilitated by the thinness of the upper and inner walls of the sinus. Penetration of infection from the ethmoid labyrinth into the orbit is facilitated by openings and fissures in the ethmoid bone, in the lower-anterior wall of the frontal, maxillary, anterolateral wall of the sphenoid sinus, through which vessels and nerves pass. Anatomical features of the structure of the paranasal sinuses are of great importance in the migration of infectious agents in the direction of the orbit. Thus, with a significant spread of the ethmoid labyrinth cells, their closer contact with the cranial cavity, orbit, lacrimal sac and optic nerves is created, which is also facilitated by the insignificant resistance to the inflammatory process of the paper plate of the ethmoid bone. With large sizes of the frontal sinus, it spreads to the entire surface of the orbital roof, borders on the small wings of the sphenoid bone, its sinus, the optic canal, forming its upper wall. Such a structure of the frontal sinus is a significant risk factor for both the occurrence of banal frontal sinusitis and its orbital and intracranial complications. The upper wall of the sphenoid sinus, depending on its thickness and pneumatization, can be in very close contact with the optic canals and optic chiasm, which often leads, even in sluggish chronic sphenoiditis, to the involvement of the arachnoid membrane surrounding the optic nerves and the nerves themselves in the toxic-infectious process, causing such forms of the disease as retrobulbar neuritis of the optic nerves and optic-chiasmatic arachnoiditis.

In the case of pyogenic orbital complications, the odontogenic factor should be taken into account, since it is possible for the infection to spread from the affected teeth into the orbit through the upper wall of the maxillary sinus, into which the infection enters from the sockets of the 1st and 2nd molars, where the bone separating the socket from the sinus is very thin and porous. It should also be borne in mind that between the alveoli of the canines and premolars there are bone canals leading to the inner angle of the orbit. Premolars and the 1st molar are especially dangerous for the eyes, less often canines and almost never incisors and 8th teeth.

The main routes of infection from the face and anterior paranasal sinuses are the extensive arterial and especially venous connections of these areas with the orbital organs. The orbital arterial system anastomoses widely with the vessels of the face, nose, paranasal sinuses, teeth, and brain. For example, the orbit and paranasal sinuses are supplied with blood by the ethmoidal, external maxillary arteries, and branches of the external carotid artery. These arterial vessels anastomose with each other through the posterior nasal artery. The arteries of the teeth, mainly branches of the external maxillary artery, are also connected with the orbital arteries.

A large number of venous plexuses of the nasal cavity, dental system, face and pharynx are connected with the venous systems of the orbit and cranial cavity, which determines the possibility of a combination of orbital and intracranial complications. In this regard, the connections of the ethmoid veins with the ophthalmic vein, and the latter with the veins of the dura mater and cavernous sinuses, are of great importance. Thus, one of the branches of the anterior ethmoid vein penetrates through the ethmoid plate into the cranial cavity to the venous plexus of the pia mater, thereby forming a ring connection between the venous system of the nasal cavity, skull and orbit. The venous system of the frontal sinus is connected with the veins of the dura mater by means of venous emissaries. And the veins of the maxillary sinus have anastomoses with the ophthalmic vein through the angular vein, which is a branch of the facial vein. The small venous network of the maxillary sinus is more developed on the upper and inner walls of this sinus and carries blood through the facial vein into the orbital or infraorbital veins.

Of no small importance in the spread of infection towards the orbit is the lymphatic vascular system, the orbital part of which begins with the cracks in the orbital tissue, connected to the lymphatic system of the nose through the vessels of the ethmoid labyrinth and the nasolacrimal canal. From the paranasal sinuses and the dental system, the lymphatic pathways lead to the lymphatic vessels of the face, submandibular and deep cervical lymph nodes.

The nasal cavity, paranasal sinuses and orbit have common sympathetic and parasympathetic and sensory innervation from the I and II branches of the trigeminal nerve through the superior cervical sympathetic, trigeminal, ciliary, pterygopalatine nodes, which determines the possibility of their combined reflex reactions. The close proximity of the posterior wall of the maxillary sinus to the sphenopalatine ganglion and its branches, to the pterygoid plexus, maxillary artery and its branches creates conditions for the transition of the inflammatory process from this sinus to the posterior cells of the ethmoid labyrinth, sphenoid sinus and through the veins of the pterygoid plexus to the veins of the orbit and cavernous sinus.

