Occupational blast injury resulting in traumatic ... - Wiley Online Library

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003

Letters to the Editor Ultrasound biomicroscopic evaluation in Sturge Weber syndrome without glaucoma Ramanjit Sihota, Viney Gupta and Harish C. Agarwal RP Centre for Ophthalmic Sciences, All India Institute of Medical Sciences, Delhi, India

Sir,

A

9-year-old girl was referred to us by a paediatrician for an ophthalmological check-up. She was known to have Sturge Weber syndrome and had consulted the paediatrician for treatment of the port wine stain on her face. On examination, apart from the angiomas present bilaterally along the distribution of the ophthalmic and maxillary division of the trigeminal nerve, we did not find any other lesions on the body. There was no history of seizures or any other neurological deficit. Her intellectual development was normal. The family history was non-contributory. The patient did not have any visual complaints and her visual acuity was 20/20 with 1 diopter sphere in both eyes. Slit-lamp examination revealed an extensive episcleral vascular plexus in the nasal part in the left eye and a similar plexus of vessels temporally and inferiorly in the right eye. Conjunctival vascular malformations were also evident in the same areas and at the limbus, extending from 5 o’clock to 10 o’clock nasally in the left eye and from 6 o’clock to 10 o’clock in the right eye (Fig. 1). There were patches of episcleral pigmentation superiorly in both eyes. However, there were no associated pigmented patches on the skin of the face, nor on the nasal or buccal mucosa. The subject’s intraocular pressure (IOP) measured after diurnal variation was 12 mmHg in both eyes. Gonioscopy of both eyes showed an open angle with a densely pigmented trabecular meshwork (Fig. 2) and a vascular arcade of anomalous vessels seen anteriorly in the sclera. Both eyes had a 0.5 : 1 cup : disc ratio with a healthy neuroretinal rim. There was no evidence of any retinal vascular tortuosity, nor was there any

408

difference in the colour of the fundus of each eye on indirect ophthalmoscopy. Fluorescein angiography of the anterior segment revealed a filling up of the extremely tortuous limbal and episcleral vascular plexus. Fundus angiography ruled out choroidal haemangiomas. On ultrasound biomicroscopy, we observed a layer of prominent episcleral vessels and a localized area of intrascleral vascular malformation near the irido-corneal angle in both eyes (Fig. 3). Humphrey 30–2 automated field analysis was within normal limits and a computer tomography (CT) scan of the head was also normal. The patient was advised regular follow-up.

Increased episcleral venous pressure is an important cause of glaucoma in Sturge Weber syndrome and vascular haematomas indicate the presence of increased venous pressure. The other hypothesis regarding the pathogenesis of glaucoma in Sturge Weber syndrome concerns the presence of angle anomalies such as a poorly developed scleral spur, thickened uveal meshwork, anterior insertion of the iris root in the trabecular meshwork (Weiss 1973) and incomplete development of Schlemm’s canal (Dunphy 1935). Clusters of abnormal vessels in the trabecular meshwork have also been reported on histological examination (Mwinula et al. 1994).

Fig. 1. Limbal vascular malformations inferiorly in the right eye.

Fig. 2. Goniophotograph of the inferior angle. The thin arrow shows the vascular plexus in the sclera. The arrowhead shows dense pigmentation of the angle.

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 However, their patient had full-blown glaucoma and had already been treated by cyclocryotherapy and surgery. Moreover, the vessels shown by Kranemann et al. (1998) were not at the limbus. In cases of Sturge Weber syndrome, early detection by gonioscopy and ultrasound biomicroscopy of vascular malformations at the limbus, and serial follow-up for enlargement, may alert the ophthalmologist to the possibility of the development of increasing episcleral venous pressure.

References

Fig. 3. Ultrasound biomicroscopic visualization of the intrascleral vascular haematoma (two thin arrows) and episcleral plexus of vessels (thick curved arrow).

The dense pigmentation seen on gonioscopy in this patient is possibly a milder expression of an angle cleavage anomaly. Weiss (1973) found vascular haematomas of the anterior episclera and conjunctiva in each of his series of Sturge Weber patients and we believe in his hypothesis that a combination of increased episcleral venous pressure and a congenital angle malformation contribute in variable proportions to the development of raised IOP. Vascular malformations of the conjunctiva and episclera are frequently found in Sturge Weber patients without glaucoma; however, the vessels become very prominent in eyes that have devel-

oped glaucoma. Although the patient described did not have glaucoma, this could be because the episcleral venous pressure was not raised to the point at which it might cause glaucoma. This was evident from the fact that the vascular malformations were localized and not prominent. Ultrasound biomicroscopic evidence of vascular malformations, especially near the angle, should also be looked for, as should the presence of episcleral vascular malformations. The presence of dilated superficial and intrascleral vessels on ultrasound biomicroscopy in a case of Sturge Weber syndrome was first described by Kranemann et al. (1998).

Dunphy EB (1935): Glaucoma accompanying nevus flammaeus. Am J Ophthalmol 18: 709–712. Kranemann CF, Pavlin CJ & Trope GE (1998): Ultrasound biomicroscopy in Sturge Weberassociated glaucoma. Am J Ophthalmol 125: 119–121. Mwinula JH, Sagawa T, Tawara A & Inomata H (1994): Anterior chamber angle vascularization in Sturge Weber syndrome. Report of a case. Graefes Arch Clin Exp Ophthalmol 232: 387–391. Weiss DI (1973): Dual origin of glaucoma in encaphalotrigeminal angiomatosis. Trans Ophthalmol Soc UK 93: 477–493.

Correspondence: Dr Ramanjit Sihota Dr RP Centre for Ophthalmic Sciences All India Institute of Medical Sciences New Delhi India Tel: þ 91 011 65 61 123 Fax: þ 91 011 68 52 919 Email: [email protected]

Lens luxation and prolapse into the surgical wound region during trabeculectomy Nina Sagara, Akira Kimura, Kazue Arimura, Masahiro Yonemura and Hidenobu Tanihara Department of Ophthalmology, Kumamoto University School of Medicine, Kumamoto, Japan

Sir,

I

ntraoperative complications that can occur during trabeculectomy include haemorrhage (Bregeat 1975; David & Sachs 1981), vitreous prolapse (Bregeat 1975; Realini & Vaphiades

2002), and lens damage (Advanced Glaucoma Intervention Study (AGIS) 2001; Realini & Vaphiades 2002). In glaucomatous eyes with a tight eyelid, elevated vitreous pressure may cause

vitreous prolapse. We report a rare case in which the lens was dislocated during a surgical procedure and herniated into the surgical wound region that resulted from the trabeculectomy.

