Chapter 138 – Choroidal Hemorrhage
MICHAEL A. KAPUSTA
PEDRO F. LOPEZ
• A hemorrhage in the suprachoroidal space that occurs spontaneously, intraoperatively, or traumatically, or is associated with intraocular vascular anomalies.
• One or more dome-shaped choroidal protrusions.
• Forward movement of the iris, lens, and vitreous body.
• Elevated intraocular pressure.
• Darkening of the red reflex.
• Excessive bleeding of conjunctiva and episcleral tissues.
• Severe pain, even under local anesthetic.
• Breakthrough vitreous hemorrhage.
• Rhegmatogenous, exudative, or tractional retinal detachment.
Choroidal hemorrhage is a serious ocular condition, which may be associated with permanent loss of visual function. Both limited and massive choroidal hemorrhages may occur as complications of most forms of ocular surgery, as well as from trauma. Intraoperative choroidal hemorrhage may progress to expulsion of intraocular tissues through the surgical wound. In some cases, expedient wound closure and appropriate application of pressure can prevent total loss of the globe. Despite modern vitreoretinal techniques, choroidal hemorrhage is associated with visual loss in most cases.
EPIDEMIOLOGY AND PATHOGENESIS
Choroidal hemorrhage may occur in a limited form or as a massive event. Massive choroidal hemorrhage is of sufficient volume to cause extrusion of intraocular contents outside the eye or to move retinal surfaces into or near apposition (“kissing”). Massive choroidal hemorrhage may be expulsive or nonexpulsive, immediate (intraoperative), or delayed hours to weeks postoperatively; it may occur spontaneously, with choroidal mass lesions (e.g., choroidal hemangioma), or with surgical or noniatrogenic trauma.   
Limited choroidal hemorrhage occurs in over 3% of intracapsular cataract extractions and in 2.2% of nucleus-expression extracapsular cases.  Massive choroidal hemorrhage has complicated 0.2% of cataract extractions and 0.73% of glaucoma filtering procedures ; it may occur even more frequently with keratoplasty. Scleral buckling procedures, as well as pars plana vitrectomy, may be complicated by either limited or massive choroidal hemorrhage.
Choroidal hemorrhage may occur when a fragile vessel is exposed to sudden compression and decompression events. An intact posterior lens capsule may serve as a tamponade against such intense intraocular decompression during surgery.  Retrobulbar anesthetic injection, retrobulbar hemorrhage, or excessive pressure on the globe during surgery may impede vortex venous outflow and lead to choroidal effusion and hemorrhage. Decompression hypotony, created when the eye is entered, and repeated fluctuations in intraocular fluid dynamics may add further insult to these fragile vessels. The resultant suprachoroidal effusion progresses to stretch the suprachoroidal space and cause further tension on the ciliary vessels. Alternatively, chronic hypotony may facilitate the extension of a pre-existing suprachoroidal effusion toward the anterior ciliary arteries. Either pathway may result in vessel wall rupture and suprachoroidal hemorrhage.
Systemic conditions which may serve as risk factors for expulsive choroidal hemorrhage include advanced age, arteriosclerosis, hypertension, diabetes mellitus, blood dyscrasias, and obesity. Ocular risk factors include previous surgery, aphakia, glaucoma, uveitis, high myopia, trauma, vitreous removal, laser photocoagulation, and choroidal sclerosis. A scleral buckle placed during vitrectomy is a risk factor for postoperative choroidal hemorrhage. A history of choroidal hemorrhage serves as a risk factor for surgery on either eye. Intraoperative risk factors include increased intraocular pressure, increased axial length, open-sky procedures, and Valsalva maneuvers. Intraoperative tachycardia has been identified as a significant risk factor or an early symptom of expulsive hemorrhage. It is unclear whether local anesthetic agents pose more risk than general anesthesia.
The risks of choroidal hemorrhage may be minimized by control of known risk factors. Preoperative massage and a Honan balloon may be used to control intraocular pressure. Intraoperative temporary security sutures may be placed before expression delivery of the lens. The water-tight wound created for phacoemulsification helps to maintain intraocular turgor; it may reduce the incidence and limit the severity of suprachoroidal hemorrhage. Blood pressure and heart rate should be monitored carefully.
