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The most complete possible rhinogenic ocular complications are presented in the classification proposed by B.V. Shevrygin and N.I. Kuranov (1976). It includes the following complications:
- reactive edema of the fiber of the eye socket and eyelids;
- diffuse non-purulent inflammation of the fiber of the eye socket and eyelids;
- periostitis (osteoperiostitis);
- subperiostal abscess;
- abscess of the eyelids;
- fistulas of the eyelids and orbital wall;
- retrobulbar abscess;
- phlegmon of the eye socket;
- vein thrombosis of the orbit.
However, this classification does not cover a number of severe ocular and visual complications arising from the pathology of the paranasal sinuses. These should include such well-known nosological forms as optic neuritis, retrobulbar neuritis and optochiasal arachnoiditis, which are essentially different stages of one disease (Sokolova, O.N. et al., 1990). Visual disturbances can be caused by cystic (mucocele, piocele) or air (pneumosinus) stretching of the paranasal sinuses. The defeat of the organ of vision with optochiasal arachnoiditis and with sinus thrombosis of the cavernous sinus are considered among intracranial complications. Orbital complications and visual disturbances are manifested by general and local symptoms, the severity of which depends on the nature of the pathological process in a particular paranasal sinus, the type of complication and localization of the focus in the orbit itself. The severity of the disease increases with the progression of the disease and the development of purulent options for the defeat of the orbit - subperiosteal, retrobulbar abscess, orbit phlegmon.
The most mild orbital complication in inflammatory diseases of the paranasal sinuses is reactive swelling of the orbit and eyelids, as well as their diffuse non-purulent inflammation. This pathology among all rhinosinusogenic orbital complications takes the first place in frequency of occurrence (B. Shevrygin and N. I. Kuranov, 1976). Especially often, this form of orbital complications develops in childhood with acute ethmoiditis that occurs against the background of a respiratory infection (Kozlov M. Ya., 1985). With this disease, swelling and redness of the skin in the eyelids, narrowing of the palpebral fissure, hyperemia and swelling of the conjunctiva, eyelids and eyeball are noted. In cases of diffuse non-purulent inflammation of the fiber of the eye socket and eyelids, chemosis and even exophthalmos can be observed with the eyeball moving in one direction or another, depending on the location of the affected sinus. However, unlike the purulent process, these changes are very unstable and fleeting. Initiated treatment that improves the outflow of pathological contents from the paranasal sinuses quickly eliminates the symptoms of orbital complications.
A more pronounced clinical pathology is inflammation of the walls of the orbit - periostitis (osteoperiostitis). There are simple (non-purulent) and purulent forms. It is clinically difficult to distinguish simple periostitis from the reactive edema and diffuse non-purulent inflammation of the eye socket and eyelids discussed above.
Simple periostitis is observed with catarrhal sinus inflammation, purulent - with empyema. The clinical manifestation of simple periostitis is limited to inflammatory tissue infiltration in the form of eyelid edema, conjunctival vascular injection. The localization of painful swelling depends on the localization of the inflammatory process in the paranasal sinuses. With the elimination of the latter, the clinical manifestations of periostitis quickly pass.
Purulent periostitis is more difficult. It is characterized by a pronounced general reaction (high body temperature, general weakness, headache). Locally, on one of the walls of the orbit, a painful infiltrate forms, in which the periosteum can be detached from the bone with the formation of a subperiosteal (periorbital) abscess.
The anatomical features of the structure of the tissues of the orbit determine the direction of distribution of pus, which, as a rule, does not occur inside the orbit, but outwards, forming a purulent fistulous passage (Kozlov M. Ya., 1985). The localization of the subperiosteal (periorbital) abscess becomes clear after the formation of the fistulous course. In frontal sinusitis, an abscess is opened in the middle of the upper orbital edge (Fig. 2.9.1) or in the region of the upper inner corner of the orbit, above the inner ligament of the eyelids. A fistula can also be located there with inflammation of the ethmoid labyrinth, and with a disease of the maxillary sinus - in the lower orbital region.
Subperiosteal abscess of the deep sections of the orbit is more difficult. They occur more often with purulent processes in the posterior ethmoid cells and the sphenoid sinus, as well as when pus breaks out of the maxillary sinus through the posterior sections of its inner wall. In this case, the development of visual disturbances (central scotomas), a violation of the mobility of the eyeball (paresis of the abducent and oculomotor nerve) and its protrusion (exophthalmos) are possible. A subperiosteal abscess resulting from a lesion of the deep paranasal sinuses can be complicated by a retrobulbar abscess and phlegmon of the orbit. When pus breaks into retrobulbar cellulose and its subsequent osumkovka, a retrobulbar abscess develops. In the case of a large virulence of microbes and weakening of the body's resistance, understanding of the abscess may not occur, and then phlegmon of the orbit develops.
Phlegmon orbits are the most severe and dangerous of all the rhinosinusogenic ocular complications discussed above. Its development is always accompanied by a stormy general reaction of the body: the body temperature rises significantly (up to 39 - 40? C), headache intensifies, nausea and vomiting are possible. Pain in the orbit increases, swelling and hyperemia of the eyes increase, chemosis becomes significantly pronounced (Fig. 2.9.2). There is always exophthalmos with limited mobility of the eyeball. Perhaps the development of blindness due to a violation of the blood supply to the retina. Phlegmon of the orbit may be preceded by thrombosis of its veins, which is manifested by similar symptoms.
