X-ray anatomical analysis of the temporal bone. Method for intraoperative determination of sigmoid sinus presentation How a thrombus occurs
The invention relates to medicine, in particular to otorhinolaryngology, and is intended to determine the presentation of the sigmoid sinus. To do this, evaluate the severity of the supraorbital fossa using a four-point system, and measure its longitudinal and transverse dimensions. And if it is not expressed or poorly expressed and the longitudinal size is 3, 20, 3 mm, transverse - 2, 80, 2 mm, then the presentation of the sigmoid sinus is established. The method makes it easier, more reliable, and more reliable to identify the presentation of the sigmoid sinus.
The invention relates to medicine, namely to otorhinolaryngology, and can be used for intraoperative determination of the presentation of the groove of the sigmoid sinus relative to the petrous part of the temporal bone. Determining the presentation of the groove of the sigmoid sinus is necessary for the otosurgeon for adequate surgical intervention on the ear, prevention of intra- and postoperative complications. Injury to the sigmoid sinus can lead to such a serious complication as the development of bleeding from the sigmoid sinus, which leads to the need for sinus tamponade. Sinus tamponade, in turn, can cause thrombosis and sepsis. The prototype is an X-ray examination of the temporal bone of the skull according to Schuler, with which one can determine the presentation of the sigmoid sinus relative to the petrous part of the temporal bone. Disadvantages of the prototype: in some cases, the image of the sigmoid sinus groove is unclear, and in some cases it is not determined. On radiographs of the temporal bone, the groove of the sigmoid sinus is often poorly differentiated; many structures of the temporal bone overlap each other, which makes it difficult to differentiate its individual elements. We are the first to propose a method for intraoperative determination of the presentation of the sigmoid sinus, which consists in assessing the severity of the supraductal fossa, measuring its longitudinal and transverse dimensions, and if the severity is 0-1 points, the longitudinal dimension is 3.20.3 mm, the transverse dimension is 2.80.2 mm, the presentation of the sigmoid sinus is established. The shape of the skull base has a significant influence on the location of the sigmoid sinus. The shape of the skull in craniology is determined using the cranial (head) index, which represents the ratio of the transverse diameter (width) of the skull to its longitudinal diameter (length), expressed as a percentage. There is also a basilar (main) index, which describes the shape of the base of the skull. We considered it appropriate to use not the cranial, but the basilar (main) index, since the temporal bone, based on its development, belongs to the bones of the base of the skull. The basilar index is calculated as the percentage ratio of the transverse diameter (width) of the skull base to its longitudinal diameter (length). The width of the base of the skull is the biauricular distance measured between the two aurions (the point that is located on the root of the zygomatic process of the temporal bone at the intersection of its vertical line drawn through the center of the external auditory canal). The length of the skull base is the distance between the nasion (where the midplane intersects the frontonasal suture) and the opisthion (where the midplane intersects the posterior edge of the foramen magnum). Depending on the size of the basilar index, skulls with a long base are distinguished - dolichobasilar (if the basilar index is less than 88.9%), with a short base - brachybasilar (if the basilar index is more than 99%) and a medium shape (basilar index is at least 89% and no more 98.9%). We conducted studies according to which the average value of the distances from the most prominent point on the mastoid process to the deepest point of the sigmoid sinus groove in three groups of skulls: brachybasilar, dolichobasilar and mesobasilar had significant differences. On turtles with a brachybasilar index, the average value was 14.90.44 mm on the left, 15.00.32 mm on the right, with dolichobasilar - on the left 19.40.48 mm, on the right 19.40.49 mm, with mesobasilar - on the left 17.70 .35 mm, right 17.90.36 mm. Thus, on skulls with a brachybasilar index, in contrast to skulls with dolicho- and mesobasilar indexes, the distance was the smallest, and thus we can talk about the presentation of the sigmoid sinus. Thus, it is possible to resolve the issue of the presentation of the sigmoid sinus by measuring the shape of the base of the patient’s skull (adjusted for the soft tissues of the head). During planned preparation of the patient for surgical intervention, this is easy to do, but during emergency it is not possible due to lack of time and the need for urgent surgical intervention. We have established a relationship between the shape of the base of the skull, and consequently, the location of the groove of the sigmoid sinus relative to the petrous part of the temporal bone and the supra-ductal fossa. In the intraoperative method we propose, the morphometric characteristics of the supraductal fossa are assessed: dimensions (longitudinal and transverse) and severity (assessed on a four-point system: 0 points - the supraductal fossa is not expressed at all, 1 point - poorly expressed, 2 points - well expressed, 3 points - very well expressed). If the supraductal fossa is smoothed, poorly defined (0-1 point), round in shape, and has small dimensions (longitudinal size on average 3.20.3 mm, transverse size - 2.80.2 mm), then this is a brachybasilar skull, and one can expect presentation of the sigmoid sinus. On the contrary, if this fossa is well defined (2-3 points), oblong in shape, the longitudinal size prevails over the transverse, averaging 5.50.3 mm and 4.30.3 mm, this is a dolichobasilar skull and there is no need to be afraid during surgical interventions his presentation. In cases where the supraductal fossa is well defined, has a longitudinal size of 3.80.3 mm, a transverse size of 3.20.3 mm, this indicates a mesobasilar shape of the skull and the presentation of the sigmoid sinus is also not noted. We measured 100 skulls of men and women aged 22 to 60 years from the collection of the Anatomy Museum of SSMU. At 98, there was a correlation between the morphometric characteristics of the supracortal fossa and the location of the sigmoid sinus groove. We tested this method on 6 patients. At the same time, during the operation the morphometric characteristics of the supracortal fossa were assessed. Selected examples. Example 1. Patient A. Was admitted to the ENT clinic on April 14, 2001 with a diagnosis of right-sided chronic purulent epitympanitis. On April 20, 2001, conservative-radical surgery on the ear was performed. The longitudinal size of the supraductal fossa is 4.9 mm, the transverse size is 3.9 mm. The fossa is well defined (2-3 points). It can be assumed that the sigmoid sinus is not present. During the operation, presentation of the sigmoid sinus was not noted. Example 2. Patient B. Was admitted to the ENT clinic on August 22, 2001 with a diagnosis of left-sided purulent otitis media and mastoiditis. On August 22, 2001, for emergency reasons, radical surgery was performed on the left ear. The longitudinal size of the supraductal fossa is 3.0 mm, the transverse size is 2.6 mm. The fossa is poorly defined (1 point). The presentation of the sigmoid sinus was expected. The operation was performed with caution, the presentation of the sigmoid sinus was noted, the sinus was exposed, but not opened (injury to the sinus was avoided). Based on the above, we concluded that our proposed method is reliable, reliable, easy to use and can be used in clinical practice. Sources of information 1. Guide to otorhinolaryngology //Ed. I.B. Soldatova. 2nd ed., - M.: Medicine. - 1997. - 608 p. 2. Speransky B.S. Fundamentals of medical craniology. M.: Medicine, 1988. - 287 p.
