INTRODUCTION — Septic dural sinus thrombosis is an uncommon condition with only several hundred cases reported in the English medical literature during the antibiotic era. Since this disorder is rare, each clinician is likely to encounter only one or a few cases during his or her career. The combination of lack of familiarity and the myriad of potential symptoms and signs often leads to misinterpretation of the clinical manifestations.
Dural sinus thrombosis includes three syndromes:
●Cavernous sinus thrombosis
●Lateral sinus thrombosis
●Superior sagittal sinus thrombosis
All three syndromes result in severe headache, which is the most common complaint that brings the patient to the clinician. An exception is the older adult (over age 65 years) who may present with an alteration in mental status without antecedent headache [1-3]. The other clinical manifestations of each syndrome reflect the anatomy of the specific sites.
This topic discusses septic dural sinus thrombosis. Aseptic dural sinus thrombosis is discussed separately:
SEPTIC CAVERNOUS SINUS THROMBOSIS — The cavernous sinus is the most frequent dural sinus to become infected and thrombosed .
Anatomy — The cavernous sinuses are the most centrally located of the dural sinuses, positioned just lateral to the base of the sella turcica and to the sphenoid paranasal sinuses. These irregularly shaped sinuses contain multiple trabeculae that act as sieves to trap bacteria; this characteristic explains the higher risk of infection of the cavernous sinuses as compared with the other dural sinuses. The cavernous sinuses are connected by two intercavernous sinuses that pass anteriorly and posteriorly to the sella turcica and the pituitary gland; thus bilateral infection is not uncommon, particularly if treatment is delayed.
A number of cranial nerves are located within a dural sleeve, lateral to the cavernous sinus: oculomotor nerve (cranial nerve III), trochlear nerve (cranial nerve IV), and ophthalmic (V1) and maxillary branches (V2) of the trigeminal nerve (figure 1). The abducens nerve (cranial nerve VI) is located more medially within the cavernous sinus and abuts the cavernous segment of the internal carotid artery .
Pathogenesis — The cavernous sinuses receive blood from the facial veins and pterygoid plexus via the inferior and superior ophthalmic veins. Infections of the face, including the nose, orbits, tonsils, and soft palate, can spread to the cavernous sinus by this route.
Three sites of primary infection are the most likely to lead to septic cavernous sinus thrombosis:
●Sphenoid and/or ethmoid sinus infections have increasingly been reported with cavernous sinus thrombosis . Sphenoid sinusitis is the most common predisposing factor for cavernous sinus thrombosis . Infection can arise via the emissary veins or, in the case of sphenoid sinusitis, can spread by breaking through the porous lateral air sinus wall [2,7,8]. Sphenoid sinus infection is particularly difficult to diagnose, and treatment is often delayed, providing time for the infection to spread to the cavernous sinus . (See "Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis".)
Ethmoid sinus infection can extend laterally to the orbit and subsequently spread to the cavernous sinus via the superior ophthalmic vein.
●Facial infections are implicated in septic cavernous sinus thrombosis, especially those that involve the so-called danger zone (medial third of the face [ie, the areas around the nose]) that drains into the ophthalmic veins (figure 2). Nasal furuncles are the most common facial infection to produce this complication, particularly if the furuncle is squeezed or drained in the absence of antibiotic coverage .
●Dental infection less commonly results in this complication; infection spreads to the cavernous sinus via the pterygoid venous plexus . (See "Epidemiology, pathogenesis, and clinical manifestations of odontogenic infections".)
●Otitis media and mastoiditis – Otitis media and its related complication, mastoiditis, rarely result in cavernous sinus disease despite the frequency of these infections as a cause in the pre-antibiotic era [5,10,11]. Mastoid infection can spread first to the lateral and sigmoid sinuses before reaching the cavernous sinuses via the inferior and superior petrosal sinuses. Infection can spread in a retrograde direction in this manner, depending upon the pressure gradients, because the dural sinuses contain no valves.
Conditions that cause immunosuppression (eg, diabetes, chronic alcohol abuse, long-term glucocorticoid therapy) may be risk factors for septic cavernous sinus thrombosis .
Microbiology — The organisms associated with septic cavernous sinus thrombosis reflect the primary sites of infection as outlined above [2,12-14]:
●Staphylococcus aureus accounts for 70 percent of all infections and is the etiologic pathogen in nearly all cases associated with facial infection or sphenoid sinusitis.
Community-acquired methicillin-resistant S. aureus (MRSA) is reported with increasing frequency .
●Streptococci (including S. pneumoniae, S. milleri, and viridans group streptococci) are less commonly found.