409


A

B

Fig. 1. (A) Slit photograph of the left eye. The zonule of Zinn was torn (arrow), the lens (asterisk) was swollen and dislocated into the trabeculectomy region of the sclera. (B) Ultrasound biomicroscopic observation revealed that the thick lens (asterisk) with the tear of the zonule of Zinn (arrow) was dislocated into upper temporal region.

A 50-year-old man was diagnosed in a clinic with angle closure glaucoma. Visual acuity (VA) was 16/20 in the right eye and 3/20 in the left. Intraocular pressure (IOP) was 56 mmHg in the right eye and 62 mmHg in the left.

After laser iridotomy, IOP decreased to 15 mmHg in the right eye, but remained high (42 mmHg) in the left eye. Trabeculectomy with mitomycin C (MMC) was performed using sub-Tenon’s anaesthesia with 1 ml of 2% xylocaine.

During the peripheral iridectomy, the patient attempted to close his eye because of severe ocular pain. The elevated vitreous pressure caused the lens to be dislocated, resulting in herniation into the region of the surgical wound at

Fig. 2. Photograph of the surgery. Pars plana lensectomy was performed. The lens was herniated into the wound of previous trabeculectomy (arrow).

410

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 the trabeculectomy site. Due to the swollen lens, postoperative deterioration resulted in ocular inflammation and elevated IOP. The patient was subsequently referred to our hospital. In our department, we found VA to be 20/20 in the right eye and finger counting only in the left. Intraocular pressure was 18 mmHg in the right eye and 12 mmHg in the left. The anterior chamber in the left eye was shallow despite the relief from the pupillary block. No filtration bleb was recognized. The lens was swollen and white, and dislocated into the upper temporal region (Fig. 1A). Ultrasound biomicroscopic observation revealed herniation of the thick lens into the trabeculectomy region of the sclera (Fig. 1B). We performed pars plana lensectomy using a vitreous cutter. Subsequently, the anterior vitreous was removed and sulcus fixation of the intraocular lens (IOL) was performed (Fig. 2). Ocular inflammation in the left eye drastically decreased after the surgery, and IOP levels dropped below 20 mmHg following administration of antiglaucoma

medications. At 6 months postoperatively, VA was 6/20 and, with medication, IOP was 17 mmHg in the operated eye. To the best of our knowledge, this is the first report of an intraoperative complication for this surgical modality where lens herniation into the region of the surgical wound of the trabeculectomy occurred. We hypothesize that the combination of the vulnerable lens zonule with ocular pain-associated elevation in vitreous (lid) pressure during filtration surgery was the cause of this serious complication. To prevent occurrence of this complication, we recommend confirmation of adequate anaesthesia and careful manoeuvres on the iris in order to prevent inadvertent irritation of the iris during trabeculectomy.

References Advanced Glaucoma Intervention Study (AGIS) (2001): The Advanced Glaucoma Intervention Study. 8: Risk of cataract for-

mation after trabeculectomy. Arch Ophthalmol 119: 1771–1779. Bregeat P (1975): Cataract surgery and trabeculectomy at the same time. [Author’s translation.] Klin Monatsbl Augenheilkd 167: 505–515. David R & Sachs U (1981): Quantitative trabeculectomy. Br J Ophthalmol 65: 457–459. Realini T & Vaphiades MS (2002): Infusion misdirection syndrome during trabeculectomy for primary trabeculodysgenesis. Am J Ophthalmol 133: 138–139.

Correspondence: Akira Kimura MD Department of Ophthalmology Kumamoto University School of Medicine Honjo 1-1-1 Kumamoto City Kumamoto 860-8556 Japan Tel: þ 81 96 373 5247 Fax: þ 81 96 373 5249 Email: [email protected]

Kaposi’s sarcoma of the conjunctiva leads to a diagnosis of acquired immunodeficiency syndrome Katharina Schmid,1 Thomas Wild,1 Matthias Bolz,2 Reinhard Horvat,1 Wolfgang Jurecka3 and Martin Zehetmayer2 1

Department of Pathology, University of Vienna, Austria Department of Ophthalmology, University of Vienna, Austria 3 Department of Dermatology, University of Vienna, Austria 2

Sir,

W

e report the case of a 34-yearold man who presented at the Department of Ophthalmology, University of Vienna in September 1999 with a 2-month history of a growing, bluish-red, painless tumour of the conjunctiva in the left eye. The lesion measured 10 mm in diameter and appeared as a solitary, highly vascularized, palpable mass located at the temporal bulbar conjunctiva (Fig. 1). Additional ophthalmic evaluation revealed no pathological findings. No other lesions localized on the skin or the mucous membranes were found. The patient had an unremarkable med-

ical history. No serological test for HIV had been performed previously. The first differential diagnosis at the time of presentation was haemangioma but Kaposi’s sarcoma (KS) was also considered. The patient underwent perioperative blood tests. Surgical resection of the ocular lesion was carried out with special care because of a possible HIV infection. The resected tissue was fixed in formalin, embedded in paraffin and sections were stained with haematoxylin-eosin. Histopathology showed the morphology of KS (Fig. 2). The tumour was composed of proliferating spindle cells

and numerous vascular slits, surrounded by a single layer of endothelium. Haemorrhage and haemosiderin depositions were observed around the small vessels. Immunohistochemistry was performed; the endothelial cells reacted positively with antibodies against CD 34 and Podoplanin, documenting the vascular and lymphatic origin of the endothelial cells (Breiteneder-Geleff et al. 1999). Polymerase chain reaction provided evidence of an HHV-8 infection. Shortly before the histological diagnosis of KS was established, blood tests (ELISA and Western Bloting)

411


Fig. 1. Preoperative appearance of Kaposi’s sarcoma, located at the left inferior epibulbar conjunctiva.

demonstrated the presence of an HIV1 infection. The patient was consequently sent to our AIDS department for retroviral therapy. In 2001 he developed another KS located on the left arm, which was also resected. No recurrence of KS was seen up to January 2003.

