Literature DB >> 23741139

Postoperative suprachoroidal hemorrhage in a glaucoma patient on low molecular weight heparin.

Dora H AlHarkan1, Ibrahim A AlJadaan.   

Abstract

Suprachoroidal hemorrhage is a complication associated with intraocular surgery that can occur both intraoperatively and postoperatively. Several intraoperative or postoperative risk factors have been identified. The use of low-molecular weight heparin (LMWH) is considered one of the risk factors in surgical cases (ocular or non ocular) and non-surgical cases. Here we present a case of suprachoroidal hemorrhage in a glaucoma patient that occurred after preoperative prophylactic LMWH for deep venous thrombosis. The use of LMWH has been reported to cause suprachoroidal hemorrhage even in patients without any risk factors. The use of LMWH continues to increase, hence it is important to be aware of the possibility of suprachoroidal hemorrhage and to determine the risk/benefit ratio, especially in patients with other risk factors.

Entities:  

Keywords:  Glaucoma; Suprachoroidal Hemorrhage; low-Molecular Weight Heparin

Mesh:

Substances:

Year:  2013        PMID: 23741139      PMCID: PMC3669497          DOI: 10.4103/0974-9233.110618

Source DB:  PubMed          Journal:  Middle East Afr J Ophthalmol        ISSN: 0974-9233


INTRODUCTION

Suprachoroidal hemorrhage is a devastating complication associated with intraocular surgery. It can occur both intraoperatively and postoperatively. Risk factors for suprachoroidal hemorrhage include axial length greater than 25 mm, high myopia independent of axial length, advanced age, atherosclerosis, elevated blood pressure, aphakia, pseudophakia, and anticoagulant medications.1–6 Anticoagulants such as low-molecular weight heparin (LMWH) is a risk factor for suprachoroidal hemorrhage in surgical cases (ocular or non-ocular) or non-surgical cases.1–4 Here we report a case of suprachoroidal hemorrhage in a patient who was treated preoperatively with LMWH for deep venous thrombosis prior to glaucoma surgery.

CASE REPORT

A 61-year-old Saudi female patient presented to the Glaucoma clinic at King Khalid Eye Specialist Hospital, (Riyadh, Kingdom of Saudi Arabia) with high-uncontrolled intraocular pressure (IOP) in the right eye. The patient had a history of bronchial asthma on remission without any current systemic medication. She was a monocular patient with phthisis bulbi of the left eye and had advanced secondary glaucoma with high myopia in the right eye. Past history of ocular surgery of the right eye included: A complicated cataract surgery and development of corneal decompensation postoperatively resulting in explantation of the intraocular lens. Subsequently she developed aphakic bullous keratopathy which required two penetrating keratoplasties. Then she developed secondary glaucoma which was managed with an Ahmed implant. Trans-scleral diode laser cyclophotocoagulation was performed for uncontrolled IOP. On examination at presentation, the vision in the right eye was 20/100 that improved with pinhole to 20/70 and the left eye had no light perception (NLP). The IOP was 39 mm Hg in the right eye on maximum topical anti-glaucoma therapy. Slit lamp examination of the right eye showed normal lid, thinning of the conjunctiva over the Ahmed tube without exposure, clear corneal graft centrally [Figure 1a], deep anterior chamber centrally with areas of peripheral anterior synechia. The Ahmed tube was in place away from the corneal graft with vitreous strands blocking it [Figure 1b], and she was aphakic. Fundus examination showed myopic changes with a pale disc and advanced cupping.
Figure 1

(a) Eye with advanced secondary glaucoma, high-uncontrolled intraocular pressure and thinning over an Ahmed glaucoma tube. (b) Eye with advanced secondary glaucoma, high-uncontrolled intraocular pressure, with vitreous strands blocking an Ahmed glaucoma tube

(a) Eye with advanced secondary glaucoma, high-uncontrolled intraocular pressure and thinning over an Ahmed glaucoma tube. (b) Eye with advanced secondary glaucoma, high-uncontrolled intraocular pressure, with vitreous strands blocking an Ahmed glaucoma tube Due to high-uncontrolled IOP even with maximal tolerated anti-glaucoma medications, triamcinolone assisted anterior vitrectomy with removal of the vitreous strands from the tube under local anesthesia was planned. The retinal consultant concurred with surgical plan with guarded prognosis. After discussion with the patient about the expected complications, risks and benefits, the patient signed an informed consent. The medical team gave the patient prophylactic LMWH (Clexane; Sanofi-Aventis, Bridgewater, NJ, USA) 4000 IU SC 2 h preoperatively. The surgery was uneventful [Figure 2]. On the first postoperative day, the patient complained of severe pain. Examination of the right eye indicated NLP with IOP of 70 mm Hg. Slit lamp examination showed an edematous cornea with flat anterior chamber and the retina was abutting the cornea. B-scan ultrasonography showed massive suprachoroidal hemorrhage with bullous choroidal detachment [Figure 3]. The patient received stat oral diamox and intravenous mannitol with methylprednisolone and topical anti-glaucoma medications. Due to the severe pain and high IOP, the retina team performed a drainage for the suprachoroidal hemorrhage with anterior chamber reformation. In the operating room, the retina was incarcerated in the tube and did not flatten. On the following day, the patient was discharged home with NLP vision. At two weeks follow-up, the vision was NLP and IOP was 8 mm Hg.
Figure 2

