Suprachoroidal Hemorrhage

Suprachoroidal hemorrhage (SCH) is a rare yet alarming complication that poses a significant threat to vision. It occurs when the long and short ciliary arteries rupture, resulting in the accumulation of blood within the suprachoroidal space [1]. The presence of SCH can result in the forward displacement of the lens-iris diaphragm and aqueous humor accumulation in the posterior chamber, leading to a vicious cycle with extraordinarily high intraocular pressure (IOP) which is challenging to control [2]. In addition to its acute destructive effects, it can lead to cyclodialysis, ciliary body dysfunction, and phthisis bulbi for an extended period [3]. The first case report of SCH in ophthalmic surgery was by Baron de Wetzl in 1760. The term “expulsive hemorrhage” (ECH) was coined by Terson in 1894. Later in 1915, Verhoeff first reported successfully managing a case of ECH [4]. SCH often occurs as a secondary complication following intraocular surgeries such as cataract surgeries, glaucoma filtration procedures, vitrectomy, scleral buckling, and keratoplasty [5]. This can happen either acutely during the surgery or in a delayed manner postoperatively [6]. The most significant risk factor is hypotony or the sudden IOP drop in or after surgery [5], leading to choroidal effusion, stretching, and rupture of ciliary arteries [7]. Stretching of ciliary nerves leads to severe ocular pain [8]. SCH has also been reported following ocular trauma or spontaneously in individuals with specific ocular or systemic risk factors [2, 9]. SCH can be categorized in various ways, including its etiology, the extent of the hemorrhage measured in quadrants, and the degree of elevation. When the elevation of two opposing sides is significant enough to cause contact between the inner retinas, it is called appositional or kissing SCH [10, 11]. We conduct a review of the literature to explore the risk factors, clinical manifestations, and effective management strategies associated with SCH.

The lamina fusca, serving as the posterior boundary of the choroid, is characterized by a thickness of approximately 35 μm. It facilitates a transition from the loosely structured choroidal stroma to the densely woven scleral fibers. This unique layer plays a crucial role in regulating IOP by orchestrating protein flow through the scleral tissue, thereby contributing to the formation of the uveoscleral outflow tract. Lamina fusca is separated from choroid by a potential space known as suprachoroidal space which contains about 10 μL of fluid [12]. When blood or serous fluid accumulates within this space, it can lead to the occurrence of SCH or effusion. The rupture of the long and short ciliary arteries, traversing the suprachoroidal region, is primarily responsible for the onset of SCH. The confined nature of this accumulation prevents its spread through the tightly adhered scleral spur anteriorly and optic nerve posteriorly [13]. The choroid has firm adherence to the sclera at the vortex vein ampullae.

The main pathogenetic mechanism is said to be IOP fluctuations, particularly hypotony. There is development of a high trans-arterial pressure gradient due to sudden hypotony which can lead to rupture of the short or long posterior ciliary artery which causes bleeding in the suprachoroidal space [4, 8]. It can also lead to development of choroidal effusion as the decreased IOP is unable to compensate for the choroidal vessel pressure and leakage. The progressive choroidal effusion leads to overstretching of the ciliary arteries and choroidal vessels with subsequent rupture and bleeding. Long posterior ciliary arteries are more prone to stretching because their connection between the outer choroid and scleral exit is shorter [14]. Severe pain is secondary to overstretching of the ciliary nerves. In rabbit models, pathogenesis of expulsive SCH has been developed. Beyer et al. [15] have suggested four stages of expulsive SCH-choriocapillaris engorgement, serous suprachoroidal effusion mainly in the posterior pole, stretching and tearing of ciliary vessels while the effusion increases, and massive bleeding from torn ciliary vessels leading to SCH and expulsion of intraocular contents. In human autopsy eyes, Wolter and Garfinkel showed ciliochoroidal effusion changing to an ECH in a perforated eye [14]. Other possible mechanisms for SCH are obstruction of venous outflow from vortex veins and direct damage to choroidal vessels [16].

