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Journal of Postgraduate Medicine, Vol. 47, Issue 4, 2001 pp.262-263 Unilateral Central Retinal Artery Occlusion Following Intravenous Streptokinase Potdar NA, Shinde CA, Murthy GG Department of Ophthalmology, B.Y.L. Nair Hospital, Mumbai – 400 008, India. Code Number: jp01076 Abstract A 38-year-old male with acute myocardial infraction who had received streptokinase presented with acute painless diminution of vision in the left eye. Examination revealed features of central retinal artery occlusion on the left side with vision of perception of light. Treatment in the form of systemic and local intraocular pressure lowering agents, retrobulbar xanthinol nicotinate and systemic injection of B-complex resulted in improvement of vision to counting fingers up to one meter. In this case thrombolytic therapy itself led to embolism into the left central retinal artery resulting in its occlusion and eventually optic atrophy and blindness. Key Words: Myocardial infarction. Streptokinase, Central Retinal Artery Occlusion, Cholesterol Embolisation syndrome. Today the spectrum of indications for fibrinolytic agents like Urokinase or Streptokinase comprises of acute myocardial infarction, lung embolism, ischaemic stroke, deep vein thrombosis and acute arterial occlusions of lower limbs. They have been tried in non-life threatening situations like central retinal artery and central retinal vein occlusion. Systemic administration of fibrinolytic agents is associated with haemorrhagic risks like cerebral haemorrhage, gastrointestinal bleeding, cardiogenic shock and unusual complications like splenic rupture, aortic dissection and cholesterol embolisation.(1) We are describing a case where thrombolytic therapy with intravenous streptokinase in acute myocardial infarction resulted in embolic phenomenon in the central retinal artery leading to sudden blindness.Case
History A 38-year-old male, non-hypertensive, non-diabetic, chronic smoker,
diagnosed with acute anterolateral wall myocardial infarction was treated with
injection streptokinase within an hour of the admission in a private hospital.
The patient developed sudden painless diminution of vision in left eye within
two hours of receiving injection streptokinase and arrived 24 hours later to
this institution. History suggested trauma to the right eye 20 years ago. On the
day of examination visual acuity in right eye was hand movements and left eye
was perception of light. Right eye had traumatic cataract that was membranous
and partially absorbed, with pupil reacting to light. Left eye had Marcus-Gunn
pupil and rest of the anterior segment was normal. Fundus examination revealed
diffuse arteriolar constriction with retinal pallor and cherry red spot at macula
suggesting of central retinal artery occlusion (CRAO). Fundus of right eye was
not visualised due to the cataract. Intraocular pressure in both eyes was normal.
Ultrasonography (B Scan) of right eye revealed posterior vitreous detachment
without any evidence of retinal detachment. Coronary angiography confirmed complete
block in left anterior descending artery just after the origin. Left circumflex
and right coronary artery were normal. Left ventricular angiography showed hypokinesia
of anterior, lateral, apical and septal areas. The left ventricular ejection
fraction was 35%. There was no thrombus in left ventricle, which was confirmed
on echocardiography.
ECG showed sinus rhythm and extensive q waves confirming anterolateral wall
myocardial infarction. His blood pressure was stable throughout. Laboratory
investigations showed elevated LDH, SGOT, SGPT levels. The lipid profile showed
triglycerides to be 249 mg/dl. His blood counts and peripheral smear were within
normal limits. Patient was treated with systemic Acetazolamide 250 mg three
times with local Betoxolol 0.5% eye drops. Retrobulbar injection of xanthinol
nicotinate 1cc (150mg) was given on alternate day (5 injections). With the above
treatment there was some improvement in the visual acuity in the left eye (counting
fingers at one meter). At the end of four months the left eye had complete pallor
of optic disc (Figure 1).Cataract surgery
performed later in the right eye showed normal fundus. Discussion
Cases of disseminated cholesterol embolisation syndrome have been
reported after intravenous streptokinase administration in patients of myocardial
infarction. Most of the reported cases manifested with cyanosis, ulcers, gangrene
of hands and feet, myalgias, intestinal infarction, eosinophilia and renal failure.(2-5)
The probable mechanism suggested is dissolution of cholesterol containing thrombi
resulting in the release of cholesterol crystals into the peripheral vasculature.(2)
Some workers have postulated that thrombolytic agents might promote embolisation
by destabilising the protective thrombus over ulcerating atheromatous plaques
and favouring continuous dissemination of atheromatous fragments into the arterial
circulation.(3) Cholesterol embolisation may also remain silent in majority
of the cases.(6) The present case developed embolisation in left retinal artery
and this being his only seeing eye, the sudden decrease in vision was immediately
appreciated. Symptoms suggestive of any other organ involvement were absent.
No thrombus was demonstrated in the left ventricle either on angiography or
on echocardiogram. Hence the most possible cause could be that the cholesterol
embolus had occluded the central retinal artery following injection of streptokinase.
So the most likely culprit of CRAO in the present case appears to be cholesterol
embolism, although a definite cause and effect relationship between streptokinase
and CRAO could not be established, as the crystals were not evident on fundus
examination. As such cholesterol embolisation syndrome is a rare event, but
the extensive use of I.V. Streptokinase may increase the possibility of such
an event. In the absence of any positive diagnostic serological investigation,
a high index of suspicion is required to diagnose this condition.(6) Hence increased
awareness of the diagnosis and more research into the underlying pathophysiological
mechanism are necessary to understand this entity and thereby reduce the patient
morbidity and mortality. Isolated CRAO has not been reported in the literature.
The present case developed consecutive optic atrophy in the left eye. There
are studies where fibrinolytic agents themselves are used as therapy for ischaemic
central retinal vein occlusion and central retinal artery occlusion.(7) However
in this case the complication of central retinal artery occlusion occurred following
intravenous streptokinase injection used for lysis of thrombus in the coronaries
after myocardial infarction - “a clinical ironical situation”. The poor visual
outcome warrants the awareness of blindness as a complication of I.V. Streptokinase
injection given in acute myocardial infarction. References
This article is also available in full-text from http://www.jpgmonline.com/ © Copyright 2001 - Journal of Postgraduate Medicine The following images related to this document are available:Photo images[jp01076f1.jpg] |
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