Phlebitis of the sigmoid sinus: causes, symptoms, diagnosis, treatment

According to V.T. Palchun et al. (1977), the sigmoid and transverse sinuses are most frequently affected (79%), then the jugular bulb (12.5%), the remaining cases occur in the cavernous and petrosal sinuses.

Pathological anatomy. The inflammatory process in the sinus can begin with periphlebitis or endophlebitis, depending on the route of infection.

Periphlebitis occurs when infection directly penetrates from the affected area of the middle ear. In this case, the sinus color changes from bluish to yellow-gray, its outer wall can be covered with granulations and fibrinous plaque, and an abscess can form nearby. Periphlebitis can be limited or widespread. In the latter case, the inflammatory process spreads to the bulb of the jugular vein and below, and upwards - along the transverse sinus to the dura mater covering the cerebellum, giving rise to pachymeningitis of the posterior cranial fossa. Sometimes periphlebitis spreads along the collaterals of the transverse and sigmoid sinuses (petrous and sagittal sinuses, emissary veins of the mammillary process), and as a result of necrotic perforation of the dura mater, SDA occurs.

Endophlebitis occurs most often when infection penetrates the sinus cavity through an emissary, for example, through the mastoid vein, which enters directly into the sigmoid sinus. Endophlebitis can occur as a result of damage to the sinus wall caused by periphlebitis. The condition for the occurrence of endophlebitis is damage to the sinus wall throughout its entire thickness, which creates conditions for the formation of first a parietal (parietal endophlebitis), and then a total thrombus (obliterating endophlebitis). Once formed, the thrombus continues to grow in both directions, sometimes reaching the opposite lateral sinus, on the one hand, and, having penetrated the bulb of the jugular vein and the internal jugular vein, descends into the innominate vein. The thrombus can transform into a fibrous plug, tightly fused with the sinus wall (sinus obliteration), which is often discovered during surgery on the mastoid process with exposure of the sinus. However, more often the thrombus becomes infected and suppurates, which often leads to very dangerous complications (meningitis, brain abscess, septicopyemia, lung abscesses). Purulent emboli, getting into the systemic circulation, can cause purulent inflammation in various parts of the body and internal organs. According to various authors, the frequency of metastatic abscesses in thrombophlebitis of the sigmoid sinus ranges from 30 to 50%.

Pathogenesis of sigmoid sinus phlebitis. The most common cause of sigmoid sinus and jugular bulb phlebitis is chronic purulent inflammation of the middle ear (caries, cholesteatoma, mastoiditis). In rarer cases, acute purulent otitis media and acute mastoiditis may cause sinusojugular phlebitis. Intraoperative and domestic trauma in the presence of chronic purulent otitis media may contribute to sigmoid sinus phlebitis.

Symptoms of thrombophlebitis of the sigmoid (lateral) sinus consist of local and general symptoms. Local symptoms are weakly expressed: slight swelling in the parotid region (Griesinger's symptom), pain with 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; when phlebitis and thrombus spread to the superior longitudinal sinus, there is an overflow of blood in the emissaries to the convexital surface of the head and an overflow of the veins of the head surface, their expansion and increased tortuosity (Medusa's head symptom). General symptoms are typical for phlebitis of any intracranial sinus and reflect the general septic state of the body.

The onset of the disease is usually sudden: against the background of acute or exacerbation of chronic purulent otitis, severe chills with a rise in temperature to 40°C occur. Sometimes the intensity of the chills increases gradually, along with the rise in body temperature, from attack to attack, reaching a peak at a temperature of 40°C. Sometimes the chills are preceded by increasing hemicrania on the side of the affected ear, which can serve as an early sign of the onset of phlebitis of the cerebral sinus. After the debut, a characteristic clinical picture is established, which for phlebitis of the lateral (sigmoid) sinus can occur in several forms - from latent and the mildest to severe septic.

The latent form occurs without septicemia with very scanty symptoms. It is often detected only during surgery on the mastoid process. Sometimes mild signs of the Griesinger symptom, Quekenstedt (a sign of impaired circulation of cerebrospinal fluid in the sigmoid and transverse sinuses: in healthy people, compression of the jugular vein increases intracranial pressure, which is seen by the increased frequency of dripping during lumbar puncture; in the presence of sigmoid sinus occlusion caused by thrombosis, tumor, this is not observed) with a positive Stacky test (Stacky symptom - when pressing through the abdominal wall on the inferior vena cava, the pressure of the cerebrospinal fluid increases). In this form, the size of the thrombus in the sigmoid sinus is limited to the site of osteitis of the bone wall of the sinus canal, and its proximal end remains uninfected.

The pyemic form is characterized by septic fever, severe chills and signs of sepsis.

The typhoid form differs from the previous ones by a constant high body temperature without pronounced swings. The patient develops a general severe condition with periodic loss of consciousness, insomnia, toxic disorders of the cardiovascular and respiratory activity, an enlarged spleen, multiple intradermal hemorrhages are detected.