Both serous and hemorrhagic choroidal detachments usually cause decreased vision. Serous choroidal detachment may be asymptomatic; however, hemorrhagic choroidal detachment often is extremely painful. Slit-lamp examination reveals a shallow anterior chamber with mild cells and flare. Ophthalmoscopy demonstrates a smooth, bullous, orange-brown elevation of the retina and choroid. Choroidal detachment that occurs anterior to the equator often extends in an annular fashion around the globe; whereas postequatorial choroidal detachment often is unilobulated or multilobulated, secondary to the periequatorial attachment of the choroid at the vortex vein ampullae. Visualization of the ora serrata without scleral depression may be a sign of pre-equatorial choroidal detachment ( Fig. 138-1 ).
Figure 138-1 Hemorrhagic choroidal detachment viewed ophthalmoscopically. A, The extent of choroidal protrusion, as evidenced by a fundus photograph focused on the optic nerve. B, The dome-shaped lobules and orange-brown color of a choroidal detachment. C, A closer view demonstrates no subretinal fluid, helping to establish that this is a choroidal detachment, not a retinal detachment.
Serous choroidal detachment, or effusion, occurs most frequently after recent glaucoma surgery. It also may develop, however, under the same conditions that lead to hemorrhagic choroidal detachment. Serous choroidal detachments are more frequent and generally subside within 3 weeks without alteration in vision. Serous choroidal detachment may be differentiated from rhegmatogenous retinal detachment by the absence of retinal breaks or outer retinal hydration lines and usually can be differentiated from hemorrhagic choroidal detachment by the low intraocular pressure and ready transillumination of serous choroidal detachment. Eyes with limited and massive (delayed) hemorrhagic choroidal detachments generally have elevated intraocular pressure and the detachments do not transilluminate. Serous choroidal detachments often are confined to the pre-equatorial suprachoroidal space, with limited postequatorial extension. Hemorrhagic choroidal detachments may extend to the posterior pole and are more voluminous posterior to the equator.
The initial intraoperative symptoms of massive choroidal hemorrhage may be paroxysmal onset of severe intraoperative pain despite akinesia and previously adequate analgesia. Classically, the pain radiates from the brow to the vertex of the head along the V1 dermatome and is often refractory to further retrobulbar analgesia. The intraoperative signs of massive choroidal hemorrhage may include tachycardia and excessive iris movement or prolapse. This usually is accompanied by
Figure 138-2 A-scan echogram. This demonstrates intravitreal opacities and the highly reflective, double-peaked, wide spike characteristic of choroidal detachment.
forward movement of the lens and vitreous body, as the globe tenses. Darkening of the red reflex may precede or accompany a choroidal elevation that protrudes into the operative field. Expulsion of intraocular contents may ensue.
DIAGNOSIS AND ANCILLARY TESTING
The intraoperative diagnosis of massive choroidal hemorrhage is based on recognition of early signs and changing ocular dynamics. Such recognition requires a high index of suspicion. Similarly, the diagnoses of delayed massive choroidal hemorrhage and limited choroidal hemorrhage are made after recent ocular surgery by consideration of the risk factors, symptoms, and signs. Measurement of intraocular pressure, gonioscopy, slit-lamp biomicroscopy, and dilated fundus examination, comparing both eyes, lead the examiner toward the diagnosis. Transillumination may be employed to differentiate serous from hemorrhagic choroidal detachment.
When the media is opaque or clear, echography may help to establish an accurate diagnosis. An A-scan echogram demonstrates a lesion with medium–high internal reflectivity and a steeply rising, 100% high spike. At low gain, this is observed to be a double-peaked wide spike characteristic of choroidal detachment ( Fig. 138-2 ). The first peak may represent the surface of the overlying detached retina or the anterior surface of the choroid. Alternatively, the double peak may represent both the anterior and posterior surfaces of the choroid. On B-scan echograms, a choroidal detachment typically appears as a smooth, thick, dome-shaped membrane in the periphery that exhibits little, if any, aftermovement on kinetic evaluation. Fresh blood clots are seen echographically as a high-reflective, solid-appearing mass, with irregular internal structure and irregular shape. Serial ultrasonography may demonstrate liquefaction of hemorrhage; the suprachoroidal space is filled with low-reflective mobile opacities, which have replaced the hemorrhagic clot. Serous elevation of the retina may accompany choroidal detachment and often resolves spontaneously. Choroidal melanoma may be distinguished from choroidal hemorrhage by its low–medium reflectivity on A-scan echography and its typical collar-button configuration and decreased reflectivity at the tumor base on B-scan echography.