Thus, the spread of infection from the ENT organs and oral cavity to the orbit can occur through contact, hematogenous (thrombophlebitis of small veins) and lymphogenous routes.

Ophthalmic complications in acute sinusitis.

In acute sinusitis, compression or blockage of the nasolacrimal canal may occur, which manifests itself as a reflexive fear of air and lacrimation. In the case of odontogenic sinusitis, accompanied by periostitis of the alveolar process of the upper jaw, swelling of the cheek, eyelids and chemosis of the conjunctiva on the side of inflammation are also observed.

In acute frontal sinusitis, ophthalmic complications are more severe than in other sinusitis. The onset of the process is manifested by swelling of the skin of the forehead and eyelids in the upper-inner corner of the eye as a result of a violation of the collateral outflow of venous blood. Neuralgic pain appears in the area of the first branch of the trigeminal nerve: in the forehead and root of the nose, eye, increasing with pressure on the infraorbital foramen. There is also lacrimation, diplopia when looking up. Thrombophlebitis of the veins anastomosing with the venous plexus of the orbit can lead to its phlegmon.

Acute ethmoiditis manifests itself with symptoms similar to other sinusitis. The difference is that with acute ethmoiditis, the pressing pain is localized deep in the root of the nose, at the inner corner of the eye, the bridge of the nose, and in the area of the branching of the second branch of the trigeminal nerve. Patients experience intense lacrimation, swelling of both eyelids, and hyperemia of the conjunctiva. In cases of difficult outflow of pus into the nose, especially with closed empyemas of the posterior cells of the ethmoid labyrinth, which is more common in children with scarlet fever, orbital complications in the form of non-purulent or purulent ophthalmitis are possible.

Acute sphenoiditis is often combined with damage to the posterior cells of the ethmoid labyrinth. This combination is characterized by pain deep in the orbit, radiating throughout the skull. The pain increases sharply with pressure on the eyeball. The proximity of these sinuses to the optic canal, the connection between the venous plexuses of the sphenoid sinus and the sheaths of the optic nerves can cause rhinogenic retrobulbar neuritis. Due to the proximity of the sphenoid sinus to the oculomotor nerves, their isolated paralysis or superior orbital fissure syndrome are possible. The latter is characterized by a discrepancy between relatively poor clinical symptoms and a sharp decrease in visual acuity due to early involvement of the optic nerves in the inflammatory process. Rhinogenic choroiditis and chorioretinitis are also possible.

In chronic sinusitis, orbital complications are caused by the influence of nearby foci of infection or in connection with progressive changes leading to the development of meningocele and pyocele of one or another sinus. In exacerbations of chronic sinusitis, the same complications may arise as in acute processes.

Inflammation of the soft tissues of the eyelids can be simple (non-purulent) and purulent. Non-purulent inflammation of the eyelids belongs to the category of reactive processes that occur either as a result of the toxic action of catabolites - products of the inflammatory process, or as a result of a violation of the outflow of lymph and venous blood from some area of tissue or organ. In this case, edema and hyperemia of the skin of the eyelids occur, more than the upper one, spreading to the lateral surface of the nose. It is observed more often in young children who have developed catarrhal ethmoiditis or frontal sinusitis against the background of some childhood infection (scarlet fever, measles) or flu. With this complication, the eye usually does not suffer. The general condition of the patient is determined by the current general infection.