●Anaerobes are occasionally cultured, including Bacteroides spp and Fusobacterium spp, and are most often found with accompanying sinus, dental, or tonsillar infections.
Clinical manifestations — Headache is the most common early symptom and generally precedes fever and periorbital edema by several days. The character of the headache is generally sharp; the pain progressively increases in severity, interferes with sleep, and is not relieved by pain medications. The pain is usually unilateral, involving the retro-orbital and frontal areas with occasional radiation to the occipital region . The severe nature of the headache is the most common reason for patients to seek medical attention. Clinicians frequently misdiagnose the pain as migraine headache when the patient presents early in the course of the disorder, before the onset of neurologic deficits.
Patients often develop symptoms in addition to headache, including:
●Fever is present in most patients (94 percent according to one review) .
●Eye swelling that begins as a unilateral process but within 24 to 48 hours spreads via the intercavernous sinuses to produce swelling in the other eye; in one series, this was reported in 73 percent of patients .
●Diplopia is a presenting complaint in some patients but is less common than documented oculomotor deficits on examination .
●Alterations in mental status such as drowsiness, confusion, and coma can rapidly follow eye complaints, reflecting spread to the meninges. A depressed mental status occurs more commonly in older adult patients and in fatal cases .
In typical patients, symptoms progress over a few to several days. Rarely, cavernous sinus infection can be a subacute or chronic process, in which headache can be present for several months prior to the onset of eye findings .
Less common complaints include photophobia and eye tearing . Rare complications include seizures, stroke, and hypopituitarism . Loss of visual acuity can arise from optic nerve involvement. Blindness caused by compression of the optic nerve by a mycotic aneurysm of the intercavernous segment of the internal carotid/ophthalmic artery has been reported . These uncommon complications are more common when treatment is delayed but can occur on antimicrobial therapy.
Evaluation and diagnosis — The early symptoms of septic cavernous sinus thrombosis are not specific, but the presence of cranial nerve signs (particularly lateral gaze palsy) on physical examination in a patient with headache should alert the clinician to the possibility of cavernous sinus involvement and prompt imaging studies, which are in most cases diagnostic. The evaluation should proceed promptly, as delays to treatment may be associated with morbidity and mortality.
Physical examination — When cavernous sinus septic thrombosis is fully manifest, the majority of patients present with fever and the classic constellation of bilateral ptosis, proptosis, chemosis, and ocular muscle paralysis. However, the physical findings may be considerably subtler when patients present earlier in the disease course. A careful eye and neurologic examination, with particular attention to the cranial nerves, is necessary in order to make a diagnosis at an earlier stage.
Periorbital edema may be the earliest physical finding and should prompt a more detailed examination in patients with headache:
●Funduscopic exam is abnormal in two-thirds of patients. Papilledema or dilated tortuous retinal veins are noted in almost two-thirds of patients .
●Extraocular muscle weakness is an important finding present in 50 to 88 percent of cases [2,3] and results from dysfunction of cranial nerves III, IV, and VI. The following signs should be sought:
•Lateral gaze palsy (isolated cranial nerve VI [abducens] dysfunction) may precede full-blown ophthalmoplegia, particularly in cases of chronic sphenoid sinusitis.
•Drooping of the eyelid (ptosis), dilation of the pupil (mydriasis), and eye muscle weakness result from cranial nerve III dysfunction. Total palsy of the nerve leads to an eye that is facing down and lateral.
●Exophthalmos (anterior bulging of the eye) and chemosis (conjunctival edema) are thought to result from occlusion of the ophthalmic veins and generally occur just before or at the same time as ophthalmoplegia. One or both of these findings is present in most patients .
●Hypo- or hyperesthesia in the dermatomes served by the ophthalmic (V1) and maxillary (V2) branches of the fifth cranial nerve (trigeminal nerve) can be subtle .
Imaging — In patients presenting with headache and cranial nerve signs localized to the cavernous sinus, a diagnostic neuroimaging study is urgent. Contrast-enhanced magnetic resonance imaging (MRI) and magnetic resonance venography are the imaging tests of choice and have been reported to be superior to computed tomography (CT), because MRI can detect all stages of thrombus in septic cavernous sinus thrombosis (image 1) . If MRI is not readily available, high-resolution orbital CT with contrast can also demonstrate septic cavernous thrombosis [23,24]. The early venous phase following administration of contrast demonstrates thickened cavernous sinus walls and decreased or irregular intrasinus enhancement (image 2) [25,26].
MRI and CT can also simultaneously detect associated paranasal sinus infection. The presence of paranasal sinus infection should prompt consultation for possible surgical intervention. (See 'Surgery' below.)
