|Year : 2015 | Volume
| Issue : 3 | Page : 155-158
Orbital and intracranial hemorrhage following thrombolysis: A case report
Karuppannasamy Divya1, Kanagaraju Vikrant2, Andavar Raghuram1, Tamilmani Yazhini1
1 Department of Ophthalmology, Peelamedu Sama Naidu Govindasamy Naidu Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
2 Department of Radiodiagnosis, Peelamedu Sama Naidu Govindasamy Naidu Institute of Medical Sciences and Research, Coimbatore, Tamil Nadu, India
|Date of Web Publication||20-Aug-2015|
Department of Ophthalmology, PSG Institute of Medical Sciences and Research, Coimbatore - 641 004, Tamil Nadu
Source of Support: None, Conflict of Interest: None
Thrombolytic therapy has been a major advance in the treatment of acute myocardial infarction to achieve coronary reperfusion and improve survival. Bleeding is the most common complication following thrombolytic therapy which can occur spontaneously and at multiple sites. We report a case of orbital and subsequent intracranial hemorrhage in a 55- year old male who had undergone thrombolytic therapy for suspected myocardial infarction. He presented with severe proptosis and visual loss 6 hours after thrombolysis. Urgent orbital decompression in the form of lateral canthotomy and cantholysis resulted in visual recovery. The possibility of orbital hemorrhage should be considered in any patient presenting with proptosis and visual loss after administration of systemic thrombolytic agents. Also, Ophthalmologists and emergency physicians should be familiar with the technique of lateral canthotomy and cantholysis for orbital decompression since prompt treatment is essential to prevent permanent visual loss.
Keywords: Cantholysis, canthotomy, orbital hemorrhage, thrombolysis
|How to cite this article:|
Divya K, Vikrant K, Raghuram A, Yazhini T. Orbital and intracranial hemorrhage following thrombolysis: A case report. J Clin Ophthalmol Res 2015;3:155-8
|How to cite this URL:|
Divya K, Vikrant K, Raghuram A, Yazhini T. Orbital and intracranial hemorrhage following thrombolysis: A case report. J Clin Ophthalmol Res [serial online] 2015 [cited 2020 Jul 13];3:155-8. Available from: http://www.jcor.in/text.asp?2015/3/3/155/163301
Orbital hemorrhage usually occurs following trauma, surgeries around the orbit or retrobulbar injections. Non traumatic orbital hemorrhage is uncommon and has been reported to occur in patients with vascular malformations of the orbit, increased venous pressure, hypertension or bleeding diathesis.  Use of thrombolytic agents have been associated with a variety of haemorrhagic complications hours to days after an uncomplicated ocular surgery. , Very few cases of orbital hemorrhage following thrombolysis have been reported in patients without any previous history of surgery or trauma. ,
We report a case of orbital and subsequent intracranial hemorrhage after thrombolysis in a patient with no history of surgery or trauma. To the best of our knowledge no similar case has been reported in literature.
| Case Report|| |
A 55- year old non diabetic, normotensive male was referred to the ophthalmology department of our hospital for sudden onset of pain, swelling and decrease in vision in right eye which developed 6 hours after thrombolysis done elsewhere. He had presented to a local hospital earlier with low grade fever and syncope where he was diagnosed with anterior wall ST segment elevation myocardial infarction (STEMI) based on electrocardiogram (ECG) and thrombolysed with 1.5 million international unit (IU) of streptokinase. He denied previous history of trauma or recent ocular surgery.
On ocular examination, his visual acuity was perception of light in right eye. The eye was found to be tense with proptosis, ecchymosis of eyelids, and subconjunctival hemorrhage [Figure 1]. Cornea was clear with normal anterior chamber depth. Pupil was 4 mm and revealed relative afferent pupillary defect. Fundus examination revealed normal optic disc and macula. Extraocular movements were restricted in all directions. The intraocular pressure by Goldmann applanation tonometry was 36 mmHg. The left eye had a visual acuity of 20/40 and was essentially normal.
|Figure 1: Clinical photograph showing lateral canthotomy wound along with proptosis, ecchymosis and subconjunctival haemorrhage in right eye.|
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The patient was diagnosed to have acute retrobulbar hemorrhage following thrombolysis, severe enough to compromise the optic nerve. Urgent decompression in the form of lateral canthotomy and inferior cantholysis was done under local anaesthesia. He was also treated with tablet acetazolamide 500 mg stat to reduce the intraocular pressure. His vision immediately improved to 20/200 and the intraocular pressure dropped to 26 mmHg. Four hours later, visual acuity was 20/80 with an intraocular pressure of 20 mmHg.
