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 Table of Contents  
CASE REPORT
Year : 2019  |  Volume : 57  |  Issue : 4  |  Page : 319-322

Endogenous orbital cellulitis with optic neuropathy secondary to an intramuscular abscess in poorly controlled diabetes mellitus


Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Puducherry, India

Date of Submission30-Jul-2019
Date of Decision17-Sep-2019
Date of Acceptance24-Oct-2019
Date of Web Publication26-Dec-2019

Correspondence Address:
Dr. Muthukrishnan Vallinayagam
Department of Ophthalmology, Mahatma Gandhi Medical College and Research Institute, Puducherry
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/tjosr.tjosr_66_19

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  Abstract 


Orbital cellulitis is an inflammation of soft tissue posterior to the orbital septum. The predisposing factors are sinusitis, dacryocystitis, hordeolum, dental infections, and penetrating trauma. The hematogenous spread of infection from a distant source is unusual. A 50-year-old diabetic male with poor glycemic control presented with sudden visual loss and swelling of the left eye for 3 days. An intramuscular abscess in the upper arm was the primary source of infection. Clinical examination disclosed orbital cellulitis with optic neuropathy, confirmed on magnetic resonance imaging. Methicillin-resistant Staphylococcus aureus was isolated from the blood culture and pus culture. The patient showed a dramatic resolution with fasciotomy and abscess drainage, adequate glycemic control, parenteral clindamycin, and oral corticosteroids. An expeditious approach is vital to circumvent visual loss due to optic neuropathy. Endogenous orbital cellulitis can occur secondary to an intramuscular abscess. A distant source of infection should be vigilantly excluded in orbital cellulitis.

Keywords: Endogenous orbital cellulitis, intramuscular abscess, methicillin-resistant Staphylococcus aureus, uncontrolled diabetes


How to cite this article:
Vallinayagam M, Sahu J, Krishnagopal S, Kumar N V. Endogenous orbital cellulitis with optic neuropathy secondary to an intramuscular abscess in poorly controlled diabetes mellitus. TNOA J Ophthalmic Sci Res 2019;57:319-22

How to cite this URL:
Vallinayagam M, Sahu J, Krishnagopal S, Kumar N V. Endogenous orbital cellulitis with optic neuropathy secondary to an intramuscular abscess in poorly controlled diabetes mellitus. TNOA J Ophthalmic Sci Res [serial online] 2019 [cited 2020 Jan 19];57:319-22. Available from: http://www.tnoajosr.com/text.asp?2019/57/4/319/273976




  Introduction Top


Orbital cellulitis is an inflammation of soft tissue posterior to the orbital septum. The infection originates from the contiguous foci of infection. Orbital cellulitis secondary to hematogenous spread from a distant source is uncustomary.[1] Infective endocarditis, septicemia, and cellulitis of distant sites are infrequently reported as etiological factors.[2]

Orbital cellulitis is fraught with complications including optic neuropathy, cavernous sinus thrombosis, meningitis, frontal abscess, and osteomyelitis.[3] Uncontrolled diabetes in the setting of orbital cellulitis results in serious morbidity.[4] A poorly controlled diabetic presenting with orbital cellulitis and optic neuropathy, secondary to an intramuscular abscess, is discussed.


  Case Report Top


A 50-year-old diabetic male presented with complaints of sudden visual loss and swelling of the left eye for 3 days. He reported a painful swelling in the left upper arm for 5 days, with features of localized cellulitis. The perception of light was absent in the left eye. Clinical examination revealed ptosis, proptosis, periorbital edema, chemosis, and congestion. There was complete restriction of extraocular movements [Figure 1]. A relative afferent pupillary defect was observed. Fundus examination was normal. The right eye examination was clinically unremarkable.
Figure 1: Left eye ptosis, proptosis, congestion, and restriction of extraocular movements

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The patient was febrile, conscious, and oriented, with no signs of meningeal irritation. The upper arm swelling was diagnosed as an intramuscular abscess [Figure 2]. Surgical referral and fasciotomy with drainage of the abscess was done. The drained specimen and a blood sample were sent for microbiological evaluation. The blood glucose was recorded to be 420 mg/dl. Diagnostic nasal endoscopy ruled out the evidence of sinusitis and mucormycosis.
Figure 2: Intramuscular abscess in the left upper arm (postfasciotomy)

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Magnetic resonance imaging (MRI) revealed foci of hyperintensities and thickening of soft tissue in preseptal and periorbital regions. Proptosis with the expansion of retro-orbital fat and thickening of the left optic nerve was noted [Figure 3] and [Figure 4]. This confirmed the diagnosis of orbital cellulitis. There was no enlargement or enhancement in the cavernous sinus.
Figure 3: T2-weighted magnetic resonance imaging showing foci of hyperintensities and thickening in preseptal and periorbital region (arrow)

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Figure 4: T1-weighted magnetic resonance imaging showing proptosis with the expansion of retro-orbital fat and thickening of the left optic nerve (arrow)

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The patient was empirically treated with a parenteral combination of piperacillin and tazobactam. A sliding scale of insulin was initiated. Methicillin-resistant Staphylococcus aureus (MRSA) was isolated from the blood culture and pus culture, which was sensitive to clindamycin. The therapy was augmented with intravenous clindamycin. Oral prednisolone in a dose of 40 mg was administered after achieving good glycemic control.