Blood cultures and other studies — Two sets of blood cultures should be sent prior to initiation of antibiotics, and they are positive in approximately 70 percent of cases .
The peripheral white blood cell count (WBC) is commonly elevated, suggesting an acute bacterial infection.
Lumbar puncture — A lumbar puncture is typically not performed unless there is concern that the patient has developed a complicating meningitis. (See 'Clinical manifestations' above.)
When performed, lumbar puncture reveals inflammatory cells in 75 percent of cases. In half of these cases, the cerebrospinal fluid (CSF) profile is most suggestive of a parameningeal focus (elevated WBC with a predominance of polymorphonuclear neutrophils [PMNs] and/or mononuclear cells, normal glucose, elevated or occasionally normal protein, and negative culture). In one-third of patients, the CSF profile is identical to that found in bacterial meningitis (elevated WBC with a predominance of PMN, low glucose, high protein, culture positive) [2,16]. In rare patients, the CSF profile is normal.
If a lumbar puncture is performed, Gram stain and culture should be performed; however, the CSF culture is rarely positive .
Differential diagnosis — A number of conditions are considered in the differential diagnosis of septic cavernous sinus thrombosis, including those that are considered in the differential diagnosis of painful ophthalmoplegia (table 1). Signs of orbital congestion (proptosis, conjunctival injection, and chemosis) usually accompany diseases involving the orbit. Most of these can be distinguished by neuroimaging evaluation and/or clinical symptoms. Among the more common conditions to consider are:
●Orbital cellulitis – Orbital cellulitis and septic cavernous sinus thrombosis have overlapping symptoms including periorbital eye swelling, chemosis, and ophthalmoplegia. Also, in rare cases, septic cavernous sinus thrombosis is a complication of orbital cellulitis (see "Orbital cellulitis", section on 'Clinical manifestations'). Clinical characteristics that increase the probability of involvement of the cavernous sinus include:
•Dilated pupil or pupils
•Fifth cranial nerve dysfunction
•Bilateral eye involvement
•Inflammatory cells in the CSF
High-resolution CT or MRI can readily differentiate between the two diseases by demonstrating involvement of the cavernous sinus. (See 'Imaging' above.)
●Intraorbital abscess – This typically presents acutely with periorbital swelling, proptosis, chemosis, ophthalmoplegia, fever, decreased vision, and pain; however, it usually has an absence of papilledema and papillary involvement. Imaging studies are able to differentiate abscess from cavernous sinus thrombosis.
●Intracavernous carotid artery aneurysm or arteriovenous fistula – These entities are often accompanied by proptosis, pain with a pulsatile feeling, bruit, and engorgement of blood vessels. Patients do not have fever or other signs of infection. Neuroimaging findings are distinctive. (See "Carotid-cavernous fistulas", section on 'Diagnosis and imaging findings'.)
●Neoplastic or inflammatory infiltration of the cavernous sinus from meningioma or metastasis, as well as neurosarcoid, IgG4-related disease, idiopathic pachymeningitis or granulomatosis with polyangiitis, and Tolosa-Hunt syndrome. These can present with headache, periorbital pain and external ophthalmoplegia; however, fever is usually mild or absent. (See "Tolosa-Hunt syndrome", section on 'Differential diagnosis'.)
●Aseptic cavernous sinus thrombosis – Septic cavernous sinus thrombosis is typically distinguished from aseptic disease by the presence of fever on examination as well as associated finding of infection in the sinus, mastoid, or face on imaging and/or examination. (See "Cerebral venous thrombosis: Etiology, clinical features, and diagnosis", section on 'Syndromes associated with isolated sinus or vein thrombosis'.)
Treatment — The mainstay of therapy for septic cavernous sinus thrombosis is antibiotics; anticoagulation and surgery are appropriate adjunctive treatments in selected cases. Treatment should be started urgently as delays to treatment may be associated with morbidity and mortality.
Antibiotics — Intravenous (IV) antibiotics should be instituted emergently and directed at the probable organisms causing this type of infection. (See 'Microbiology' above.)
The regimens listed below are for patients with normal renal function. Dose adjustments for patients with reduced kidney function can be found in the Lexicomp drug information topics within UpToDate.
●Empiric and directed regimens – Empiric therapy should include coverage for community-acquired MRSA. Appropriate empiric parenteral regimens include:
•Ceftriaxone (2 g IV every 12 hours); OR
•Cefepime (2 g IV every 8 to 12 hours). Cefepime (2 g IV every eight hours) should be used if Pseudomonas coverage is desired (eg, in patients with chronic sinusitis and known colonization of the sinus with pseudomonas).
