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ARTICLES
Year : 1985  |  Volume : 33  |  Issue : 4  |  Page : 239-241

Orbital mucormycosis (phycomycosis)


Department of Ophthalmology, Dayanand Medical College and Hospital Ludhiana, India

Correspondence Address:
R K Grewal
Department of Ophthalmology, Dayanand Medical College and Hospital, Ludhiana
India
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Source of Support: None, Conflict of Interest: None


PMID: 3842832

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How to cite this article:
Grewal R K, Grewal S S, Zachariah R M. Orbital mucormycosis (phycomycosis). Indian J Ophthalmol 1985;33:239-41

How to cite this URL:
Grewal R K, Grewal S S, Zachariah R M. Orbital mucormycosis (phycomycosis). Indian J Ophthalmol [serial online] 1985 [cited 2020 Nov 27];33:239-41. Available from: https://www.ijo.in/text.asp?1985/33/4/239/30799

Phycomycosis is caused by a group of mycose, eumycetes (true fungi) of class phycomycetes. The agents causing invasive infections of eye and orbit are typically absidia, mucor and rhizopus. They are members of the order mucorales; hence the term mucormycosis. Orbital mucormycosis is the most urgent form of oculomycosis and manifests as unilateral orbital cellulitis, proptosis of the globe and orbital apex syndrome, VII N involvement, oedema and necrosis of the ocular adenexa. Extension through the internal carotid artery, brain and meninges and generalised sepsis may be the terminal events.


  Case report Top


12 years old boy was admitted to the hospital with low grade fever, vomiting and diabetic ketoacidosis. He had omitted insulin dose the previous day. 2 days later he developed a pea-size swelling near the left medial canthus with slight pain and tenderness. After another 2 days he developed ptosis Visual acuity and fundus were normal. On 15th day x-ray revealed cloudy ethomoidal sinuses. He was diagnos­ed as a case of ethmoiditis and was treated with oral Septran (Burrough Wellcome) and Erthromycin for one week without improve­ment.

On the 21st day he complained of sudden diminution of vision of left eye and was transferred to the Eye ward. Ocular examina­tion revealed no perception of light and pupil was dilated. Direct reaction to light was absent but consensual reflex was present. In addition he had full-blown left orbital apex syndrome (cranial nerves II, III, IV, V-1, 2), VI N palsy and infranuclear facial palsy [Figure - 1]a. Fundus showed occlusion of the central retinal artery. Ophthalmodyna­mometry showed left ophthalmic artery insufficiency. Left preauricular lymph nodes were enlarged and tender. A small ulcer with cheesy greyish escher was seen on the septum of nose on left side. He was febrile (100°F) and urine reduction was red.

Lacrimal sac washings, conjunctival smear and scrapings from septum of nose and nasopharynx were taken. A fresh KOH smear from the nose showed aseptate hyphae, typical of phycomycosis. Culture of scrapings from the septum of nose showed rhizopus growth after 7 days, in Sabauroud's medium [Figure - 1]b. Intravenous Amphoteri­cin-B was started immediately with a dose of 0.25 mg/kg body weight (in 500 cc of 5% dextrose over 6 hours) which was increased daily by 0.25/kg body weight till a maximum dose of 1 mg/kg body weight was reached.

After one month of hospitalization, patient developed cord-like supraorbital and supratrochlear veins. A small firm swelling, 10X5 mm with irregular margins and fixed to the underlying bone was felt in the superomedial rim of left orbit which increased in size and became fluctuant and tender and later burst forming a sinus. No growth of the organism was found from the pus. The patient was put on Potassium iodide solution (KI) 20 gms dissolved in 20 cc of water orally - 5 drops thrice daily initially, and the dose was raised by 3 drops daily till a maximum of 30 drops daily was given. Ampicillin capsule 500 mg 6 hrly for one week was also given. The sinus healed in 2 weeks time. After three months, he was discharged after completing a dose of 2 grams of Amphoteri­cin B. KI was continued for another four weeks. X-ray of paranasal sinuses was normal.

Extraocular muscle movements became normal after one year and there was no residual facial palsy [Figure l]c. Direct reac­tion to light in the left pupil was still absent. The retina showed degenerative changes consequent to the central retinal artery occlusion. Now 3 years after his treatment was stopped, the patient has had no relapses or. complications. His diabetes is con­trolled.


  Discussion Top


A century has passed since Paltauf reported mucormycosis in man in 1885 but the first case of rhino-orbitocerebral mucor­mycosis was published[1]. Debilitating con­ditions are predisposing factor. However, phycomycosis may develop in otherwise healthy individuals with mild or unrecognis­ed diabetes mellitus.

The usual portal of entry is the nose, It proliferates and spreads to the paranasal sinuses and then to the orbit by direct extension or intravascular dissemination. It also spreads to the cavernous sinus, leptomeninges and frontal lobe. The byphae invade the arteries,and veins to produce a thrombosing vasculitis with extensive ischaemic necrosis. The early visual loss and central retinal artery occlusion of orbital mucormycosis are not found in pyo­genic cavernous sinus thrombosis and help to differentiate the two syndromes. Though our patient had a characteristic picture of central retinal artery occlusion, ophthalmo­dynamometry showed only insufficiency of left ophthalmic artery. Ferry and Abedi[2] have discussed a similar case in their series where pathological examination of the eye revealed the lumen of the central retinal artery to be patent throughout the entire extent of its course in the optic nerve indicat­ing that the vascular obstruction had occurred more proximally.

The strictly unilateral involvement is characteristic. The peripheral 7th nerve weakness with early ecchymosis and necrosis of ocular adenexae distinguish this disease from other causes of orbital cellulitis and orbital apex syndrome[3]. But Ferry and Abedi state that proptosis and formation of black eschar were only seldom found among the initially apparent features.

Customarily, the cases are treated with surgical debridement and intravenous Amphotericin-B, However not all authori­ties agree that extensive debridement is necessary. Two cases of survival, who were treated with Amphotericin-B alone without exenteration despite prominent orbital involvement, have been documented by Ferry and Abedi[2]. With early diagnosis, systemic antifungal therapy, surgical debride­ment and control of the underlying disease, the prognosis ranges from 44-85%[4].

The present case report is interesting in that (1) it documents another survival with I/V Amphotericin-B and concurrent supple­mentary KI therapy, (2) we were able 4o culture the fungus rhizopus successfully, (3) ecchymosis and necrosis of ocular adenexa were absent (except for the grey eschar on the nasal septum) in spite of starting Amphotericin-B almost 3 weeks after the disease had apparently started, (4) to our knowledge this is the first case where motility of the affected extiaccular muscles has returned to their full extent and (5) the patient is still healthy after 3 years.


  Summary Top


A rare case of recovery and survival of 12 years old child having left orbital apex syndrome due to mucormycosis treated with Amphotericin-B and Potassium iodide without any surgical intervention has been described.

 
  References Top

1.
Ferry,. A.P, 1961, Surv. Ophthalmol 6: 1-24.  Back to cited text no. 1
    
2.
Ferry, A.P., Abedi, S. 1983, Ophthal­mology. 90 : 1096 1104.  Back to cited text no. 2
    
3.
Jones, D.B.. 1974, Ocular inflammatory disease, B. Golden, ed. p, 238, Publisher Charles C. Thomas, Springfield. Illinois.  Back to cited text no. 3
    
4.
Leherer, R.I. and Howard, D.H., 1980, Ann. Intern Med. 93 : 93-108.  Back to cited text no. 4
    


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