Lateral sinus thrombosis with cranial nerves palsies

Lateral sinus thrombosis with cranial nerves palsies

International Journal of Pediatric Otorhinolaryngology Extra (2007) 2, 165—168 www.elsevier.com/locate/ijporl CASE REPORT Lateral sinus thrombosis ...

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International Journal of Pediatric Otorhinolaryngology Extra (2007) 2, 165—168

www.elsevier.com/locate/ijporl

CASE REPORT

Lateral sinus thrombosis with cranial nerves palsies B. Viswanatha * Department of E.N.T., Victoria Hospital and Bangalore Medical College, Bangalore 560002, Karnataka, India Received 23 March 2007; received in revised form 3 May 2007; accepted 3 May 2007

KEYWORDS Lateral sinus; Thrombosis; Cranial nerve palsy

Summary Lateral sinus thrombosis is a well-known complication of otitis media. The classical picture is often modified by previous antibiotic therapy, making the diagnosis and management difficult. A 14-year-old male patient with attico antral type of otitis media presented with fever, headache, deviation of left eye and deviation of tongue to left on protrusion. On investigation patient was found to have lateral sinus thrombosis, petrous apicitis, meningitis and internal jugular vein thrombosis along with cranial nerves palsies. Patient underwent radical mastoidectomy and intravenous antibiotics were given for 2 weeks. Patient recovered well in 1 month. Lateral sinus thrombosis is now a rare intracranial complication of otitis media. The presence of lateral sinus thrombosis mandates further investigation for additional complication. Here a case of lateral sinus thrombosis with internal jugular vein thrombosis, petrous apicitis, abducent and hypoglossal nerves palsies is presented for its rarity. # 2007 Elsevier Ireland Ltd. All rights reserved.

1. Introduction Lateral sinus thrombosis is a well-known otogenic complication with serious consequences if left untreated [1]. The involvement of lateral sinus during the course of ear infection was a very well-known complication in preantibiotics days [2]. The dramatic drop in the incidence of lateral sinus thrombosis can be attributed to the introduction of antibiotics, earlier diagnosis and prompt effective treatment [1]. The classical picture is * Correspondence address: 716, 10th Cross, 5th Main, M.C. Layout, Vijayangar, Bangalore 560040, Karnataka, India. Tel.: +91 80 2338 1567. E-mail address: [email protected].

often modified because of previous antibiotic therapy making the diagnosis of the occasional case of lateral sinus thrombosis more difficult by altering the expected clinical course [2—4]. The remarkable decrease in incidence of this complication has gradually reduced the suspicion and hence the diagnosis of lateral sinus thrombosis. Otologists should, however, realize that this complication will be encountered occasionally and must be managed properly [2]. In the present case patient presented with both intracranial and extra-cranial complication secondary to cholesteatoma. Along with lateral sinus thrombosis patient had, petrous apicitis meningitis, internal jugular vein thrombosis and cranial nerves palsies.

1871-4048/$ — see front matter # 2007 Elsevier Ireland Ltd. All rights reserved. doi:10.1016/j.pedex.2007.05.001

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B. Viswanatha

2. Case report A 14-year-old boy presented with history fever and headache of 20 days duration and deviation of left eye and difficulty in speech and mastication of 3 days duration. Patient also had ear discharge for the past 3 years. Ear discharge started 3 years back, continuous, yellowish, foul smelling, small quantity and not blood stained. It was associated with decreased hearing. Fever started 20 days back and it was associated with generalised headache. It was not associated with chills and rigors. Patient developed deviation of left eye and speech and eating difficulty since 3 days. Patient had difficulty in chewing food on the left side. There was no history of aspiration or regurgitation of food. Patient complained of deviation of tongue to the left side on protrusion. On examination patient was conscious, febrile and speech is slurred. There was lateral rectus paralysis on the left side (Fig. 1). Left hypoglossal nerve was paralysed. Facial and other cranial nerves were normal. There was no sensory or motor deficit. On examination of left ear, there was mastoid tenderness. Yellowish foul smelling discharge was present in the external auditory canal. Deeper part of the external auditory canal and attic was filled with granulation. Tympanic membrane was not visualised. Right ear was normal. Tuning fork test showed conductive deafness on the left side. Nose, sinuses and throat (except for tongue movements) examinations were normal. On neck examination, left internal jugular vein was palpable in the upper part of the neck and it was tender on palpation. Rest of the neck examination was normal. Routine blood and urine examinations were normal. On MRI left lateral sinus was occluded with thrombus and dilated (Fig. 2). MRI venogram showed non-filling of lateral sinus on the left side. Small T1 hypo intense region, suggestive of cholesteatoma was seen in the left mastoid region. Axial T2

Fig. 1 Photograph showing lateral rectus palsy on the left side.

Fig. 2 MRI showing (arrow) occlusion and dilatation of left lateral sinus.

weighted MRI showed hyper intense region in the left petrous apex (Fig. 3). Post contrast enhancement of sinus wall was present (Fig. 4). Mild dural enhancement was seen at the prepontine cistern and signals suggestive of exudates were seen in the left cerebral hemisphere. Culture and sensitivity of ear discharge showed pseudomonas organisms sensitive to ceftriaxone and amikacin. The CSF picture was that of meningitis and patient had raised intracranial tension. Mastoid exploration was done under general anesthesia. Mastoid and middle ear were filled with

Fig. 3 Axial T2 weighted MRI showing hyper intense region (arrow) in the left petrous apex.

