Otogenic Lateral Sinus Thrombosis

Updated: Mar 21, 2019
Author: B Viswanatha, DO, MBBS, PhD, MS, FACS, FRCS(Glasg); Chief Editor: Arlen D Meyers, MD, MBA 



Otogenic lateral sinus thrombosis is a well-known intracranial complication of otitis media. It occurs in combination with other intracranial complications. Before the advent of antibiotics, which brought about a decline in this condition, most lateral sinus thrombosis was attributable to acute otitis media. Now, however, chronic otitis media predominates in most published reports.

An image depicting otogenic lateral sinus thrombosis can be seen below.

MR venogram that shows nonfilling of the lateral s MR venogram that shows nonfilling of the lateral sinus on the left side.

History of the Procedure

Lateral sinus thrombosis was first described in 1826. Three decades later, the pathology of lateral sinus thrombosis was first described by Lebert. In 1888, Lane performed the first successful surgery for lateral sinus thrombosis.


Lateral sinus thrombosis is a potentially fatal condition in which early diagnosis may be difficult because of previous antibiotic therapy. In the antibiotic era, the presentation of lateral sinus thrombosis has changed from pronounced signs and symptoms to vague and nonspecific symptoms. The decreased incidence and change in presentation requires clinicians to maintain a high index of suspicion to make the diagnosis.

Lateral sinus thrombosis should be suspected in patients who have persistent fever, otorrhea, and headache despite adequate antibiotic treatment.



Lateral sinus thrombosis accounts for 6% of all intracranial complications in the era of antibiotic treatment of suppurative ear disease.


The proximity of the middle ear and mastoid air cells to the dural venous sinuses predisposes them to thrombosis and thrombophlebitis secondary to infection and inflammation in the middle ear and mastoid.

Lateral sinus thrombosis usually develops as a complication of chronic otitis media caused by the direct dissemination of the infection through the neighboring eroded bone. It has been reported in a patient with an intact sigmoid plate, indicating propagation by the thrombophlebitic spread through the small emissary vein. It may also develop as a complication of acute suppurative otitis media by thrombophlebitic dissemination through the emissary vein in the intact bone. Lateral sinus thrombosis was ranked second to meningitis in the preantibiotic era as the most frequent fatal complication of otitis media and lateral sinus thrombosis occurred largely as a complication of acute otitis media. It is less often a disease of children in association with acute otitis media. More often, it is seen in the adult patient after a long history of chronic ear disease.

A retrospective study by Schneider et al suggested that pediatric patients with otogenic lateral sinus thrombosis secondary to acute otitis media and mastoiditis may have an underlying thrombophilic condition. The investigators found that three out of seven individuals in the study (43%) demonstrated evidence of thrombophilia; these signs, which differed among the patients, included elevated factor IX levels, reduced protein C and S activity levels, and elevated levels of antibodies to cardiolipin.[1]

Similarly, a retrospective study by Scorpecci et al found that out of 25 pediatric patients with otogenic lateral sinus thrombosis, 24 (96%) demonstrated a thrombophilia-related genetic abnormality.[2]


Initially, a perisinus abscess is formed, and, as the infection penetrates the dura and approach intima, a mural thrombus develops. Damage to the intima of blood vessels, hypercoagulation, and decreased blood flow are contributory factors in the formation of thrombus within the vessels. Damage to the tunica intima is the predominant factor in septic sinus thrombosis because the inflammatory process initiates fibrin formation and aggregation of blood platelets. The thrombogenic properties of bacteria are supposed to accelerate the process. Unless effective treatment is properly instituted, the mural clot grows and necrotizes, forming an intramural abscess. A mural thrombus then develops within the lumen of the sinus, propagates proximally and distally, and may become infected. The lumen of the vessel is eventually occluded by the propagating thrombus, and infected material may be embolized into the systemic circulation, causing septicemia.