Purulent inflammation of the eyelids is characterized by the formation of an abscess or phlegmon in their tissue due to a breakthrough of pus from the ethmoid labyrinth or maxillary sinus. At the onset of the disease, eyelid edema occurs, then a dense limited infiltrate, which after some time transforms into a fluctuating abscess. The infiltrate can diffusely spread throughout the eyelid, transforming into phlegmon. The skin over the abscesses is hyperemic, cyanotic. As the infiltrate develops, patients complain of sharp pulsating pain in the eyeball, radiating to the temporal region and upper jaw. Ptosis develops. The process ends with a breakthrough of pus to the outside with the formation of a cutaneous fistula, sometimes communicating with the sinus cavity. Usually the process ends with scarring and deformation of the eyelid, its cicatricial fusion with the bony edge of the orbit, deformation of the palpebral fissure (lagophthalmos), leading to the development of keratitis.

Retrobulbar edema occurs mainly when the collateral outflow of venous blood is impaired in posterior sinusitis, especially purulent sinusitis. In this case, children have a fever, headache, vomiting, eyelid edema, conjunctival chemosis, exophthalmos, outward immobility of the eyeball due to paralysis of the fourth nerve, and diplopia. These symptoms are very similar to cavernous sinus thrombosis, but retrobulbar edema is distinguished from the latter by the child's generally satisfactory condition and the absence of changes in the fundus. In adults, general symptoms are weak or absent altogether, but temporary decreased visual acuity and partial strabismus are possible.

Purulent-inflammatory processes in the orbit. One of the most formidable orbital rhinogenic complications are purulent-inflammatory processes in the orbit. In descending order of frequency of occurrence of orbital complications, frontal sinusitis is in first place, then sinusitis and ethmoiditis, and in third place is spheioiditis.

The spread of the inflammatory process to the orbit, in addition to hematogenous, is possible by contact, especially when sinusitis acquires a closed character due to the blockade of their anastomoses with the nasal cavity. According to M.M. Zolotareva (1960), inflammation of the mucous membrane of the nose and paranasal sinuses leads to the same process first in the superficial and then in the deep layers of the bone. Osteo-periostitis is accompanied by thrombophlebitis of small venous trunks penetrating the orbit and flowing into the orbital veins. Orbital complications are distinguished by certain features depending on the type of complication that occurs. The resulting osteoperiostitis of the orbit can be simple and purulent.

Simple osteoperiostitis is local in nature and occurs mainly in acute empyemas of the frontal sinus or ethmoid labyrinth as a complication of some infectious disease (flu, scarlet fever, etc.). Symptoms such as swelling of the skin in the upper inner corner of the orbit and in the forehead area, injection of the conjunctival vessels and sechemosis occur. In the early period, transient paresis or paralysis of the corresponding muscles may cause limited eye mobility and diplopia. Decreased visual acuity is possible due to toxic edema of the retrobulbar tissue and optic neuritis. In simple periostitis of the sphenoid sinus and posterior cells of the ethmoid labyrinth, damage to the optic nerves occurs especially early and is more profound.

Purulent periostitis is characterized by an acute onset, increased body temperature, headache, and general weakness. With empyema of the posterior sinuses, eyelid edema, conjunctival hyperemia, and exophthalmos with displacement of the eyeball to the side opposite to the localization of the process and limited mobility toward the empyema develop. Diplopia, optic neuritis, and decreased visual acuity occur. With damage to the apex of the orbit, decreased visual acuity may be combined with central or paracentral scotoma. Visual impairment usually disappears with the elimination of the inflammatory process in the sinuses and orbit, but in particularly severe cases the process ends with secondary atrophy of the optic nerves and blindness. Severe exophthalmos may be complicated by keratitis. Purulent periostitis in the area of the frontal sinus with involvement of the upper wall of the orbit is manifested by swelling of the upper eyelid, hyperemia and chlamydia of the conjunctiva of the eye in the upper part of the eyeball, moderate exophthalmos, downward displacement of the eye and impaired upward mobility.