Anaerobic coverage should be added if a dental or sinus infection is suspected. IV metronidazole (500 mg every six to eight hours) is highly effective for this purpose.
If a cephalosporin or metronidazole (if indicated) cannot be used, the combination of vancomycin (table 2) and meropenem (2 g IV every eight hours) is a reasonable empiric regimen for most patients. If meropenem is not available, imipenem (1 g IV every six hours) can be used; however, we prefer meropenem since imipenem may increase the risk of seizures. Patients with severe beta-lactam allergies (eg, Stevens Johnson syndrome) may require a different regimen. (See "Penicillin allergy: Delayed hypersensitivity reactions" and "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics" and "Immediate cephalosporin hypersensitivity: Allergy evaluation, skin testing, and cross-reactivity with other beta-lactam antibiotics" and "Cephalosporin hypersensitivity: Clinical manifestations and diagnosis".)
Antifungal therapy is rarely required and should only be utilized if invasive fungal infection is proven by biopsy.
If susceptibility testing reveals methicillin-susceptible S. aureus, therapy should be changed to nafcillin (2 g IV every four hours) or oxacillin (2 g IV every four hours). First-generation cephalosporins (eg, cefazolin) should be avoided for treatment of central nervous system infections because of poor CSF penetration.
If the organism is methicillin resistant S. aureus, vancomycin should be continued (table 2) [27-29]. If vancomycin cannot be used or is ineffective based on a lack of improvement of clinical manifestations (eg, fever, bacteremia, changes in mental status) over the course of seven days, reasonable alternatives include ceftaroline (600 mg IV every 8 to 12 hours) , daptomycin (6 to 10 mg/kg IV once daily), linezolid (600 mg IV or orally twice daily) [15,31-33], and trimethoprim-sulfamethoxazole (5 mg/kg [based on the trimethoprim component] IV every 8 to 12 hours) [34-36].
●Duration – Because thrombus may limit the penetration of antibiotics, prolonged IV antibiotics are recommended. A minimum of three weeks of treatment is generally required to assure sterilization. The duration may need to be extended longer based upon the presence of other factors, such as bacteremia with S. aureus (see "Clinical approach to Staphylococcus aureus bacteremia in adults", section on 'Completing antibiotic therapy') or if significant ophthalmoplegia or edema of the eye remains at the end of planned therapy. We use clinical rather than imaging parameters to guide this decision, as improvement in imaging is often delayed.
Anticoagulation — We suggest immediate anticoagulation in patients with unilateral cavernous sinus thrombosis in order to prevent bilateral extension. This practice is based on limited and conflicting data. For patients with bilateral disease, we do not use anticoagulation.
For patients treated with anticoagulation, we suggest continuous-infusion heparin anticoagulation, adjusting the dose to maintain a partial thromboplastin time ratio of 1.5 to 2.5 . There are no reports of low-molecular-weight heparin being used in this setting; however, hemorrhagic complications have been observed in two patients who were receiving low-molecular-weight heparin for septic lateral sinus thrombosis (see 'Septic lateral sinus thrombosis' below). Warfarin should be avoided in the acute phase of the illness because of the difficulty in rigorously maintaining safe anticoagulation levels.
The duration of anticoagulation has not been determined. We continue anticoagulation until the infection as well as the symptoms and signs of cavernous sinus thrombosis (eg, periorbital edema, fever, leukocytosis) have resolved or significantly improved.
Although the use of anticoagulants in septic cavernous sinus thrombosis is controversial and there are limited data on this issue, one retrospective study observed a reduction in mortality in patients with unilateral involvement who presented early and who received heparin (14 percent) compared with those who did not receive heparin (36 percent) . In a second retrospective analysis, the addition of early anticoagulation to antibiotic treatment did not affect mortality but did decrease morbidity, including ophthalmoplegia, blindness, stroke, hypopituitarism, and seizures .
Complications associated with anticoagulation were rare. In another cohort of 57 patients who had central nervous system venous thrombosis associated with head or neck infections, use of heparin was not associated with an increase in intracranial hemorrhage in patients receiving heparin compared with patients not receiving heparin (26 versus 25 percent) .
Surgery — Surgical drainage of sphenoid sinus infection that has been documented on imaging should be strongly considered and, if done, should be performed emergently . Debridement of the infected sphenoid can be followed by rapid improvement. Although controlled studies are lacking, the improved mortality from this condition over the past decade is likely attributable in part to improved imaging and earlier surgical drainage .
Lack of role for glucocorticoids — We do not favor the use of glucocorticoids for septic cavernous sinus thrombosis.