Lateral sinus thrombosis with cranial nerves palsies

Fig. 4 MRI showing (arrow) post contrast enhancement of the sinus wall on the left side.

foul smelling pus and granulation. Attic was filled with cholesteatoma. Tympanic membrane and ossicles were destroyed. Sinus plate was eroded and sinus was covered with granulation. Granulations were removed from the middle ear and mastoid. On needle aspiration of sinus, there was absence of blood flow. A longitudinal incision was made on the sinus wall. Sinus was filled with thrombus and pus which was removed. There was no free blood flow from both the ends. Radical mastoidectomy and a wide meatoplasty was done. Patient was given intravenous antibiotics for 2 weeks. Patient was also treated for meningitis and raised intracranial pressure. Eye movements became normal after 2 weeks. Tongue movements became normal after 1 month.

3. Discussion 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 [5]. It has been reported in patient with an intact sigmoid plate indicating propagation by the thrombophlebitic spread through small emissary vein [4,5]. The first successful surgery for lateral sinus thrombosis was performed by Lane in 1888. Until then the mortality for this complication has been 100%. Operative intervention reduced the mortality to 50%. Between 1932 and 1940 when antibiotic were introduced, a combination of antibiotics and surgical management reduced the mortality rate to 25% [6].

167 The most frequent presenting symptoms were headache, otalgia, fever and vomiting and pain in the neck [1,7]. With the occlusion of the lumen of the sinus, interruption of cortical venous circulation results in headache, papilloedema and increased intracranial pressure. Tenderness and edema over mastoid (Griesinger’s sign) are pathagnomonic of lateral sinus thrombosis and reflex thrombosis of mastoid emissary vein [8]. Internal jugular vein thrombosis can manifest as tender mass in the neck along or across sternocleidomatoid muscle [9]. 9th, 10th, 11th cranial nerve may be paralised by the presence and pressure of clot in the jugular bulb (jugular foramen syndrome). Hypoglossal nerve is spared because it travels in separate hypoglossal canal [8]. Our patient presented with otorrhoea on left side, fever and headache. There was left abducent nerve palsy. MRI showed involvement of the petrous apex by the disease process. Abducent nerve palsy was due to petrous apicitis (Gradenigo’s syndrome). In series of patients with petrous apicitis the predominant causative organism was found to be pseudomonas aeruginosa [8]. In our case also pseudomonas was responsible for the infection. The lateral sinus exits the skull through the jugular foramen to become internal jugular vein. Deep cervical lymph nodes are closely adjacent to the vein throughout its course. Thrombosis of internal jugular vein can manifest as tender mass in the neck along or across strnocleidomastoid muscle [9]. In our case there was paralysis of hypoglossal nerve on the left side and left internal jugular vein was palpable as tender mass in the upper part of the neck. Hypoglossal nerve palsy could be due to the mass causing pressure over the hypoglossal nerve in the upper part of the neck. Basal meningitis often presents as multiple cranial nerve palsies [10]. In our case also CSF analysis showed features of meningitis. MRI showed mild dural enhancement at prepontine cistern and signals suggestive of exudates was seen in the left cerebral hemisphere. Hypoglossal nerve palsy may also be due to basal meningitis. The antibiotic era has seen a change in not only the clinical presentation of lateral sinus thrombosis, but also bacteriology [3]. Beta haemolytic streptococcus is no longer dominant organism [3,11]. Since chronic, rather than acute infection more commonly precede lateral sinus thrombosis, cultures characteristically yields mixed flora including bacteroids, staphylococcus, enterobacteriaceae, proteus, pseudomonas and others species [3,5,7]. Since antibiotics are commonly used during the prodromal ear infection, blood culture is often negative [2,3].

168 CT and MRI are the investigations of choice in making diagnosis. MRI is more sensitive than CT in detecting the thrombus [12]. This is the investigation of choice, and should be performed in conjunction with CT, there by fully evaluating associated otologic and cerebral pathology [13]. Once the diagnosis is made, combination of antibiotics and surgical treatment is necessary to keep the mortality rate at 25% [6]. Surgery includes mastoid exploration, exposure of sinus, incision and drainage and removal of as much clot as possible [3,5]. Free bleeding from both ends is desirable. If there is no bleeding, evacuation of as much as clot as possible will suffice [3,14]. Canal wall down mastoidectomy should be done for cholesteatomatous ears presenting with lateral sinus thrombosis [1]. Most authors agree that there is no place for anticoagulants in the management of lateral sinus thrombosis [3,8]. Unless thrombus propagates after surgery, anticoagulants are not recommended [7,11]. Recent authors are of the opinion that with modern antibiotic therapy internal jugular vein ligation is not required [4]. Internal jugular vein ligation should reserved for those cases in which septicemia and embolisation do not respond to initial surgery and antibiotic treatment [6,14].

4. Conclusion Lateral sinus thrombosis is now a rare intracranial complication of otitis media. The presence of lateral sinus thrombosis mandates further investigation for additional complication. In our case patient had meningitis, petrous apicitis, internal jugular vein thrombosis and cranial nerves palsies along with lateral sinus thrombosis.

B. Viswanatha

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