Visual disturbances caused by cystic deformities (expansion) of the paranasal sinuses can occur in the form of a displacement of the eyeball and its exophthalmos, double vision (diplopia), and a decrease in its severity as a result of developed atrophy of the optic nerve.
Mucocele and piocele are cystic extensions of the paranasal sinuses.
Most clinicians attribute the development of cystic sinus enlargement to the closure of the anastomosis between the sinus and nasal cavity, and therefore sterile mucus (mucocele) or pus containing a low-virulent flora (piocele) accumulates in it. A predisposing factor to the development of this disease is an injury that violates the patency of the anastomosis of the sinus with the nasal cavity. Most often, the sinuses are affected, having narrow and long excretory channels and openings. That is why most often (80% of cases) there is a cystic expansion of the frontal sinus (Likhachev A.G., 1963).
The disease manifests itself in an increase in the volume of the affected sinus and displacement of the eyeball, depending on the localization of the process (Fig. 2.9.3). When the frontal sinus is affected, the eyeball moves down and out, when the trellised labyrinth is damaged, it moves outward and forward, and when the sphenoid sinus is damaged, it moves forward. Patients complain of a feeling of heaviness in the area of the affected sinus and orbit. In some cases, patients are concerned only with an increasing cosmetic defect.
With the localization of the disease in the region of the ethmoid bone, the function of the tear ducts is impaired, which is accompanied by lacrimation.
Thinning of the bone walls caused by cystic enlargement of the sinus also determines the symptom of "parchment" crunch observed in some cases during palpation. It is also possible the formation of defects in the bone walls of the cystic dilated sinus. Then, in the resulting defect, the mucous membrane of the sinus with its mucous contents prolapses, like a hernia.
It is necessary to point out another reason for the cystic expansion of the paranasal sinuses, which can lead to visual impairment up to its complete loss - their air expansion. Such an airy sinus enlargement should not be called pneumocele, but pneumatic sine (Feldman A.I., 1926). Pneumocele is an air tumor formed as a result of the accumulation of air in the cranial cavity in case of violation of the integrity of the walls of the pneumatic cavities (paranasal sinuses, cells of the mastoid process), which usually happens with fractures. Pneumatosinus is defined as the air expansion of any paranasal sinus with the absolute integrity of its bone walls. The pneumosinus of the frontal sinus was described in detail in Russian literature by A.I. Feldman (1926). The pneumosinus of the sphenoid sinus was described by A.S. Kiselev, D.V. Rudenko and T.A. Lushnikova (1995). At the same time, a triad of symptoms characteristic of the pneumosinus of the sphenoid sinus was established:
1) increased pneumatization of the sphenoid sinus with the presence of an arcuate deformation of its upper wall, convex facing up, and its displacement in the cranial direction; 2) preservation of airiness of the sinus; 3) a progressive decline in debate caused by atrophy of the optic nerves. As an illustration, a radiograph of a patient suffering from atrophy of the optic nerves that developed as a result of the pneumatosine of the sphenoid sinus is given (Fig. 2.9.4).
Treatment of rhinogenic inflammatory ocular complications should be carried out in a hospital with the participation of ENT and ophthalmologists, and in some cases with the involvement of other specialists. It should be comprehensive and often completely urgent, covering a wide range of activities, depending on the nature of the orbit and the pathological process in the paranasal sinuses.
In non-purulent forms of orbital complications (reactive swelling of the orbital fiber and eyelids, diffuse non-purulent inflammation of the orbital fiber, purulent osteoperiostitis) resulting from acute sinusitis, conservative treatment is performed. It should include the active rehabilitation of the paranasal sinuses through their effective drainage, the appointment of antibacterial and antihistamine therapy. With the same complications, but developed as a result of exacerbation of chronic inflammation of the paranasal sinuses, conservative methods of treatment can be combined with gentle surgical intervention.
In purulent processes in the orbit or in the presence of symptoms of visual impairment, in particular, optic neuritis or retrobulbar neuritis, irrespective of the nature of the pathological process in the paranasal sinuses, a wide opening of the affected paranasal sinuses and simultaneously elimination of the purulent focus in the orbit are necessary (if any) using additional orbitotomy. Currently, in connection with the possibilities of modern endonasal surgery using endoscopes, opening an orbital abscess and draining the purulent foci, as well as operations on the affected paranasal sinuses, they are successfully performed with the endonasal approach (StammbergerH., 1991; Kozlov V.S., 1997) . Surgical treatment is accompanied by active antibiotic therapy. With severe intoxication, dehydration and detoxification therapy is necessary. In case of thrombosis of the orbit veins, anticoagulants are used.
The treatment of mucocele and piocele is prompt. With damage to the frontal sinus and ethmoid labyrinth, the extranasal paraorbital approach is most appropriate. The same lesion of the sphenoid sinus requires an autopsy with endonasal transeptal access for guaranteed rehabilitation.
In case of atrophy of the optic nerves caused by the pneumosinus of the sphenoid sinus, we also recommend an endonasal transeptal opening of the sphenoid sinus with careful curettage (evisceration) of the mucous membrane. This principle in the treatment of pneumosinus is based on modern ideas about the process of formation of the paranasal sinuses, in which the mucous membrane lining them is actively involved (Takahashi R, 1983, Speransky V.S., 1988). Our clinical observations confirm these theoretical concepts. So, after evisceration of the mucous membrane of the sphenoid sinus, we managed, in some cases, to stop further decrease in vision caused by atrophy of the optic nerves as a result of the progressive expansion (pneumosinus) of this sinus.
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