Ocular involvement in fully developed AIDS is seen in up to 70% of HIV-infected patients. It mainly presents as microvascular retinal syndrome, cytomegalovirus chorio-retinitis, sicca syndrome and KS, and is usually a sign of poor prognosis (Holland et al. 1983; Rosenberg et al. 1983). Kaposi’s

sarcoma is the most common tumour of AIDS-related diseases and occurs as a frequent manifestation of AIDS (in 25% of cases). Of these cases, 20% involve the eye area. In extremely rare cases the initial clinical manifestation of AIDS-related KS can be recognized by ophthalmic examination (Shuler et al. 1989). Haye et al. (1987) and Soll & Redovan (1989) reported the first two cases of KS of the ocular adnexa as the first manifestation of AIDS. In both cases the KS was located on the eyelid. Kurumety & Lustbader (1995) published a case of KS on the bulbar conjunctiva as the initial clinical manifestation of AIDS in an HIV-infected man. To our knowledge, the case presented here is the first report of KS on the ocular adnexa that led to the diagnosis of HIV infection. It shows the importance of ophthalmic examination in regard to AIDS-related diseases. We strongly suggest that ophthalmologists consider KS among their differential diagnoses of ocular neoplasms. Such a lesion may be mistaken for granuloma pyogenicum, cavernous haemangioma, foreign body granuloma, chronic subconjunctival haemorrhage, malignant melanoma (lymph-)angioma or metastatic tumour (Macher et al. 1983).

References

Fig. 2. Histopathology of conjunctival Kaposi’s sarcoma. Covered by conjunctival epithelium, thin-walled vessels and slit-like spaces are separated by a stroma composed mainly of spindle cells (H&E staining; original magnification 40).

412

Breiteneder-Geleff S, Soleinman A, Kowalski H et al. (1999): Angiosarcoma express mixed endothelial phenotypes of blood and lymphatic capillaries. Am J Pathol 154: 385–394. Haye C, Dhermy P, Chic F & Schlienger P (1987): Kaposi’s sarcoma of the eyelid as a manifestation of AIDS. Bull Soc Ophthalmol Fr 87: 233–236. Holland GN, Pepose JS, Pettit TH, Gottlieb MS, Yee RD & Foos RY (1983): Acquired immunodeficiency syndrome: ophthalmic manifestations. Ophthalmology 90: 859–873. Kurumety UR & Lustbader JM (1995): Kaposi’s sarcoma of the bulbar conjunctiva as an initial clinical manifestation of acquired immunodeficiency syndrome. Arch Ophthalmol 113: 978. Macher AM, Palestine A, Masur H, Bryant G, Chan C, Nussenblatt RB & Rodrigues MM (1983): Multicentric Kaposi’s sarcoma of the conjunctiva in a male homosexual with acquired immunodeficiency syndrome. Ophthalmology 90: 879–884. Rosenberg PR, Uliss AE, Friedland GH, Harris CA, Small CB & Klein RS (1983): Acquired immunodeficiency syndrome:

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 ophthalmic manifestations in ambulatory patients. Ophthalmology 90: 874–878. Shuler JD, Holland GN, Miles SA, Miller BJ & Grossmann I (1989): Kaposi’s sarcoma of the conjunctiva and the eyelid associated with acquired immunodeficiency syndrome. Arch Ophthalmol 107: 858–862. Soll DB & Redovan EG (1989): Kaposi’s sarcoma of the eyelid as the initial manifest-

ation of AIDS. Ophthal Plast Reconstr Surg 5: 49–51.

Correspondence: Martin Zehetmayer MD Department of Ophthalmology University of Vienna

Waehringer Guertel 18-20 A-1090 Vienna Austria Tel: þ 43 1 40 400 79 63 Fax: þ 43 1 40 400 28 62 Email: [email protected]

Bilateral optic disc swelling as the presenting sign of Waldenstro¨m’s macroglobulinaemia Antonio Pinna,1 Stefano Dore,1 Fausto Dore,2 Andrea Salis3 and Francesco Carta1 1

Institute of Ophthalmology, University of Sassari, Italy Institute of Haematology, University of Sassari, Italy 3 Institute of Radiology, University of Sassari, Italy 2

Sir,

W

aldenstro¨m’s macroglobulinaemia is a malignant proliferation of plasma cells, which secrete monoclonal

IgM, bind to each other and form serum protein aggregates that increase serum viscosity. It is slightly more common in

men and occurs with increased incidence with age (median 64 years). The onset is insidious with weakness, fatigue and

Fig. 1. T1-weighted SE MRI coronal scan shows tissue with decreased signal intensity in the lesser wings of the sphenoid (circles) and jaw (asterisks). Arrows show optic nerves in the optic canals. Findings are consistent with a bone marrow malignancy.

413

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 epistaxis observed. Recurrent infections, congestive heart failure, diarrhoea, weight loss, visual disturbances and neurological symptoms may be present. Pallor, hepatosplenomegaly, peripheral adenopathy and purpura are the most common abnormalities seen. Serum hyperviscosity is responsible for retinopathy, neurological symptoms and congestive heart failure. Waldenstro¨m’s macroglobulinaemia is diagnosed by observing the typical signs and symptoms, monoclonal IgM production and bone marrow abnormalities (Longo 1994). We report a case of Waldenstro¨m’s macroglobulinaemia with bilateral optic disc swelling at the onset. A 38-year-old woman with a history of psoriasis presented with a 2-month history of blurred vision. Physical examination showed pallor, laterocervical lymphadenopathy and psoriasis. Best

corrected visual acuity was 20/25 bilaterally. Anterior segment examination was unremarkable. Fundus examination revealed florid optic disc swelling, dilated retinal veins and scattered, flame-shaped retinal haemorrhages bilaterally. Fluorescein angiography showed bilateral disc leakage. Automated perimetry disclosed bilateral blind spot enlargement. Laboratory evaluation revealed normocytic, normochromic anaemia with haemoglobin of 6.8 g/dl (normal range 12–16 g/dl). Serum protein electrophoresis showed elevated gamma globulin (4.57 g/dl; normal range 1.34–2.34 g/dl). Immunoglobulin electrophoresis yielded elevated IgM (4340 mg/dl; normal range 43–279 mg/dl). Magnetic resonance imaging (MRI) of the head showed hypointense tissue in the jaw, diploe and sphenoid (Fig. 1). Lymph node biopsy showed proliferation of small

and medium-sized cells with round nuclei and extracellular eosinophilic material. Immunohistochemical evaluation disclosed the presence of lambda light chains and IgM. Accordingly, a diagnosis of Waldenstro¨m’s macroglobulinaemia was made. The patient was given packed red blood cells (two units) and started treatment with intravenous fludarabin (25 mg/m2 daily for 3 days), cyclophosphamide (300 mg/m2 daily for 3 days), and prednisone (60 mg daily for 1 week), repeated at 4-week intervals. After six courses of treatment, laboratory, radiological and ophthalmic abnormalities had reversed almost completely (Fig. 2). The patient showed no signs of active disease at 14-months follow-up. Manifestations of Waldenstro¨m’s macroglobulinaemia have been described in the conjunctiva, cornea and retina

Fig. 2. Post-treatment T1-weighted SE MRI coronal scan taken at 9-months follow-up. The scan reveals almost normal signal intensity in the lesser wings of the sphenoid and jaw.

