Acute ethmoidosphenoiditis: causes, symptoms, diagnosis, treatment

Acute craniobasal sinusitis (acute ethmoidosphenoiditis). These diseases include inflammation of the mucous membrane of the posterior cells of the ethmoid bone and sphenoid sinuses, which in most cases occur simultaneously, and in most cases the onset of the disease is rhinogenic inflammation of the posterior cells of the ethmoid bone, which communicate quite freely with the sphenoid sinus. Therefore, in foreign literature, the term acute ethmoidosphenoiditis is most widely used.

Acute ethmoidosphenoiditis is an acute non-specific inflammation of the mucous membrane of the posterior cells of the ethmoid bone and sphenoid sinus, which occurs either primarily on the basis of acute banal or influenza rhinitis, or as a consequence (very rarely) of acute transient inflammation of the anterior paranasal sinuses. Mostly adults are affected.

Etiology and pathogenesis. Most often, acute ethmoidosphenoiditis is a consequence of acute epidemic rhinitis of viral or bacterial etiology, occurring against an allergic background. In this case, most often the disease takes the form of pansinusitis. If the specified rhinitis acquires a malignant clinical course, characterized by high body temperature, hemorrhages, purulent ulcerative-necrotic lesions of the nasal mucosa and bone tissue of the ethmoid labyrinth, then the infection easily penetrates into the sphenoid sinus and causes its acute inflammation. Lesions of the nasal mucosa in glanders, meningococcal infection, syphilis, childhood infections can also lead to acute ethmoidosphenoiditis. As noted by A.S. Kiselev (1997), at present, great importance in the development of inflammatory diseases of the paranasal sinuses is given to rhinoviruses combined with bacterial microbiota. Traumatic lesions of the middle floor of the nasal cavity can also cause infection of the posterior cells of the ethmoid bone and the mucous membrane of the sphenoid sinus. Tumors of the rhinoethmoidal and nasopharyngeal region, the base of the skull, when they grow in the ethmoidosphenoid direction and the drainage function of the outlet openings of the sphenoid sinus is impaired, cause the appearance of transudate in them, which subsequently becomes infected and leads to their acute purulent inflammation.

An important factor in the pathogenesis of acute ethmoidosphenoiditis is the degree of pneumatization of the sphenoid sinus and posterior cells of the ethmoid bone. As already noted, there is a direct dependence of the frequency and severity of inflammatory diseases of the paranasal sinuses on their size. To a large extent, this also applies to the sphenoid sinus.

Symptoms and clinical course. Acute ethmoidosphenoiditis is classified into the following clinical forms:

1. open and closed forms; the first is characterized by the presence of functioning outlet openings and a mild clinical course; the second - by blockage of the outlet openings, accumulation of inflammatory exudate in the sphenoid sinus and a severe acute clinical course, often requiring emergency surgical intervention; it is with this form that severe intracranial complications of acute ethmoidosphenoiditis occur;
2. etiological and pathogenetic forms - bacterial, viral, specific, allergic;
3. pathomorphological forms - catarrhal, serous, purulent, osteonecrotic;
4. complicated forms - basal OXA with optic neuritis, meningoencephalitis, brain abscesses.

The deep location of the sphenoid sinus, its proximity to important anatomical structures determine the features of the symptoms, clinical course and complications that arise in acute and chronic sphenoiditis. Acute ethmoidosphenoiditis is characterized by a veiled clinical course, which does not manifest itself in the initial stages with bright symptoms that clearly indicate the localization of the pathological process, therefore, its diagnosis is often difficult, which is also facilitated by not always clear radiological data.

Subjective symptoms that occur with acute ethmoidosphenoiditis are most often assessed as signs of acute ethmoiditis, which is more clearly diagnosed by radiographic examination.

Patients with acute ethmoidosphenoiditis complain of a feeling of pressure and distension in the deep parts of the nose, spreading to adjacent areas and the eye sockets. The pains that arise in this area are of a painful, bursting nature, radiating to the crown, to the occipital bone area and often to the frontal area. The pains are predominantly constant, periodically sharply aggravating, causing nausea and vomiting. When shaking the head, they sharply intensify, synchronizing with the vibrations of the head. The genesis of headaches in acute ethmoidosphenoiditis is determined both by the inflammatory exudative process itself, which causes the accumulation of pathological contents in the cavities of the sphenoid bone, and by the resulting toxic neuritis of the nerve fibers innervating the sphenoid sinus: the posterior ethmoid nerve (from the first branch of the trigeminal nerve), the nasal nerves (from the second branch of the trigeminal nerve, causing the irradiation of pain to the frontal region) and the branches of the pterygopalatine ganglion).

Other important subjective symptoms of acute ethmoidosphenoiditis include decreased olfactory acuity and decreased vision. The former is the result of an inflammatory process in the posterior cells of the ethmoid bone, the latter is a consequence of perivascular edema occurring in the optic canal. In the open form of acute ethmoidosphenoiditis, a characteristic symptom appears - the presence of constant discharge in the nasopharynx, provoking the patient to cough it up and spit it out, which is also typical for inflammation of the posterior cells of the ethmoid bone.