Formula of invention
A method for intraoperative determination of the presentation of the sigmoid sinus, including assessment of the severity of the supraductal fossa using a four-point system, measurement of its longitudinal and transverse dimensions and if the severity is 0-1 point, and in the longitudinal dimension 3.20.3 mm, in the transverse dimension - 2.80.2 mm establish the presentation of the sigmoid sinus.
Indirect signs of sigmoid sinus presentation may be: a) small mastoid process; b) convex surface of the mastoid process; c) close location of the mastoid-squamosal fissure to the posterior wall of the auditory canal.
Sign atypical position of the dura mater The middle cranial fossa can be determined by the close location of the supramastoid crest to the upper bony wall of the auditory canal and the supracastal spine.
Higher literature data were provided that high bulb domes and large jugular fossae are more common than small ones (in our practice we found the opposite). A high jugular fossa poses a surgical hazard. The large jugular fossa can be located in front and in the middle of the mastoid portion of the facial nerve canal or occupy the entire retrolabyrinthine space.
Very wide jugular the fossa can reach the stem posterior semicircular canal or lie between it and the dura mater. The large jugular fossa can contact the aqueduct of the vestibule and the aperture of the cochlear duct, deform the ducts, simulate their diameter, and even change their anatomical course.
By using X-ray methods The study can reliably measure the width of the jugular foramen and the base of the jugular vein bulb. However, often only on the operating table can one accurately determine the position of the sigmoid sinus, the distance between the sinus and the bulb of the jugular vein, as well as the height of the bulb in the tympanic cavity.
Dimensions of the jugular vein bulb and distance to the sigmoid sinus.
How to determine jugular vein bulb dimensions and the distance from it to the sigmoid sinus, we will show on the cavity where anthromastoidotomy was performed.
From the bottom of the middle cranial fossa We draw the main axis, line (1), in the center of the mastoid cavity to the apex of the process. Distance (1) is 35 mm.
By relative to the main axis(1) we restore four perpendiculars: line (2) runs from the lower wall of the ear canal; line (3) - from the middle of the fold of the digastric tendon; line (4) - from the lower base of the fold of the digastric tendon; line (5) - from the apex of the mastoid process.
Segment(2-5) corresponds to the distance from the lower wall of the ear canal to the apex of the process and ranges from 20 to 22.5 mm. Perpendicular lines drawn to the main axis divide the distance (2-5) into three segments.
Subsequently we installed that the segment (2-3) is the distance from the lower wall of the auditory canal to the top of the jugular vein bulb. The interval (2-4) corresponds to the distance from the lower wall of the ear canal to the base of the vein bulb. Distance (3-4) shows the height of the jugular vein bulb. Section (4-5) is equal to the distance from the base of the bulb to the apex of the mastoid process. As we can see, the segments turned out to be almost equal and each had a length on average of 7.3 mm (fluctuations 6.7 ± 1.2 mm) (see Fig. 52).
Define width of jugular vein bulb possible along line (4). To do this, measure the distance from the lower base of the fold of the digastric muscle tendon to the main axis (1), which will correspond to the width of the base of the bulb. In our calculations, the width of the base of the bulb was 10 mm. The point of intersection of line (4) with axis (1) indicates the place of transition of the sigmoid sinus into the bulb of the jugular vein.
Define jugular vein bulb height possible along line (4). To do this, divide the width of the base of the bulb (the distance from the lower base of the digastric muscle fold to the main axis) in half and restore the perpendicular to the line (3) in the center. The perpendicular line will correspond to the height of the vein bulb.
Perpendicular line length(H), or the height of the bulb, is equal to the distance (3-4). Thus, the height of the bulb is 7.3 mm. The point of intersection of the perpendicular (H) with line (3) corresponds to the apex of the jugular vein bulb.
Next we define distance between jugular vein bulb and sine. To do this, we divide line (3) into three parts: from the center of the fold of the digastric muscle to the top of the bulb (3a), from the top of the bulb to the main axis (3b) and from the main axis to the anterior slope of the sigmoid sinus (Sv).
We got almost equal segments- 5.5 mm each (5 ± 1.3 mm). As we can see, the distance from the anterior wall of the mastoid cavity to the apex of the bulb is 5.5 mm, from the apex of the bulb to the slope of the sigmoid sinus is 11 mm (10 ± 2.2 mm).
Thus, the distance from the lower wall of the ear canal to the top of the jugular vein bulb, the height of the bulb itself and the distance from the base of the bulb to the highest point of the apex of the mastoid process were equal and averaged 7.3 mm.
Presented mathematical model We performed it on forty mastoid processes 35 mm long. Therefore, we suggest turning to more extensive statistical material. These are the results obtained by J. Nadol (1991) and A. Asian (1997) in a study of thousands of pyramids of the temporal bone.
With a length of the mastoid process of 35 mm, the height of the jugular vein bulb is 8 ± 2 (mm), from the lower wall of the external auditory canal to the top of the bulb - 9 ± 2 (mm).
