Rhinogenic ophthalmic complications: causes, symptoms, diagnosis, treatment

Occurrence of rhinogenic ophthalmologic complications is facilitated by close anatomic connections of the nose and paranasal sinuses with the orbit and its contents. The commonness of their bone walls is not a significant obstacle to penetration from the paranasal sinuses into the orbit, even a deep-lying sphenoid sinus is often the focus of a spreading infection to the base of the skull and to the cerebral membranes through which the cranial nerves pass. Transition of infection from the maxillary sinus to the orbit is facilitated by the fineness of the upper and inner walls of the sinus. Penetration of infection from the latticed labyrinth into the orbit is facilitated by holes and cracks in the latticed bone, in the inferior-anterior wall of the frontal, maxillary, anterior-lateral wall of the sphenoid sinus, through which the vessels and nerves pass. Important in the migration of infectious agents in the direction of the orbit have anatomical features of the structure of the paranasal sinuses. Thus, with a considerable spread of the cells of the latticed labyrinth, their closer contact with the cranial cavity, orbit, lacrimal sac and optic nerves is created, which is facilitated by insignificant resistance to the inflammatory process of the plate of the lattice. With large frontal sinuses, it extends to the entire surface of the roof of the orbit, bordering on the small wings of the sphenoid bone, its sinus, the visual channel, forming its upper wall. This structure of the frontal sinus is an important risk factor for the emergence of banal frontalitis, as well as its ophthalmic and intracranial complications. The upper wall of the sphenoid sinus, depending on its thickness and pneumatization, can very closely contact with the visual canals and the visual crossover, which often leads even when the current chronic sphenoiditis is sluggishly to involve the arachnoid shell surrounding the optic nerves in the toxic-infectious process, such forms of the disease as retrobulbar neuritis of optic nerves and optic-chiasmal arachnoiditis.

In the event of pyogenic ophthalmic complications, the odontogenic factor should be taken into account, since it is possible to spread infection from the affected teeth to the orbit through the upper wall of the maxillary sinus into which the infection comes from the wells of the 1-2 molar, where the bone separating the socket from the sinus is very thin and porous . It should be borne in mind also the fact that between the alveoli of canines and premolars there are bone ducts leading to the inner corner of the orbit. Especially dangerous for the eyes are premolars and the first molar tooth, less frequently canines and almost never - incisors and 8 teeth.

The main ways of spreading infection from the face and anterior paranasal sinuses are the extensive arterial and especially venous connections of these regions with the orbit organs. The orbital system of the orbit widely anastomoses with the vessels of the face, nose, paranasal sinuses, teeth and brain. For example, the orbit and paranasal sinuses are supplied with blood in the latticed, external maxillary arteries, as well as branches of the external carotid artery. These arterial vessels anastomose with each other through the posterior nasal artery. The arteries of the teeth, mainly the branches of the outer maxillary artery, are also connected to the arteries of the orbit.

A large number of venous plexuses of the nasal cavity, dentofacial system, face and pharynx is associated with the venous systems of the orbit and the cranial cavity, which makes it possible to combine orbital and intracranial complications. In this respect, the connection of the latticed veins with the orbital vein, and the latter with the veins of the dura mater and the cavernous sinuses, are of great importance. Thus, one of the branches of the anterior latticed vein through the trellis plate penetrates into the cranial cavity to the venous plexus of the soft medulla, thereby forming an annular 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 rigid meninges through venous emissaries. And the veins of the maxillary sinus have anastomoses with the orbital vein through the angular vein, which is the branch of the vein of the face. The fine 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.

Important role in the spread of infection in the direction of the orbit has a lymphatic vascular system, the orbital part of which begins with the slits in the fiber of the orbit, is associated with the lymphatic system of the nose through the vessels of the latticed maze and the tear-nasal canal. Of the paranasal sinuses and dentoalveolar system, lymphatic pathways lead to the lymphatic vessels of the face, submandibular and deep cervical lymph nodes.

