Conjunctival haemangiopericytoma

1 Croxatto JO, Font RL. Hemangiopericytoma of the orbit: aclinicopathologica study of 30 cases. Hum Pathol 1982; 13:210-8.

2 Roth SI, August CZ, Lissner GS, O'Grady RB. Hemangio-pericytoma of the lacrimal sac. Ophthalmology 1991; 98:925-7.

3 Papale JJ, Frederick AR, Albert D. Intraocular hemangio-pericytoma. Arch Ophthalmol 1993; 101: 1409-11.

4 Grossniklaus HE, Green R, Wolff SM, Iliff NT. Hemangio-pericytoma of the conjunctiva. Ophthalmology 1986; 93:265-7.

5 Stout AP, Murray MR. Hemangiopericytoma: a vasculartumour featuring Zimmerman's pericytes. Ann Surg 1942;116: 26-33.

6 Enzinger FM, Smith BH. Hemangiopericytoma; an analysis of106 cases. Hum Pathol 1976; 7: 761-81.

7 Enzinger FM, Weiss SW. Soft tissue tumours. St Louis: Mosby,1988: 596-611.

8 Pandya A, Dayal Y, Singhal V, Pattnaik NK. Haemangioperi-cytoma. BrJ Ophthalmol 1984; 68: 124-7.

9 Yu CCW, Hall PA, Fletcher CDM, Camplejohn RS, WaseenNH, Lane DP, et al. Haemangiopericytomas, the prognosticvalue of immunohistochemical staining with a monoclonalantibody to proliferating cell nuclear antigen (PCNA).Histopathology 1991; 19: 29-33.

10 Henderson JW, Farrow GM. Primary orbital haemangioperi-cytoma; an aggressive and potentially malignant neoplasm.Arch Ophthalmol 1978; %: 666-73.

11 Nemas Z. Differentiation markers in hemangiopericytoma.Cancer 1992; 69: 133-9.

12 Ahern VA, Roberts SJ. Hemangiopericytoma, QueenslandRadium Institute experience and a review of the literature.Australas Radiol 1991; 35: 248-52.

British journal ofOphthalmology 1994; 78: 499-501

Treatment of aphakic malignant glaucoma usingNd:YAG laser posterior capsulotomy

B C Little

Malignant glaucoma is the term introduced in1869 by von Graefel to describe one of the moreserious but rare complications of anteriorsegment surgery. It is best known followingtrabeculectomy but has been reported after awide variety of anterior segment procedures.

It is notoriously refractory to medical treat-ment alone2 3 and surgical intervention has hadonly limited success.45 An additional treatmentoption in pseudophakic eyes or aphakic eyes withan intact posterior capsule is that of short pulsedNd:YAG laser posterior capsulotomy which isminimally invasive, carries little risk and can re-establish forward flow of posteriorly misdirectedaqueous through into the drainage angle of theanterior chamber.26 Successful use of Nd:YAGposterior capsulotomy can obviate the need forfurther surgical intervention.A case is reported of malignant glaucoma

developing post-trabeculectomy which persisteddespite surgical treatment. Long term pressurecontrol was established following Nd:YAGposterior capsulotomy.

Moorfields Eye Hospital,City Road, LondonEC1V 2PDB C LittleAccepted for publication13 December 1993

Case reportA 69-year-old woman presented in 1987 withocular hypertension and narrow drainage anglesfor which topical ,3 blocker (timolol drops0 25%) treatment was required the followingyear. Intraocular pressure (IOP) control wasunsatisfactory and unresponsive to bilateral 360degree argon laser trabeculoplasty. Adjunctivetopical treatment using an adrenergic agonist(dipivefrin drops) did not improve IOP control(30mm Hg bilaterally) and automated perimetryrevealed an early arcuate scotoma in her righteye. A right trabeculectomy was performed inSeptember 1992.On the first postoperative day she had diffuse