SCH can be classified based on precipitating factors, timing of occurrence with relation to surgery, and size and extent of hemorrhage [4]. SCH classification based on precipitating factors includes spontaneous SCH, surgical SCH, traumatic SCH. SCH occurring during intraoperative surgery is called acute intraoperative SCH and is typically expulsive due to expulsion of intraocular contents through the surgical incisions. SCH occurring postoperatively is called postoperative or delayed SCH which usually occurs in a closed system and is not usually expulsive. Based on size and extent, SCH can either be limited or massive; the latter can be massive enough to cause choroidal and retinal apposition [4]. Wirostko et al. [17] classified SCH based on severity: non-appositional SCH without vitreous or retinal incarceration; central appositional SCH without vitreous or retinal incarceration; SCH with associated vitreous incarceration; and SCH with associated retinal incarceration.

SCH can result from several systemic risk factors, which can cause fragile choroidal or posterior ciliary vasculature or mechanical forces. The most common factors include advanced age, hypertension, arteriosclerosis, increased venous pressure during the Valsalva maneuver, hemodialysis, liver disease, diabetes mellitus, chronic hypercapnia, blood dyscrasia, polycythemia, thrombocytopenia, and antiplatelet and anticoagulant medication use [5, 18‒21].

In addition to systemic risk factors, several ocular risk factors can contribute to the development of SCH. The most important is ocular hypotony. The other risk factors which increase the likelihood of SCH include longer axial length, previous intraocular surgery, vitrectomized eyes, uncontrolled high IOP, aphakia, pseudophakia, prior SCH in the presenting or fellow eye, choroidal lesions, intraocular malignancy, age-related macular degeneration (AMD), hard nucleus cataract surgery, ocular comorbidities such as uveitis or past trauma [5, 22‒24].

Advanced age and uncontrolled hypertension are well-established systemic risk factors for spontaneous SCH due to the fragility of the choroidal or posterior ciliary vasculature and mechanical forces that can tear these delicate vessels in the eye [23, 25, 26]. Valsalva maneuvers such as coughing, straining, etc. can also increase the likelihood of SCH [18, 27].

Several reports of spontaneous cases were predisposed to bleeding because of systemic antithrombotic therapy in subjects treated with warfarin, heparin, thrombolytic agents, or bleeding tendency [2, 22, 23, 25, 28‒34]. Combining systemic antithrombotic agents with the Valsalva maneuver may further increase the risk of spontaneous SCH [2, 23, 28, 35]. This is especially challenging in patients with mechanical valves who cannot be off warfarin and are prone to ocular bleeding [36].

SCH is also associated with new direct oral anticoagulants such as rivaroxaban and dabigatran, which are alternatives to vitamin K antagonists and heparin and used for thromboembolic diseases and stroke prevention in atrial fibrillation patients [37, 38]. COVID-19 infection or vaccination may be associated with SCH, which can be related to microvascular choroidal changes [39, 40].

High myopia is an ocular risk factor for spontaneous SCH secondary to increased choroidal vascular fragility in an eye with more axial length. Retinal detachment (RD) in a high-myopic eye may cause a dramatic decrease in IOP, which may be associated with SCH. Additionally, SCH in eyes with longer axial lengths may be secondary to vortex vein varices [41‒43].

Uveal melanoma may present with spontaneous SCH. The posterior ciliary arteries rupture due to tumor necrosis, leading to massive intraocular hemorrhage, and in cases of SCH without significant risk factors, this possibility should be considered [44]. AMD is a predisposing risk of SCH, especially when using systemic anticoagulants or antiplatelet agents, and it is crucial to warn AMD patients about the predisposing risk of SCH [23].

SCH-related ocular surgeries are classified as “acute intraoperative SCH” or “delayed postoperative SCH.” It is related to IOP changes and is reported in most intraocular surgeries, including keratoplasty, cataract surgeries, glaucoma, and vitreoretinal surgery [6]. Additional factors that may contribute to this condition are congestion of the choroidal vasculature due to retrobulbar or peribulbar anesthesia and the presence of atherosclerotic vessels [45]. The incidence of intraoperative SCH for all surgeries is about 0.29% [46].

SCH has been reported in association with penetrating and lamellar keratoplasty [47, 48]. The risk factors for penetrating keratoplasty include perforated corneal ulcer, large-size graft, therapeutic keratoplasty, and combined surgeries [49].

