Orbit, 2013; 32(5): 330–332 ! Informa Healthcare USA, Inc. ISSN: 0167-6830 print / 1744-5108 online DOI: 10.3109/01676830.2013.814686


Septic Cavernous Sinus Thrombosis with Diffuse Spread Leading to Cerebral Ischemia Pooja Sethi, Scott T. Jones, and Alejandra A. Valenzuela

ABSTRACT Introduction: Septic cavernous sinus thrombosis (CST) is a rare disease with many etiologies and a diffuse array of initial presentation leading to high mortality. Case: A 25-year-old male with a history of a nasal furuncle presents with an acute onset of fixed and dilated pupils, bilateral exophthalmos, hemorrhagic chemosis, elevated intraocular pressures, restricted extraocular motility, and unresponsiveness. A retinal septic emboli in the left eye is present on dilated fundoscopic exam while an exudative retinal detachment is present in the right eye. MRI/MRV revealed extensive thrombosis of cavernous sinuses, distal sigmoid dural sinuses, and proximal internal jugular veins with associated cerebral edema and multifocal areas of venous infarction. Blood cultures grew Methicillin-resistant Staphylococcus aureus and the patient suffered multi-system organ failure. Despite treatment with full dose systemic anticoagulation and broad spectrum antibiotics the patient suffered a cardiopulmonary arrest and expired. Comment: The acuity of onset coupled with the multiple risk factors for septic cavernous sinus thrombosis in this patient led to a fulminant presentation of this disease and ultimate poor outcome. Keywords: Cavernous sinus thrombosis, furunculosis, venous infarction, septic emboli

Septic cavernous sinus thrombosis (CST) is a rare disease with many etiologies and a diffuse array of initial presentation leading to high mortality. We describe a presentation of septic CST with in a young male presenting with bilateral ophthalmoplegia, exophthalmos, chemosis, elevated intraocular pressures, exudative retinal detachment and septic retinal emboli. MRI/MRV revealed extensive thrombosis of cavernous sinuses, distal sigmoid dural sinuses, and proximal internal jugular veins with associated cerebral edema and multifocal areas of venous infarction.

treated), latent hepatitis-C, and distant IV drug abuse. The patient sought medical attention for a furuncle on his right anterior nares 2 days prior but declined treatment (per family the furuncle had been present for at least 5 days). In the emergency room he had 40.5  C of temperature of unknown duration and was tachycardic and tachypnic with mildly reactive pupils and nuchal rigidity. His Glascow Coma Scale was 6 at admission and he was therefore intubated. On ophthalmic examination, which occurred three hours after admission, he presented with marked bilateral periorbital edema, ophthalmoplegia, fixed dilated pupils, bilateral chemosis, exophthalmos (25-23/118 by Naugle) and disc edema (Figure 1). Forced duction exam was significant for restriction in extraocular motility in all directions in both eyes. His intra-ocular pressures were 47 and 39 mmHg, respectively. An exudative retinal detachment traversing the macula was present on the right and a

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Department of Ophthalmology, Tulane Medical School, New Orleans, Louisiana, USA

CASE REPORT A 25-year-old male was referred for bilateral proptosis and chemosis after presenting to the emergency room with unresponsiveness. Past medical history was significant for respiratory tuberculosis (successfully

Received 2 December 2012; Revised 1 April 2013; Accepted 10 June 2013; Published online 30 July 2013 Correspondence: Alejandra A. Valenzuela, MD, Department of Ophthalmology, Tulane University, 1430 Tulane Avenue, SL-69, New Orleans, LA 70112, USA. E-mail: [email protected]


Septic Cavernous Sinus Thrombosis


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FIGURE 1. (a) Clinical picture of the male patient with bilateral periocular swelling, chemosis, showing a right nasal furuncle. (b) Clinical picture demonstrating bilateral proptosis though more extensive on the right, and hemorrhagic chemosis, clearly indentified on the left temporal palpebral commissure.

FIGURE 2. (a) Axial MRI image depicting sphenoid sinusitis (arrowhead), cerebellar infarcts (arrow), proptosis and deformity of the posterior globes bilaterally. (b) Posterior-to-anterior view of MRV with multiple areas of dural sinus attenuation and thrombus (arrowheads) and no perfusion into internal jugular veins bilaterally.

well-circumscribed 0.6DA retinal lesion with central clearing, suspicious for septic emboli, was present in the left fundus. The patient was HIV negative and had a leukocytosis of 15.5 with the presence of immature band neutrophils. CT revealed diffuse cerebral edema and pansinusitis with abnormal contour of both globes (Figure 2a). Magnetic resonance imagining and magnetic resonance venography of the brain and orbits revealed thrombosis of cavernous sinuses, distal sigmoid dural sinuses, proximal internal jugular veins, and vasculature along the Sylvian fissures bilaterally (Figure 2b). There were focal ischemic infarcts in the cerebellar hemispheres and pons. Diffuse cortical ischemia and anoxic injury, and mass effect with sulcal effacement secondary to cerebral edema were also present. Based on these findings, a diagnosis of septic cavernous sinus thrombosis (CST) with diffuse intracranial dissemination was made. Anticoagulation with unfractionated intravenous heparin was started, as well as intravenous vancomycin, piperacillin/ tazobactam, and amphotericin-B. One day after admission his blood cultures grew Methicillin !

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resistant Staphylococcus aureus with no cardiac source of emboli on echocardiogram. Due to the advanced nature of his multi-systemic illness the patient went into septic shock and ventricular fibrillation arrest requiring resuscitation. Four days after he failed the apnea test and was declared brain dead, life support was withdrawn, and he died. An autopsy was not performed due to family wishes.