With a process length of less than 35 mm, the height of the jugular vein bulb is 5.3 ± 3 (mm), from the lower wall of the external auditory canal to the top of the bulb - 6.6 ± 3.5 (mm).
With a process length of more than 35 mm, the height of the jugular vein bulb is 6 ± 2.9 (mm), from the lower wall of the auditory canal to the top of the bulb - 8.5 ± 3.7 (mm).
IMAGES OF THE TEMPORAL BONE IN AN OBLIQUE PROJECTION (according to SCHÜLLER)
Purpose of the photo. The image is used to study the structure of the mastoid process, identify abnormalities in the development of the temporal bone, assess the condition of the temporomandibular joint and determine longitudinal fractures of the temporal bone.
Information content of the photo. The image shows the anterior and posterior surfaces of the temporal bone pyramid, the apex of the mastoid process, its pneumatic cells, and the temporomandibular joint. The bright enlightenment with clear edges in the center of the pyramid image is due to the projectionally coinciding external and internal auditory openings. The image makes it possible to evaluate the structure of the mastoid process and identify changes associated with the development of an inflammatory process or tumor. It must be borne in mind that in healthy people there are two variants of the structure of the mastoid process: pneumatic and sclerotic. Sclerotic mastoid can also be the result of chronic inflammation. During the inflammatory process, the transparency of the cells decreases, the partitions between them are destroyed; sclerosis increases, against which residual veiled cells or cavities are sometimes visible. An image of the temporal bone according to Schüller allows one to determine anomalies in the structure of the temporal bone, which are important during surgical intervention. Among the various types of anomalies, the presentation of the sigmoid sinus is of greatest practical importance - its displacement forward, deeper into the pyramid. The Schuller image clearly shows the temporomandibular joint. Therefore, this image can be used to study this joint. In case of skull injuries, vertically running cracks in the parietotemporal region often move to the base of the skull, leading to a longitudinal fracture of the pyramid with damage to the structures of the middle ear. These changes can also be detected on a Schuller image.
IMAGES OF THE TEMPORAL BONE IN THE AXIAL PROJECTION (according to MAYER)
Purpose of the photo. The image is used mainly to study the condition of the middle ear, mainly the mastoid cave (antrum). In case of injuries (in the case of a longitudinal fracture of the pyramid), the image makes it possible to determine damage to the structures of the middle ear.
Information content of the photo. In a picture of the temporal bone according to Mayer, the mastoid cave (antrum) is clearly identified - the largest cell of the mastoid process. The image of the mastoid cave is located next to the posterior wall of the external auditory canal and appears as a clearing with wavy contours, on which small air cells located around it are layered. Up from the mastoid cave, the pneumatic structure of the mastoid process is determined. With chronic inflammatory processes, the image of the mastoid cave changes dramatically: its transparency decreases, and bone sclerosis develops around it. With the development of cholesteatoma, the mastoid cave, as a rule, stretches, its walls straighten, and a clear end plate is formed along the edge. An axial view of the temporal bone (according to Mayer) makes it possible to determine the nature of the operation performed on the middle ear, as well as to determine the degree of damage to the structures of the middle ear during a longitudinal fracture of the pyramid.
IMAGES OF THE TEMPORAL BONE IN THE TRANSVERSE PROJECTION (STEENVERS)
Purpose of the photo. A transverse view of the temporal bone (according to Stenvers) is intended to study the pyramid of the temporal bone, its apex and the internal auditory canal, mainly for the purpose of identifying a tumor of the cerebellopontine angle. The image is also used to determine the transverse fracture of the pyramid.
Information content of the photo. The image clearly shows the pyramid of the temporal bone, including its apex, without significant projection distortions. The contours of the internal auditory canal are clearly defined. Often, changes in the internal auditory canal can only be determined by comparison with data from a similar image of the opposite side. Therefore, photographs of the temporal bones in the transverse projection (according to Stenvers) must be performed on both sides under the same physical and technical shooting conditions. The expansion of the internal auditory canal with corresponding neurological symptoms indicates the presence of an acoustic neuroma. The labyrinth and cochlea are also visible in the photographs, but it is not possible to recognize the changes occurring here from the photographs.(
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Otogenic intracranial complications are caused by the anatomical and topographic proximity of the middle ear to the brain and its vascular formations. The ear communicates with the cranial cavity through numerous vascular and nerve canals, as well as the “water conduits” of the ear labyrinth, dehiscences and microcracks, which during otogenic infection serve as a gateway for its penetration into the cranial cavity (Fig. 1).
Rice. 1. Ways of spread of infection in purulent otitis media: a - Bezold's mastoiditis: 1 - destruction of the apex of the mastoid process; 2 — abscess formation of mastoid cells; b — extradural abscess 1 — osteolysis of the internal bone plate of the upper wall of the supratympanic space; 2 - protective granulation tissue; c — thrombosis of the sigmoid sinus: 1 — focus of osteolysis; 2 - zone of thrombosis of the sigmoid sinus; d - brain abscess: 1 - focus of inflammation in the mastoid process; 2 - abscess of the temporal lobe; 3 - cerebellar abscess
The most common intracranial complications include: otogenic meningitis, extradural and subdural abscess, temporal lobe abscess and cerebellar abscess, as well as thrombophlebitis of the sigmoid sinus and, as its complication, sepsis.
Otogenic meningitis
Meningitis ( meningitis otica; from Greek meninx- meninges) is an inflammation of the meninges, which is differentiated into three forms in accordance with which of the three meninges is affected: meningitis- inflammation of the soft membrane, pachymeningitis- hard shell, arachnoiditis- arachnoid membrane. Based on their origin, meningitis is divided into primary and secondary. Otogenic meningitis refers to secondary inflammation of the meninges, occurring in most cases as a diffuse inflammatory process.
Etiology. The causative agent of meningitis can be any pathogenic microorganism (staphylococcus, streptococcus, diplococcus, meningococcus, tuberculosis bacillus, spirochete pallidum, etc.). Meningitis can occur with influenza, typhoid fever, brucellosis, leptospirosis, tularemia, etc. As for otogenic meningitis, most often the etiological factor is hemolytic, mucous and pyogenic streptococcus, pneumococcus and other flora that grow in the primary focus of inflammation.