Patient was under intensive care treatment where a subsequent ECG revealed no ischemic changes. He underwent a complete cardiac evaluation and no significant cardiac pathology was detected. Coagulation studies revealed a platelet count of 1,50,000/uL(normal:150000-400000/uL), activated partial thromboplastin time(APTT) of 33.3 seconds(normal:27-35 seconds) prothrombin time (PT) of 16.1 seconds (normal:11-15 seconds) and prothrombin time INR (PT/INR) 1.23 (normal range-0.9-1.1) which was essentially within normal limits except for marginal increase in PT and PT/INR. On the second day of admission, he developed drowsiness and weakness of the left upper limb. Computed tomography (CT) scan of the orbits and brain was done which showed a well defined, lentiform hematoma along the lateral wall of right orbit near lateral rectus muscle [Figure 2]. Intracerebral hemorrhage in the right frontal lobe and subarachnoid hemorrhage in the anterior interhemispheric fissure were also noted [Figure 3]. Magnetic resonance imaging (MRI) revealed hyperintensity along the extraconal space on T2 weighted images and fluid attenuated inversion recovery (FLAIR) sequences confirming orbital hemorrhage [Figure 4]. Repeat platelet count, prothrombin time, and PT/INR were within normal limits. (151000/uL, 13.9 seconds and 1.07 respectively).
|Figure 2: Axial CT scan of the orbits showing mild proptosis and lentiform hematoma along the lateral wall of right orbit (arrow) near lateral rectus|
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|Figure 3: Axial CT image showing intracerebral haemorrhage in right frontal lobe and subarachnoid haemorrhage in the anterior interhemispheric fissure (arrows)|
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|Figure 4: T2 Weighted axial MR image of the orbits showing hyperintense biconvex lesion along lateral wall of right orbit (arrow)|
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He continued to be under intensive care for the neurological status and was managed conservatively. Ocular examination at one week revealed a healing canthotomy wound. Visual function could not be assessed because of his critical condition. Detailed examination at one month follow up revealed a best corrected visual acuity of 20/40 in right eye with healed canthotomy wound, brisk pupil, full extraocular movements and intraocular pressure of 16 mmHg. Repeat CT scan of the orbits showed complete resolution of the hematoma [Figure 5].
|Figure 5: Follow up axial CT at one month showing resolution of proptosis and orbital hematoma|
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| Discussion|| |
Orbital hemorrhage is a true ophthalmic emergency since it can lead to the development of orbital compartment syndrome.  Orbital compartment syndrome occurs due to acute rise in volume within confined space of the bony orbit which results in an acute rise in orbital tension. Visual loss can occur from central retinal artery occlusion, direct compressive optic neuropathy or compromise of vascular supply to the optic nerve.  The presence of normal retinal vessels in our patient excluded the possibility of central retinal artery occlusion. The visual loss in our patient was the result of optic nerve dysfunction, most probably due to ischemia following increased orbital pressure.
The diagnosis of orbital compartment syndrome is completely clinical and early recognition and emergent orbital decompression (even prior to imaging) is essential in preventing permanent visual loss. In our patient lateral canthotomy and inferior cantholysis resulted in prompt reduction of the intraorbital pressure and dramatic visual recovery. This involves cutting the lateral canthal tendon along its length to the orbital rim and disinserting the inferior limb of the tendon from the bony orbit. Several studies have demonstrated immediate and significant reduction in intraorbital pressure after this procedure. , If the vision does not improve following lateral canthotomy and cantholysis, surgical evacuation of the haematoma is warranted.
The development of pain or decrease in vision in any patient after thrombolytic therapy should alert the clinician to the possibility of an ocular or an adnexal hemorrhage. Thrombolytic therapy restores coronary blood flow by activation of plasmin, the enzyme responsible for fibrin degradation. The commonly used thrombolytic agents include streptokinase, recombinant tissue plasminogen activators (tPA) like alteplase, reteplase and tenecteplase. While the action of tPA is fibrin specific,  the streptokinase- plasminogen complex is non selective, activating plasminogen whether it is associated with clot or not, producing a systemic lytic state. Hence the major limitation of thrombolytic therapy is hemorrhage. Mechanisms of hemorrhage following thrombolysis include dissolution of haemostatic plugs, depletion of clotting factors and loss of vascular integrity. 
The most common site of spontaneous bleeding following thrombolysis is gastrointestinal tract.  Symptomatic intracranial hemorrhage following thrombolysis is rare with reported incidence rates varying between 0.7-1%. , The single large study evaluating the ocular haemorrhagic complications of thrombolysis revealed only 12 cases (0.03%) of ocular hemorrhage among 41,021 patients.  However none of the twelve patients had associated intracranial hemorrhage.
Our patient presented with orbital hemorrhage initially and later developed intraparenchymal and subarachnoid hemorrhage which is extremely rare.
Although the survival benefits are significant, the major risk of thrombolytic therapy is hemorrhage which is mostly procedure related. However hemorrhage can also occur spontaneously at multiple sites as in our patient. Hence continued monitoring for haemorrhagic complications is essential after administration of thrombolytic therapy.
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[Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5]