The nasal cavity, paranasal sinuses and the orbit have a common sympathetic and parasympathetic and sensitive innervation from the I and II branches of the trigeminal nerve through the nodes of the upper cervical sympathetic, trigeminal, ciliary, and pterygopalus, which determines the possibility of their combined reflex reactions. The close proximity of the posterior wall of the maxillary sinus with the wedge-palatal node and its branches, with the pterygoid plexus, the maxillary artery and its branches creates conditions for the transition of the inflammatory process from this sinus to the posterior cells of the latticed labyrinth, the 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 the oral cavity into the orbit can be carried out by contact, hematogenous (thrombophlebitis of small veins) and lymphogenous pathways.

Glaucous complications in acute sinusitis.

In acute sinusitis, compression or blockage of the tear duct can occur, which is manifested by self-fear of reflex character and lacrimation. In the case of odontogenic sinusitis accompanied by a periostitis of the alveolar process of the maxilla, swelling of the cheek, eyelid and chemosis of the conjunctiva on the side of the inflammation are observed.

With acute frontal ophthalmic complications are more severe than with other sinusitis. The onset of the process is manifested by edema of the skin of the forehead and eyelids in the upper-inner corner of the eye as a result of the violation of the collateral outflow of venous blood. There is a neuralgic pain in zone I of the branch of the trigeminal nerve: in the forehead and root of the nose, the eyes, which is strengthened by pressing on the infraorbital aperture. There are also lacrimation, diplopia when looking up. Thrombophlebitis of the veins anastomosing with the venous plexus of the orbit can lead to its phlegmon.

Acute etomoiditis is manifested by similar symptoms with other sinusitis. The difference is that with acute etmoiditis, the pressing pain is localized in the depth of the root of the nose, at the inner corner of the eye, the bridge of the nose and in the branching zone of the second branch of the trigeminal nerve. In patients there is intense lacrimation, edema of both eyelids, hyperemia of the conjunctiva. In cases of debilitating outflow of pus in the nose, especially with closed empyema of the posterior cells of the trellis labyrinth, which is more common in children with scarlet fever, orbital complications in the form of a non-purulent or purulent ophthalmitis.

Acute sphenoiditis is often combined with damage to the posterior cells of the trellis labyrinth. This combination is characterized by pain in the depth of the orbit, radiating across the entire skull. Pain sharply increases with pressure on the eyeball. The proximity of these sinuses to the visual canal, the connection between the venous plexuses of the wedge-shaped sinus and the optic nerve shells can be the cause of rhinogenic retrobulbar neuritis. Due to the proximity of the sphenoid sinus to the oculomotor nerves, isolated paralyzes or upper globular cavity syndrome are possible. For the latter, there is typically a discrepancy between relatively poor clinical symptoms and a sharp decrease in visual acuity due to early involvement in the inflammatory process of the optic nerves. It is also possible the occurrence of rhinogenic choroiditis and chorioretinitis.

In chronic sinusitis, ocular complications are caused by the influence of nearby foci of infection or in connection with progressive changes leading to the development of menigothic and piocele of one or another sinus. With exacerbations of chronic sinusitis, the same complications can occur as in acute processes.

Inflammation of the soft tissues of the eyelids is simple (purulent) and purulent. Puffy inflammation of the eyelids belongs to the category of reactive processes that arise either as a result of the toxic effects of catabolites - the products of the inflammatory process, or as a result of a violation of the outflow of lymph and venous blood from any part of the tissue or organ. This causes swelling and hyperemia of the skin of the eyelids, more than the upper, extending to the lateral surface of the nose. It is observed more often in young children, who have a catarrhal ethmoiditis or frontal infection against a background of any childhood infection (scarlet fever, measles) or influenza. 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 appearance of an abscess or phlegmon in their cellulose due to the breakthrough of pus from the latticed labyrinth or maxillary sinus. At the beginning of the disease, there is an edema of the eyelid, followed by a tight limited infiltrate, which after a while turns into a fluctuating abscess. The infiltrate can spread diffusely throughout the entire age, transforming into phlegmon. The skin over the abscesses is hyperemic, cyanotic. With the development of infiltration, patients complain of sudden pulsating pains in the eyeball, radiating to the temporal region and the upper jaw. Ptosis develops. The process ends with a breakthrough of pus outward with the formation of a dermal fistula, sometimes communicating with the sinus cavity. Usually the process ends with scarring and deformation of the eyelid, its cicatricial fusion with the bone edge of the orbit, deformation of the eye gap (lagophthalmus) leading to the appearance of keratitis.