Pathological anatomy. Damage to the dura mater can manifest itself as simple inflammation and edema, as well as external and internal inguinal meningitis, accompanied by adhesions. At the beginning of inflammation, the pia mater becomes rigid, then infiltrated by purulent stripes running along the vessels. The cerebral cortex also becomes inflamed and infiltrated, the ventricles of the brain expand due to overproduction of cerebrospinal fluid and disruption of its circulation. The inflammatory process is most pronounced in the vicinity of the otogenic focus, but it can quickly spread to the convex or basal meninges. The formation of adhesions blocks the purulent process, resulting in the formation of extensive extra- or subdural abscesses.
Pathogenesis. Otogenic meningitis most often occurs as a complication of chronic purulent epitympanitis in the acute stage, in the presence of cholesteatoma and bone caries. However, just as often it occurs as a complication of acute purulent otitis media with hypervirulent flora, the presence of a number of anatomical and other contributing conditions, for example, as a result of intraoperative trauma to the dura mater, with injuries to the temporal bone with damage to its internal cortical layer. Otogenic meningitis can occur with petrositis, labyrinthitis, thrombophlebitis of the sigmoid sinus, or as a complication of a primary brain abscess.
There are the following ways of spreading infection (in order of frequency):
A) bone path, in which the destructive process spreads to the posterior wall of the cave near the sigmoid sinus, the roof of the cave and the tympanic cavity, the perilabyrinthine and periapical cells of the pyramid;
b) labyrinthine path occurs as a result of labyrinthitis complicating acute or chronic purulent otitis media; this path also includes the internal auditory canal, the aqueducts of the cochlea and vestibule, and the endolymphatic sac;
V) vascular pathway- venous, arterial and lymphatic; most often the venous route is realized through phlebitis of the sigmoid sinus;
G) performed paths- dehiscence in the roofs of the antrum and tympanic cavity, lying in the petrosquamosal suture, bone canals of the facial and petrosal nerves and branches of the tympanic plexus, unobliterated rockomastoid canal of Moore (Mouret); Performed pathways should also include lines of consolidated fractures of the pyramid, which usually heal only with the help of fibrous tissue.
A contributing factor for otogenic meningitis is a general weakening of the body as a result of an intercurrent infection (viral infections, childhood diseases, immunodeficiency conditions, vitamin deficiency, alcoholism, head and ear trauma).
Clinical picture. Otogenic meningitis occurs in three periods - initial, peak and terminal.
Initial period creeps up unnoticed and is characterized by an increase in headache, which becomes so severe that the patient screams from it (a symptom of meningitis scream). Sometimes the pain syndrome is accompanied by vomiting of central origin, which is characterized by the absence of previous nausea and suddenness. The general condition deteriorates slightly, the pulse rate is increased and corresponds to body temperature (38-38.5 ° C). Mental disorders are manifested by anxiety and agitation. Loud sounds and bright lights cause irritation (hyperacusis, photophobia). Knitzk's symptoms (pain when pressing on the retromandibular area) and Kulenkampf's symptoms (pain when pressing on the back of the neck) may be detected.
High period is characterized by the generalization of the inflammatory process with its transition to the brain substance (encephalitis) and is manifested by a number of subjective and objective signs and inflammatory changes in the cerebrospinal fluid.
Subjective signs: severe diffuse headache caused by increased intracranial pressure, aggravated by the slightest movements of the patient. In children, headaches manifest themselves as so-called hydrocephalic cry- sudden screaming during sleep.
Objective signs are manifested by general cerebral and focal symptoms. TO general cerebral symptoms include (especially in children) epileptiform seizures, convulsions, hyperesthesia in relation to pain, smell, light and sound stimuli, under the influence of which “convulsive readiness” is activated. With severe intoxication, mental disorders occur, manifested by stupor, irritability, tearfulness, isolation, detachment from the outside world, and sometimes delirious-oneiric states. In infants, due to developing cerebral edema and hydrocephalus, the fontanelles protrude; Percussion of the head reveals a characteristic “watermelon” sound.
Focal symptoms caused by damage to brain tissue and cranial nerves located in the area of the inflammatory process. Functional dysfunction is very common oculomotor nerves, manifested by strabismus, sometimes complete ophthalmoplegia. Ptosis and anisocoria may occur. In 30% of cases with otogenic meningitis, neuritis occurs optic nerve.
When the infectious process spreads to the substance of the spinal cord, a picture of spinal motor disorders arises, for example, Brown-Séquard syndrome— symptom complex for unilateral transverse spinal cord injury: spastic paralysis of the muscles with a disorder of deep sensitivity on the affected side and weakening of pain and temperature sensitivity on the opposite side.
Tonic muscle contraction- the most striking and typical sign of meningeal syndrome. An early and persistent symptom of meningitis is stiff neck, as a result of which the head is thrown back, its movements are difficult, attempts to tilt the head to the chest cause pain in the spine due to the tension of the inflamed meninges.
Meningeal syndrome is detected by a number of tests. Thus, the patient’s voluntary attempt to touch the chest with his chin fails. With a passive tilt of the head to the chest in a patient lying on his back, a reflex flexion of the legs occurs in the knee and hip joints ( upper, or occipital, Brudzinski's sign). When one leg passively flexes at the knee and hip joints in a patient lying on his back, the other limb involuntarily bends at these joints ( inferior Brudzinski's sign). Kernig's sign (I) lies in the fact that after preliminary extension of the leg in the hip joint (adduction of the thigh to the abdomen) and flexion of the lower leg in the knee joint, it becomes impossible to straighten this lower leg in the knee joint while maintaining the position of the thigh: an attempt to straighten the lower leg causes sharp pain in the cervico-occipital region due to tension of the affected meninges. With acute meningitis, another sign of meningeal syndrome is expressed - “ pointer dog pose": the head is thrown back, the torso is in a hyperextension position, the legs are brought to the stomach. This position is most often observed in young children and is most characteristic of epidemic cerebrospinal meningitis.