The incidence of SCH related to endothelial keratoplasty has been estimated to be about 0.05% [50, 51]. Minor fluctuations in IOP observed in Descemet Stripping Automated Endothelial Keratoplasty (DSAEK) and Descemet Membrane Endothelial Keratoplasty (DMEK) have been shown to reduce the risk of SCH compared to open-sky surgical approaches [6, 52, 53]. Table 1 shows various studies of SCH in different types of keratoplasties.

The estimated prevalence of SCH during extracapsular cataract extraction ranges from 0.13 to 4%, while the prevalence during phacoemulsification ranges from 0.013 to 0.5% [46, 61]. Phacoemulsification involves 1–3 mm corneal self-sealing wounds and a closed irrigation-aspiration (I-A) system which has been shown to reduce the incidence of severe hypotony. As a result, cataract surgery by phacoemulsification decreases the risk of SCH and avoids the expansion of SCH to an ECH [8], but sudden IOP fluctuations in poorly constructed wounds can lead to SCH [8]. SCH has also been reported in femtosecond laser-assisted phacoemulsification secondary to multiple attempts at docking leading to sudden hypotony [62].

The independent risk factors contributing to acute intraoperative SCH include a history of glaucoma, increased IOP, and increased intraoperative pulse rate and blood pressure. Elevated episcleral vessel pressure in the carotid cavernous fistula, cataract maturity, posterior capsular rupture, vitreous loss, and recent COVID-19 infection may increase the risk of SCH during operation. There is no confirmation to recommend that anticoagulation is a risk factor for acute SCH in cataract surgeries [8, 40, 63]. Increased retro-orbital pressure after local anesthetic block can cause compression of the vortex veins, leading to impendence of flow, choroidal stasis, and subsequent hemorrhage [8].

Recent data from the Royal College of Ophthalmologists’ National Ophthalmology Database showed that acute intraoperative SCH had an incidence of 0.03%, with risk factors including posterior capsular rupture, raised IOP, glaucoma, and advanced age, especially >90 years. Intracameral anesthetic addition appeared to be protective compared to topical anesthesia alone [64]. Table 2 shows various studies of SCH in different types of cataract surgeries.

High preoperative IOP with sudden decrease makes glaucoma surgeries the most common ocular surgery related to SCH. The incidence of SCH varies from 0.7% to 6.1% in different studies [87‒90]. In tube shunt surgeries, the risk of SCH is twice as trabeculectomy [45]. This difference may be explained by the fact that cases requiring drainage devices have more severe glaucoma with higher IOP, leading to more significant postoperative ocular hypotonia [89, 91, 92]. Using antimetabolites during glaucoma surgery is associated with a higher risk of SCH because it may cause lower IOP [93].

The XEN gel implant represents advancement in minimally invasive glaucoma surgery. This implant is designed to decrease the risk of SCH through its inner diameter, providing an outflow resistance of 6–8 mm Hg. Despite these theoretical benefits, reports of SCH occur in patients who have undergone the minimally invasive glaucoma surgery procedure using the XEN gel implant [94, 95]. Delayed SCH may present following YAG laser goniopuncture [96]. It is also reported after micropulse cyclophotocoagulation diode therapy [97]. Previous cyclodestruction procedures, such as cyclophotocoagulation and cyclocryodestruction, may lead to late-onset hypotony and SCH after the implantation of glaucoma drainage devices [98].

The risk of SCH after glaucoma surgeries in Sturge-Weber syndrome is more than in other cases. Multiple methods have been recommended to reduce this risk, including preoperative IOP management, prophylactic sclerotomy, anterior chamber (AC) formation with viscoelastic devices, and prophylactic laser photocoagulation or radiotherapy to treat choroidal hemangioma [99]. Table 3 shows various studies of SCH in different types of glaucoma surgeries.

During pars plana vitrectomy (PPV) procedures, SCH incidence rates are 0.06–4.3% in various studies [3, 124‒126]. An incidence of 1% is reported in scleral buckling [12].

Factors associated with an increased risk of SCH include longer axial length, aphakic or pseudophakic, surgical treatment of RD, scleral buckling, RD, anticoagulant drug use, and cryotherapy [3, 5, 127]. SCH may be associated with quadrants of RD involvement [128]. Vitrectomized eyes undergoing intraocular surgery are prone to SCH due to the absence of vitreous support and increased susceptibility to IOP fluctuation [3]. In a study by Mo et al. [3], 21.43% had >20/200 visual acuity. They suggested various reasons for good prognosis of SCH associated with PPV such as lower traction in vitrectomised eye leading to localized SCH and lesser chances of RD, reduced chances of postoperative proliferation and subsequent RD, presence of internal perfusion during PPV which can be increased when SCH occurs to reduce hypotony, and more controllable postoperative increase in IOP due to absence of vitreous. SCH associated with PPV is thus more localized and has better visual prognosis. However, massive SCH in PPV has also been reported [129]. Table 4 shows various studies of SCH in vitreoretinal surgeries.

