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 Table of Contents  
CASE REPORT
Year : 2016  |  Volume : 28  |  Issue : 1  |  Page : 61-64

A case of cavernous sinus thrombosis complicating orbital cellulitis


Department of Ophthalmology, Little Flower Hospital and Research Centre, Angamaly, Kerala, India

Date of Web Publication11-Nov-2016

Correspondence Address:
J K Ann
Department of Ophthalmology, Little Flower Hospital and Research Centre, Angamaly, Kerala
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0976-6677.193869

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  Abstract 


A 47-year-old patient with a swelling of the left upper eyelid, redness, proptosis, and defective vision of few days duration was seen in our clinic. The history, examination, and investigations were suggestive of cavernous sinus thrombosis complicating orbital cellulitis. The patient was admitted and treated by a team of specialists including ophthalmology, neurosurgery, and hematology. Patient recovered fully after 3 weeks of treatment. This case report is being presented to highlight the importance of careful clinical examination and high index of suspicion in recognizing such a serious complication.

Keywords: Cavernous sinus thrombosis; orbital cellulitis; proptosis.


How to cite this article:
Ann J K, Sreedhar A, Jacob MC. A case of cavernous sinus thrombosis complicating orbital cellulitis. Kerala J Ophthalmol 2016;28:61-4

How to cite this URL:
Ann J K, Sreedhar A, Jacob MC. A case of cavernous sinus thrombosis complicating orbital cellulitis. Kerala J Ophthalmol [serial online] 2016 [cited 2019 Mar 25];28:61-4. Available from: http://www.kjophthal.com/text.asp?2016/28/1/61/193869




  Introduction Top


Cavernous sinus thrombosis (CST) in the septic form results from an infection of the face, sphenoid, ethmoidal sinuses, or oral cavity. Rarely, otitis media or orbital sinuses is the cause. Reported incidence of cavernous sinus thrombosis as a complication of orbital cellulitis is 1%. Before the availability of antimicrobial agents, the mortality from CST was 100%, however, it markedly reduced to 20–30% during the antibiotic era.[1] Nevertheless, the threat of death and serious morbidity continues to necessitate early recognition, diagnosis, and treatment of CST to minimize risks to the patient.


  Case Report Top


A 47-year-old male came to our outpatient department with complaints of pain and swelling in his left eye of 1 week duration. He was under treatment from a local hospital (some tablets and ointment) for these complaints. There, he underwent incision and curettage of the swelling. Thereafter, he noticed increase in swelling associated with drooping of eyelid. Redness slowly increased and eye slightly bulged forwards, for which he came to our hospital. There was associated headache also. There was no increase in proptosis with coughing, sneezing, or with Valsalva; there was no postural variation. He had no dental or ear, nose, throat complaints. He was on medication for hypertension and hyperlipidemia.

His right eye vision was 6/6 and left eye was 2/60. There was lid edema, complete ptosis, eccentric proptosis (down and out) of 6 mm and limitation of all extraocular movements in the left eye [Figure 1] and [Figure 2]. Cornea was edematous and pupillary reaction was sluggish to both direct and consensual light. On fundus examination, there was disc edema of 1 DD with venous engorgement in the left eye. Examination of the right eye was within normal limits. He had sensory loss of supraorbital area on the left side (V th cranial nerve).
Figure 1: (a) LE lid edema, ptosis (b) eccentric proptosis (down and out)

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Figure 2: Limitation of extra ocular movements in LE

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At this point, our provisional diagnosis was orbital cellulitis with orbital apex syndrome in view of multiple cranial nerve palsy, II nd, III rd, IV th, V th, and VI th. We ordered a routine blood examination and computed tomography (CT) of the brain and orbit. He had a leukocytosis with thrombocytopenia. Peripheral smear showed thrombocytopenia with large platelets. Blood culture was negative. CT orbit showed proptosis with soft tissue inflammation in left orbit and dilated left superior ophthalmic vein [Figure 3]. In the left frontal lobe, there was a hypoechoic lesion seen in the inferior part suggestive of hemorrhage. Magnetic resonance imaging (MRI) with contrast confirmed these findings as well as cavernous sinus thrombosis on the left side [Figure 4] and [Figure 5].
Figure 3: Proptosis with soft tissue inflammation in left orbit and dilated left superior ophthalmic vein

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Figure 4: MRI brain showing cavernous sinus thrombosis of left side

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Figure 5: MRI brain showing hypoechoic lesion in left frontal lobe inferior part suggestive of hemorrhage