414

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 (Carr & Henkind 1963; Orellana & Friedman 1981). Retinal findings, caused by serum hyperviscosity, have been observed in 30–67% of patients (Orellana & Friedman 1981). The progression of retinal changes begins with dilated, tortuous veins. As congestion increases, flame-shaped or punctate haemorrhages appear, as does an increase in venous diameter. Finally, the retina demonstrates venous occlusions with confluent haemorrhages and disc swelling (Carr & Henkind 1963; Orellana & Friedman 1981). In this report, MRI showed infiltration of the lesser wings of the sphenoid, which probably caused optic nerve compression with resultant disc swelling. In Waldenstro¨m’s macroglobulinaemia, disc oedema may also be caused by serum hyperviscosity-related

central retinal vein occlusion (Orellana & Friedman 1981). However, our patient showed no angiographic signs of vein occlusion, suggesting that disc swelling was provoked by nerve compression in the optic canal. To our knowledge, compressive optic neuropathy has never been associated with Waldenstro¨m’s macroglobulinaemia. Disc swelling due to compressive optic neuropathy, along with retinal haemorrhages and dilated retinal veins, may represent the presenting sign of Waldenstro¨m’s macroglobulinaemia.

References Carr RE & Henkind P (1963): Retinal findings associated with serum hyperviscosity. Am J Ophthalmol 56: 23–31.

Longo DL (1994): Plasma cell disorders. In: Isselbacher KJ, Braunwald E, Wilson JD et al. (eds). Harrison’s Principles of Internal Medicine. 13th edn. New York: McGraw-Hill. Vol. 2; Chap. 280. Orellana J & Friedman AH (1981): Ocular manifestations of multiple myeloma, Waldenstro¨m’s macroglobulinaemia and benign monoclonal gammopathy. Surv Ophthalmol 26: 157–169.

Correspondence: Dr Antonio Pinna Via Casula 6 07100 Sassari Italy Tel: þ 39 079 22 82 51 Fax: þ 39 079 22 84 84 Email: [email protected]

Dehydration is a risk factor for central retinal vein occlusion in young patients Peter J. Francis, Miles R. Stanford and Elizabeth M. Graham Medical Eye Unit, St Thomas’ Hospital, London, UK

Sir,

C

entral retinal vein occlusion (CRVO) is a common cause of visual morbidity known to have several systemic and local risk factors (Eye Disease Case-Control Study Group 1996). Recently, there has been interest in determining whether hypercoagulable states and inherited thrombophilias also play a role in CRVO (Lahey et al. 2002). In this report, we describe four young patients who developed CRVO following an episode of dehydration. No other cause could be established despite exhaustive laboratory blood analysis.

Case 1 A 40-year-old white male awoke with blurred vision in his right eye the morning after a particularly hot summer night following an evening of heavy alcohol intake. He had not rehydrated. Examination identified a CRVO in the right eye. His vision improved to 6/9 within 3 months.

Case 2 A 55-year-old black male developed decreased right vision during his observation of the Christian festival of Lent. For the preceding 7 days, he had been fasting and abstaining from all but essential fluids. Examination revealed a non-ischaemic CRVO with no macula oedema. The subject’s vision improved spontaneously to 6/9 by 6 months.

Case 3 A 24-year-old white male Olympic rower noted blurred right vision after a strenuous training session during an Australian summer’s day. He had not rehydrated. Examination revealed a CRVO with macula oedema. His vision remains at 6/60.

Case 4 A 47-year-old white male presented with blurred vision in both eyes after a hot bath following a long run. He had

not rehydrated and had experienced mild flu-like symptoms with a fever for the preceding 2 days. Examination revealed a right CRVO and left inferior hemi-vein occlusion. There has been no significant visual recovery in either eye.

Discussion Virchow’s classic axiom states that thrombosis will occur in a blood vessel when there are disturbances in the blood flow, the vessel wall or coagulation. Why such abnormalities are common at the point where the central retinal vein traverses the lamina cribrosa is unclear. In elderly patients, it is likely that changes in blood flow brought about by compression of the adjacent arteriosclerotic central retinal artery result in clotting. While similar processes appear important in younger patients, there is evidence that procoagulant states such as thrombophilia also play a role. Increased blood viscosity resulting in abnormal erythrocyte aggregation has been established as a cause of venous

415

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 thrombosis in other parts of the body (Gilbert 2001). The retinal venous circulation is characterized by low flow in the presence of high vascular resistance. This combination should make the central retinal vein particularly susceptible to thrombosis in hyperviscosity states and indeed conditions such as polycythaemia and multiple myeloma have been associated with CRVO (Fong & Schatz 1993). In our patients, who experienced profound visual loss, the severe dehydrational episode would be expected to raise the blood haematocrit, producing a state of acute hyperviscosity (further exacerbated by exercise in Case 3) (Gibbs et al. 2001), resulting in venous thrombosis. The confirmation that dehydration is a risk factor for CRVO in healthy individuals (Alghadyan 1993) reinforces

the need for careful history taking in these patients. As a preventive measure, it has been recommended to these patients that they avoid dehydration.

References

Gilbert H (2001): Current management in polycythaemia vera. Semin Hematol 38: 25–28. Lahey J, Tunc M, Kearney J, Modlinski B, Koo H, Johnson R & Tanaka S (2002): Laboratory evaluation of hypercoagulable states in patients with central retinal vein occlusion who are less than 56 years of age. Ophthalmology 109: 126–131.

Alghadyan A (1993): Retinal vein occlusion in Saudi Arabia: possible role of dehydration. Ann Ophthalmol 25: 394–398. Eye Disease Case-Control Study Group. (1996): Risk factors for central retinal vein occlusion. Arch Ophthalmol 114: 545–554. Fong A & Schatz H (1993): Central retinal vein occlusion in young adults. Surv Ophthalmol 37: 393–417. Gibbs C, Blann A, Edmunds E, Watson R & Lip G (2001): Effects of acute exercise on haemorheological, endothelial and platelet markers in patients with chronic heart failure in sinus rhythm. Clin Cardiol 24: 724–729.