There has been interest in using glucocorticoids in patients with septic cavernous sinus thrombosis to potentially reduce cranial nerve edema and orbital inflammation, but the limited data available suggest they are not useful [37,41,42]. In one prospective observational study of 624 patients with cerebral venous thrombosis, poor outcome defined as death or dependence at six months was similar in patients treated with steroids compared with patients not treated with steroids (odds ratio 1.7; 95% CI 0.9 to 3.3) .
Outcome — The overall mortality rate associated with septic cavernous sinus thrombosis has been reported to be 30 percent . An additional 30 percent of patients in that series suffered serious sequelae including persistent oculomotor weakness, blindness, hemiparesis, or pituitary insufficiency. The morbidity and mortality (50 percent, respectively) are particularly high in cases of cavernous sinus thrombosis associated with sphenoid sinus infection [2,7]. More recent case series and reviews provide a small number of patients for analysis, but the prognosis appears to be more favorable, with estimated mortality rates of 9 to 16 percent and morbidity rates of 15 to 38 percent [40,43].
SEPTIC LATERAL SINUS THROMBOSIS — Lateral sinus thrombosis, a complication of acute or chronic otitis media, is now uncommon, except in developing countries . (See "Acute otitis media in children: Epidemiology, microbiology, and complications", section on 'Complications and sequelae'.)
Pathogenesis — Lateral sinus thrombosis most often occurs as a complication of acute or chronic otitis media. If otitis media is not treated appropriately in a timely manner, the infection can spread to the mastoid and ultimately to the epidural space. Mastoid air cell infection can lead to thrombosis of the lateral sinus, which may then propagate to the internal jugular vein and other dural sinuses [2,45,46].
Interruption of venous circulation may lead to increased intracranial pressure .
Septic pulmonary embolism may also occur as a complication of lateral sinus thrombosis [47-49].
In children, hypercoagulable conditions appear to be a risk factor. Although the magnitude of this risk has not been quantified systematically, in one series of septic dural sinus thrombosis in the setting of otitis media, more than 70 percent had a prothrombotic condition .
Microbiology — Infection is often polymicrobial, containing both aerobes and anaerobes. The principal pathogens associated with this complication reflect the bacteriology of chronic otitis media. Traditionally, Proteus spp have been most common, followed by S. aureus, Escherichia coli, and anaerobes (Bacteroides fragilis and anaerobic streptococci) ; however, more recent case series suggest that streptococcal infections are increasing in incidence . Pseudomonas has been identified as a pathogen in intraoperative cultures in a few cases; however, when Pseudomonas is cultured from the external ear canal, it cannot be assumed that this is the infecting organism [45,52].
Clinical manifestations — Septic lateral sinus thrombosis has a subacute onset. Symptoms generally begin several weeks before presentation and reflect the underlying infection as well as the development of septic lateral sinus thrombosis.
Symptoms — Symptoms include :
●Earache is generally the first symptom, persisting for several weeks prior to the onset of headache.
●Headache is generally severe, persistent, and localized to the side of the ear infection. Pain is thought to be a manifestation of a developing epidural abscess, irritation of the fifth cranial nerve, or thrombosis of the lateral sinus. (See "Intracranial epidural abscess".)
●Nausea and vomiting develop in nearly half of cases and can be mistaken for severe gastroenteritis. This manifestation may reflect irritation of brainstem nuclei or cranial nerves, or elevated cerebrospinal fluid (CSF) pressure.
●Other symptoms include vertigo, diplopia, photophobia, and neck pain and stiffness.
●Less commonly, patients can present with headache and neurologic manifestations in the absence of ear pain and have radiologic findings consistent with chronic otitis media that may be accompanied by a cholesteatoma .
●Some patients develop cough productive of bloody sputum that results from septic pulmonary emboli, an uncommon complication of lateral sinus thrombosis .
●Fever is present in 80 percent of cases, and patients often appear ill . High-spiking "picket" fence fevers are considered characteristic ; however, fever may be less prominent in those associated with chronic otitis media .
●An abnormal ear examination is found in most patients; 40 percent have a ruptured tympanic membrane and 20 percent have a dull, erythematous tympanic membrane .
Posterior auricular swelling is found in over half of the cases and is caused by occlusion of the mastoid emissary veins. This finding is called the Griesinger sign and is considered pathognomonic for septic lateral sinus thrombosis .
●Bilateral papilledema (the result of elevated CSF pressure) is also present in half of the cases and may be associated with retinal hemorrhage . Accompanying loss of visual acuity develops in 15 percent.
●Unilateral sixth nerve dysfunction is reported in over a third of cases and is thought to be caused by compression of the nerve by swelling of the inferior petrosal sinus within the closed space of Dorello canal [2,51].