Spontaneous SCH mainly presents with severe unilateral ocular pain and headache, sudden severe vision loss, shallowing of the AC, and dilated and fixed pupil [2, 135]. Intraoperative SCH presents with AC shallowing, hardening of the globe, rapidly progressing black shadow from the back of the eye and absence of red reflex, elevated IOP, posterior capsule stretching, and prolapse of intraocular contents such as the iris, lens/intraocular lens, vitreous, and retina [65, 77]. Delayed onset SCH presents about a week after surgery with complaints of acute loss of vision, severe ocular pain, headache, nausea, and vomiting, with findings of elevated IOP [136].

Intraoperatively, SCH can be seen as a dark-brown convex elevation at the periphery of the retina with visualization of ora serrata and pars plana accompanied by bleeding into the suprachoroidal space. Postoperatively, slit lamp examination can show shallowing of AC, vitreous prolapse into the AC in aphakia and pseudophakia, and loss of red reflex. In clear media, fundus examination shows dark elevated dome-shaped CDs peripherally, at the equator, or even extending posteriorly which do not transilluminate [4]. There may be increase in IOP secondary to angle closure. A diagrammatic representation of development of SCH with progressive shallowing of the AC due to forward movement of the iris-lens diaphragm is depicted in Figure 1.

The diagnosis of SCH is usually clinical, but imaging helps aid in the diagnosis, especially in opaque media with no visualization of the retina. The gold standard for SCH diagnosis is an ultrasound B scan.

Ultrasound B scan serves as the best tool for diagnosis and management of SCH. On B scan, SCH typically shows dome-shaped choroidal detachment with multiple low reflective dot echoes behind the membrane suggestive of hemorrhage, in one or more quadrants, as shown in Figure 2. Corresponding A scan shows a double-peaked high reflective spike, i.e., M spike from the retina and choroid, behind which there are low reflective spikes suggestive of hemorrhage [40, 70]. When the CDs are highly elevated and touching each other, they are known as “kissing choroidals.” SCH needs to be differentiated from serous CDs, which typically are hypoechoic behind the membrane.

Wang et al. used an ultrasound-based system for grading the severity of SCH. In their system, the axial scan with the largest volume of CD was selected to determine the SCH ratio, aka “SH ratio,” which was the vertical distance of the detached choroid divided by the diameter of the equator of the eyeball in the selected B-mode scan image. These were then graded and divided into the following grades.

• • Grade I: SH ratio ≤1:4.

• • Grade II: SH ratio >1:4 to ≤1:2.

• • Grade III: SH ratio >1:2, but no central apposition.

• • Grade IV: Kissing choroidals with central apposition.

Ultrasound is used for monitoring clot lysis or liquefaction. At first evaluation, SCH appears as highly reflective, solid heterogenous mass with irregular internal shape and structure. At subsequent follow-up visits, clot lysis occurs which appears to have lower and less irregular internal reflectivity. Kinetic scans show the movement of fluid hemorrhage within the CD as liquefaction begins. At around 1–2 weeks, complete clot lysis can be expected which is seen on B scan as low reflective mobile dot echoes [4]. This is accompanied by decrease in height of SCH over time. Ultrasound helps decide about second surgical intervention based on clot lysis and reduction in height of SCH [5]. In cases of second surgery, ultrasound helps determine the quadrant of highest CD where drainage should be attempted.

Computed tomography can help identify and differentiate between serous and hemorrhagic CDs. The latter has higher attenuation values compared to serous and serosanguineous CDs [137].

On magnetic resonance imaging, subacute SCH appears as moderately hyperintense image in T1-weighted MR scans and as hypointense in T2-weighted scans. Chronic SCH is seen as hyperintense image in T1- and T2-weighted scans. Serous CDs and choroidal effusion are moderately hyperintense in T1- and T2-weighted scans [138].