Anterior vitrectomy and removal of the vitreous strands that obstruct the tube

Figure 3

B-scan showing diffuse suprachoroidal hemorrhage

Anterior vitrectomy and removal of the vitreous strands that obstruct the tube B-scan showing diffuse suprachoroidal hemorrhage

DISCUSSION

Suprachoroidal hemorrhage can occur intraoperatively or postoperatively. Although it is quite rare, it can severely limit visual potential with a very poor prognosis without timely intraoperative and postoperative management. The overall incidence of intraoperative suprachoroidal hemorrhage ranges from 0.05% to 0.40%, with most series reporting an incidence of 0.20%. Choroidal hemorrhage has been reported with various types of intraocular surgeries including cataract extraction, glaucoma filtering surgeries, suture fixation of secondary IOL, penetrating keratoplasty, and retinal detachment surgery.5 The most important risk factors associated with the development of suprachoroidal hemorrhage is an elevated preoperative intraocular pressure, usually greater than 30 mm Hg or a history of glaucoma. Preoperative use of anticoagulants in ophthalmic surgery is a risk factor for complications such as hemorrhage associated with local anesthetic injections, intraoperative hemorrhage, or delayed postoperative hemorrhage. The use of LMWH has increased as prophylaxis for deep venous thrombosis for patients undergoing any surgery. LMWHs such as clexane comprise a group of antithrombotic agents which offer potential advantages over unfractionated heparin because they are given in fixed doses, are readily bioavailable when injected subcutaneously and can be equally effective for the treatment and prevention of thromboembolic processes, as well as acute coronary syndromes.7 Law et al.,2 reported that patients receiving chronic anti-coagulants therapy (ACT) have a statistically significant increased rate of hemorrhagic complications during and after glaucoma surgery. Patients who continued ACT during glaucoma surgery had the highest rate of hemorrhagic complications.2 An additional risk factor for hemorrhagic complications in patients on anticoagulation or antiplatelet aggregation therapy is a high preoperative IOP.2 Neudorfer et al.,1 reported a spontaneous massive choroidal hemorrhage in a patient who presented with unstable angina pectoris who was treated with subcutaneous enoxaparin (Clexane) for several days. The patient in the current case report had many risk factors for suprachoroidal hemorrhage; however, the use of LMW heparin has been reported to cause suprachoroidal hemorrhage even in patients without any risk factors.8 As LMWH are gaining in popularity, it may increase the risk of suprachoroidal hemorrhage in predisposed eyes. Hence, it is important to be aware of the possibility of this devastating ocular complication and to weigh the risks over the benefits, especially in those known to have other risk factors.
  7 in total

1.  Spontaneous suprachoroidal haemorrhage in a patient receiving low-molecular-weight heparin (fraxiparine) therapy.

Authors:  J S Wong
Journal:  Aust N Z J Ophthalmol       Date:  1999-12

2.  Survey of risk factors for expulsive choroidal hemorrhage: case reports. Substantiation of the risk factors and their incidence.

Authors:  Y Sekine; K Takei; H Nakano; T Saotome; S Hommura
Journal:  Ophthalmologica       Date:  1996       Impact factor: 3.250

Review 3.  Low-molecular-weight heparins in the management of acute coronary syndromes.

Authors:  P J Zed; J E Tisdale; S Borzak
Journal:  Arch Intern Med       Date:  1999-09-13

4.  Massive choroidal hemorrhage associated with low molecular weight heparin therapy.

Authors:  M Neudorfer; I Leibovitch; M Goldstein; A Loewenstein
Journal:  Blood Coagul Fibrinolysis       Date:  2002-04       Impact factor: 1.276

5.  Orbital hemorrhage and compressive optic neuropathy in patients with midfacial fractures receiving low-molecular weight heparin therapy.

Authors:  Basem T Jamal; Robert J Diecidue; Daniel Taub; Allen Champion; Jurij R Bilyk
Journal:  J Oral Maxillofac Surg       Date:  2009-07       Impact factor: 1.895

6.  Spontaneous suprachoroidal hemorrhage associated with age-related macular degeneration and anticoagulation therapy.

Authors:  Yu-Yen Chen; Ying-Ying Chen; Shwu-Jiuan Sheu
Journal:  J Chin Med Assoc       Date:  2009-07       Impact factor: 2.743

7.  Hemorrhagic complications from glaucoma surgery in patients on anticoagulation therapy or antiplatelet therapy.

Authors:  Simon K Law; Brian J Song; Fei Yu; Kristina Kurbanyan; Tien-An Yang; Joseph Caprioli
Journal:  Am J Ophthalmol       Date:  2008-02-06       Impact factor: 5.258

  7 in total

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