Differential diagnosis consists of choroidal effusion, rhegmatogenous retinal detachment, and melanoma or metastatic tumor of choroid or ciliary body.
The management of serous choroidal detachment usually is conservative. Postoperative serous choroidal detachments often resolve on their own within days. Cycloplegia and topical corticosteroids are general management measures. Most commonly, serous choroidal detachments occur after excessive leakage from a wound or after glaucoma filtering surgery. These cases
usually respond to measures that reduce over-filtration and consequent hypotony, such as pressure patching and glue or bandage contact lens use. Surgical management of serous choroidal detachment may be indicated for refractory progressive shallowing or flattening of the anterior chamber—particularly in association with marked inflammation, which may promote the formation of peripheral anterior synechiae. The threat of corneal decompensation after lens–cornea touch or the apposition of retinal surfaces in kissing choroidal detachment are other potential indications for surgical intervention.
Delayed nonexpulsive limited choroidal hemorrhage generally carries a good prognosis. Limited choroidal hemorrhage usually resolves spontaneously within 1–2 months without ophthalmoscopic evidence of damage. Management remains conservative in this situation and includes the use of cycloplegics and topical corticosteroids. The management of delayed, nonexpulsive, massive choroidal hemorrhage, by contrast, remains controversial. Systemic corticosteroids are employed by some investigators. Some reports suggest that massive choroidal hemorrhage that follows glaucoma surgery can be observed, with spontaneous resolution to preoperative vision levels. Others suggest that delayed massive choroidal hemorrhage after filtering or seton surgery may result in irreversible loss of vision when intervention does not take place within 1 week. Surgical drainage should be considered in the following circumstances:
• Massive choroidal hemorrhage associated with severe pain
• Elevated intraocular pressure
• Persistently flat anterior chamber
• Suprachoroidal hemorrhage under the macula
• Extension of hemorrhage into the subretinal space or vitreous cavity
Significant vitreous incarceration in the surgical wound and kissing choroidal detachments, which may lead to secondary subacute traction or rhegmatogenous detachment after resolution of the suprachoroidal hemorrhage and its classic “buckle-like” effect, also are potential indications for surgical drainage.
In 1915, Voerhoeff introduced posterior sclerotomy to release suprachoroidal blood for the management of massive choroidal hemorrhage. Intraoperative massive choroidal hemorrhage is managed by tamponade of the eye with direct digital pressure and rapid wound closure. After penetrating keratoplasty, a Cobo temporary keratoprosthesis may be useful to prevent expulsion of intraocular contents. Posterior sclerotomy may be necessary, at the time of surgery, to permit adequate wound closure. Sclerotomies should be performed by careful cut-down incisions to the suprachoroidal space, beginning posterior to the muscle insertions. The vortex veins and long posterior ciliary vessels should be avoided, to minimize the risks of recurrent choroidal hemorrhage postoperatively.  The goal of rapid wound closure is to prevent expulsion or loss of the intraocular contents and incarceration of vitreous or retina in the surgical wound.
Choroidal hemorrhage that occurs postoperatively, recurs, or meets indications for further surgical intervention should be managed by a vitreoretinal surgeon. The successful management of affected eyes requires that vitreous or retinal incarceration be relieved completely. Patients who have vitreous incarceration are at high risk of developing retinal detachment. Eyes with concurrent vitreous and retinal detachment, at the time of diagnosis, may not be amenable to surgical repair or may be at high risk for proliferative vitreoretinopathy. Surgical intervention to drain choroidal hemorrhage ideally is conducted after liquefaction of the suprachoroidal hemorrhage, which may be assessed by serial echography.  Three-dimensional reconstruction of the B scan is possible with modern ultrasonography. This may assist in localization of the best sites for surgical drainage ( Fig. 138-3 ).