Correspondence: Dr E. M. Graham Consultant Ophthalmologist Medical Eye Unit 9th Floor, North Wing St Thomas’ Hospital Lambeth Palace Road London SE1 7NH UK Tel: þ 44 20 7928 9292 Fax: þ 44 20 7922 8165 Email: [email protected]

Occupational blast injury resulting in traumatic corneal endothelial rings Mahiul M. K. Muqit, Clifford Weir and Stuart Osborne Tennent Institute of Ophthalmology, Gartnavel General Hospital, Glasgow, UK

Sir,

T

raumatic corneal endothelial rings are unusual phenomena that occur following non-penetrating blast injuries. They were first reported by (Pichler 1916) and classically appear as transient, greyish, ring-shaped opacities of the corneal epithelium (Payrau & Raynaud 1965). Of the few reports that exist in the literature, mechanisms of injury have included bullet cartridge explosion (Cibis et al. 1978), gunshot powder explosion (Wittpenn et al. 1982; Stulting et al. 1986) and firework explosion (Forstot & Gasset 1974). Because these corneal endothelial rings are reported to occur in the wake of non-penetrating blast injuries inflicted at modest velocities of below 1000 p.s.i. (pounds per square inch), we report the case of an engineer who developed this condition following a high velocity occupational blast injury. A 35-year-old male naval engineer suffered a high velocity air blast injury while handling part of an air purifier within a submarine periscope system, which uses high pressure air at

416

3000 p.s.i. He was wearing no eye protection. The system malfunctioned during routine servicing and an explosion occurred approximately 0.5 m from his face. He attended our Ophthalmic Casualty Department the following day, complaining of a red and irritable left eye, associated with slightly blurred vision. On examination, his visual acuity was found to be 6/5 in both eyes. The left side of his face was peppered with tiny abrasions consistent with blast injury. His left conjunctiva was mildly injected and he was noted to have five small corneal epithelial defects with subepithelial foreign bodies, associated with endothelial ring-shaped opacities (Fig. 1A, B). The anterior chamber was quiet and intraocular pressure (IOP) was within normal limits. Fundoscopy was unremarkable and examination of the right eye was normal. The corneal foreign bodies were removed under slit-lamp and the subject was prescribed chloramphenicol eye ointment to be used four times daily. He was reviewed 1 week later,

by which time his ocular symptoms had resolved completely and, subjectively, his vision had returned to normal. The corneal epithelial defects had healed and the traumatic endothelial rings had disappeared. The patient was reviewed on one further occasion 3 months later, when his ocular examination remained normal. He was advised to wear suitable eye protection when operating machinery in future. To our knowledge, traumatic corneal endothelial rings due to accidental occupational air blast injury at this velocity have not been reported previously. These unusual signs are thought to result from the high velocity impact of tiny desiccant particles on the corneal epithelium. This produces a concussive force, which is transmitted through the corneal stroma and Descemet’s membrane to the endothelium and subsequently produces transient endothelial cell dysfunction. Maloney et al. (1979) reported localized areas of corneal oedema and persistent endothelial damage in cases of severe velocity of impact.


Fig. 1. (A) Grey corneal endothelial ring opacity; low magnification. (B) Dark appearance of endothelial rings in retroillumination; high magnification.

Fortunately, and in keeping with previous reports, our patient’s signs were self-limiting and resolved within 1 week. This case illustrates the fact that traumatic corneal endothelial rings are transient phenomena, which, although they arise from potentially serious insults, resolve with conservative management.

References Cibis GW, Weingeist TA & Krachmer JH (1978): Traumatic corneal endothelial rings. Arch Ophthalmol 96 (3): 485–458.

Forstot SL & Gasset AR (1974): Transient traumatic posterior annular keratopathy of Payrau. Arch Ophthalmol 92: 527–528. Maloney WF, Colvard DM & Bourne WM (1979): Specular microscopy of traumatic corneal endothelial posterior annular keratopathy. Arch Ophthalmol 97: 1647–1650. Payrau P & Raynaud G (1965): Lesions de la corneé par souffle´. Corps e´trangers perforants microscopiques: anneaux veloute´s posterieurs. Ann Ocul (Paris) 198: 1054–1074. Pichler A (1916): Die Casparache Ringtrubung der Hornhaut. Z Augenheilkd 36: 311–313. Stulting RD, Rodriques MM & Nay RE (1986): Ultrastructure of traumatic corneal endothelial rings. Am J Ophthalmol 101 (2): 156–159.

Wittpenn JR, Hirst LW & Green WR (1982): Histopathologic study of traumatic corneal endothelial rings. Md Med 31 (6): 43–45.

Correspondence: Mahiul M. K. Muqit Tennent Institute of Ophthalmology Gartnavel General Hospital 1053 Great Western Road Glasgow G12 0YN UK Tel: þ 44 141 211 3000 Fax: þ 44 141 211 2054 Email: [email protected]

417


Retinal neovascularization and vitreous haemorrhage in a patient with acute myeloid leukaemia and haematopoietic stem cell transplantation Angel Salinas-Alamań,1 Jose´ Rifoń-Roca2 and Alfredo Garcı´ a-Layana1 1 2

Ophthalmology Department, Clinical University of Navarra, Pamplona, Spain Haematology Department, Clinical University of Navarra, Pamplona, Spain

Sir,

R

etinal neovascularization and secondary vitreous haemorrhage have been seen, albeit rarely, in some forms of leukaemia. Nevertheless, to our knowledge no prior case has been reported in a patient diagnosed with acute myeloblastic leukaemia. A 30-year-old man was referred to our Retina Unit with a 2-week history of decreased visual acuity (VA) in his right eye. The patient had been treated for acute myeloblastic leukaemia for 2 years. He was in complete remission after standard chemotherapy, and treatment was consolidated with an haematopoietic stem cell transplant from a human leucocyte antigen (HLA) identical sibling. The patient did not receive radiation treatment. The course after transplantation was uncomplicated at first, but after 4 months graft failure was diagnosed, causing the patient to require a second transplant

from the same donor. After the second transplant, acute grade 3 graft versus host disease with gastrointestinal and liver involvement occurred, but was successfully treated with high dose corticosteroids. A complete remission of the patient’s haematological process was achieved, and subsequently no other systemic disease was diagnosed. Ophthalmological examination demonstrated VA of finger counting in the right eye (RE) and 20/20 in the left eye (LE). The anterior segment was normal in both eyes. A massive retrohyaloid haemorrhage was present in the posterior segment of the RE. In the LE, multiple punctate haemorrhages and microvascular anomalies were present. Fluorescein angiograms demonstrated two neovascular tufts in the nasal midperipheral retina of the LE and hyperfluorescence behind a retrohyaloid haemorrhage in the RE

A

B

C

D

(Fig. 1). This suggested that the retrohyaloid haemorrhage in the RE was secondary to retinal neovascularization. Vitrectomy and panretinal photocoagulation was performed in the RE and panretinal photocoagulation was performed in three sessions in the LE. At follow-up, the response was considered adequate (Fig. 2). Retinal abnormalities such as retinal haemorrhages and cotton-wool spots are frequently observed in adult patients with acute myeloid leukaemia (Specchia et al. 2001). Retinal neovascularization has been described in patients with chronic myelocytic and acute lymphocytic leukaemia (Wiznia et al. 1994). Nevertheless, the patient we describe represents, to our knowledge, the first case of acute myeloid leukaemia and retinal neovascularization to be reported.