The edema of the retrobulbar fiber appears mainly when the collateral outflow of venous blood is disturbed in the posterior sinusitis, especially purulent. In this case, children's body temperature rises, headache, vomiting, eyelid edema, conjunctival chemosis, exophthalmos, eyeball immobility outside due to IV nerve palsy, diplopia. These signs are very similar to thrombosis of the cavernous sinus, but the edema of retrobulbar fiber is distinguished from the latter by the general satisfactory state of the child, no changes on the fundus. In adults, the general symptoms are weak or nonexistent, but temporary visual acuity and strabismus squint may be temporary.

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

The spread of the inflammatory process to orbit, in addition to the hematogenous, is possible by contact, especially when the sinusitis acquires a closed character due to the blockade of their anastomosis with the nasal cavity. According to MM Zolotareva (1960), inflammation of the nasal mucosa and paranasal sinuses leads to the same process at first in the surface and then in the deep layers of bone. Osteochiourism is accompanied by thrombophlebitis of small venous trunks penetrating into the orbit and flowing into the ophthalmic veins. Orbital complications differ in certain features, depending on the type of complication that arises. The resulting osteoperostitis of the orbit can be simple and purulent.

Simple osteoperiostitis is local in nature and occurs mainly with acute empyema of the frontal sinus or the latticed labyrinth as a complication of any infectious disease (influenza, scarlet fever, etc.). There are such symptoms as swelling of the skin in the upper-right corner of the orbit and in the forehead, the injection of conjunctival vessels and hemochems. In the early period, due to transient paresis or paralysis of the corresponding muscles, there may be a restriction of the mobility of the eye and diplopia. Because of the toxic edema of retrobulbar fiber and neuritis of the optic nerves, a decrease in visual acuity is possible. With a simple periostitis of the sphenoid sinus and the posterior cells of the latticed labyrinth, the defeat of the optic nerves arises especially early and has a deeper character.

Purulent periostitis is characterized by a sharp onset, an increase in body temperature, headache, and general weakness. With the empyema of the posterior sinuses, edema of the eyelids, conjunctival hyperemia, exophthalmus with an eyeball shift in the direction opposite to the localization of the process develops, and its mobility is limited to the empyema. There is diplopia, optic neuritis, visual acuity reduction. When the top of the orbit is damaged, a decrease in visual acuity can be combined with a central or paracentral scotoma. Visual disturbances, as a rule, with the elimination of the inflammatory process in the sinuses and orbit pass, but in especially severe cases the process ends with a secondary atrophy of the optic nerves and blindness. A pronounced exophthalmos can be complicated by keratitis. Purulent periostitis in the frontal sinus with the involvement of the upper wall of the orbit in the process is manifested by the edema of the upper eyelid, hyperemia and chasmosis of the conjunctiva of the eye in the upper part of the eyeball, moderate exophthalmos, displacement of the eye downward and impaired mobility upward.