Clinical features vary according to the stage of the disease. Patients present with headache, fever, and otorrhea. The classic case of lateral sinus thrombosis in the preantibiotic era typically produced a picket fence fever curve, due to the periodic release of hemolytic streptococci from the septic sinus thrombus. With the occlusion of the lumen of the sinus, an interruption of the cortical venous circulation results in headache, papilledema, and increased intracranial pressure. Involvement of the torcular and sagittal sinus can result in otitic hydrocephalus.

Tenderness and edema over the mastoid (the Griesinger sign) are highly suggestive of lateral sinus thrombosis and reflex thrombosis of mastoid emissary vein. With the extension of thrombophlebitis into the jugular bulb and internal jugular vein, pain may be present in the neck, particularly on rotation. Internal jugular vein may be palpated in the neck as a tender cord. The 9th, 10th, and 11th cranial nerve may be paralyzed by the presence and pressure of a clot in the jugular bulb (jugular foramen syndrome).

Because the right transverse is usually dominant, the symptoms are more likely to occur when this sinus is involved. Recovery depends on the development of collateral circulation or possibly recanalization of the sinus. Because of this, the presence of anastomotic channel is important for recovery.


See Medical therapy.

Relevant Anatomy

The lateral sinus is formed by the confluence of the superior petrosal sinus and the transverse sinus. The right transverse sinus is usually a continuation of the sagittal sinus, and the left transverse sinus is a continuation of the straight sinus. The lateral, or sigmoid, sinus exits the skull through the jugular foramen to become the internal jugular vein. It is called the lateral sinus because it is encountered laterally in mastoid surgery.



Laboratory Studies

The following laboratory studies are indicated:

  • Culture and sensitivity of purulent material

  • CBC count and differential count

  • Blood culture

The antibiotic era has seen a change in not only the clinical presentation of lateral sinus thrombosis but also bacteriology. This change in bacteriology is thought to be due to the fact that the disease more commonly proceeds by chronic rather than acute ear infection. Beta hemolytic streptococcus is no longer a dominant organism. Since chronic, rather than acute, infection more commonly precedes lateral sinus thrombosis, cultures characteristically yield mixed flora, including Bacteroides, Staphylococcus, Enterobacteriaceae, Proteus, Pseudomonas, and other species. Because antibiotics are commonly used during the prodromal ear infection, blood culture is often negative.

Imaging Studies

Imaging studies have been considered diagnostic aids for lateral sinus thrombosis, and definitive diagnosis can be made at surgery. Present imaging techniques and experiences enable clinicians to have relatively precise view of lateral sinus thrombosis before surgeries.

CT is particularly important for demonstrating pathology in the mastoid and cranial cavity and excluding existing intracranial complication. CT scanning with contrast can demonstrate a filling defect in thrombosed sinus and ring enhancement or the “delta sign” around the thrombosed sigmoid sinus. CT scan usually demonstrates the "delta sign," an empty triangle at the level of sigmoid sinus that consists of a clot surrounded by a high-intensity rim of contrast-enhanced dura, when thrombus is present. However, this sign is not always detectable and not all thrombus can be demonstrated by CT scanning.

MRI is more sensitive than CT scanning in detecting the thrombus. It shows blood flow, sinus obstruction, and the subsequent reversal of flow. On gadolinium-enhanced MRI, thrombus appears as soft tissue signal associated with vascular bright appearance of the dural wall (the "delta" sign, as seen with gadolinium enhanced MRI). This is the investigation of choice and should be performed in conjunction with CT scanning, thereby fully evaluating the associated otologic and cerebral pathology.

With the presence of significant sinus thrombosis, an MRI and magnetic resonance venogram (MRV) are warranted, because they can be used serially for clot progression and resolution.

Other Tests

Audiologic tests



Medical Therapy

Treatment of lateral sinus thrombosis is universally agreed to be with a combination of antibiotics and surgery. In selected cases of lateral sinus thrombosis, medical therapy alone with intravenous antibiotics may be successful.