Fig. 1. (A) Retrohyaloid haemorrhage partially occult details in funduscopic image of the RE. (B) Colour photograph shows retinal vascular abnormalities in the posterior pole of the LE. (C) Fluorescein angiography of the RE shows hyperfluorescence behind a retrohyaloid haemorrhage. (D) A neovascular tuft can be seen in the nasal retina of the LE.

418


A

B

Fig. 2. Funduscopic image of right and left eyes after vitrectomy in the RE and panretinal photocoagulation in both eyes.

Chemotherapy has been implicated in the pathogenesis of retinal and optic disc neovascularization in myeloproliferative diseases. Lopez et al. (1991) described a series of patients with acute leukaemia who developed a form of retinopathy associated with bone marrow transplantation. They suggested that high dose chemotherapy may increase susceptibility for the development of retinopathy at otherwise safe radiation doses. However, our patient had not received radiation treatment. In our patient, the leukaemia was in complete remission before the ocular pathological findings were detected, but subclinical retinal abnormalities during the phase of active leukaemia or during chemotherapy or stem cell transplantation may represent the basis for neovascularization in the post-transplant period. Retinal neovascularization is thought to occur in response to hypoxic insults,

which lead to changes in the existing vasculature and compensatory new capillary growth. It has recently been demonstrated that transplanted adult stem cells provide endothelial progenitor cell activity that contributes to retinal neovascularization (Grant et al. 2002). Other recent studies show that angiogenesis and angiogenic factors play an important role in haematological malignancies (Keyhani et al. 2001). Possibly, increased angiogenesis in patients with acute myeloid leukaemia may play a role in the pathogenesis of retinal neovascularization.

References Grant MB, May WS, Caballero S et al. (2002): Adult haematopoietic stem cells provide functional haemangioblast activity during retinal neovascularization. Nat Medicine 8: 607–612.

Keyhani A, Jendiroba DB & Freireich EJ (2001): Angiogenesis and leukaemia. Leuk Res 25: 639–645. Lopez PF, Sternberg P, Dabbs CK, Vogler WR, Crocker I & Kalin NS (1991): Bone marrow transplant retinopathy. Am J Ophthalmol 112: 635–646. Specchia G, Albano F, Guerriero S et al. (2001): Retinal abnormalities in newly diagnosed adult acute myeloid leukaemia. Acta Haematol 105: 197–203. Wiznia RA, Rose A & Levy AL (1994): Occlusive microvascular retinopathy with optic disc and retinal neovascularization in acute lymphocytic leukaemia. Retina 14: 253–255.

Correspondence: Angel Salinas-Alamań MD Departamento de Oftalmologı´ a Clı´ nica Universitaria de Navarra Avenue Pı´ o XII 36 31080 Pamplona, Spain Tel: þ 34 948 296 290 Fax: þ 34 948 296 500 Email: [email protected]

Spontaneous carotid-cavernous sinus fistula diagnosed by ophthalmodynamometry Jost B. Jonas1 and Christoph Groden2 1

Department of Ophthalmology, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany 2 Department of Neuroradiology, Faculty of Clinical Medicine Mannheim, University of Heidelberg, Mannheim, Germany

Sir,

T

he episcleral veins communicate upstream through the aqueous veins with Schlemm’s canal in the eye, and downstream via the superior ophthalmic vein with the cavernous sinus. A spontaneous dilatation of episcleral veins can pose diagnostic problems, especially if imaging techniques are

unremarkable. The present report describes a patient who presented with dilated episcleral veins of primarily unknown aetiology, and in whom ophthalmodynamometric determination of the central retinal vein collapse pressure was diagnostically helpful.

A 59-year-old female patient experienced binocular diplopia and increasing redness of both eyes. Ophthalmologic examination revealed bilaterally dilated episcleral veins, blood staining of Schlemm’s canal upon gonioscopy, slightly dilated retinal veins, a reduction in horizontal motility of the left eye

419

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 corresponding with sonographic thickening of the left horizontal rectus muscles, and slight exophthalmos of 3 mm. Cerebral nuclear magnetic imaging was unremarkable. A preliminary diagnosis of endocrine orbitopathy was made and treated accordingly. Dilatation of the episcleral veins increased, however, and intraocular pressure (IOP) was elevated to 25 mmHg. A choroidal detachment developed in the left eye. Visual acuity remained unchanged at 20/20. Modified ophthalmodynamometry was performed as follows. Under topical anaesthesia, a conventional Goldmann contact lens with a pressure sensor mounted into its holding ring was put onto the cornea (Fig. 1). The contact lens was slightly pressed onto the cornea and the pressure values at the time when the central retinal vein or artery started to pulsate were noted. The measurements were repeated nine times, and the mean of the 10 values was taken for further statistical analysis. A previous study determined the reproducibility of the technique for measurements of the collapse pressures of the central retinal vein and artery to be 16.3 11.4% and 8.5 4.1%, respectively (Jonas 2003). The method has already been described in detail (Jonas & Niessen 2002; Jonas 2003; Jonas & Harder 2003). Central retinal vein collapse pressure (OD: 24.1 4.8 relative units; OS: 88.0 6.3 relative units) measured significantly (p ¼ 0.02) higher in the patient presented in this report than in a normal control group (6.1 8.4 relative units) consisting of 27 subjects with a mean age of 69.6 12.5 years. Central retinal artery collapse pressure did not vary significantly between the patient of the present report and the subjects of the control group (88.8 1.7 relative units versus 78.0 19.2 relative units; p ¼ 0.44). As the central retinal vein

Fig. 1. Photograph depicting the ophthalmodynamometer consisting of a conventional Goldmann contact lens and a pressure sensor mounted into the holding ring grip.

and the episcleral veins drain into the same intracranial venous system, suggesting an abnormality in the cavernous sinus, neuroradiological examination was repeated. Cerebral angiography indicated a carotid-cavernous sinus fistula as the reason for increased central retinal vein pressure and dilatation of the episcleral veins. After endovascular embolization of the shunt with detachable platinum coils, exophthalmos, ocular motility, dilatation of the episcleral veins and IOP were reduced or normalized. After 4 months follow-up, IOP has remained normal, and the dilatation of the episcleral veins has regressed. The present report shows that using a modified type of ophthalmodynamometry for estimation of central retinal vein collapse pressure can be helpful in the diagnosis of carotid-cavernous sinus fistula. It is paralleled by other studies in which ophthalmodynamometric measurement of central retinal vein collapse pressure was shown to be useful in determining increased intracerebral pressure (Firsching et al. 1998; Jonas & Harder 2003).