Optical coherence tomography (OCT) can be used in cases of limited SCH with the view of the retina. SCH can be seen as a low-to-moderate reflective region between the choroid and sclera in swept-source OCT (SSOCT) images or enhanced depth imaging OCT (EDI-OCT) which have deeper penetration and better visualization of choroidal layers [139]. This space corresponds to the accumulated blood between these layers. OCT imaging may show an increased choroidal thickness compared to the unaffected eye or baseline measurements. In some cases, SCH may result in the accumulation of subretinal fluid. EDI-OCT is an important tool to differentiate SCH from choroidal tumors [27].

Ultrasound biomicroscopy (UBM) can reveal swelling of the ciliary body due to filling by circumferential high-density materials with ciliochoroidal effusion and shallow AC angle [140].

There are no remarkable features in fundus fluorescein angiography (FFA), indocyanine green angiography (ICG), and fundus autofluorescence (FAF). However, they can help in differentiating SCH from other choroidal mass lesions [70].

Choroidal mass lesions are the main differential diagnosis of SCH. Choroidal melanoma is one of the differential diagnoses but is usually painless, with double circulation in FFA and ICG, shaggy photoreceptors on OCT, and low internal reflectivity on ultrasound B scan. Additionally, transillumination demonstrates shadowing in melanoma. Another differential diagnosis is granuloma with early hypo- and late hyperfluorescence in FFA and ICG and low internal reflectivity on ultrasound B scan. Choroidal hemangioma is the other differential with early and late hyperfluorescence and washout pattern in FFA and ICG and high internal reflectivity on B scan. Posterior scleritis may be mistaken for SCH. It also presents with pain. It has zonal hyperfluorescence with pinpoint leakage in FFA and ICG and low internal reflectivity with a characteristic “T sign” on ultrasound [31, 70].

Perioperative prophylactic measures should be taken to prevent the occurrence of SCH. This begins with a complete ocular and systemic examination to rule out any pre-existing risk factors, as mentioned above for SCH. It is preferable to avoid aspirin and other anticoagulants prior to surgery. Proper systemic control of blood pressure, diabetes, and treatment of blood dyscrasias is essential before planning surgery. Preoperative topical phenylephrine drops should be avoided. High IOP should be managed with appropriate medications as increased IOP and sudden globe decompression during surgery play a role in SCH occurrence. Preoperative intravenous hyperosmotic agents such as mannitol or carbonic anhydrase inhibitors can be administered for decreasing the IOP. Valsalva maneuvers such as coughing, straining, vomiting, and compressive devices should be avoided. During the surgery, it is important that the blood pressure and heart rate are maintained at a lower level. In cases of filtering surgeries for glaucoma, it’s preferable to plan for a scleral flap rather than full-thickness procedures to avoid hypotony. Tight wound closure is recommended in all surgeries [4]. Postoperative delayed SCH can be avoided by maintaining normal IOP of the eye at the end of surgery, avoiding marked changes in blood pressure in the postoperative period, avoiding Valsalva maneuvers by prescribing laxatives or emetics, protecting the eye from trauma and eye pressure, and control of inflammation vigorously because inflammation can lead to choroidal effusion and, subsequently, SCH [4].

If acute SCH is suspected intraoperatively, the first step is to immediately tamponade the globe by applying pressure on the globe digitally which helps increase the IOP enough to prevent further bleeding [4]. This can also be achieved by rapid suturing of all incisions. This helps prevent expulsion of intraocular contents. Loosening of the eyelid speculum helps reduce pain and direct globe pressure [4]. Changing position of the patient to reverse Trendelenburg with head end elevated which can help decrease bleeding by reducing the venous and fluid passage to choroidal vessels should be considered [65]. Immediate reduction of IOP with osmotic agents such as intravenous mannitol 20% should be given on-table. It is also important to lower high blood pressure and pain with appropriate medications such as midazolam or sublingual nifedipine [65]. AC should be reformed with either air or saline to prevent prolapse of the vitreous. If there is expulsion of ocular contents, they should be immediately reposted. If that is not possible, then drainage sclerotomies should be made intraoperatively to drain the blood and reduce the IOP. It is better to avoid any further intervention as this can lead to progression in SCH. Delayed SCH drainage is advised in cases where the globe can be successfully closed and left at a normal IOP or to limit degree of increased IOP to reduce the likelihood of rebleeding. A summary of intraoperative management of SCH is shown in Figure 3.