The timing of such intervention may be altered by the presence of rhegmatogenous retinal detachment.
Figure 138-3 A 3D ultrasonogram of choroidal hemorrhage.
The primary surgical goal is to separate any kissing choroidal detachments to prevent secondary traction or rhegmatogenous retinal detachment. Additional surgical goals include posterior rotation of the lens–iris diaphragm, which results in a deepened anterior chamber and, thus, prevents peripheral anterior synechiae and secondary angle-closure glaucoma, as well as corneal endothelial damage from lens–cornea contact. Surgical goals should also include the separation of kissing choroidal detachments by one half of their original height.
The initial stages of surgical drainage of massive choroidal hemorrhage include conjunctival peritomy and isolation of the relevant rectus muscles with bridle sutures. Often, all four rectus muscles are isolated to enable exposure if posterior drainage sclerotomies are needed in multiple quadrants to evacuate adequately the suprachoroidal hemorrhage.
Figure 138-4 A self-retaining infusion cannula in the anterior chamber.
Figure 138-5 Creation of a posterior sclerotomy incision to drain a choroidal hemorrhage.
Infusion of fluid or air to pressurize the eye and allow more complete evacuation of the suprachoroidal hemorrhage generally is a useful adjunctive procedure. The anterior chamber is entered with a 25-guage or smaller needle, bent posteriorly, so that the bevel directs the infusion away from the corneal endothelium. Alternatively, a micro–vitreo-retinal blade may be used if a self-retaining or sutured infusion cannula is to be inserted ( Fig. 138-4 ). Again, flow should be directed posteriorly. Viscoelastic agents may be employed to deepen the anterior chamber sufficiently to insert the infusion cannula.
Posterior sclerotomy sites generally are created in the area of greatest choroidal elevation, with the patient in the supine (surgical) position to optimize drainage of the hemorrhage. Incisions (4–6?mm long) are created with a round or sharp blade posterior to the rectus muscle insertions, centered at the equator of the globe. Exposure is best in the inferotemporal quadrant, but other quadrants may be incised to achieve optimal drainage, as judged by inspection and ophthalmoscopy ( Fig. 138-5 ). The sclerotomy sites may be sutured closed to restore anatomical integrity and stability, or left open if further spontaneous drainage is felt likely or necessary.
If vitreous is incarcerated in the original surgical wound, a vitrectomy probe may be introduced through a second limbal incision and an anterior vitrectomy performed to minimize vitreoretinal traction during the choroidal drainage procedure. Anterior chamber lens remnants similarly may be removed. Once adequate initial drainage has been achieved, a posterior vitrectomy with scleral depression may be performed to remove residual lens fragments, cortex, and vitreous adhesion to the iris. In the absence of retinal detachment, this may be deferred to later surgical intervention. For rhegmatogenous retinal detachment, a more extensive posterior vitrectomy in conjunction with drainage of the choroidal hemorrhage usually is necessary.
Figure 138-6 Transverse B-scan of an eye after repair of a ruptured globe. The annular, flat, and diffuse hemorrhagic choroidal detachment is typical of trauma.
In these cases, the insertion of a 6?mm infusion cannula through the anterior pars plana may be necessary to prevent suprachoroidal infusion. Relaxing peripheral retinotomy or retinectomy may be necessary to relieve incarceration of the retina or severe anterior vitreous traction. The use of perfluorocarbon liquids may facilitate the drainage of suprachoroidal hemorrhage and facilitate reattachment of the retina. Scleral buckling or long-term intraocular tamponade with silicone oil may minimize the chances of recurrent retinal detachment in these eyes.
Central retinal apposition in retinal detachment that follows drainage of choroidal fluid poses a unique surgical challenge. Perfluorocarbon liquids may be used to stabilize the posterior retina. A taper-tip endocautery can preserve hemostasis as the retinal surfaces are teased or cut apart to separate them. The perfluorocarbon level can be raised further to flatten the now-separated surfaces. Endolaser treatment and gas or oil tamponade may then be used.