References Firsching R, Schutze M, Motschmann M & Behrens-Baumann W (1998): Non-invasive measurement of intracranial pressure. Lancet 351: 523–524. Jonas JB & Niessen A (2002): Ophthalmodynamometric diagnosis of unilateral ischaemic ophthalmopathy. Am J Ophthalmol 134: 911–912. Jonas JB (2003): Reproducibility of ophthalmodynamometric measurements of the central retinal artery and vein collapse pressure. Br J Ophthalmol 87: 577–579. Jonas JB & Harder B (2003): Ophthalmodynamometric estimation of cerebrospinal fluid pressure in pseudotumour cerebri. Br J Ophthalmol 87: 361–362.

Correspondence: Dr J. Jonas Universita¨ts-Augenklinik Theodor-Kutzer-Ufer 1-3 68167 Mannheim Germany Tel: þ 49 621 383 2652 Fax: þ 49 621 383 3803 Email: [email protected]

Valsalva haemorrhagic retinopathy in a pregnant woman: implications for delivery Sanjeewa S. Wickremasinghe, Paris G. Tranos and Clare Davey Department of Ophthalmology, Royal Free Hospital, London, UK

Sir,

V 420

alsalva retinopathy is caused by a sudden increase in intrathoracic

or abdominal pressure against a closed glottis (Valsalva manoeuvre). The rapid

rise in venous pressure may lead to the rupture of normal and abnormal

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 superficial retinal capillaries, resulting in haemorrhagic detachment of the internal limiting membrane and, possibly, vitreous haemorrhage (Callender et al. 1995). Visual loss can be profound if haemorrhage occurs in the premacular region. Most cases of Valsalva retinopathy resolve spontaneously over several months, with vision returning to pre-haemorrhage levels. When Valsalva haemorrhage occurs during pregnancy, there may be difficulty in determining the optimal method for delivery in order to prevent progression and recurrence. We report a 38-year-old AfroCaribbean woman, who presented to the Eye Services Department 35 weeks into her third pregnancy. Her previous pregnancies had been uneventful and the current pregnancy had been without incident until presentation. After a violent bout of vomiting, the subject noticed that vision had deteriorated in her left eye, without accompanying photopsia or visual field loss. She had no significant medical or ocular history and, in particular, no history of coagulation defects, sickle cell disease or diabetes. Examination revealed best corrected visual acuity (VA) of 6/5 in the right eye and 6/24 in the left eye. Her anterior segments were normal in appearance. The left eye had evidence of subhyaloid haemorrhage superior to the disc (Fig. 1), accompanied by vitreous haemorrhage inferiorly and nasally (not visible), with no evidence of a retinal tear or vascular anomaly. There was no sign of neovas-

cularization of the disc or elsewhere. Systemic examination revealed a blood pressure of 123/70. A diagnosis of Valsalva retinopathy was made, with the mild vitreous haemorrhage accounting for the decrease in VA. Management consisted of rest and avoidance of non-steroidal anti-inflammatory medications. The remainder of the pregnancy passed without further incident and 4 weeks later the subject spontaneously delivered a healthy 3.39 kg male after 2 hours, 19 mins of labour. Four months after delivery, the patient’s VA had improved to 6/9 and the preretinal haemorrhage had largely resolved (Fig. 2). The Valsalva haemorrhage in this case most likely occurred as a result of the violent bout of vomiting experienced by the patient. The sudden associated elevation of intra-abdominal pressure probably led to a systemic increase in venous pressure and subsequent transmission to and rupture of the superficial retinal capillaries within the left eye. Although the haemorrhage was extra-macular, VA was reduced as a result of the accompanying vitreous haemorrhage. Breaches within the internal limiting membrane account for the spread of the blood from the retina to the vitreous cavity. Although most cases of Valsalva retinopathy resolve spontaneously within a few months, recovery may be complicated by pigmentary changes at the macula, which preclude VA

Fig. 1. Fundus photograph of the left eye, showing a dense round retinal haemorrhage (upper arrow), a boat-shaped subhyaloid haemorrhage (middle arrow) close to the optic disc and a few nerve fibre layer haemorrhages nasal to the disc (lower arrow).

returning to normal. (Deane & Ziakas 1997). Labour is associated with a significant elevation in venous pressure secondary to increased intra-abdominal pressure against a closed glottis. There is debate as to whether spontaneous vaginal delivery is liable to exacerbate the haemorrhage. Potential interventions include elective caesarean section under epidural/general anaesthesia to prevent progression by limiting such Valsalva increases in venous pressure. In this case, as in other cases where spontaneous vaginal delivery was chosen, without epidural or other intervention (Duane 1972; Deane & Ziakas 1997), no recurrence of the haemorrhage was noted on examination post partum. Anaesthesia is required for delivery by elective caesarean section. Several cases of retinal haemorrhage have been described in association with both general and epidural anaesthesia (Bolder & Norton 1984; Ling et al. 1993). General anaesthesia may cause hypoxia and hypercarbia, both of which cause vasodilatation and an increase in retinal venous pressure. Moreover, extubation may lead to significant rises in venous pressure secondary to coughing (Chidley et al. 1998). Epidural anaesthesia has also been associated with retinal haemorrhage, possibly as a result of increases in the cerebrospinal fluid pressure (secondary to volume effects within the epidural space) leading to elevated retinal venous pressure and subsequent haemorrhage (Chidley et al. 1998). As Valsalva haemorrhage is selflimiting and is usually associated with spontaneous recovery of vision (albeit after several months), the available evidence suggests that additional obstetric or anaesthetic intervention in cases of Valsalva haemorrhage during pregnancy is unnecessary to prevent recurrence and occasionally may be harmful. Additionally, in the unlikely event of progression to the macular region after normal delivery, neodymiumYAG laser photodisruption of the internal limiting membrane overlying the subhyaloid haemorrhage may be performed to allow dispersal of the blood into the vitreous cavity and