●Otitis media, sixth nerve paralysis, and fifth cranial nerve irritation (temporoparietal and retroorbital pain) are known as Gradenigo syndrome. This is rare, but when present, this symptom complex provides strong evidence for lateral sinus thrombosis or inflammation of the petrous ridge of the temporal bone [54,55].
●Nuchal rigidity is present in one-third to one-half of patients and is probably the result of meningeal inflammation [2,51].
●Depression in mental status is noted in 14 percent of cases.
Imaging findings — Mastoid radiographs are abnormal in all patients with septic lateral sinus thrombosis, showing increased density with loss of mastoid trabeculae, bony sclerosis, and lytic lesions of the temporal and parietal bones.
Otomastoid infection can be confirmed on either computed tomography (CT) or enhanced magnetic resonance imaging (MRI). Contrast-enhanced CT or MRI with venography (CTV or MRV) detect filling defects from thrombi and absent flow in the dural sinus, respectively, in patients with septic lateral sinus thrombosis (image 3). Three-dimensional magnetic resonance gradient-echo cerebral venography has been shown to be superior to two-dimensional magnetic resonance .
Chest radiography rarely reveals rounded densities. These lesions are caused by septic emboli passing from the lateral sinus into the internal jugular vein and then passing into the pulmonary venous circulation.
Evaluation and diagnosis — The diagnosis of septic lateral sinus thrombosis should be suspected in a patient with otitis media who develops headache and neurologic signs such as vertigo and diplopia. Either contrast-enhanced MR with MRV or contrast-enhanced CT with CTV should be performed and will confirm the diagnosis, differentiating this from other complications including mastoiditis and abscess formation. (See 'Imaging findings' above and "Chronic otitis media and cholesteatoma in adults".)
Lumbar puncture and opening pressure measurement should be performed in all cases after MRI or CT has excluded the possibility of brain abscess. CSF pressures are commonly elevated to the range of 450 to 500 mm H2O in 75 percent of cases. Increased CSF pressure results from interference with CSF resorption by arachnoid villi draining into the superior sagittal sinus. The CSF analysis is normal in two-thirds of cases and reflects parameningeal inflammation in the other third. CSF should be sent for Gram stain and culture.
Two sets of blood cultures should be sent prior to initiation of antibiotics.
We do not routinely evaluate patients for hypercoagulable conditions, particularly in the typical setting in which there is a documented otitis which explains the occurrence of thrombosis. However, case series in pediatric patients suggest that between one-third to one-half of children may be found to have a hypercoagulable condition when tested [57,58].
Treatment — The mainstays of treatment of septic lateral sinus thrombosis are antibiotics and, in the absence of rapid defervescence, surgery.
Antibiotics — Intravenous (IV) antibiotics need to be administered immediately [2,59,60]. The regimens listed below are for patients with normal renal function. Dose adjustments for patients with reduced kidney function can be found in the Lexicomp drug information topics within UpToDate.
An appropriate empiric parenteral regimen includes:
●Ceftriaxone 2 g IV every 12 hours OR
●Cefepime 2 g IV every 8 to 12 hours
●Metronidazole 500 mg IV every six to eight hours
Meropenem (2 g IV every eight hours) is an acceptable alternative to one of the above regimens for most patients and is also active against Pseudomonas. If meropenem is not available, imipenem (1 g IV every six hours) can be used, but if both agents are available, we prefer meropenem since imipenem may increase the risk of seizures. Patients with severe beta-lactam allergies (eg, Stevens Johnson syndrome) may require a different regimen. (See "Penicillin allergy: Delayed hypersensitivity reactions" and "Allergy evaluation for immediate penicillin allergy: Skin test-based diagnostic strategies and cross-reactivity with other beta-lactam antibiotics" and "Immediate cephalosporin hypersensitivity: Allergy evaluation, skin testing, and cross-reactivity with other beta-lactam antibiotics" and "Cephalosporin hypersensitivity: Clinical manifestations and diagnosis".)
Methicillin-resistant S. aureus (MRSA) is rare in patients with septic lateral sinus thrombosis; however, the empiric addition of vancomycin (table 2) is typically warranted in those who have had MRSA detected in prior cultures of the mastoid and in those who are acutely ill. (See "Vancomycin: Parenteral dosing, monitoring, and adverse effects in adults".)
If an organism is identified based upon cultures from myringotomy or intraoperative specimens, therapy should be changed to target the identified organisms based upon their antibiotic sensitivities.