Eyes for which the outcomes are successful through observation, conservative measures, or surgical intervention may be considered for intraocular lens implantation for visual rehabilitation. The reduction of risk factors for choroidal hemorrhage should achieve foremost attention at the time of secondary lens implant.
Choroidal Hemorrhage in Trauma
Choroidal hemorrhage that occurs with noniatrogenic trauma or rupture of the globe may be associated with intraocular structural damage. In addition to contusive injury, fibrocellular proliferation with membrane formation may limit the visual rehabilitation of the eye. The management of these cases must take into consideration the high likelihood of retinal detachment and associated proliferative vitreoretinopathy. Surgery may require evacuation of hyphema. Corneal blood staining may necessitate the use of a temporary keratoprosthesis. The choroidal hemorrhage is drained as described above. Scleral buckling and long-term tamponade with silicone oil may be required to effect repair of an associated rhegmatogenous retinal detachment. The echographic characteristics of choroidal hemorrhages that result from trauma differ from those that arise from other causes. In general, traumatic choroidal hemorrhages tend to be more diffuse and less elevated ( Fig. 138-6 ). 
Choroidal Hemorrhage in Other Conditions
Choroidal hemorrhage may occur in association with hemoglobinopathies, with anticoagulants, or spontaneously ( Fig. 138-7 ). In one series, patients developed acute angle-closure glaucoma from forward displacement of the lens–iris diaphragm, which resulted from massive hemorrhagic detachment of the choroid and retina. Affected patients often have associated systemic hypertension or a primary or anticoagulant-induced clotting disorder. The source of “spontaneous” hemorrhage in these patients is choroidal neovascularization in a disciform lesion.
Sturge–Weber syndrome is characterized by a flat, facial hemangioma that follows the distribution of the fifth cranial nerve. Occasionally, meningeal hemangiomas may be present and can produce seizures. Choroidal and episcleral hemangiomas are
Figure 138-7 A hemorrhagic choroidal detachment seen in a patient using warfarin. (Courtesy of Jeffrey L. Marx, MD.)
seen commonly—leakage from the choroidal hemangioma can cause retinal edema. Glaucoma may be present when the facial hemangioma involves the lid or conjunctiva. Trabeculectomy in these cases is complicated by rapid expansion of the hemangioma, with effusion of fluid into the suprachoroidal and subretinal space in 17% of cases. Some surgeons recommend placement of two or three posterior sclerotomies to prevent such expansion. Definitive management includes posterior drainage sclerotomy followed by reformation of the anterior chamber.
Limited choroidal hemorrhage can be mistaken for a choroidal melanoma, particularly when it appears as a discrete, dark, posterior mass. Failure to differentiate these lesions can lead to unnecessary treatment or enucleation. Recent ocular surgery, trauma, or use of anticoagulants should alert the clinician to consider choroidal hemorrhage when malignant melanoma is suspected. Fluorescein angiography and ultrasonography may help to differentiate these entities. Serial examination by ophthalmoscopy or ultrasonography reveals diminishing size of choroidal hemorrhage, over a period of several weeks, and little or no growth of malignant melanoma. Suprachoroidal hemorrhage has been reported to occur with systemic tissue plasminogen activator. In one case, this complication occurred days after administration of the agent to a patient with acute myocardial infarction.
COURSE AND OUTCOME
Delayed, nonexpulsive, limited choroidal hemorrhage generally carries a good prognosis. Choroidal hemorrhages in cataract surgery tend to fare better than those in other forms of ocular surgery or in trauma. Retinal detachment in an eye with choroidal detachment or with choroidal hemorrhage in all four quadrants correlates with a poor visual outcome.  The extension of suprachoroidal hemorrhage into the posterior pole has been associated with worse visual and anatomical outcomes. Vitreous and, especially, retinal incarceration is associated with a poorer prognosis.  In the absence of retinal adherence, however, kissing choroidal detachments may not portend a worse outcome—the natural history of this condition has not been delineated precisely.
1. Bukelman A, Hoffman P, Oliver M. Limited choroidal hemorrhage associated with extracapsular cataract extraction. Arch Ophthalmol. 1987;105(3):338–41.