shallowing of the anterior chamber with an IOP

of 38 mm Hg and a diagnosis of malignantglaucoma was made. The following day a limitedpars plana core vitrectomy was performedand the anterior chamber reformed internallythrough a surgical cyclodialysis. On the firstpostoperative day a deep anterior chamber waspresent with a normal IOP. Two days later a totalhyphaema was present together with a peri-pherally flat anterior chamber and raised IOP.Maximum topical and systemic treatmentreduced the IOP to 25 mm Hg. The hyphaemaslowly resorbed over the following 2 weeks toabout 30% of the corneal diameter, but themalignant glaucoma persisted despite full cyclo-plegia. At this stage she was referred for furthermanagement.Her right IOP was 18 mm Hg on full medical

treatment and her acuity 6/12 with a healthy disc.There was marked diffuse conjunctival andepiscleral hyperaemia and the anterior chamberdepth measured 1 6 mm centrally (Haag-StreitAC depth meter) but was peripherally closed andno drainage bleb was present overlying thetrabeculectomy site. Over the following 4 daysthe IOP remained under 20 mm Hg on topicaland systemic treatment and the inflammationsettled on treatment with topical steroidalthough the anterior chamber remained peri-pherally flat.B scan ultrasound showed ciliary body

enlargement in the right eye but not in theunoperated left eye. The axial length of the righteye was difficult to measure accurately but that ofthe left eye wa's 21-1 mm. Her preoperativerefraction was not hypermetropic and neitherwas there anisometropia in her reading prescrip-tion.

She was discharged and reviewed 2 weeks laterwhen the anterior chamber was still flat with anIOP of 30mm Hg and an optically clear zone wasnoted behind her lens, presumed to be seques-

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Little

Figure I Flat anterior chamber with posterior capsuleherniating through capsulorrhexis.

tered aqueous. Her corrected acuity remainedgood at 6/9.

She was then booked for further pars planavitrectomy and extracapsular lens extractionwithout intraocular lens (IOL). At operation acorneal groove was cut and a 27 gauge anteriorchamber paracentesis made tangentially in theperipheral cornea. A single port pars planaOcutome vitrectomy was carried out and theanterior chamber inflated through the paracente-sis with viscoelastic. The corneal section wascompleted followed by enlargement of the peri-pheral iridectomy to a broad iridectomy whichenabled a large continuous tear needle capsulor-rhexis to be fashioned. Following hydrodissec-tion the nucleus was expressed and, afteraspiration ofthe residual cortical lens matter, thesection was closed with 10/0 nylon.On the first postoperative day the anterior

chamber had flattened and the vitreous washerniating the posterior capsule through thecapsulorrhexis, forming a 'dome' whose apexwas almost in contact with the corneal endo-thelium (Fig 1). The IOP was 10 mm Hg andthere was no leak through the cataract section

Figure 2 Deep anterior chamber immediately followingNd:YAG posterior capsulotomy.

Figure 3 Retroillumination before Nd:YAG laser posteriorcapsulotomy.

and no conjunctival bleb. The early recurrenceof malignant glaucoma was diagnosed. ANd:YAG posterior capsulotomy combined withanterior vitreolysis was performed the followingday resulting in an instantaneous forward gush offluid accompanied by simultaneous deepening ofthe anterior chamber (Fig 2). Retroilluminationhighlights the small central laser capsulotomy(pre-treatment (Fig 3) and post-treatment (Fig4)).Over a 7 month follow up period the anterior

chamber has remained deep and the IOP normaland stable in the absence of a trabeculecomy bleband, surprisingly, no antiglaucoma medication.The normal IOP despite no treatment may wellbe due to the existence of an alternative outflowpathway via the surgical cyclodialysis. The cor-rected acuity is 6/9.

CommentVon Graefe' introduced the term 'malignantglaucoma' in 1869 to describe raised intraocularpressure associated with a flat anterior chamberfollowing uneventful surgery for angle closure

Figure 4 Retroillumination immediatelyfollowingNd:YAG laser posterior capsulotomy: the capsulotomyformsa central vertical ellipse.