Three to four weeks of antibiotics are generally recommended, as mastoiditis is the most common primary infection; if the infection has been resected, a shorter duration of 10 to 14 days may be sufficient. We typically document resolution of the thrombosis with imaging.
Surgery — Patients diagnosed with lateral sinus thrombosis should have an urgent surgical consult [51,61,62]. Radical mastoidectomy should be strongly considered in all patients who fail to defervesce within 12 to 24 hours of the initiation of antibiotic treatment. The basis for this recommendation is the understanding that mortality rates were substantial prior to the institution of this practice. No studies provide comparative outcome data.
During surgery, the area overlying the lateral sinus should be explored so that infected granulation tissue or purulent collections can be drained and sent for culture. Removal of thrombus from the lateral sinus is considered in some cases; however, recanalization or the development of collateral venous drainage can occur without this intervention once the infection has been controlled [51,63,64]. Ligation of the jugular vein, a common procedure in the preantibiotic era, is not recommended in most cases .
Not all cases of lateral sinus thrombosis require mastoidectomy with drainage. In one pediatric series, three of five patients responded quickly to antibiotic therapy and myringotomy for the underlying otitis, fully recovering without more aggressive surgical intervention . However, in the absence of prompt defervescence, surgical intervention is recommended.
Anticoagulation — Anticoagulation is not part of the routine management of septic lateral sinus thrombosis.
Potential indications for anticoagulation include:
●Failure to improve clinically with extension of thrombosis despite antibiotics and surgical drainage
●Patients with a documented hypercoagulable state
The role of anticoagulation in septic lateral sinus thrombosis remains controversial. Although there may be a theoretic benefit, the stimulus precipitating thrombosis in septic cases is self-limited, resolving with antibiotic treatment, and thrombotic vessels often undergo recanalization without anticoagulation .
Also, anticoagulation carries a potential risk of intracerebral hemorrhage. One case series describes a patient with septic lateral sinus thrombosis and cortical vein thrombosis who suffered a fatal hemorrhage while receiving warfarin . Hemorrhagic complications have been reported in at least three patients who were receiving low-molecular-weight heparin for septic lateral sinus thrombosis [49,66]. Such cases are anecdotal, and the magnitude of the risk is unclear . In somewhat related patient populations, the risk appears to be low. As an example, in a report of patients with cerebral venous thrombosis associated with head and neck infections, there was no increased risk of intracranial hemorrhage associated with heparin therapy . The risk of hemorrhagic complications in patients with acute aseptic dural sinus thrombosis who receive anticoagulation appears to be low. (See "Cerebral venous thrombosis: Treatment and prognosis", section on 'Risk of new intracranial hemorrhage'.)
If anticoagulation is started, the duration is unclear. Neuroimaging can be used to document persistence or resolution of the thrombosis to guide treatment decisions. If a hypercoagulable state is documented, anticoagulation should be continued for at least six months . Prolonged anticoagulation should also be maintained for pediatric patients whose lateral sinus fails to recannulate . For others, anticoagulation can be continued until the infection as well as the symptoms and signs of lateral sinus thrombosis have resolved or significantly improved. (See "Cerebral venous thrombosis: Treatment and prognosis", section on 'Long-term anticoagulation'.)
Treatment of elevated intracranial pressure — For patients with elevated intracranial pressure, serial lumbar punctures every 48 hours and/or ventricular drain may be required to lower the CSF pressure and relieve papilledema. Persistent communicating hydrocephalus may require placement of a ventricular shunt. Follow-up imaging and intervention should be guided by the patient's clinical examination, especially their level of consciousness. (See "Evaluation and management of elevated intracranial pressure in adults".)
Outcome — The outcome is usually favorable in this disease, with a reported mortality of less than 1 percent in the past decade [2,67]. The majority of patients fully recover, although 10 to 15 percent suffer chronic sequelae including hydrocephalus, decreased visual acuity, impaired hearing, and, rarely, residual hemiparesis .
SEPTIC SUPERIOR SAGITTAL SINUS THROMBOSIS — The superior sagittal sinus is the largest venous channel in the brain. In addition to arachnoid villi (responsible for cerebrospinal fluid resorption), multiple cortical veins empty into this venous channel [2,4]. Given the large size of the superior sagittal sinus, septic thrombotic occlusion is very rare.
The most common infection associated with complete occlusion of the superior sagittal sinus is bacterial meningitis. Thrombosis of the anterior segment has been associated with frontal bacterial sinusitis occasionally. Less common associations include facial plastic surgery and oral surgery [68,69]. (See "Epidemiology of community-acquired bacterial meningitis in adults" and "Acute sinusitis and rhinosinusitis in adults: Clinical manifestations and diagnosis".)