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In consultation with our hematologist and neurosurgeon, we started him on inj. ceftazidime 1 gm IV BD, inj. betnesol 2 cc IV OD, and topical steroid antibiotic treatment. After 2 days of treatment, he was put on anticoagulants – subcutaneous injection low molecular weight (LMW) heparin 1 mg/kg. We regularly monitored platelet count and International normalised ratio (INR) to adjust the dose of anticoagulation therapy. Patient started improving, and within 2 weeks lid edema reduced; ptosis recovered completely and vision in the left eye became 6/6. Extraocular movements were full in the left eye. By the third week, congestion also reduced [Figure 6] and [Figure 7]. Patient was discharged on oral antibiotics and steroids. Oral anticoagulation continued for 3 months. At the end of 3 months, repeat MRI was taken and superior ophthalmic vein and cavernous sinus thrombosis were found to be resolved. The hemorrhage seen in frontal lobe also disappeared in repeat scan [Figure 8].
Figure 6: LE Lid edema reduced and ptosis recovered at 2 weeks

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Figure 7: Extra ocular movement full

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Figure 8: MRI brain at three months showing normal superior ophthalmic vein and resolved cavernous sinus thrombosis

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  Discussion Top


Orbital cellulitis is an infection of the soft tissues of the orbit posterior to the orbital septum. Orbital cellulitis occurs in following three conditions:

  • Extension of an infection from paranasal sinuses or other periorbital structures such as the face, globe, or lacrimal sac
  • Direct inoculation of the orbit from trauma or surgery
  • Hematogenous spread from bacteremia.


Complications of orbital cellulitis may be limited to orbit such as subperiosteal or orbital abscess, exposure or neuropathic keratitis, secondary glaucoma, optic neuritis, Central retinal Artery Occlusion (CRAO), or intracranial such as meningitis, CST, and brain abscess. CST is a potentially lethal and rare complication of orbital cellulitis.

Our patient had a history of minor surgical procedure of upper eyelid and all the clinical features of orbital cellulitis. However, severe headache, rapid progression of symptoms, and multiple cranial nerve paralysis were suspicious of intracranial extension. Imaging studies confirmed the diagnosis of CST. Radiological findings included expansion of cavernous sinus with reversal of its typical outer concave margin, asymmetrically diminished enhancement with filling defects, and narrowing of intracavernous portion of the internal carotid artery.

Owing to the rarity of occurrence, there are no randomized controlled studies published regarding the management of CST. Cavernous sinus communicates with superficial and deep venous system of face and orbit through valveless veins. This allows an easy spread of infection from the face to cavernous sinus. The organisms found are Staphylococcus aureus 70%, Streptococcus pneumoniae followed by gram negative bacilli, anaerobes, and fungi (aspergillus and Rhizopus).[2],[3] First line of treatment is third generation cephalosporins. In case of methicillin-resistant S. aureus, vancomycin is added. Metronidazole is added when anaerobic organisms are suspected as in cases of sinus infections. Intavenous antibiotics are continued till the patient shows significant improvement, and it should be continued up to 3–4 weeks.[4]

Role of steroids is controversial. Steroids are recommended in cases of severe orbital congestion, as in our case, which can reduce pressure on the optic nerve. It also improves cranial nerve dysfunction. Definite indication for systemic steroids is adrenal insufficiency secondary to pituitary dysfunction.

In regards to anticoagulation therapy, there are various school of thoughts. Most of the studies recommend anticoagulation; It reduces the morbidity and mortality.[2] However, this patient had an intracranial bleed also, in which case we should be extremely cautious regarding anticoagulation therapy. There was a temporary thrombocytopenia, which could be a secondary thrombocytopenia either due to infection or due to the drugs he has taken before. The platelet count was increasing on consecutive days and became normal within two days of admission. Patient was on oral anticoagulants for 3 months.

High index of suspicion, timely imaging, multidisciplinary approach, and appropriate treatment is necessary to reduce the morbidity and mortality of such a complication.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
  References Top

1.
Ebright JR, Pace MT, Niazi AF. Septic thrombosis of cavernous sinus. Arch Intern Med 2001;161:2671-6.  Back to cited text no. 1
    
2.
Varshney S, Malhotra M, Gupta P, Gairola P, Kaur N. Cavernous sinus thrombosis of nasal origin in children. Indian J Otolaryngol Head Neck Surg 2015;67:100-5.  Back to cited text no. 2
    
3.
Gupta MC, Ahuja OP, Kumar S. Cavernous sinus thrombosis. Indian J Med Sci 1970;24:748-53.  Back to cited text no. 3
    
4.
Swaminath D, Narayanan R, Orellana-Barrios MA, Temple B. Necrotizing fasciitis of the nose complicated with cavernous sinus thrombosis. Case Rep Infect Dis 2014;2014:914042.  Back to cited text no. 4
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8]



 

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