Objective symptoms include diffuse swelling of the nasal mucosa with all the characteristic signs of acute ethmoiditis, obstruction of the nasal passages, "posterior" rhinorrhea, hyposmia, lacrimation, photophobia, hyperemia of the sclera, impaired accommodation and visual acuity. Anterior rhinoscopy reveals scanty purulent discharge in the nasal passages, which is abundantly visible during posterior rhinoscopy, covering the posterior ends of the middle and lower nasal conchae, flowing down the posterior wall of the nasopharynx.

The nature of the clinical course is determined by the clinical forms of the disease described above. The most severe are the so-called closed forms, in which the process most often becomes purulent and purulent-necrotic and often spreads to the basal structures of the brain, causing the occurrence of acute ethmoidosphenoiditis and other intracranial complications. The evolution of acute ethmoidosphenoiditis can develop in the same directions as acute inflammatory processes in other paranasal sinuses. It is mainly determined by the virulence of the microbiota, the degree of immunity, the general condition of the body, the degree of drainage of the sphenoid sinus and ethmoid labyrinth, as well as timely initiation of adequate treatment.

General symptoms include moderate fever (38-39°C) of a remittent type with daily fluctuations in body temperature within 1.5-2°C; general weakness, loss of appetite, insomnia due to headaches that intensify at night. Blood tests reveal changes typical of a general inflammatory process (neutrophilic leukocytosis, eosinophilia in case of allergies, increased ESR, etc.). General psychoneurological signs may include increased irritability or apathy, indifference to the environment, a desire to be alone in a darkened room, and an unwillingness to communicate with people.

Diagnostics. In most cases, direct diagnostics is difficult and a final diagnosis requires weeks or even months of observation of the patient. Nowadays, with the availability of modern methods of video endoscopy, X-ray diagnostics, CT and MRI, the final diagnostic time can be limited to several days, provided the clinical course is typical. As for complicated forms, unfortunately, some of them are diagnosed in some cases only at autopsy or when irreversible organic and functional changes occur in the secondary affected organs and systems.

The clinical diagnosis is established based on the presence in the anamnesis of acute banal, influenza or specific rhinitis, immediately preceding the onset of typical pain syndrome (tearing pain deep in the nose, radiating to the crown, back of the head and eye socket). Impaired olfactory acuity that occurred at the onset of the disease can be interpreted as a symptom of nasal congestion, but the addition of eye symptoms (hyperemia of the sclera, impaired acuity and especially visual fields) with scanty discharge or their absence in loci typical of acute ethmoidosphenoiditis should indicate acute exudative sphenoiditis of the closed type. If discharge is present, it is usually determined in the upper nasal passage and flows to the posterior end of the middle turbinate and further towards the nasopharynx. The diagnosis is confirmed either by X-ray or MRI.

Acute ethmoidosphenoiditis is differentiated from inflammatory diseases of other paranasal sinuses, from cranioccipitocervical neuralgias such as neuralgia of the diseased occipital nerve, from neuralgia of the internal nasal nerve, ethmoidosphenoidal, craniobasilar and retroorbitosphenoidal tumors. The criterion for excluding acute ethmoidosphenoiditis in differential diagnostics is the ineffectiveness of non-surgical and even surgical treatment of the disease that imitates acute ethmoidosphenoiditis.

The prognosis of acute ethmoidosphenoiditis in uncomplicated clinical forms is favorable, the condition for which is timely and adequate treatment for the clinical stage. In protracted forms that have passed into the purulent-necrotic stage, complications from the optic nerves and meninges are possible. If urgent surgical intervention on the sphenoid sinus is not undertaken in this case, then there is a threat of inevitable chronicization of the process in the middle cranial fossa in the form of basal leptomeningitis and ACA, leading to serious visual impairment. The prognosis for life is serious in the event of complications such as thrombosis of the cavernous sinus and brain abscess.

Treatment of acute ethmoidosphenoiditis is primarily non-surgical, drug-based, local and general, with the use of some manipulations such as the "transfer method", sphenoid sinus catheterization, some microsurgical interventions in the area of the outlet openings of the posterior cells of the ethmoid bone to facilitate drainage of the sphenoid sinus through the opened posterior cells, etc. Important in the therapy of acute ethmoidosphenoiditis is the earliest use of local and general treatment. Antiphlogistic agents, decongestants, antiseptics, and corticosteroids are used locally with the sole purpose of reducing the severity of the inflammatory reaction in the area of the natural outlet openings of the sphenoid sinus and ensuring their satisfactory functioning. At the same time, broad-spectrum antibiotics or antibiotics adapted to a specific pathogenic microbiota obtained during sphenoid sinus catheterization are used parenterally or per os. Antihistamines, intravenous calcium chloride and ascorbic acid (to strengthen barriers and cell membranes), and detoxification therapy are also prescribed.

A very effective means of treating acute ethmoidosphenoiditis is catheterization of the sphenoid sinus, and the most appropriate is the use of a double cannula by V.F. Melnikov (1994), which is especially effective in the closed form of ethmoiditis, in which the use of a single-lumen cannula and the introduction of fluid into the sinus sharply increases the pressure in the sinus, increases pain and is fraught with the danger of fluid penetration through dehiscences, perivasal spaces and pathological erosions into the surrounding tissues.

[ 1 ]