Postoperative management can be conservative or surgical. Limited SCH without retinal or vitreous prolapse or macular involvement can be observed with conservative treatment and serial B scan ultrasounds, and they usually resolve without surgical intervention. Surgical management in the form of drainage sclerotomy with or without combined PPV is planned for uncontrolled elevated IOP with maximum treatment, severe pain, flat AC, presence of RD, appositional SCH, intraocular content prolapses, retinal or vitreous incarceration, macula involvement due to hypoxia of photoreceptor, and prolonged SCH [45, 141].

The main goal of postoperative management is IOP control. This is achieved with topical medications such as aqueous suppressants/β-blockers and oral carbonic anhydrase inhibitors. Topical steroids help reduce concomitant inflammation, and topical cyclopegics help reduce pain [45]. Additional analgesics can also be administered for pain. Antiplatelet drugs such as aspirin and non-steroidal anti-inflammatory drugs (NSAIDs) should be avoided as they can accelerate hemorrhage. Systemic steroids are also found to be beneficial for controlling inflammation and aiding clot lysis [142].

An important part of postoperative management is serial indirect ophthalmoscopy if the media is clear to look for location and progression of SCH. Serial ultrasound B scans are especially important in opaque ocular media, to look for clot lysis in SCH and determine if second surgery is needed. The requirement and appropriate time to take up resurgery should be based on amount of clot lysis which is said to occur in 10–14 days [4].

Secondary surgical management in patients with SCH depends on the extent of SCH and associated complications. Surgical intervention is indicated in cases of kissing choroidal detachment with retinal apposition, massive macula-involving SCH, high and uncontrolled IOP despite maximum medical management, intractable ocular pain, flat AC, lens dislocation, non-resolving vitreous hemorrhage, vitreous incarceration, and RD [4]. It has also been recommended that surgical intervention be considered if more than 2 quadrants posterior to the equator are involved [143].

The main goals of surgery are to drain the SCH while maintaining the IOP, relieve retinal apposition, and prevent forward movement of the iris-lens diaphragm due to SCH which can lead to angle closure [144]. The timing of second surgery is controversial. It is advisable to wait for clot lysis of the SCH confirmed on ultrasound B scan which takes 10–14 days, as attempts to drain before clot lysis may not prove successful [4]. This time allows enough time for the clot to liquefy and flow smoothly. Serial ultrasounds can help monitor clot lysis and identify quadrants with the highest height of SCH. However, in certain cases, such as kissing choroidals with retinal apposition, a longer waiting time might be associated with poorer functional outcomes, and these cases can benefit from earlier intervention. Pakravan et al. [121] performed choroidal tap and AC reformation in 7 eyes immediately after diagnosis of delayed SCH and found that visual acuity showed significant improvement by intervening immediately. Surgical management can be either drainage procedures alone to evacuate the bleed or in combination with vitreoretinal surgery to address the associated problems such as VH, retained lens material, vitreoretinal traction, RD, etc.

Drainage sclerotomies, one or more in number, are usually of 1–2 mm in size and are made 4–10 mm from the limbus in a radial manner in the quadrant of the highest choroidal elevation. The surgery is started by limited or 360-degree conjunctival peritomy, depending on the location of the highest SCH. Recti muscles are isolated to get good exposure of quadrants. Scleral incisions are 2–3 mm in size. It is important to avoid the vortex veins and place the sclerotomies anterior to them. An AC maintainer is recommended to maintain adequate IOP during the surgery [145, 146]. This can also be alternately achieved by placement of pars plana infusion cannula with 6 mm cannula [146]. Gushing of dark red blood is noted after making the scleral incisions [144]. Providing gentle mechanical pressure at the sclerotomy edge can help in the drainage of more SCH. However, small clots which can block the sclerotomy can be removed using either forceps or vitrectomy cutter external to the opening or with a cyclodialysis spatula. The sclerotomies can be left unsutured [4, 5, 56]. In case no more blood is coming out through the sclerotomy, a vitrectomy can be done with a pars plana infusion to clear the vitreous cavity. Boral and Agarwal [67] modified technique of drainage sclerotomies by multiple sclerotomies using 23 G or 25 G cannulas made more posteriorly, 10–15 mm posterior to the limbus, allowing for more posterior passive drainage of SCH. However, it is slower than conventional radial sclerotomies and unable to drain clotted blood.