Due to the destruction of the bone wall of the sinus and the development of an intraorbital fistula, a subperiosteal abscess occurs in the orbit. The clinical manifestations of which are much more pronounced than in the orbital complications described above. Depending on the affected sinus, a fluctuating swelling appears in the eyelid area, with frontal sinusitis - in the upper inner corner of the eye, with ethmoiditis - slightly lower, under the inner commissure of the eyelids or in the projection of the lacrimal sac and below. Subperiosteal orbital abscess is usually accompanied by edema of the retrobulbar tissue (exophthalmos, limited mobility of the eyeball, its displacement to the side opposite to the localization of the abscess). In patients with empyema of the frontal sinus, a breakthrough of pus into the eyelid or into the upper inner corner of the orbit is possible. However, a breakthrough of the abscess towards the orbit is possible only with a deep location of the sinus. Subperiosteal abscess in posterior sinusitis manifests itself as pain in the retrobulbar region, which intensifies with pressure on the eyeball; more severe exophthalmos than in anterior sinusitis; impaired eye mobility and its displacement to the side opposite to the location of the abscess, as well as blindness or decreased visual acuity, central scotoma. Neurophthalmic corneal ulcer or panophthalmitis occurs much less frequently. With the specified localization of subperiosteal abscess, there is a risk of pus breaking through into the orbit, and then a retrobulbar abscess develops.

In empyemas of the maxillary sinus, subperiosteal abscesses of the orbit are much less common, but this complication most often occurs in children due to damage to the teeth or osteomyelitis of the maxillary sinus. When the abscess is localized in the anterior part of the maxillary sinus, symptoms characteristic of ossoperiostitis are more intense; in the case of a deeper process, exophthalmos, upward displacement of the eye and limitation of its mobility are noted (coriander), while involvement of the optic nerves in the inflammatory process is possible with a decrease in visual acuity, up to amaurosis.

Retrobulbar abscess occurs as a result of a breakthrough into the orbit of a deeply located subperiosteal abscess, which arose with purulent sinusitis or hematogenously from a distant focus of purulent infection (furuncle of the nose and upper lip, osteomyelitis of the lower jaw, phlegmon of the floor of the mouth, peritonsillar abscess, etc.). In this complication, a pronounced general reaction of the body is observed, resembling sepsis. Local symptoms include exophthalmos, displacement of the eyeball to the side opposite to the localization of the abscess, and limited mobility towards the focus. The resulting optic neuritis leads to a decrease in visual acuity. During an X-ray examination, in addition to sinusitis, shadowing of the orbit is determined, and in the case of the transition of the process from the sinus to the orbit by contact - a defect in the bone wall of the latter, sometimes detected by palpation.

Orbital phlegmon is an acute purulent inflammation with infiltration, necrosis and purulent melting of the orbital retina.

Pathological anatomy and pathogenesis. The process begins with thrombovasculitis of the orbital vessels and the formation of small abscesses around them, which then merge. The complication most often occurs with empyema of the maxillary sinus and frontal sinus, less often with lesions of other sinuses. Orbital phlegmon often occurs as a result of metastasis of purulent emboli from other foci of infection (pneumonia, sepsis, dental diseases, furuncle and carbuncle of the nose and face, purulent processes in the maxillofacial region). This form of intraorbital purulent complication is the most dangerous in terms of the occurrence of intracranial complications.

Clinical picture. The disease is accompanied by a general severe condition of the patient with a high body temperature, bradycardia that does not correspond to it, and a septic nature of the clinical course. The patient experiences stunning chills, severe sweating, headaches, at the height of which vomiting and confusion are possible. The headache is localized in the frontal region, the orbit, intensifies with pressure on the eyeball and with attempts to move it, which are significantly limited in all directions. The eyelids are dense, tense, the skin above them is hyperemic, a thrombosed venous network of the eyelids and face is determined, the palpebral fissure is closed, the eye is sharply bulging forward, motionless due to inflammatory infiltration of the extraocular muscles, orbital tissue and motor nerves. The mucous membrane is hyperemic, sharply edematous, pinched between the closed eyelids. Diplopia occurs only in cases where orbital phlegmon was preceded by a subperiosteal abscess that displaces the eyeball to the side.