Septic thrombosis of the superior sagittal sinus results in hemorrhagic infarcts due to cortical vein thrombosis as well as in communicating hydrocephalus. When combined with the cerebral edema associated with meningitis, massive brain infarction in most cases quickly leads to transtentorial brainstem herniation .
Diagnosis is made most readily by gadolinium-enhanced magnetic resonance imaging (MRI) and MR venography (image 4). As discussed above, this diagnostic technique readily demonstrates thrombus formation and decreased venous flow. As observed for lateral sinus thrombosis, three-dimensional MR has proved to be superior to two-dimensional MR angiography .
Antibiotics, if begun early for bacterial meningitis, can prevent this complication from occurring; however, once occlusion has occurred, initiation of antibiotics is unlikely to be of significant benefit for this complication. The treatment of bacterial meningitis is discussed in detail elsewhere. (See "Initial therapy and prognosis of community-acquired bacterial meningitis in adults".)
The outcome of complete occlusion of the superior sagittal sinus is universally fatal. Occlusion of the anterior segment in association with frontal sinusitis presents with mild to moderate headache and spontaneously resolves following the development of collateral venous channels. Although anticoagulants and thrombolytic therapy are often administered in aseptic superior sagittal sinus thrombosis, their role in septic disease has not been defined, and, given the extensive intracerebral hemorrhage and the rapid progression to death, they are unlikely to be of benefit.
SUMMARY AND RECOMMENDATIONS
Septic cavernous sinus thrombosis
●The cavernous sinus is the most frequent dural sinus to become infected and thrombosed. The underlying site of infections includes the sphenoid or ethmoid sinuses, facial infections, and dental infections. (See 'Anatomy' above.)
●Staphylococcus aureus accounts for 70 percent of all infections and is the etiologic pathogen in nearly all cases associated with facial infection or sphenoid sinusitis. (See 'Microbiology' above.)
●Headache is the most common early symptom and generally precedes fever and periorbital edema by several days. Other common clinical manifestations include eye swelling and diplopia.
These symptoms are not specific, but the presence of cranial nerve signs (particularly lateral gaze palsy) on physical examination in a patient with headache should alert the clinician to the possibility of the diagnosis and prompt an urgent evaluation.
●Urgent empiric antibiotic therapy is required. For most patients, we suggest a regimen that includes vancomycin plus ceftriaxone or cefepime (Grade 2C). Metronidazole should be added if anaerobic coverage is required (eg, suspected dental or sinus infection). (See 'Antibiotics' above.)
●Surgical drainage of sphenoid sinus infection that has been documented on imaging should be strongly considered and, if done, should be performed emergently. (See 'Surgery' above.)
Septic lateral sinus thrombosis
●Septic lateral sinus thrombosis most often occurs as a complication of acute or chronic otitis media. Infection is often polymicrobial, containing both aerobes and anaerobes, reflecting the bacteriology of chronic otitis media. (See 'Pathogenesis' above and 'Microbiology' above.)
●Along with symptoms of ear infection, patients develop headache along with neurologic signs such as vertigo and fifth and sixth nerve impairment. Some patients develop increased intracranial pressure. (See 'Clinical manifestations' above.)
●The diagnosis of septic lateral sinus thrombosis is made by contrast-enhanced MRI. Other essential tests include lumbar puncture and blood cultures. (See 'Evaluation and diagnosis' above.)
●Treatment consists of antibiotic therapy and surgery in most cases; some patients require management of elevated intracranial pressure:
•Urgent empiric antibiotic therapy is required. For most patients, we suggest a regimen that includes metronidazole plus either ceftriaxone or cefepime (Grade 2C). Meropenem is an acceptable alternative. (See 'Antibiotics' above.)
•We suggest against anticoagulation in most patients with lateral sinus thrombosis, unless a hypercoagulable state is documented (Grade 2C). However, in patients not responding to antibiotic and surgical treatment, it is reasonable to provide anticoagulation treatment along with monitoring for hemorrhagic complications of anticoagulation. (See 'Anticoagulation' above.)
•For patients with increased intracranial pressure, monitoring and interventions are guided by the clinical examination. (See "Evaluation and management of elevated intracranial pressure in adults".)
Septic superior sagittal sinus thrombosis
●Septic superior sinus thrombosis is a rare complication of bacterial meningitis, bacterial sinusitis, and facial surgery. Producing hemorrhagic infarcts with cerebral edema, along with hydrocephalus, transtentorial brainstem herniation generally ensues, accounting for this condition's high mortality. (See 'Septic superior sagittal sinus thrombosis' above.)
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