Another method of drainage is using a transconjunctival trocar cannula system with 23 G or 25 G systems [147, 148]. The trocar entry is made in the quadrant of the highest SCH, ensuring that it does not cause a retinal tear. This is ensured by making the entry at an angle of 15–20° so that the tip of the cannula is in the suprachoroidal space without penetrating the retina [144]. Forceps or vents can help keep the valve open in case of valved trocars. By using a vitreous substitute and increasing the IOP, extrusion of the blood from the cavity occurs, and most of SCH can be evacuated in this manner. These vitreous substitutes can be balanced salt solution, gas, heavy liquid, or even viscoelastic [84, 113]. Active drainage using a needle has also been attempted [149, 150].

Trans-scleral drainage is recommended for uncomplicated SCH and external drainage combined with vitrectomy and silicone oil tamponade for more complex SCH with vitreoretinal involvement [56]. In cases of SCH with associated complications such as VH, RD, vitreous incarceration, vitreoretinal traction, or dislocated cataract, a combined procedure is indicated. In these combined cases, drainage of SCH is done first with simultaneous reformation with saline in AC, usually in aphakic cases or vitreous cavity in phakic or pseudophakic cases. Long 6 mm cannulas are preferred in the pars plana approach to avoid subretinal or suprachoroidal location of the cannula. Perfluorocarbon liquid (PFCL) instillation into the vitreous cavity can help in evacuating more blood through the radial sclerotomies [5]. It acts by sinking to the posterior pole of the eyeball and pushing the blood anteriorly out of the sclerotomies. PFCL is used in this manner to flatten the retina and force vitreous/vitreous debris/retained lens fragments anteriorly [4, 151]. After drainage of SCH as completely as possible, additional vitreoretinal surgery is done to take care of other pathologies. Occasionally, due to massive nature of SCH or recurrent SCh intraoperatively or appearance of subretinal hemorrhage, PFCL alone or PFCL/silicone oil sandwich can be left in the cavity of 2–3 weeks to prevent submacular hemorrhage. After 2–3 weeks, PFCL can be removed and exchanged with silicone oil. Silicone oil has advantages such as its anti-inflammatory properties to preventing proliferative vitreoretinopathy and maintaining of IOP, thus helping to reduce rebleeding [152]. Silicone oil is preferred as tamponade as expansile material during vitrectomy surgeries may increase the risk of SCH related to high systemic intravascular blood pressure levels and ocular hypotony because the nonexpansile tamponades provide more support for vascular bed due to more density than expansile tamponades [153]. Laube et al. [33] did trans-scleral drainage of SCH with PPV and silicone oil tamponade in four eyes of four patients with massive SCH, of which 2 eyes had improvement of vision from light perception to 20/20 and 20/30 [32]. They suggested that a combined approach is necessary to preserve the globe integrity and potential good visual outcomes. They also recommended that surgery should not be delayed more than 2 weeks after SCH onset. Nadarajah et al. [84] proposed a new surgical approach for massive SCH with retinal apposition. In this technique, a 180-degree inferior conjunctival peritomy is done after which all the recti are isolated. Two full-thickness triangular scleral flaps of size 3 × 3 × 3 mm are made at the equator in the inferotemporal and inferonasal quadrants. Via these flaps, partial drainage of SCH can be achieved, followed by 0.3 mL of intravitreal gas injection of 100% perfluoropropane (C3F8). The flaps are left unsutured, but overlying conjunctiva is sutured. With this technique, good visual outcomes were obtained [84].

Even with successful reattachment of the choroid, the retinal function may not completely recover from damage caused by prolonged hemorrhage due to chorioretinal fibrosis and irreversible optic nerve damage secondary to high IOP. As a result, early liquefaction and drainage of clots to decrease the damage have become treatment options in SCH, which can be achieved by applying tissue plasminogen activator (t-PA) into the suprachoroidal space, followed by drainage. This approach has been shown to result in positive visual outcomes [18, 34, 74, 75, 134]. Recombinant t-PA can be directly injected into the suprachoroidal space, avoiding systemic risks. It acts by increasing the plasminogen binding to fibrin clot and aiding in early liquefaction [134]. By aiding in early clot lysis, t-PA can help reduce retinal complications. Subtenon’s urokinase injection can also assist in the same manner [73].