In 48 h, the patient was symptomatically better with significant resolution of proptosis and periorbital edema. The extraocular movements recovered to normal range in 5 days [Figure 5]. However, the visual acuity was unchanged. The wound dressing of fasciotomy was done daily, and blood glucose levels were closely monitored. The oral corticosteroid was gradually tapered over 10 days.
Figure 5: Resolution of ptosis, proptosis, and congestion with a full range of extraocular movements

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  Discussion Top


Orbital cellulitis is an ocular emergency characterized by fever, pain, proptosis, chemosis, periorbital erythema, restriction of ocular motility, and diminution of vision. Although common in children, it is not an unusual infection in adults. The common triggers for orbital cellulitis are contiguous spread from rhinosinusitis, dacryocystitis, hordeolum, dental infection, trauma, and orbital surgeries. The hematogenous spread of infection from a distant site is relatively unusual.[1]

A case of bilateral orbital cellulitis caused by  Neisseria More Details gonorrhoeae has been reported.[1] Infective endocarditis with the dissemination of septic emboli leading to orbital cellulitis is documented. Bilateral orbital cellulitis has been described as a sequelae of hematogenous spread from foot ulcer in an uncontrolled diabetic.[2] Uncontrolled diabetes with orbital cellulitis is more predisposed to neurological complications.[4] The precipitating cause in this patient was an intramuscular abscess in the upper arm.

The mechanisms of visual loss from optic nerve involvement are due to optic perineuritis, direct compression by an abscess, or occlusion of vessels supplying the optic nerve. Intraocular infections may advance from endophthalmitis to panophthalmitis. In some cases, extensive orbital soft-tissue inflammation occurs in the absence of ocular involvement.[1] Ischemic optic neuropathy resulting from a rapidly progressive orbital infection was presumably the cause of total visual loss in this case.

Radiographic imaging constitutes a crucial diagnostic tool. Computed tomography (CT) provides information regarding the paranasal sinuses, extent of orbital involvement, orbital abscess, and intracranial involvement. MRI is superior to CT scan in disclosing intracranial complications such as cavernous sinus thrombosis.[2]

The most common organisms implicated are Streptococcus pneumoniae, S. aureus, Haemophilus influenza, and nonspore forming organisms.[2] In a study conducted in a tertiary care hospital in South India, S. aureus was the most common organism isolated. MRSA was cultured from the majority of cases followed by coagulase-negative staphylococcus and S. aureus.[5] Infections with MRSA usually occur in individuals with well-established risk factors such as recent hospitalization, multiple antibiotic treatments, or chronic debilitating illness.[6] MRSA was isolated from the blood and pus culture in this case.

The most commonly used antibiotics in orbital cellulitis are broad-spectrum antibiotics such as cephalosporins and metronidazole.[2] MRSA is susceptible to non-β-lactam antibiotics such as clindamycin, tetracyclines, and cotrimoxazole. Linezolid, tigecycline, daptomycin, and vancomycin are especially effective for potentially severe clinical forms.[5] The adjunctive use of oral steroids in orbital cellulitis may hasten the resolution of inflammation with a low risk of exacerbating the infection.[7] The patient showed a dramatic resolution of inflammation with parenteral clindamycin and oral corticosteroids.

An expeditious approach is vital to circumvent serious complications of orbital cellulitis such as optic neuropathy, cavernous sinus thrombosis, meningitis, brain abscess, and sepsis.[5] The advent of high-resolution imaging, newer antibiotics, and early surgical intervention for orbital abscess have substantially declined the risk of visual loss.[2]

An aggressive management and prompt surgical intervention addressing the distant source of infection would have obviated the visual loss in this patient. The delay in presentation resulted in an irreversible visual compromise.


  Conclusion Top


This report is highlighted as an unusual case of orbital cellulitis secondary to hematogenous spread from an intramuscular abscess. It demonstrated a favorable response to fasciotomy with abscess drainage and systemic antibiotics. Adequate glycemic control is of prime importance to prevent grave consequences in diabetic patients. It is to be emphasized that a distant source of infection should be vigilantly excluded in orbital cellulitis.

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.



 
  References Top

1.
Sundar G, Hegde R. Orbital cellulitis-A review. TNOA J Ophthalmic Sci Res 2017;55:211.  Back to cited text no. 1
  [Full text]  
2.
Parija S, Banerjee AC, Sen S. Bilateral orbital cellulitis due to hematogenous spread from a rare site-A case report. IP Int J Ocular Oncol Oculoplasty 2018;4:58-60.  Back to cited text no. 2
    
3.
Chaudhry IA, Al-Rashed W, Arat YO. The hot orbit: Orbital cellulitis. Middle East Afr J Ophthalmol 2012;19:34-42.  Back to cited text no. 3
[PUBMED]  [Full text]  
4.
Colapinto P, Aslam SA, Frangouli O, Joshi N. Undiagnosed type 2 diabetes mellitus presenting with orbital cellulitis. Orbit 2008;27:380-2.  Back to cited text no. 4
    
5.
Pandian DG, Babu RK, Chaitra A, Anjali A, Rao VA, Srinivasan R. Nine years' review on preseptal and orbital cellulitis and emergence of community-acquired methicillin-resistant Staphylococcus aureus in a tertiary hospital in India. Indian J Ophthalmol 2011;59:431-5.  Back to cited text no. 5
[PUBMED]  [Full text]  
6.
Charalampidou S, Connell P, Fennell J, Lynch M, Acheson R. Preseptal cellulitis caused by community acquired methicillin resistant Staphylococcus aureus (CAMRSA). Br J Ophthalmol 2007;91:1723-4.  Back to cited text no. 6
    
7.
Pushker N, Tejwani LK, Bajaj MS, Khurana S, Velpandian T, Chandra M, et al. Role of oral corticosteroids in orbital cellulitis. Am J Ophthalmol 2013;156:178-830.  Back to cited text no. 7
    


    Figures

  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]



 

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