Myotonic signs of central origin include Lasègue's symptom (hanging symptom): if you lift a child with meningitis by the armpits, an involuntary bending of the legs at the knees and bringing the hips to the stomach occurs, while a healthy child actively moves his legs as if walking on air. An acute inflammatory process of the meninges is characterized by a number of other symptoms ( Babinsky, Oppenheimer, Rose - Nylen etc.).
Sensory disorders are central in nature and, as a rule, are accompanied by hyperesthesia or hypoesthesia of the skin. Acute meningitis is also characterized by a complex of autonomic disorders, which often causes a severe clinical course of the disease and, in extremely severe cases, leads to death. The main manifestations of vegetative syndrome concern disruption of the cardiovascular and respiratory systems.
Often, with meningitis of the posterior cranial fossa, swallowing disorders are observed due to damage to the caudal group of cranial nerves (this group includes the accessory, hypoglossal, vagus and glossopharyngeal nerves), and a partially inhibited state of the patient.
Vegetative syndrome in meningitis also includes pupillary disorders, manifested either by unstable anisocoria, or by a violation of the pupillary reaction to light, as well as by a violation of accommodation and convergence.
Due to general intoxication of the body, the lability of the vasomotor system (Trousseau's symptom) sharply increases: in response to touch or pressure, red and white spots or even pinpoint hemorrhages appear on the skin, indicating an increase in the permeability of the vascular wall.
Cerebrospinal fluid changes play a decisive role not only in establishing the final diagnosis of acute meningitis, but also in determining its form, which is important for prognosis and treatment. Changes in the cerebrospinal fluid are determined by a number of signs, such as pressure, cellular and biochemical composition, color, consistency, the presence of a certain microbiota, etc.
Terminal period characterized by a gradual increase in the symptoms of the height of the period, the stiffness of the neck muscles gradually turns into opisthotonus, consciousness is completely lost, breathing takes on a Cheyne-Stokes character, the pulse is 120-140 beats per minute, arrhythmic. Involuntary passage of feces and urination occur. With increasing signs of increased intracranial pressure, death occurs within 1.5-2 minutes when breathing stops and cardiac activity stops.
Forecast. Currently, despite the use of highly effective antibiotics and modern methods of surgical treatment of the primary lesion, the prognosis remains serious.
Diagnosis and differential diagnosis. The diagnosis is not difficult during the height of the disease; it is established on the basis of anamnesis, the presence of acute or chronic (in the acute stage) purulent otitis media, complicated by cholesteatoma, bone caries, labyrinthitis, etc. Otogenic meningitis follows differentiate from other forms of inflammation of the meninges:
A) tuberculous meningitis, which is characterized by the presence of a tuberculosis infection, a longer course, specific changes in the cerebrospinal fluid (CSF), in which there is a sharp decrease in chlorides and an increase in protein fractions, the presence of a tuberculosis bacillus and a large number of lymphocytes;
b) syphilitic meningitis, which is characterized by other specific signs of syphilis, clear, microflora-free CSF, positive Bordet-Wassermann, Nonne-Appelt and Pandi reactions;
V) epidemic cerebrospinal meningitis, which is characterized by an epidemiological situation, the presence of meningococcus in the CSF and in the mucus of the upper respiratory tract, and a higher incidence in children's groups;
G) pneumococcal meningitis, which is characterized by the absence of an otogenic focus of infection;
d) traumatic and toxic(poisoning) meningitis - according to medical history;
e) lymphocytic meningitis, in which there is no otogenic focus of infection and pyogenic flora in the CSF, it sometimes occurs in acute epidemic viral parotitis;
and) meningism- meningeal syndrome, which occurs with toxic (aseptic) and traumatic irritation of the meninges due to increased intracranial pressure, cerebral edema, and traumatic brain injury. Characterized by headache, neck stiffness, Kernig sign, vomiting and dizziness. Unlike meningitis, these phenomena are less pronounced; no pathological changes are detected in the CSF.
Treatment with otogenic meningitis it is divided into conservative And surgical with supportive therapeutic treatment.
Conservative treatment consists in the mandatory prescription of sulfonamides and antibiotics. From drugs sulfonamide series, for example, you can use sulfalene meglumine, produced in ampoules of 5 ml in the form of an 18.5% solution for injection. This is a drug with a prolonged, broad bacteriostatic spectrum of action. It is used for various forms of purulent infections, including severe septic conditions, purulent meningitis and meningoencephalitis, as well as for the prevention of complications of bacterial infection in the postoperative period, for example after extended radical ear surgery performed with exposure of the dura mater or sigmoid sinus . The drug is prescribed intramuscularly or intravenously in a stream or drip, depending on the severity of the disease. For purulent meningitis, use 1.0 ml once a day during the entire course of treatment. Other sulfonamides may be used sulfate, sulfatima-SS And sulfatima-DS.
Among antibiotics, broad-spectrum drugs are used (fluoroquinolone series, semi-synthetic penicillins, cephalosporins, aminoglycosides, macrolides, etc.). For meningitis caused by Pseudomonas aeruginosa, it is advisable to use carbenicillin, polymyxin, gentamicin. From the group of macrolides it is possible to use sumameda, highly active against both gram-positive (staphylococci, streptococci, pneumococci) and gram-negative microorganisms (enterococci, Escherichia coli, hemophilus influenzae, shigella, salmonella), as well as mycoplasmas, chlamydia, legionella and bacteroides.
To combat toxicosis in all forms of meningitis (otogenic purulent, tuberculous, epidemic cerebrospinal, etc.), heavy drinking is prescribed, as well as intravenous administration of glucose, water-salt and protein solutions with simultaneous dehydration therapy (Lasix, Diacarb, mannitol, etc.) , preventing cerebral edema.
Surgical treatment used depending on the type and form of the primary source of infection, complicated by meningitis.
