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Cavernous Sinus Thrombophlebitis: Case Report

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Cavernous Sinus Thrombophlebitis: Case Report CASE REPORTS Cavernous Sinus Thrombophlebitis: cose and protein levels, 10 white cells (9 mononuclear cells and 1 neutro­ Case Report phil), and negative gram stain and cul­ ture. The opening pressure was 22 cm of water. The peripheral white cell count was 13,000. The erythrocyte sed­ Timothy C. Kriss, M .D ., Vesna M artich Kriss, M .D ., imentation rate was 82. CSF, blood, urine, and sputum cultures were Benjamin C. Warf, M.D. Downloaded from https://academic.oup.com/neurosurgery/article/39/2/385/2884550 by guest on 29 September 2021 negative. Departments of Surgery (Division of Neurosurgery) (TCK, BCW), Radiology (VMK), and Magnetic resonance imaging (MRI) Pediatrics (VMK), University of Kentucky Medical Center, Lexington, Kentucky revealed enlargement and abnormal en­ hancement of the left cavernous sinus, with enhancement and increased T2 sig­ OBJECTIVE AND IMPORTANCE: Cavernous sinus thrombophlebitis is a rare, nal extending posteriorly to the petrous apex and clivus. The sphenoid sinus dangerous, and historically difficult condition to diagnose and treat. Knowl­ was opacified. The intracavernous left edge of the imaging findings and the importance of early diagnosis and internal carotid artery was markedly treatment are emphasized. narrowed. Figure 1, A through D, shows CLINICAL PRESENTATION: We present a case of cavernous sinus thrombo­ the results of the MRI performed before phlebitis caused by sphenoid sinusitis. Previously undescribed magnetic treatment. resonance imaging findings of cavernous sinus thrombophlebitis include Intravenous broad-spectrum antibiot­ enlargement of the cavernous sinus, abnormal enhancement and increased ics (nafcillin, cefotaxime, and metroni­ T2 signal of the petrous apex and clivus, and marked narrowing of the dazole) were started immediately. En­ cavernous portion of the internal carotid artery. Resolution of cavernous doscopic left sphenoidotomy with sinus sinus thrombophlebitis is also documented by magnetic resonance imaging. drainage and ethmoidectomy were per­ INTERVENTION: The anatomy of the cavernous sinus dictates the natural formed. Fluid but no pus was obtained from the sphenoid sinus. Gram stain history and diagnosis of cavernous sinus thrombophlebitis. We review the and culture from the sphenoid sinus did literature regarding the clinical diagnosis, differential diagnosis, and treat­ not identify an organism. A cell count ment of cavernous sinus thrombophlebitis. was not obtained. CONCLUSION: We emphasize the importance of a high index of suspicion, The patient rapidly improved. MRI the potentially rapid and fatal course of the disease process, and the subse­ performed 1 week later demonstrated quent need for antibiotic therapy and selective surgery. (Neurosurgery 39: dramatic reversal of the previous mag­ 385-389, 1996) netic resonance (MR) findings: marked increase in the caliber of the left internal Key words: Cavernous sinus, Sinus thrombosis, Thrombophlebitis carotid artery with decreased abnormal enhancement of the clivus, petrous n the preantibiotic era, septic inflamma­ ache (behind her left eye) and diplopia apex, and cavernous sinus regions. F ig ­ tion/ thrombosis of the cavernous sinus for 2 weeks. She also had associated u re 2, A through C, shows the results of was uniformly fatal. In 1936, Grove (11) nausea, malaise, fatigue, and occasional the MRI examination after sphenoi­ reviewedI >400 cases with an estimated vomiting for 2 weeks, with 3 days of dotomy and antibiotic treatment. The 100% mortality. The vast majority of cases persistent low-grade fever. Her history patient completed a 6-week course of came from infections of the middle one- was significant for a recurrent sinus in­ intravenous antibiotics at home, with third of the face (7, 11, 26, 27, 30). In the fection treated with over-the-counter complete resolution of the sixth nerve postantibiotic era, morbidity and mortal­ medications (first treated 6 weeks before palsy, headache, and fever. ity rates remain high; 20 to 34% of patients admission and then again at 3 weeks still die, and >50% will suffer permanent before admission). neurological morbidity, usually a persis­ A neurological examination re­ DISCUSSION vealed a left sixth nerve palsy. A gen­ tent cranial nerve palsy, visual field defi­ Anatomy cit, or even blindness (7,18, 20, 21, 26, 27). eral physical examination revealed nothing remarkable, with the excep­ The diagnosis, pathophysiology, and tion of an oral temperature of 101°F; natural history of cavernous sinus CASE REPORT no meningismus was present. Cere­ thrombophlebitis are dictated by the An 8-year-old female patient pre­ brospinal fluid (CSF) from a lumbar anatomy of the cavernous sinus. The sented with slowly progressive head­ puncture demonstrated normal glu­ Vlth cranial nerve is the only cranial Neurosurgery, Vol. 39, No. 2, August 1996 385 386 Kriss et al. difficult to diagnose (7, 16, 18, 20,25,' 29). Patients with isolated sphenoid nusitis will usually have headaches ar low-grade fevers. With subsequent ca ernous sinus involvement, half