healthmedicinet

An 86 year old Caucasian lady presented to the Emergency Department (ED) of a tertiary
referral teaching hospital with sudden and persisting loss of vision in her right
eye over eight hours. The ED team reported that a hyphaema was present with ‘bleeding
through the pupil’. The patient described reduced vision after waking that morning,
which progressed during the day. She reported severe pain (6/10) and aching in the
right eye, which extended ipsilaterally down to her neck and was associated with dry
retching every 30 min. She denied any previous similar episodes.

She was on Warfarin for recurrent pulmonary emboli and had recently been prescribed
intravenous Ceftriaxone and subsequent oral Cefaclor for cellulitis of her right leg.
Her general health had been complicated by a cerebrovascular accident 30 years earlier
following a ventriculoperitoneal shunt revision originally performed for pseudotumour
cerebri. She had treated hypothyroidism and hypertension.

Her right visual acuity was light perception and left was 6/9. The right pupil response
to light was sluggish, but due to her long-standing Parinaud’s syndrome secondary
to the stroke, pupillary assessment was challenging. However, there was no evidence
of a relative afferent pupil defect, nor indeed of an indirect relative afferent pupil
defect. In the right eye there was a 1.6 mm hyphaema. Her IOP was 55 mmHg, with slight
corneal microcystic oedema. There was no evidence of pupillary block and her anterior
chamber angles were open at grade 2. There was no evidence of primary uveal melanoma.
The left eye was normal, except for a small area of temporal foveal atrophy.

B-scan ultrasound was normal with no evidence of vitreous haemorrhage or mass lesions
identified. An iris fluorescein angiogram was contemplated and would have supported
a more definitive diagnosis of iris microhaemangioma but was deemed clinically unnecessary
at the time. A computed tomography angiogram of the brain, conducted in ED to investigate
the patient’s symptoms, with a view to excluding internal carotid artery stenosis,
was also normal. Full blood count, liver function tests, blood sugar level and HbA1C
were normal. Coagulation studies revealed a supratherapeutic INR of 3.9 and electrolyte
analysis revealed elevated serum potassium of 5.9 mEq/L, both of which were deemed
iatrogenic secondary to her recent oral antibiotic use.

A 23-gauge needle anterior chamber paracentesis was performed temporally. The intraocular
pressure was lowered to 29 mmHg, and statim dilatation was carried out with guttae
(G.) Tropicamide 1 %. As the pupillary diameter increased, clot retraction occurred
with clearing of the visual axis, immediate improvement in right eye visual acuity
to 6/60, and demonstration of the ipsilateral IVTS (Fig. 1). At this point, the IVTS in the left eye also became evident. Right fundus examination
demonstrated a normal optic nerve head with a cup:disc ratio of 0.2, and with a small
area of central foveal atrophy.

Fig. 1. Iris Microhaemangiomas. Iris Microhaemangiomas on right pupil visualised after clot
retraction

The patient was commenced on hourly G. Prednisolone Acetate 1 %, G. Atropine 1 % twice
daily, and a combination of Brinzolamide, Timolol, Latanoprost and Brimonidine. With
the advice of the Haematologists, she was administered 1 mg of Vitamin K intravenously
in order to normalise her INR. With advice from the Nephrologists, 30 g of Resonium
was administered orally to reduce her serum potassium.

Her hyphaema resolved completely, and after 48 h her right visual acuity had improved
to 6/12. Subsequent scanning laser polarimetry of the retinal nerve fibre layer and
automated achromatic perimetry testing were within normal limits.

Given the absence of any significant trauma and lack of systemic associations, the
patient’s spontaneous hyphaema was attributed to her IVTs with supratherapeutic INR
as a predisposing factor. Her recent oral cephalosporin usage for lower limb cellulitis
was implicated as causal for her high INR. It is known that these antibiotics decrease
the absorption and alter the metabolism of vitamin K, thus augmenting the effects
of Warfarin. Haematology review deemed her risk of further clotting episodes to be
too high to stop warfarinisation. Counselling was given to the patient on the association
of an increased, and potentially life-threatening INR, and propensity for further
IVT bleeding.