Branch retinal artery occlusion in toxoplasma retinochoroiditis.

SIR,-The adverse effects of mydriatic agents are well documented. When using these drugs one must carefully consider the relevant medical history. The uveitic patient with early posterior synechiae and concomitant systemic disease is illustrative of this problem. We report a serious complication in a patient treated with mydriatic agents. A 26-year-old male had a 10-day history of photophobia, fatigue, and fevers for several months. On examination his vision was 20/40 and the pupils were constricted secondarily to 2700 posterior synechiae. He had hyperaemic conjunctivae, diffuse 'mutton-fat' keratic precipitates, and 3+ cells. Dilatation with topical and pledget soaked tropicamide 1% and phenylephrine 2 5% was unsuccessfully attempted. The patient returned 24 hours later, and a mixture of two drops (100 V1) each of tropicamide 1%, atropine 1%, and phenylephrine 10% was injected subconjunctivally at the inferior limbus of the right eye. This mixture comprised 7 mg of phenylephrine, 1 mg of atropine, and 1 mg oftropicamide. The patient immediately developed severe headache, dyspnoea, and diaphoresis. His pulse was 110 per minute and blood pressure of 160/110 mmHg. He was taken to the emergency room, where he was found to be in respiratory failure. Chest x-ray revealed diffuse interstitial infiltrates not present on the previous day's films. The patient

SIR,-The adverse effects of mydriatic agents are well documented. When using these drugs one must carefully consider the relevant medical history. The uveitic patient with early posterior synechiae and concomitant systemic disease is illustrative of this problem. We report a serious complication in a patient treated with mydriatic agents.
A 26-year-old male had a 10-day history of photophobia, fatigue, and fevers for several months. On examination his vision was 20/40 and the pupils were constricted secondarily to 2700 posterior synechiae. He had hyperaemic conjunctivae, diffuse 'mutton-fat' keratic precipitates, and 3+ cells. Dilatation with topical and pledget soaked tropicamide 1% and phenylephrine 2 5% was unsuccessfully attempted. The patient returned 24 hours later, and a mixture of two drops (100 V1) each of tropicamide 1%, atropine 1%, and phenylephrine 10% was injected subconjunctivally at the inferior limbus of the right eye. This mixture comprised 7 mg of phenylephrine, 1 mg of atropine, and 1 mg oftropicamide. The patient immediately developed severe headache, dyspnoea, and diaphoresis. His pulse was 110 per minute and blood pressure of 160/110 mmHg.
He was taken to the emergency room, where he was found to be in respiratory failure. Chest x-ray revealed diffuse interstitial infiltrates not present on the previous day's films. The patient was intubated, and Swan-Ganz catheterisation revealed a pulmonary wedge pressure of 8 mm. He was transferred to the intensive care unit for management of non-cardiogenic pulmonary oedema. Subsequent diagnostic testing was consistent with a diagnosis of sarcoidosis. The pulmonary oedema resorbed and the patient was discharged on topical steroids with subsequent resolution of the iritis. This is the first reported case of noncardiogenic pulmonary oedema associated with the use of mydriatic drugs. Both atropine and tropicamide are anticholinergic drugs whose actions include relaxation of the circular muscle ofthe iris and paralysis ofthe ciliary muscle. The principal adverse cardiopulmonary effect of these drugs is tachycardia. Phenylephrine, a potent, direct-acting, and selective a, agonist exerts its main mechanism ofaction by stimulation of a receptors of the dilator pupillae.' Stimulation of these receptors can cause constriction of the systemic, pulmonary, and coronary arteries, leading to severe hypertension, headache, ventricular arrhythmias, myocardial infarction, and cardiac arrest.' It is conceivable that in our patient phenylephrine may have produced severe pulmonary vasoconstriction leading to alveolocapillary damage and consequent non-cardiogenic pulmonary oedema. In addition our patient had pre-existing pulmonary sarcoidosis, which may have increased his susceptibility to lung injury from other insults.
Subconjunctival injections of mydriatic agents to forcibly dilate pupils with synechiae is recommended' and is commonly used in several eye centres. These injections, especially in hyperaemic conjunctivae, can lead to enhanced systemic absorption and' serious complications. We advise extreme caution when using this method of administering dilating agents. ILAN  Branch retinal artery occlusion in toxoplasma retinochoroiditis SIR,-Although toxoplasma retinochoroiditis may cause retinal vein occlusion, vascular remodelling, and even retinochoroidal anastomosis," retinal artery obstruction is rare."-We have recently studied a patient suffering from such a complication. An 18-year-old student attended in March 1989, 24 hours after the sudden loss of inferotemporal field in the right eye, which was confirmed by automated perimetry. A branch artery occlusion was found in a corresponding area of focal retinochoroidal inflammation. Some areas of periphlebitis were also seen peripherally. Fluorescein angiography confirmed occlusion of the artery within the area of inflammation (Fig 1). Antibodies to toxoplasma were detected by latex agglutination at serum dilutions of more than 1:1000.  The patient was treated with clindamycin, 150 mg four times a day, and prednisolone 60 mg daily, reducing over eight weeks. At the end of this period the inflammatory focus had become inactive. Repeat fluorescein angiography demonstrated reperfusion of the artery (Fig 2). However, the field defect persisted.
This case confirms that field loss in toxoplasma retinochoroiditis can result from arterial occlusion. Arterial thrombosis is presumably caused by the intense adjacent inflammation. Corticosteroid and antimicrobial therapy6 may assist resolution of the inflammatory focus and should be considered when retinal vessels are involved and therefore at risk of occlusion. If, as in this case, occlusion has already occurred, retinal function may not recover despite resolution of the inflammation and reperfusion of the blood vessel. Corneal penetration by tarantula hairs SIR,-Tarantulas are large, hairy spiders belonging to the family Theraphosidae. Their popularity as pets parallels the increasing popularity ofexotic pets in general. Although their bite is virtually harmless to humans, many species of New World tarantulas possess projectile urticating hairs on the dorsal surface of the abdomen.' When threatened, the spiders rapidly stroke their hind legs in a vibratory fashion on the dorsal hairs, catapulting a cloud of barbed hairs at the attacker. Some species may incorporate urticating hairs into their retreats or webs. These hairs, each possessing multiple barbs, are capable of penetrating deeply into skin, and causing intense and prolonged localised urticaria in humans.'2 In addition to dermatological trauma tarantula hairs are capable of embedding into the ocular tissues and producing an inflammatory reaction in the eye.34 Due to its small calibre, offending hairs could easily be overlooked without a slit-lamp examination of the anterior eye segment. A 13-year-old boy reported feeling severe foreign body sensation in both eyes within five minutes of stroking his pet tarantula. This was followed by intense pruritus, tearing, conjunctival injection, and eyelid swelling, thus prompting the patient to rub his eyes vigorously with his fingers. The eye rubbing further aggravated his discomfort. The patient was seen that day by his family physician, who treated him with antibiotic eyedrops. When the symptoms and signs showed only minimal resolution after three weeks of treatment, the patient was referred for ophthalmological con-