With orbital phlegmon, visual acuity, up to amaurosis, decreases in 1/3 of cases. Instantaneous blindness occurs due to thrombophlebitis and thrombosis of the orbital vein, thrombosis of the central retinal vein or retinal artery embolism. A progressive decrease in visual function occurs due to compression or developing toxic neuritis of the optic nerve. Ophthalmoscopic examination reveals neuritis, optic nerve atrophy (mainly with posterior sinusitis), retinal hemorrhage and rarely its detachment, thrombophlebitis of the retinal veins. Later, with moderate severity of the inflammatory process, fluctuation in the lower part of the orbit and a breakthrough of pus through the tissues of the eyelids and conjunctiva appear. The earlier the breakthrough of pus occurs, the greater the likelihood of reverse development of the process and recovery. This is also facilitated by simple orbitotomy with opening of the phlegmon. In severe cases, some patients (21% of adults and 10% of children) develop loss of corneal sensitivity with loss of neurotrophic function, followed by neurotrophic keratitis and purulent corneal ulcer. Panophthalmitis is possible as an outcome.

Orbital phlegmons are dangerous due to intracranial complications (thrombophlebitis of the transverse, superior longitudinal and cavernous sinuses, meningitis, brain abscess, etc.). Orbital phlegmons that arise from purulent sphenoiditis are especially dangerous in this regard.

Rhinogenic retrobulbar neuritis. Rhinogenic retrobulbar neuritis is caused by the proximity of the optic canal to the posterior ONI.

Thus, the posterior cells of the ethmoid labyrinth sometimes closely approach this canal, and in some cases the optic nerve penetrates these cells or the mucous membrane of the sphenoid sinus passes onto the membranes of the optic nerves, etc. In the 20s of the last century, the opinion was established that one of the most common causes of retrobulbar neuritis is inflammation of the posterior paranasal sinuses. Later, this opinion was repeatedly confirmed by the fact that improved vision and a decrease in the symptoms of retrobulbar neuritis occurred during surgical intervention on the paranasal sinuses even in cases where no obvious clinical manifestations of the disease of these sinuses were noted. However, there was and still is an opposite opinion, confirmed by factual material. Such well-known authors as M.I. Volfkovich (1937), E.Zh. Tron (1955), A.G. Likhachev (1946) and others generally considered the rhinogenic etiology of retrobulbar neuritis to be a very rare phenomenon, pointing to the leading role of multiple sclerosis in this pathological condition. In the last years of the 20th century and the beginning of the 21st century, the "theory" of rhinogenic retrobulbar neuritis again prevailed and, moreover, it is rhinogenic lesions that are credited with an important role in the occurrence of damage to the optic chiasm in optic-chiasmatic arachnoiditis.

The clinical picture of retrobulbar neuritis differs little from a similar disease of a different etiology. Retrobulbar neuritis is divided into acute and chronic. Acute rhinogenic retrobulbar neuritis is characterized by a history of acute rhinitis, a rapid decline in visual acuity and an equally rapid improvement in vision after abundant irrigation of the mucous membrane of the corresponding half of the nose with solutions of cocaine and adrenaline. The pain syndrome is not as intense as with purulent processes in the orbit: pain occurs when moving the eye, pressing on it and on the supraorbital foramen - the exit point of the supraorbital branch of the trigeminal nerve, sometimes photophobia, slight exophthalmos, and eyelid edema occur. The fundus is normal or signs of papillitis - acute or subacute inflammation of the optic disc - of varying severity, up to edema resembling congestion of the optic disc.

On the affected side, a central scotoma and sometimes narrowing of the peripheral boundaries of the visual field are determined. An increase in the size of the blind spot and its decrease under the influence of treatment (Van der Hove symptom), according to many ophthalmologists, cannot be considered a pathognomonic sign of rhinogenic retrobulbar neuritis, since this symptom is observed in retrobulbar neuritis of other etiologies. M.I. Volfkovich (1933) proposed taking into account the following data confirming the rhinogenic etiology of retrobulbar neuritis: an increase in the blind spot after tamponade of the corresponding half of the nose and its decrease after removal of the tampon; an even sharper decrease in the blind spot after cocaine-adrenaline anemia of the nasal mucosa, spontaneous nosebleed or after opening the "causative" sinus. The author of the test explained these phenomena by changes in the hemodynamic status in the nasal cavity and, accordingly, reflex and physical changes in blood circulation in the optic nerve.