A literature review by Au et al of 104 pediatric patients with lateral sinus thrombosis (using case reports from 1993-2011) found the prevalence of various management strategies to be as follows[3] :

  • Broad-spectrum antibiotics (100%)

  • Mastoidectomy (94%)

  • Anticoagulation (57%)

  • Manipulation of the thrombosed sinus (50%)

Most authors agree that anticoagulants have no place in the management of lateral sinus thrombosis. Anticoagulants have been advocated to prevent extension of the thrombus to the distal sinuses. However, they are rarely used now, because most infections can be controlled with antibiotics and surgery, and this tends to prevent the thrombus from propagating. The risks of anticoagulation include releasing septic emboli from clot breakdown and uncontrollable hemorrhage at the bleeding site. Anticoagulants arrest the spread of thrombosis but may increase the risk of venous infarctions and are therefore no longer used.

Systemic anticoagulation is not necessary unless the clot is shown to involve the sagittal sinus, or signs of increased intracranial pressure persist despite medical management.

Surgical Therapy

The management of lateral sinus thrombosis includes the combination therapy of appropriate antibiotics and surgeries. A mastoidectomy with the removal of the infected clot and thrombus in the lateral sinus is considered the standard surgical care.

Cortical mastoidectomy is sufficient for non cholesteatomatous ear disease. It allows the drainage of the initiating infection and confirms the diagnosis of lateral sinus thrombosis. Perisinus disease can be found despite a normal-appearing sinus plate. Current recommendations state that the removal of the sinus plate that overlays the sinus should always be performed.

Most cases are due to attico antral type of ear disease. Cholesteatoma is a persistent source of infection and is unresponsive to antibiotics. The early removal of this source of infection reduces the possibility of further intracranial extension, shortens the duration of illness, and provides definitive treatment. Canal wall down mastoidectomy has been used successfully in the treatment of cholesteatomatous ears with lateral sinus thrombosis.

Although an appropriate management of the thrombus in the sinus is not certain, most authors propose needling of the lateral sinus before incision in order to confirm the diagnosis. No further intervention is required, if free blood is aspirated. If blood is not returned, the diagnosis can be confirmed with incision on the sinus and evacuation of the clot, and obtaining free bleeding from the sinus is unnecessary.

Recent reports have shown that if the surrounding granulation tissue and inflammation are removed through a mastoidectomy, the sinus will recannalize without clot evacuation. Jun et al are of the opinion that the organized thrombus is an initial step for spontaneous resolution, finally inducing recanalization of a sinus.

Recent authors are of the opinion that with modern antibiotic therapy internal jugular vein ligation is not required.[4, 5, 6] Internal jugular vein ligation may possibly isolate the cause of infection and prevent embolization, thus increasing the cure rates of lateral sinus thrombosis. But internal jugular vein ligation may not eliminate septic complications because of collateral veins and may predispose the patient to retrograde-intracranial septic complications and add surgical risks of additional cervical dissections.

Internal jugular vein ligation should be reserved for those cases in which septicemia and embolization do not respond to initial surgery and antibiotic treatment. Recently, several studies showed the possibility of conservative managements with limited indications for the internal jugular vein ligation.

Intraoperative Details

Intraoperative needle aspiration of the sinus provides information on sinus patency or obstruction of blood flow. Absence of the blood return and aspiration of pus or thrombus are indications for opening the sinus. With the removal of the sinus plate, a longitudinal incision is made on the sinus and the thrombus is removed. Free bleeding from both ends is desirable. If no bleeding is found, evacuating as much of the clot as possible should suffice. Before the introduction of antibiotics, obtaining free bleeding from each end of the incised sinus was considered desirable, but now following the clot centrally to obtain free bleeding is not thought to be necessary and removing organized thrombus is also not thought to be necessary.

However, recent reports have challenged this dictum and demonstrate that if the surrounding granulation tissue and inflammation are removed through a mastoidectomy, the sinus recanalizes without clot evacuation.