Due to the destruction of the sinus bone wall and the appearance of an intraorbital fistula in the orbit, a subperiosteal abscess appears. The clinical manifestations of which are much more pronounced than with the orbital complications described above. Depending on the affected sinus in the field of the eyelids there is a fluctuating swelling, with the front - in the upper-right corner of the eye, with etmoid - a little lower, under the internal adhesion of the eyelids or in the projection of the lacrimal sac and below. Usually the subperiosteal abscess of the orbit accompanies the edema of retrobulbar fiber (exophthalmos, limitation of mobility of the eyeball, its displacement in the direction opposite to the localization of the abscess). In patients with an empyema of the frontal sinus, a pus may break through into the eyelid or into the upper sinus angle of the orbit. However, the breakthrough of the abscess toward the orbit is possible only with a deep sinus location. Subperiosteal abscess with posterior sinusitis is manifested by pain in the retrobulbar area, which is strengthened by pressure on the eyeball; more exophthalmic than in the anterior sinusitis; impaired mobility of the eye and its displacement in the direction opposite to the location of the abscess, as well as blindness or decreased visual acuity, central scotoma. Significantly less occurs neuro-ophthalmic corneal ulcer or panophthalmitis. With this location of the subperiosteal abscess, there is a danger of pus penetrating into the orbit, and then a retrobulbar abscess develops.

With empyema of the maxillary sinus, subperiosteal orbital abscesses are much less common, but more often this complication is manifested in children due to tooth lesions or osteomyelitis of the maxillary sinus. When the abscess is localized in the anterior part of the maxillary sinus, the symptoms characteristic of ossoperiostitis are more intense; in the case of a deeper process, exophthalmos are observed, the eye is shifted upward and its ciliia is limited, while it is possible to involve the optic nerves in the inflammatory process with a reduction in visual acuity, including amaurosis.

A retrobulbar abscess occurs as a result of a breakthrough into the orbit of a deeply located subperiosteal abscess that originated with purulent sinusitis or a hematogenous path from a distant focus of purulent infection (nasal and upper lip furuncles, mandibular osteomyelitis, oral cavity phlegmon, peritonsillar abscess, etc.). . With this complication, a pronounced general reaction of the organism resembling sepsis is observed. Of the local symptoms observed exophthalmos, the displacement of the eyeball in the direction opposite to the localization of the abscess, and limiting mobility toward the focus. The resulting optic neuritis leads to a decrease in visual acuity. In the X-ray examination, in addition to sinusitis, shading of the orbit is determined, and in the case of a process from the sinus to the orbit through contact - the defect of the bone wall of the latter, sometimes detectable palpation.

Phlegmon orbit is an acute purulent inflammation with infiltration, necrosis and purulent fusion of the orbital retina.

Pathological anatomy and pathogenesis. The process begins with the thrombovasculitis of the vessels of the orbit and the formation around them first of small, then merging abscesses. Complication usually occurs with empyema of the maxillary sinus and frontal sinus, less often with lesions of other sinuses. Often, the phlegmon of the orbit arises from the metastasis of purulent emboli from other foci of infection (pneumonia, sepsis, dental disease, furuncles and carbuncles of the nose and face, suppurative processes in the maxillofacial region). This form of intraorbital purulent complication is most dangerous with respect to the occurrence of intracranial complications.

Clinical picture. The disease is accompanied by a general severe condition of the patient with a high body temperature, not corresponding to her bradycardia and septic character of the clinical course. The patient has tremendous chills, a sharp sweating, headaches, at the height of which vomiting and deafening consciousness are possible. Headache is localized in the frontal region, the orbit, is strengthened by pressing on the eyeball and trying its movements, which are substantially limited in all directions. The eyelids are dense, strained, the skin over them is hyperemic, the thrombosed venous network of eyelids and faces is determined, the eye gap is closed, the eye is sharply protruded forward, immovable due to inflammatory infiltration of extraocular muscles, cellulose of the orbit and motor nerves. Mucous membrane is hyperemic, sharply edematous, it is restrained between closed eyelids. Diplopia occurs only in those cases when the phlegmon of the orbit preceded the subperiosteal abscess, shifting the eyeball to the side.