421

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 Chidley KE, Law R & Vanner RG (1998): Caesarean section following a recent retinal haemorrhage. Anaesthesia 53: 483–485. Deane JS & Ziakas N (1997): Valsalva retinopathy in pregnancy. Eye 11: 137–143. Duane TD (1972): Valsalva haemorrhagic retinopathy. Trans Am Ophthalmol Soc 52: 298–313. Ladjimi A, Zaouali S, Messaoud R, Ben Yahia S, Attia S, Jenzri S & Khairallah M (2002): Valsalva retinopathy induced by labour. Eur J Ophthalmol 12: 336–338. Ling C, Atkinson PL & Munton CGF (1993): Bilateral retinal haemorrhages following epidural injection. Br J Ophthalmol 77: 316–317.

Fig. 2. Fundus photograph of the same eye 4 months after spontaneous delivery, showing substantial resolution of the haemorrhages. Some residual preretinal haemorrhages are still present (arrow).

consequently improve acuity (Ladjimi et al. 2002). Ultimately, patients should be counselled about the possible risks of each method of delivery and their wishes should be carefully considered when making a final decision.

References Bolder BM & Norton ML (1984): Retinal haemorrhage following anaesthesia. Anesthesiology 61: 595–597. Callender D, Beirouty ZAY & Saba SN (1995): Valsalva haemorrhagic retinopathy in a pregnant woman. Eye 9: 808–809.

Correspondence: Sanjeewa Wickremasinghe Anterior Segment Service Moorfields Eye Hospital City Road London EC1V 2PD UK Tel: þ 44 (0)207 3411 Email: [email protected]

One-stop laser clinics: patients’ preferences for treatment Lynval Jones, Venkatadri Sampat and Sergio Pagliarini Paybody Eye Unit, Coventry and Warwickshire Hospital, Coventry, UK

Sir,

T

here is increasing debate on the value of ‘one-stop clinics’ in various surgical specialties (Dey et al. 2002; Dixon 2002). These clinics are assumed to be more cost-effective primarily because they reduce the number of visits needed by combining clinical assessment, investigation and treatment. The cataract surgery experience has provided a well established model for one-stop clinics in ophthalmology (Hughes et al. 2001). Patients’ preferences for a one-stop (OS) laser service for medical retina clinics have not previously been evaluated. We therefore undertook a survey to determine patient opinion on an OS laser clinic for patients visiting a medical retina clinic.

422

We carried out a descriptive crosssectional survey on 44 consecutive patients reporting to the medical retina clinic at Paybody Eye Unit, Coventry and Warwickshine Hospital in January 2002. We conducted face-to-face interviews with each patient using structured, precoded questions with precoded responses. This allowed us to probe fully for responses and to clarify any ambiguities, especially with patients from different cultural and ethnic backgrounds and those with whom an interpreter was used. We described our usual clinic (UC) model as consisting of an initial consultation, followed by two to three other visits for investigations and possible treatment. We then described the concept of an OS ser-

vice as consisting of a package including an initial consultation, investigations which might include fundus photography and fundus angiography, followed by laser treatment if indicated. We explained that this might mean spending up to 3 hours in the department as opposed to approximately 1 hour for each visit in the UC model. We asked patients whether they would prefer the OS service or the UC model. Results were analysed using the statistical package for social sciences (SPSS for Windows 98). The patient sample included 30 males (68.2%) and 14 females (31.8%), with a mean age of 56.64 years (range 14–89 years). The average distance travelled was 4.9 miles (standard deviation

ACTA OPHTHALMOLOGICA SCANDINAVICA 2003 5.85 miles). Sixteen patients travelled by bus, 26 by car, one by train and one by ambulance. Fourteen patients (31.8%) had diabetes. In all, 89% (n ¼ 39) of patients preferred an OS service (x2 ¼ 26.273, d.f. ¼ 1, p ¼ 0.001). Our survey showed that most patients prefer an OS laser service for medical retina clinics, despite the fact that they may need to spend up to 3 hours in the department. This finding challenges the UC model of multiple hospital visits, with its inherent greater economic costs and waiting lists for investigations and treatment. Patients on waiting lists may be at risk of losing their vision while they wait for laser treatment (Diabetic Retinopathy Study Research Group 1981). About a third of the patients in our survey were referred for diabetic retinopathy (31.8%); those with high risk proliferative diabetic retinopathy/maculopathy underwent laser treatment at the initial visit. A significant reduction in the number of retinal risk factors occurs within 3 weeks of laser treatment (Doft & Blankenship 1984). In the UC

model, it is unlikely that patients would be investigated and treated within 3 weeks. Furthermore, patients preferred to be treated at the first visit. Other possible benefits of OS laser clinics include: a reduction in absenteeism following initial laser treatment (requires further evaluation); a reduction in the time taken up by retrieval of case notes; more effective use of staff time, and no waiting lists for laser treatment. The average cost of travelling to the clinic and the hospital resource costs are similar for each model. Thus, an OS service that reduces the number of visits to the first treatment episode from three to one has potential savings. In conclusion, given the choice, patients visiting a medical retina clinic preferred a one-stop medical retina service.

References Dey P, Bundred N, Gibbs A et al. (2002): Costs and benefits of a one-stop clinic compared

with a dedicated breast clinic: randomized controlled trial. BMJ 324: 507–510. Diabetic Retinopathy Study Research Group (1981): Photocoagulation treatment of proliferative diabetic retinopathy: clinical application of diabetic retinopathy study (DRS) findings. DRS Report 8. Ophthalmology 88: 583–600. Dixon JM (2002): One-stop clinics should not be abandoned. BMJ 324: 510. Doft BH & Blankenship G (1984): Retinopathy risk factor regression after laser pan-retinal photocoagulation for proliferative retinopathy. Ophthalmology 91: 1453–1457. Hughes EH, Forrest F & Diamond JP (2001): One-stop cataract surgery: the Bristol Eye Hospital experience 1997–99. Eye 15: 306–308.

Correspondence: Lynval D Jones 104 Codsall Road Tettenhall Wolverhampton WV6 9QJ UK Tel: þ 44 7968 526184 Fax: þ 44 1902 742852 Email: [email protected]

423