A study by Ryan et al of seven pediatric patients with otogenic lateral sinus thrombosis indicated that the condition can be successfully treated with aggressive management of the mastoid cavity, with no thrombectomy required. All of the study’s patients achieved good recovery without major sequelae after undergoing treatment with intravenous antibiotics and mastoidectomy, with the sigmoid sinus unroofed and a tympanostomy tube placed. None of the children underwent sinus exploration with thrombectomy. Five of the patients were treated with perioperative anticoagulation without complication.[7]

Postoperative Details

After the thrombus has been evacuated, the patient should be maintained on antibiotics for 2-3 weeks and a repeat MRI and MR venogram should be performed to rule out the development of secondary intracranial complication such as brain abscess, or propagation of thrombus in to the superior sagittal sinus.


Follow-up MRI of the brain should be obtained to detect late embolic abscess or other delayed intracranial complications.


The presence of lateral sinus thrombosis mandates further investigation for additional intracranial complication. Before the antibiotic era, lateral sinus thrombosis had associated complications in 80% of the patients. The development of antibiotics has led to a decrease in the incidence of complications, which is now 20%.

Usually associated complications are seen on the same side as the diseased ear. Viswanatha et al have reported a case of attico antral disease with ipsilateral lateral sinus thrombosis and contralateral occipital lobe abscess.[8] The development of abscess in one hemisphere following infection in the contralateral mastoid can presumably occur from hematogenous spread of organisms.

Otitic hydrocephalus is known to complicate a significant number of lateral sinus thrombosis cases.

The aforementioned literature review by Au et al of 104 pediatric patients treated for lateral sinus thrombosis found the mortality rate to be 0.96% (one patient in 104). Contributing to the 10% morbidity rate were conditions such as cranial nerve palsy, sensorineural hearing loss, stroke, and septic hip joint.[3]

Outcome and Prognosis

The first successful surgery for lateral sinus thrombosis was performed by Lane in 1888. Until then, the mortality for this complication was 100%. Operative intervention reduced the mortality to 50%. Between 1932 and 1940, when antibiotics were introduced, a combination of antibiotics and surgical management reduced the mortality rate to 25%.

In the era of antibiotics, mortality averaged up to 10% of surgically treated cases and close to 100% for untreated cases.

In studies by Samuel et al (1987), Amirmajdi (1988), O'Connell (1990), Syms et al (1999), Bardley et al (2003), Ooi et al (2003), and Viswanatha (2007), no mortalities were found.[9, 10, 11, 12, 5, 13, 14]

Future and Controversies

Before the advent of antibiotics, ligation of the internal jugular vein was performed almost routinely in order to avoid dissemination of thrombophlebitic process and septic emboli. Internal jugular vein ligation is controversial.

In 1939, Cody summarized the argument for internal jugular vein ligation as follows[15] :

  • This procedure isolates the source of infection from the general circulation.

  • This procedure protects against the possibility of the mural thrombus embolizing.

  • This procedure does not alter the favorable course of the disease or add undue burden to the patient.

In 1935, Lyman summarized the argument against internal jugular vein ligation as follows[16] :

  • Numerous cases of symptomless lateral sinus thrombosis were found during mastoid surgery.

  • Septic complication often followed internal jugular vein ligation because the ligation above the entrance of the facial vein does not block off collateral circulation.

  • In the presence of collateral circulation, ligation may cause retrograde thrombosis and interruption of the venous return from the head, resulting in intracranial infection.

  • Operative interventions on the internal jugular vein exposed the patient to damage to the vagus, accessory, and hypoglossal nerves.

Today internal jugular vein ligation is indicated for the following specific reasons:

  • When the clots extends beyond the mastoid area.

  • When septicemia and pulmonary complications persist despite initial treatment with surgery and antibiotics.

  • When infection or thrombosis of the internal jugular vein is found.

In 2011, Ropposch et al published a retrospective study report on the management of lateral sinus thrombosis.[17] They are of the opinion that anticoagulant therapy is a safe treatment option to prevent extension of the thrombosis and development of other intracranial complications.