The meningeal form is characterized by signs of meningitis and inflammatory changes in the cerebrospinal fluid.

Thrombosis of the bulb of the jugular vein most often occurs in acute otitis in children. It manifests itself as painful swelling and hyperemia of the skin in the area of the apex of the mastoid process, behind the angle of the lower jaw, at the upper end of the sternocleidomastoid muscle. These phenomena can easily be mistaken for the onset of mastoiditis, which delays the true diagnosis of thrombophlebitis of the bulb of the jugular vein. When the infection spreads in the direction of the lacerated opening, the nerves located here (glossopharyngeal, vagus, hypoglossal) can be involved in the inflammatory process, which is manifested by partial signs of Berne's syndrome (alternating paralysis developing due to damage to the pyramidal tract in the medulla oblongata, manifested by contralateral spastic hemiparesis, homolateral paralysis of the soft palate, swallowing muscles and muscles of the larynx). Sometimes thrombophlebitis of the jugular bulb does not manifest itself with local symptoms; its presence can be suspected only on the basis of septicopyemia and detected during surgery on the mastoid process.

Jugular vein thrombosis is manifested by pain in the neck on the side of inflammation when turning the head, as well as swelling of the tissue along 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). If the jugular vein thrombus extends to the confluence with the subclavian vein, then signs of the development of collateral circulation can be detected, manifested by an increase in the venous pattern on the corresponding half of the neck, as well as the absence of a blowing sound during auscultation of the jugular vein.

Diagnosis of lateral sinus thrombophlebitis 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.

Treatment of otogenic sinus thrombosis is determined by the condition of the primary source of infection, the severity of the general septic syndrome, and the presence or absence of remote pyemic complications. In almost all cases, after appropriate preoperative rehabilitation preparation, treatment begins with emergency elimination of the primary source of infection. An integral part of the treatment are non-surgical measures, including massive antibiotic therapy (intravenous or intra-arterial), normalization of blood rheological parameters and electrolyte content, 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 of sigmoid sinus thrombosis. This treatment is urgent even at the slightest suspicion of the occurrence of this disease. In any type of intervention on the middle ear and mastoid process, it is necessary to remove as completely as possible all the cells of the mastoid process, all the pathologically changed bone, expose and open the sigmoid sinus within its pathological changes. After opening the sinus, the further course of surgical intervention is dictated by the pathological changes in the sinus and the general condition of the patient. Here, various options are possible.

1. The sinus is outwardly normal: its pulsation is determined, its color is bluish, there are no fibrinous deposits or granulations on its surface. In this case, two paths are possible:
   1. further intervention on the sinus is stopped and the operation is completed with extended RO; with this alternative there is a risk of subsequent development of sinus thrombosis;
   2. a sinus puncture is performed, after washing the wound with a sterile antiseptic solution (furacilin, rivanol) and a solution of the appropriate antibiotic and treating the sinus surface with a weak alcohol solution of iodine. If normal venous blood is found in the sinus puncture, the sinus is not opened.
2. The sinus surface is hyperemic, covered with granulation or fibrinous plaque, there is no pulsation, sinus puncture is mandatory. The appearance of fresh blood in the syringe indicates that the pathological process is limited to parietal phlebitis and, possibly, parietal thrombus. In this case, the sinus is not opened, and the wound is treated openly. If it is not possible to obtain the contents of the sinus by suction or pus is released through the needle, then further surgical intervention depends on the general clinical signs of sinus thrombophlebitis:
   1. in the absence of septicemia, some authors recommend not to open the sinus and not to remove the thrombus, which in this case initially plays a biologically protective role, being a barrier to infection, but to take a wait-and-see attitude; in the case of purulent melting of only the central part of the thrombus (in the absence of signs of septicemia), this tactic involves removing the purulent focus by suction through puncture;
   2. in the presence of septicemia, the sinus is opened or a part of its wall is removed (window) with the thrombus removed along its entire length, until fresh blood appears in its proximal part; if the thrombus is large enough to prevent its complete removal, then only the most infected central part is removed; the thrombus is removed only after the sinus is excluded from circulation by tamponade of its upper and lower ends, limited by the size of the longitudinal incision in the sinus wall; for this, an ear gauze turunda is inserted between the sinus and the outer bone wall until the sinus is completely compressed; the operation is completed with loose tamponade of the surgical wound with iodoform; usually after such surgery the sinus becomes empty and sclerotic; if the signs of septicemia do not disappear within a few days, then the pathologically altered internal jugular vein is ligated and removed.

The prognosis for limited thrombophlebitis of the sigmoid sinus and timely surgery, as well as effective complex drug treatment, is favorable for life. The prognosis is cautious and even questionable in septicemia and septicopyemia, especially when distant foci of infection occur in internal organs. Often, such foci of infection lead to chronic sepsis, the treatment of which can last for many months.

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