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Treatment ofaphakic malignant glaucoma usingNd:YAG laserposterior capsulotomy

glaucoma. It is now recognised to comprise thediagnostic triad of a diffusely flat anteriorchamber, high intraocular pressure, andaqueous pooling that is sometimes visible in or infront of the anterior vitreous.

Malignant glaucoma is notoriously difficult totreat and carries a generally poor prognosis forlong term control of intraocular pressure.

It is thought to involve the mechanisms ofciliolenticular block of aqueQus flow leading tothe misdirection of aqueous posteriorly into, orin front of, the vitreous gel leading to thecharacteristic diffuse shallowing of the anteriorchamber accompanied by an often precipitousrise in intraocular pressure. Medical treatmentalone is rarely successful in establishing controlof the IOP.23 Pars plana vitrectomy has beenused in the surgical management of malignantglaucoma with some definite but limited successin phakic as well as pseudophakic eyes.45However, when malignant glaucoma develops

in pseudophakic eyes (with posterior chamberIOLs) there exists an additional treatment option

of Nd:YAG laser capsulotomy and/or vitreo-lysis26 which can be effective in arresting thespiralling rise in IOP by redirecting aqueous flowanteriorly thereby avoiding the need for acutesurgical intervention with its inevitably highermorbidity. The same reasoning can be appliedto aphakic eyes that have an intact posteriorcapsule, with similar chances of a successfuloutcome.

1 von Graefe A. Bietrage zur pathologie und therapie desglaucoms. Arch Ophthalmol 1869; 15: 108.

2 Tomey KF, Senft SH, Antonios SR, Shammas IV, Shihab SM,Traverso CE. Aqueous misdirection and flat chamber afterposterior chamber implants with and without trabeculec-tomy. Arch Ophthalmol 1987; 105: 770-3.

3 Schrader CE, Belcher CD III, Thomas JV, Simmons RJ,Murphy EB. Pupillary and iridovitreal block in pseudo-phakic eyes. Ophthalmology 1984; 91: 831-7.

4 Weiss H, Shin DH, Kollarits CR. Vitrectomy for malignant(ciliary block) glaucomas. Int Ophthalmol Clin 1981; 21: 113.

5 Lynch MG, Brown RH, Michels RG, Pollack IP, Stark WJ.Surgical vitrectomy for pseudophakic malignant glaucoma.AmJ Ophthalmol 1986; 102: 149-53.

6 Little BC, Hitchings RA. Pseudophakic malignant glaucoma:Nd:YAG capsulotomy as a primary treatment. Eye 1993; 7:102-4.

British Journal ofOphthalmology 1994; 78: 501-503

Nasolacrimal obstruction and facial bonehistopathology in craniodiaphyseal dysplasia

Dominic A McHugh, Geoffrey E Rose, Alec Gamer

Moorfields Eye Hospital,City Road, LondonEC1V 2PDD A McHughG E RoseA GarnerCorrespondence to:Mr G E Rose.Accepted for publication10 January 1994

Craniodiaphyseal dysplasia is a rare, severe, andprogressive bone dysplasia characterised bythickening, distortion, and enlargement of thecranium and face.'2 Epiphora and recurrentdacrycystitis can occur in this and other suchbone diseases owing to nasolacrimal ductstenosis.4 The management of such a caseprovided an opportunity to obtain material foranalysis, with the aim of gaining more informa-tion on the aetiology and possible treatment ofthis condition.

Case reportThe patient was a female, aged 3 years in whom adiagnosis of craniodiaphyseal dysplasia had been

made soon after birth, from the typical clinical(Fig IA) and radiological appearances (Fig 1B).A low calcium diet had been commenced andcalcitriol therapy administered in an attempt to

Figure I (A) Clinicalappearance ofa patient withcraniodiaphyseal dysplasia.Note the paranasal bossingand hypertelnim, whichhas arisen as a result of theunderlying bonyabnormnality. (B)Radiograph ofthe skull ofthe patient shown in Figure1. Hyperostosis and sclerosisofthe facial skeleton resultedin left nasolacrimalobstruction.

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Fig IA

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