At acute purulent otitis media, when signs of otogenic meningitis appear during the first week of the disease or when acute otitis is complicated by mastoiditis and then meningitis, a wide tympanotomy is performed to expose the meninges of the temporal lobe and cerebellum. At chronic purulent otitis media(otomastoiditis) an extended radical operation is performed with exposure of the dura mater in places of pathologically altered bone.
To examine the CSF, reduce pressure in the subarachnoid space and prevent cerebral edema, as well as to remove pus and toxins from this space and administer antibiotics and other medications, a lumbar or suboccipital puncture is performed, as well as, if indicated, a puncture of the third or fourth ventricle of the brain. In an infant, CSF is obtained by puncture of the fontanel.
Extradural abscess
Otogenic extradural abscess (see Fig. 1, b) appears in the form of limited purulent pachymeningitis located in the area of carious (osteomyelitis) lesions of the internal cortical layer of the bone wall of the tympanic cavity or the mastoid process, bordering the middle or posterior cranial fossa, respectively. The accumulation of pus occurs between the skull bone and the outer surface of the dura mater; its integrity is not broken. Extradural abscess in 3/4 of cases develops as a complication of acute purulent otitis media. Contributing factors are a well-developed cellular system of the temporal bone, the presence of perforated bone tracts (dehiscences), reduced immunity, vitamin deficiency, allergies, etc. Young people are more often affected.
Clinical picture. Extradural abscess can occur in three forms: latent, subacute and acute. Most often occurs latent form, which is masked by clinical manifestations of mastoiditis or exacerbation of chronic purulent epitympanitis. This form is often discovered during radical surgery or mastoidotomy. Subacute form differs from latent in the appearance of paroxysmal headaches on the affected side. With this form, deep palpation of the mastoid region can identify typical pain points.
Acute form proceeds rapidly with high hectic temperature, sometimes acquiring a septic character, with chills, meningeal symptoms and signs of increased intracranial pressure. It is this form that is often complicated by generalized meningitis and brain abscess.
Diagnosis extradural abscess is established on the basis of the presence of persistent headaches localized in the temporal region, profuse purulent discharge from the ear with a fetid odor, severe inflammatory changes in the blood, meningeal symptoms, data from lumbar puncture and computed tomography.
Differentiate extradural abscess with primary meningitis (absence of otitis media) and brain abscess (presence of focal symptoms).
Treatment exclusively surgical: extended radical surgery on the ear, maximum opening of the mastoid cells, exposure of the dura mater, identification of the abscess and its removal, followed by drainage of its cavity. Granulations on the dura mater should not be removed, as they play a protective role. If a subdural abscess is suspected, a puncture is performed from the side of the normal dura mater in the direction of the suspected subdural abscess (after thoroughly removing the pus, washing the extradural abscess cavity with disinfectant solutions and disinfecting the puncture site with 5% tincture of iodine). At the same time, conservative treatment is carried out, as for meningitis.
Subdural abscess
The causes of subdural abscess are the same as extradural ones. The abscess cavity is located between the dura and arachnoid membranes and the pia mater adjacent to the brain tissue. In the middle cranial fossa, a subdural abscess occurs when the upper wall of the epitympanic recess is damaged. In the posterior cranial fossa it forms as a complication of purulent labyrinthitis, anthritis or thrombophlebitis of the sigmoid sinus.
Pathomorphology and pathogenesis. A subdural abscess is one or more interthecal abscesses immured in adhesions, containing foul-smelling, greenish, creamy pus. The dura mater over the abscess is thinned, loses its natural bluish color and becomes pale yellow or yellow-green. The brain tissue under the abscess is swollen with symptoms of local encephalitis.
Clinical picture determined by the relationship of the subdural abscess to the source of infection, the location of the abscess and its prevalence. There are general, cerebral and focal symptoms. General symptoms: fever, inflammatory changes in the blood, weakness, increased fatigue, lack of appetite. Brain symptoms: persistent constant headache, mainly on the side of the abscess, nausea and vomiting of a central nature, congestive optic discs (increased intracranial pressure), meningeal symptoms and moderate pleocytosis in the cerebrospinal fluid.. With severe cerebral symptoms, stupor, confusion, and coma are observed.
Focal symptoms are caused by local encephalitis: when it is localized in the middle cranial fossa, these symptoms manifest themselves as mild pyramidal signs on the opposite side (transient weakness or flaccid paresis of the upper limb). When a subdural abscess is localized in rear cerebellar symptoms occur in the cranial fossa (undulating nystagmus, impaired coordination of movements, adiadochokinesis, etc.). When a subdural abscess is localized in the area of the apex of the pyramid, symptoms characteristic of Gradenigo syndrome occur.
Diagnosis. With pronounced brain symptoms, diagnosis is very difficult; contributes to the diagnosis of the presence of a purulent process in the middle ear. A definitive diagnosis can only be made with CT or MRI. The final topographic-anatomical diagnosis is established only on the operating table.
Forecast serious, depending on the timeliness of diagnosis, the virulence of the flora, the general condition and state of the body’s immune system, the presence or absence of other intracranial complications.
Treatment exclusively surgical by removing the primary focus, exposing the dura mater, opening it, removing the subdural abscess and non-viable parts of the meninges, draining the abscess cavity and washing it with antibiotic solutions using them intramuscularly, intralumbarally or suboccipitally. At the same time, measures are taken to strengthen the general condition of the body and immunity.
Otogenic brain abscess
The localization of an otogenic brain abscess is most often determined by the location of the inflammatory process in the middle ear system. With anthritis and mastoiditis, as a rule, a cerebellar abscess occurs; with epitympanitis, an abscess of the temporal lobe occurs. When infection spreads hematogenously, abscesses can occur at a considerable distance from the primary source of infection. In 80% of cases, otogenic brain abscesses arise as complications of chronic purulent otitis media, complicated by cholesteatoma and bone caries, and account for 50-60% of all brain abscesses of various origins. Otogenic abscesses of the cerebrum are 5 times more common than cerebellar abscesses. Most often, these complications occur at the age of 20-30 years.