of t patients will develop meningisnu which can easily distract the phvsici from diagnosing the true source oft problem, the sphenoid sinusitis. B cause of these difficulties, the diagno- of cavernous sinus thrombophlebitis often delayed, with ominous ramificDownloaded from https://academic.oup.com/neurosurgery/article/39/2/385/2884550 by guest on 29 September 2021 tions (7, 16, 18, 20, 25). A high index suspicion is critical for both spheno sinusitis and cavernous sinus thromb phlebitis (6, 16, 18, 20, 25). Other cau- of cavernous sinus thrombophlebitis i elude infections of the middle third the face and dental infections (by way emissary veins and the pterygoid pie us), although the latter is much les common (7, 27). The differential diagnosis of caven ous sinus thrombophlebitis focuses o other causes of periorbital edema i multiple cranial nerve palsies. Otherir flammatory orbital conditions includ orbital cellulitis, infraorbital abscess, a! lergic blepharitis, ocular migraine,anc Tolosa-Hunt syndrome (14). In pa­ tients with cranial nerve signs, the di: ferential diagnosis would favot FIG U RE 1. A, Tl-weighted, contrast-enhanced coronal MR image demonstrating trauma, internal carotid artery aneu abnormal enhancement of the cavernous sinus with marked narrowing of the cali­ rysm, carotid-cavernous fistula, tumoi ber of the cavernous portion of the left internal carotid artery (arrow). Note the (meningioma or nasopharyngeal), pi­ sphenoid sinusitis. Axial MR images without (B) and with (C) contrast enhance­ tuitary abscess, mucormycosis, or as­ ment, showing the abnormal enhancement of the cavernous sinus, clivus, and pergillosis of the sphenoid sinus. petrous apex (arrows). T2-weighted axial image (D) demonstrating increased signal of the clivus and petrous apex (arrow), as well as the sphenoid sinusitis (arrowhead). Diagnosis The diagnosis of cavernous sinus nerve that actually runs within the cav­ nous connections, the cavernous sinus is thrombophlebitis is clinical and can b ernous sinus; all other cranial nerves of uniquely positioned to transmit infec­ predicted from the anatomy (2, 4,6. the cavernous sinus (III, IV, V„ V2) run tion or thrombus from the face or sphe­ 13, 17, 25-27). Obstruction of the supe within the lateral dural wall of the sinus. noid sinus into the dural sinuses and rior orbital vein causes proptosis, die- The intracavernous portion of the inter­ central nervous system. Cranial nerves mosis, and orbital edema. These Iocs nal carotid artery (along with its accom­ III, IV, VI, Vv and V2 and the intracav­ eye signs and symptoms, in conjunct^ panying sympathetic plexus) is the only ernous internal carotid artery (and its with a Illrd, IVth, or Vlth cranial nerve other structure within the sinus (12, 15). sympathetic plexus) are directly ex­ palsy, suggest the diagnosis of cavern­ Each cavernous sinus receives blood posed to any inflammatory process in ous sinus thrombophlebitis (2,4,6,7, U from the orbit via the superior and infe­ the cavernous sinus. The nearby optic 25-27). Progression from unilateral or rior ophthalmic veins. There are no nerve and V3 are also at risk. bital signs to bilateral involvement is valves in any of the dural sinuses (7, 26), ominous indicator that is essentially p-1 which has important implications for Pathogenesis thognomonic (25). the spread of infection or thrombus. Be­ Headache, often from s p h e n o i d sinU' cause of its central location adjacent to Sphenoid sinusitis is the most com­ itis, is present in >90% of the p a tie n ts (- the thin-walled sphenoid sinus (15) and mon modern cause of cavernous sinus 7, 17, 18, 20, 25-27). It typically has • its myriad potentially bidirectional ve­ thrombophlebitis, but it is notoriously unilateral and retro-orbital or front Neurosurgery, Vol. 39, No. 2, August 1996 Cavernous Sinus Thrombophlebitis 387 phy (CT) is the test of choice to diagnose sphenoid sinusitis (6, 20, 25, 28). MRI is the best imaging method for suspected cavernous sinus thrombo­ phlebitis (5, 7, 17, 24). The signal inten­ sities of the sinus can vary significantly as a result of infection, inflammation, and clot evolution (13, 19, 24). Inflamed meninges may worsen (13). Sphenoid sinus opacification with increased T2 signal is consistent with sphenoid sinus­ Downloaded from https://academic.oup.com/neurosurgery/article/39/2/385/2884550 by guest on 29 September 2021 itis. The cavernous sinus may be en­ larged, and the absence of flow void in the sinus suggests thrombosis (13, 19, 24). MRI in our case demonstrated para- meningeal enhancement and increased T2 signal along the clivus and petrous apex. This parameningeal enhance­ FIG U RE 2. A, follow-up MR scan after 1 ment, however, can also be seen in week of treatment (sphenoidotomy and other subacute and chronic inflamma­ antibiotics), showing normal caliber of tory processes. The dramatic decrease the cavernous portion of the left carotid artery (arrow) on the contrast-enhanced in the diameter of the intracavernous T1-weighted coronal image. Axial MR internal carotid artery was also docu­ images without (B) and with (C) contrast mented by MRI, as was its subsequent enhancement, demonstrating decreased resolution.
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