With the phlegmon of the orbit, the visual acuity, down to the amaurosis, decreases in 1/3 of the cases. Instant blindness occurs due to thrombophlebitis and thrombosis of the orbital vein, central vein thrombosis of the retina or embolism of the retinal artery. The increasing decline in visual function occurs due to compression or developing toxic optic neuritis. Ophthalmoscopically reveal the phenomena of neuritis, atrophy of the optic nerves (mainly in the posterior sinusitis), hemorrhage into the retina and rarely its detachment, thrombophlebitis of the retina veins. In the future, with an average severity of the inflammatory process, there is a fluctuation in the lower part of the orbit and a breakthrough of pus through the tissues of the eyelids and conjunctiva. The earlier the breakthrough of pus occurs, the more likely the reverse development of the process and recovery. This is also facilitated by a simple orbitotomy with phlegmon opening. In severe cases, some patients (in 21% of adults and 10% of children) develop loss of sensitivity of the cornea with loss of neurotrophic function, then develop neurotrophic keratitis and purulent corneal ulcer. In the end, panophthalmitis is possible.

Phlegmon orbits are dangerous intracranial complications (thrombophlebitis of the transverse, upper longitudinal and cavernous sinuses, meningitis, brain abscess, etc.). Especially dangerous in this respect are the phlegmon of the orbit arising from the soil of purulent sphenoiditis.

Rinogenous retrobulbar neuritis. Rinogenous retrobulbar neuritis is due to the proximity of the optic nerve channel to the posterior ones.

Thus, the posterior cells of the latticed labyrinth sometimes come very close to this channel, and in some cases the optic nerve permeates these cells or the mucous membrane of the sphenoid sinus passes over to the optic nerve shells, etc. In the 20s of the last century, the opinion was established that one of the The most common causes of retrobulbar neuritis are inflammation of the posterior paranasal sinuses. Later this opinion was repeatedly confirmed by the fact that the improvement in vision and the decrease in the phenomena of retrobulbar neuritis occurred during surgery on the paranasal sinuses even in those cases when there were no obvious clinical manifestations of the disease of these sinuses. However, there is and still exists an opposite opinion, supported by factual material. Such well-known authors as MIVol'kovich (1937), E.Zh.Tron (1955), AGLikhachev (1946) and others generally considered the rhinogenetic etiology of retrobulbar neuritis to be very rare, indicating a leading role in this the pathological state of multiple sclerosis. In the last years of the XX century. And the beginning of the XXI century. The "theory" of rhinogenous retrobulbar neuritis has again prevailed and, moreover, it is to the rhinogenic lesions that it is attributed an important role in the onset of lesion of the optic chiasm in optic-chiasmal arachnoiditis.

The clinical picture of retrobulbar neuritis differs little from a similar disease of another etiology. Retrobulbaric neuritis is divided into acute and chronic. For acute rhinogenic retrobulbar neuritis, a history of an acute rhinitis, a rapid drop 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 are characteristic. Pain syndrome is not as intense as in purulent processes in the orbit: pain occurs when the eye moves, pressure on it and on the supraorbital opening - the place of the exit of the supraorbital branch of the trigeminal nerve, and sometimes there is photophobia, small exophthalmos, eyelid edema. The ocular fundus without features or signs of papillitis - acute or subacute inflammation of the optic disc - of varying severity, up to an edema resembling a stagnant disk of optic nerves, can be observed.

On the side of the lesion, the central scotoma is determined, sometimes narrowing the peripheral boundaries of the field of vision. The increase in the size of the blind spot and its decrease under the influence of treatment (the Van der Hove symptom), according to many ophthalmologists, can not be considered a pathogmous sign of rhinogenic retrobulbar neuritis, since this symptom is observed in retrobulbar neuritis of other etiologies. MI Vol'kovich (1933) suggested 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 a decrease in it after the extraction of the tampon; an even sharper decrease in the blind spot after cocaine-adrenaline anemia of the nasal mucosa, spontaneous nasal bleeding, or after the opening of the "causal" sinus. These phenomena, the author of this trial explained by changes in hemodynamic status in the nasal cavity and, respectively, reflex and physical changes in the circulation in the optic nerve.