2. Welch JC, Spaeth GL, Benson WE. Massive suprachoroidal hemorrhage. Ophthalmology. 1988;95(9):1202–6.
3. Ingraham HJ, Donnenfeld ED, Perry HD. Massive suprachoroidal hemorrhage in penetrating keratoplasty. Am J Ophthalmol. 1989;108(6):670–5.
4. Beyer CF, Peyman GA, Hill JM. Expulsive choroidal hemorrhage in rabbits. Arch Ophthalmol. 1989;107(11):1648–53.
5. Speaker MG, Guerriero PN, Met JA, et al. A case-control study of risk factors for intraoperative suprachoroidal expulsive hemorrhage. Ophthalmology. 1991; 98(2):202–10.
6. Chu TG, Cano MR, Green RL, et al. Massive suprachoroidal hemorrhage with central retinal apposition. Arch Ophthalmol. 1991;109(11):1575–81.
7. Chu TG, Green RL. Suprachoroidal hemorrhage. Surv Ophthalmol. 1999;43: 471–86.
8. Wheeler TM, Zimmerman TJ. Expulsive choroidal hemorrhage in the glaucoma patient. Ann Ophthalmol. 1987;19(5):165–6.
9. Lambrou FH, Meredith TA, Kaplan HJ. Secondary surgical management of expulsive choroidal hemorrhage. Arch Ophthalmol. 1987;105(9):1195–8.
10. Ariano ML, Ball SF. Delayed nonexpulsive suprachoroidal hemorrhage after trabeculectomy. Ophthalmic Surg. 1987;18(9):661–6.
11. Canning CR, Lavin M, McCartney ACE, et al. Delayed suprachoroidal hemorrhage after glaucoma operations. Eye. 1989;3(3):327–31.
12. Davidson JA. Vitrectomy and fluid infusion in the treatment of delayed suprachoroidal hemorrhage after combined cataract and glaucoma filtering surgery. Ophthalmic Surg. 1987;18(5):334–6.
13. Lakhanpal V, Schocket SS, Elman MJ, et al. A new modified vitreoretinal surgical approach in the management of massive suprachoroidal hemorrhage. Ophthalmology. 1989;96(6):793–800.
14. Iverson DA, Ward TG, Blumenkranz MS. Indications and results of relaxing retinotomy. Ophthalmology. 1990;97(10);1298–304.
15. Desai UR, Peyman GA, Chen CJ, et al. Use of perfluoroperhydrophenanthrene in the management of suprachoroidal hemorrhages. Ophthalmology. 1992;99(10): 1542–7.
16. Awan KJ. Intraocular lens implantation following expulsive choroidal hemorrhage. Am J Ophthalmol. 1988;106(3):261–3.
17. Liggett PE, Mani N, Green RL, et al. Management of traumatic rupture of the globe in aphakic patients. Retina. 1990;10:S59–S64.
18. Pepsin SR, Katz J, Augsburger JJ, et al. Acute angle-closure glaucoma from spontaneous massive hemorrhagic retinal or choroidal detachment. Ophthalmology. 1990;97(1):76–84.
19. Hoskins HD Jr, Kass MA. Developmental and childhood glaucoma. In: Becker–Shaffer’s diagnosis and therapy of the glaucomas, ed 6. St Louis: Mosby; 1989:355–403.
20. Morgan CM, Gragoudas ES. Limited choroidal hemorrhage mistaken for a choroidal melanoma. Ophthalmology. 1987;94(1):41–6.
21. Khawly JA, Ferrone PJ, Holck DEE. Choroidal hemorrhage associated with systemic tissue plasminogen activator. Am J Ophthalmol. 1996;121(5):577–8.
22. Reynolds MG, Haimovici R, Flynn HW, et al. Suprachoroidal hemorrhage. Clinical features and results of secondary surgical management. Ophthalmology. 1993;100(4);460–5.
23. Tabandeh H, Sullivan PM, Smahliuk P. Suprachoroidal hemorrhage during pars plana vitrectomy. Ophthalmology. 1999;106:236–42.
24. Wirostko WJ, Han DP, Mieler WF, et al. Suprachoroidal hemorrhage: outcome of surgical management according to hemorrhage severity. Ophthalmology. 1998; 105:2271–5.