Risk factors in patients with chronic suppurative otitis media include: traumatic brain injury, pregnancy, pneumatic type of structure of the temporal bone, presentation of the sigmoid sinus, low position of the middle cranial fossa, general infections (influenza, pneumonia, etc.), vitamin deficiency, immunodeficiency and dystrophic states, etc.
Clinical picture. According to the clinical course, otogenic abscess of the temporal lobe is a threefold “insidious” disease: at the onset it is masked by signs of the underlying disease; the second time it misleads with its light gap (formation of a dense protective capsule and elimination of perifocal encephalitis); The third danger is that with ongoing low-grade inflammation in the event of unfavorable conditions (influenza, acute respiratory infections, traumatic brain injury, etc.), the process flares up with renewed vigor and often ends in death, especially when pus breaks through into the ventricles of the brain.
The period of pronounced clinical manifestations usually occurs suddenly and is characterized by three syndromes: toxic, cerebral and focal.
Toxic syndrome manifested by the following symptoms: increased body temperature with fluctuations from 37.5 to 40 ° C and bradycardia (a symptom of temperature-pulse dissociation); cessation of suppuration from the ear with an increase in clinical symptoms of a septic nature; gastrointestinal disorders (constipation, rotten belching); changes in peripheral blood (increased ESR, polynuclear leukocytosis, increasing anemia).
Brain syndrome is determined by an increase in intracranial pressure: headache with paroxysms of hemicrania, coinciding with the cessation of otorrhea (abscess drainage). Cephalgia crises are accompanied by nausea and vomiting; bradycardia (40-50 beats/min at body temperature 39-40 °C); mental disorders manifest themselves either in the form of lethargy, drowsiness, weakening of attention and memory while maintaining intelligence, or in a deeper form with a decrease in intellectual and mental activity, prostration, etc.
Children may experience epileptiform seizures; ocular symptoms depend on the size of the abscess and the degree of increase in intracranial pressure (strabismus, spontaneous nystagmus, anisocoria; in the fundus - congestive discs, venous stasis, arterial spasm and pinpoint hemorrhages); signs of meningeal irritation are variable and often weakened, but with concomitant purulent meningitis they become significant.
Focal symptoms appear later and are caused by spreading perifocal encephalitis, edema and pressure from the increasing abscess on areas of the brain located at some distance from the abscess cavity. Focal symptoms are manifested by motor, sensory disorders, hearing, speech, and smell disorders.
Terminal period occurs when pus breaks through into the ventricles of the brain or into the subarachnoid convexital space, with compression of the brain stem.
Diagnosis acute abscess of the temporal lobe is established on the basis of the presence of acute or chronic purulent otitis media in the acute stage, a sudden deterioration in general condition, the appearance of the above-described symptoms and MRI data. Clinical picture chronic abscess this localization is little expressed. There is a period of light that can last for months or years. The abscess can progress to the stage of fibrosis with complete recovery. In such cases, the diagnosis is made post factum, either by X-ray of the brain for some other reason, or by autopsy.
Forecast serious, especially in acute cases and in children, with metastatic abscesses localized near the ventricles of the brain, convexital subarachnoid space, in the brain stem, in persons with immunodeficiency conditions (HIV), in diabetes, weakened by chronic diseases. With timely surgical treatment and appropriate drug therapy, recovery is the most common outcome of the disease.
Treatment carried out in several directions: a) sanitation of the primary focus of infection and abscess by draining it in fresh cases, when rupture of an unformed capsule is almost inevitable, or in the presence of a dense capsule - by its extracapsular removal; b) massive antimicrobial therapy using antibiotics; c) measures aimed at preventing or eliminating hydrocephalus and cerebral edema, strengthening the immune system, etc.; d) elimination of cardiac and respiratory function disorders; ensuring the normal functioning of the digestive and excretory systems, as well as adequate nutrition orally or through the parenteral administration of modern nutritional cocktails.
Otogenic thrombophlebitis of the cerebral sinuses. Otogenic sepsis
The routes of spread of otogenic infection to the cerebral venous sinuses are determined by their topographic relationship to the anatomical formations of the middle and inner ear. There are phlebitis of the sigmoid sinus, jugular vein bulbs, thrombophlebitis of the cavernous sinus and phlebitis of other venous systems of the brain. In purulent diseases of the middle ear, the sigmoid sinus is most often affected, then the bulb of the jugular vein; the remaining cases occur in the cavernous and other venous sinuses of the brain.
Phlebitis of the sigmoid sinus and jugular vein bulb (flebitis sinuso-jugularis)
Pathological anatomy. The inflammatory process in the sinus (see Fig. 1, c) can begin with peri- or endophlebitis. Periphlebitis occurs when infection penetrates from the affected area of the middle ear. The color of the sinus wall becomes yellow-gray, it is covered with granulations and fibrinous plaque, and an abscess may form nearby. Endophlebitis occurs most often when the infection enters the sinus cavity through an emissary, for example through mastoid vein, entering directly into the sigmoid sinus. First, a parietal thrombus is formed (parietal endophlebitis), which increases in both directions and completely clogs the sinus (obliterating endophlebitis); penetrating into the bulb of the jugular vein and into the internal jugular vein, it can reach innominate vein. The blood clot can fester, which often leads to complications such as meningitis, brain abscess, septicopyemia, multiple abscesses of the lung and other internal organs.
Clinical picture thrombophlebitis of the sigmoid sinus consists of local and general symptoms.
Local symptoms: swelling in the postauricular area (Griesinger's symptom), pain on deep palpation of the posterior edge of the mastoid process and the exit site of its emissaries, pain, swelling and hyperemia of the skin along the common jugular vein when phlebitis spreads to this vein. With the spread of phlebitis and thrombus to the upper longitudinal sinus, stagnation occurs in the emissaries coming from the veins of the convexital surface of the head, expansion and increased tortuosity of these veins on the surface of the head (symptom of the “head of Medusa”).