COMMENT CST poses a challenge for even the modern-day clinician due to its diffuse array of initial presentation in signs, symptoms, and acuity. The estimated annual incidence is 3–4 cases per 1 million people.3 Survivors of CST may suffer from blindness, orbital movement disorders such as permanent cranial nerve damage, and external ophthalmoplegia.1,6 In adults infection is the cause of CST in 6–12% of cases,4 resulting from hematogenous spread through the network of veins draining into the cavernous sinus which are continuous and anatomically predisposed to impaired drainage. Forward flow of blood

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332 P. Sethi et al. through this system of veins depends heavily on the pressure gradient within the venous system.6 We believe our patient being in a supine position immediately prior to the acute change in his neurologic status exacerbated this venous stasis. As the paranasal and cavernous sinuses are confluent, septic CVT may be also be caused by sinusitis. The limitation in forced duction exam for this patient suggests orbital infiltrative involvement which could have extended from the pansinusitis. Given the patient’s history of pulmonary tuberculosis, empiric Amphotericin B was started to cover Aspergillosis, which has been implicated in cases of sinusitis leading to CST. However given the blood culture results, it is likely that the implicated pathogen was Staphylococcus aureus, which is not only a common etiology of sinusitis but also furunculosis.10 Widespread thrombosis causes vasogenic and cytotoxic cerebral edema as a result of extravascation of intravascular contents.8 Massive edema in a closed space, such as the skull, causes an acute rise in intracranial pressure, impairs blood perfusion, ultimately leading to cerebral ischemia. This phenomenon has been previously described as ‘‘venous infarction’’ and usually causes hemorrhagic infarcts, but on occasion may be ischemic.2,7 Typically the areas of cortical ischemia do not correlate with an arterial blood supply; this case demonstrated multi-focal areas of ischemia in the cerebellum and pons not consistent with one main arterial distribution. A unique aspect of this case was the presence of a septic retinal emboli. Gupta et al.5 described CST in association with a carotid vasculitis resulting in recurrent episodes of micro-emboli leading to vision loss and branch retinal vein occlusion. While our patient did not have any evidence of retinal artery occlusions or carotid disease/thrombus at presentation, this phenomenon of septic emboli originating from an infectious vasculitic source remains a possible etiology for a septic emboli.9 As our case also had a markedly deceased ejection fraction and underwent cardiopulmonary arrest, it is possible that there were other foci of septic emboli in the pulmonary vasculature as well. It is also possible that repeat imaging of the brain and neck 24–48 hours after presentation would reveal emboli-related ischemia and carotid pathology, however this could not be obtained due to the patient’s rapid clinical deterioration. This case report emphasizes the acuity of CST onset, fast progression, and a plethora of

ophthalmologic findings, suggesting the ultimate diagnosis. The barriers to successful outcome in the case of this patient included the virulence of the organism and advanced presentation, likely related to a delay in seeking care in the setting of medical noncompliance.

DECLARATION OF INTEREST The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper. The authors would like to acknowledge Natalie Weil, MD and Kate Hust, MD for their contributions.

REFERENCES 1. Absoud M, Hikmet F, Dey P, et al. Bilateral cavernous sinus thrombosis complicating sinusitis. J R Soc Med 2006; 99(9):474–476. 2. Al-Shami A, Merrill CR, Kar-Purkayastha S. Cerebral venous sinus thrombosis causing stroke—an underdiagnosed entity. Int J Clin Pract 2007;61(9):1582–1584. 3. Bhatt A, Ingole J, Kumar S, Jain A. Bilateral Proptosis: Unusual presentation of Cortical Sinus Thrombosis. Internet J Intern Med 2009;8(1). DOI: 10.5580/924. 4. Bousser MG, Russell RR. Cerebral venous thrombosis. In: Major Problems in Neurology. Warlow CP, Van Gijn J, eds. London: WB Saunders, 1997. pp.27, 104. 5. Gupta A, Jalali S, Bansal RK, Grewal SP. Anterior ischemic optic neuropathy and branch retinal artery occlusion in cavernous sinus thrombosis. J Clin Neuroophthalmol 1990; 10(3):193–196. 6. Hoshino C, Satoh N, Sugawara S, et al. Septic cavernous sinus thrombosis complicated by narrowing of the internal carotid artery, subarachnoid abscess and multiple pulmonary septic emboli. Intern Med 2007;46(6):317–323. Epub 2007 Mar 15. 7. Kamouchi M, Wakugawa Y, Okada Y, et al. Venous infarction secondary to septic cavernous sinus thrombosis. Intern Med 2006;45(1):25–27. Epub 2006 Feb 1. 8. Pavlovich P, Looi A, Rootman J. Septic thrombosis of the cavernous sinus: two different mechanisms. Orbit 2006; 25(1):39–43. 9. Zaninetti M, Stangos AN, Abdo G, Pournaras CJ. Cavernous sinus thrombosis elicited by a central retinal vein venous stasis retinopathy. Graefes Arch Clin Exp Ophthalmol 2005;243(8):834–836. Epub 2005 Mar 9. 10. Zeyad M, Muhammad S, Quick Cadric A. Multiple bilateral orbital abscesses secondary to nasal furunculosis. Int J Pediatr Otorhinolaryngol 2001;58(2):167–171.


Septic cavernous sinus thrombosis with diffuse spread leading to cerebral ischemia.

Septic cavernous sinus thrombosis (CST) is a rare disease with many etiologies and a diffuse array of initial presentation leading to high mortality...
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