General symptoms. The onset of the disease is sudden. Against the background of acute or exacerbation of chronic purulent otitis media, severe chills occur with a temperature rise of up to 40 ° C. After the debut, a characteristic clinical picture is established, which for phlebitis of the sigmoid sinus can occur in several forms - from latent and mild to severe septic.
Latent form proceeds without septicemia with very scanty symptoms. Sometimes mild signs of Griesinger's and Queckenstedt's symptoms may appear. The latter is as follows: in healthy people, compression of the jugular vein increases intracranial pressure, which causes increased droplets during lumbar puncture; in the presence of occlusion of the sigmoid sinus (thrombosis, tumor), an increase in droplets is not observed. At the same time, a positive Knock test is observed: with pressure through the abdominal wall on the inferior vena cava, the pressure of the cerebrospinal fluid and the frequency of droplets during lumbar puncture increase.
Pyemic form characterized by septic fever, severe chills, and signs of sepsis.
Typhoid form differs from the previous ones in a constant high body temperature without pronounced swings. The patient develops a general serious condition with periodic loss of consciousness, insomnia, toxic disorders of cardiovascular and respiratory activity, an enlarged spleen, and multiple intradermal hemorrhages.
Meningeal form characterized by signs of meningitis and inflammatory changes in the CSF.
Thrombosis of the jugular vein bulb occurs more often with acute otitis media in children. It manifests itself as painful swelling and hyperemia of the skin in the area of the apex of the mastoid process and behind the angle of the lower jaw. These phenomena can easily be mistaken for incipient mastoiditis. When the infection spreads in the direction of the lacerated foramen, the cranial nerves located here (glossopharyngeal, vagus, sublingual) may be involved in the inflammatory process, which is manifested by partial signs of Verne's syndrome.
Jugular vein thrombosis manifested by pain in the neck on the side of inflammation when turning the head, as well as swelling of the tissue surrounding the jugular vein, spreading along the outer edge of the sternocleidomastoid muscle, the presence of a dense and mobile cord in this area (compaction of the vein and surrounding tissue).
Diagnosis thrombophlebitis of the sigmoid sinus does not cause any particular difficulties if it develops as a consequence of inflammation of the middle ear, mastoiditis and manifests itself with the symptoms described above. Differential diagnosis is carried out with other otogenic intracranial complications, mastoiditis and its cervical complications, for example, Bezold’s “cervical” mastoiditis (see Fig. 1, a).
Treatment otogenic sinus thrombosis is determined by the state of the primary focus of infection, the severity of the general septic syndrome, the presence or absence of distant purulent complications. Treatment begins with emergency elimination of the primary source of infection. Conservative measures include massive antibiotic therapy (intravenous or intraarterial), normalization of blood rheological parameters and the content of electrolytes in it, detoxification of the body, saturation with vitamins, and strengthening of the immune system. In severe cases, they resort to the production and use of antitoxic and antimicrobial serums specific to pathogenic microbiota.
Surgical treatment for sigmoid sinus thrombosis is urgent even at the slightest suspicion of the occurrence of this complication. The sigmoid sinus is exposed and opened within the limits of its pathological changes. After opening the sinus, the further course of the surgical intervention is dictated by the pathological changes in the sinus and the general condition of the patient. The main goal of surgical intervention is to completely eliminate the source of infection and prevent its spread through the venous tract.
Forecast with limited thrombophlebitis of the sigmoid sinus and timely surgery, as well as with effective complex drug treatment, life is favorable. The prognosis is cautious and even doubtful for septicemia and septicopyemia, especially when distant metastatic foci of infection occur in the internal organs. Often such foci of infection lead to chronic sepsis, the treatment of which can last for many months.
Labyrinthitis
Acute and chronic purulent otitis media can be complicated by labyrinthitis, an inflammation of the membranous formations of the inner ear. Labyrinthitis occurs in two forms - serous And purulent. Serous form with timely medical and surgical treatment of the primary source of infection, it can undergo reverse development without noticeable functional disorders in the organ of hearing and vestibular apparatus. Purulent form leads to a total shutdown of these sensory organs and is fraught with intracranial complications. The route of spread of complications lies through the endolymphatic sac and the internal auditory canal.
The clinical picture of acute serous labyrinthitis is manifested by a violent Meniere-like syndrome: dizziness, spontaneous nystagmus, imbalance, nausea, vomiting, severe autonomic disorders, hearing loss and tinnitus. Specific vestibular reactions are initially directed towards the diseased ear (dizziness, spontaneous nystagmus, etc.), but as the inflammatory process develops, the causal labyrinth is suppressed and the vector of these reactions changes to the opposite. At the height of the clinical manifestations of serous labyrinthitis, it is impossible to conduct any vestibular diagnostic tests. In cases where the process reaches the purulent phase and the labyrinth is switched off without intracranial complications, the vestibular syndrome subsides, but the vestibular function of this labyrinth remains switched off, and the function of the vestibular analyzer as a whole is realized due to the other labyrinth remaining intact and the compensatory reaction of the vestibular nuclei.
With precocious serous labyrinthitis As a complication of acute otitis media, a more extended than usual paracentesis is sometimes used, which often leads to the reverse development of the inflammatory process in the labyrinth. However, if signs of switching off the labyrinth occur (perceptual deafness, spontaneous nystagmus in the healthy ear), an extended radical operation with trepanation of the labyrinth is performed (Piquet operation). At purulent labyrinthitis extended radical surgery is supplemented by opening the anterior and posterior segments of the labyrinth (Hautan, Neumann or Gaston operations). In exceptional cases, if antibiotic therapy is ineffective, they resort to translabyrinthine opening of the internal auditory canal. In case of post-traumatic purulent otitis media and concomitant fracture of the base of the skull with a rupture of the dura mater, plastic closure of the membrane defect with an autograft from the fascia lata is used.
Otorhinolaryngology. V.I. Babiyak, M.I. Govorun, Ya.A. Nakatis, A.N. Pashchinin