The prognosis of SCH depends on various factors including the timing of presentation, location, severity, and extent of SCH. Limited and localized SCH not involving the posterior pole has better visual prognosis of >6/60. However, expulsive SCH has a grimmer prognosis with a less than 50% chance of vision >6/60 despite appropriate surgical management. Nil perception of light has been reported in 12–57% of the cases despite second intervention [4, 127, 154].

Prognostic factors for bad visual outcomes include preoperative visual acuity, kissing choroidals with longer duration of retinal apposition, vitreous incarceration, 360-degree SCH, and RD at the time of SCH [127, 142, 155]. A recent study of 52 eyes of ECH during cataract surgery showed that eyes with limited ECH had better visual outcomes than those with full-blown ECH [66]. Scott et al. [155] described 51 cases of appositional SCH and found that vitreous incarceration in the wound, concurrent or delayed RD, afferent pupillary defect on presentation, poorer initial VA, and longer duration of central retinal apposition were the factors associated with poor visual outcomes. They also found that eyes which had postoperative SCH had better final VA than eyes which had intraoperative or traumatic SCH [155].

In a meta-analysis conducted by Liu et al. [11] of 68 studies to study the visual and anatomic outcomes of SCH, it was found that 72% achieved a 3-line improvement in ETDRS VA, almost 40% had a final VA of 20/200 or better, and 75.5% achieved anatomic success. Nonspontaneous SCH and eyes receiving systemic steroids had better visual and anatomic outcomes. Eyes that were treated surgically were associated with better VA improvement [11].

Future advances in the management of SCH include the development of advanced imaging techniques, such as wide-field high-resolution OCT, allowing for earlier and more precise detection of hemorrhage. Minimally invasive surgical techniques may also be developed, reducing the invasive current options while effectively managing SCH. Additionally, the utilization of targeted drug delivery systems and novel therapeutic agents could improve treatment outcomes by promoting faster resolution of SCH and reducing associated complications. Uncovering potential predictive markers for SCH with help aid in risk assessment and personalized management strategies. AI-powered imaging analysis and predictive algorithms can be utilized improving early detection and management outcomes for SCH. Systemic anticoagulants inherently carry a potential risk of intraocular bleeding. However, implementing refined strategies for achieving optimal internalized normal ratio control and individualized dosage adjustments under the guidance of a cardiologist can effectively mitigate this risk.

SCH is a rare but potentially sight-threatening complication. Due to its low incidence, maintaining a high level of suspicion is essential for early detection and prompt intervention. SCH can occur spontaneously, as a result of trauma, or in association with various intraocular surgeries, presenting with characteristic signs such as shallow or flat AC, elevated IOP, and prolapse of intraocular contents. The management of SCH involves a multidisciplinary approach, including control of systemic risk factors, IOP control, and potential surgical intervention based on the severity of the condition. In cases where the hemorrhage is small and localized without involvement of the macula, conservative management may lead to resolution. However, certain indications necessitate surgical intervention, such as uncontrolled elevated IOP, severe pain, flat AC, kissing SCH, retinal or vitreous incarceration, presence of RD, and macula involvement. The optimal timing for surgical intervention in SCH remains a topic of debate, but it can be guided by ultrasound evidence of clot lysis. Early surgical intervention may be necessary in cases where there is a significant risk of irreversible visual impairment. In summary, early detection, vigilant monitoring, and appropriate management are crucial in addressing SCH. Through a comprehensive understanding of the condition and timely intervention, the potential blinding consequences can be minimized, improving patient outcomes.

J.C.: Allergan, Salutaris, and Biogen. All the other authors have no conflicts of interest to declare.

We confirm that no funding was received for the execution of this manuscript.

Sashwanthi Mohan, Elham Sadeghi, and Madhuvanthi Mohan: acquisition, analysis and interpretation, drafting, final approval of work, and accountable for all aspects of the work. Danilo Iannetta: analysis and interpretation, revising and critical review, final approval of work, and accountable for all aspects of the work. Jay Chhablani: conception and design, revising and critical review, final approval of work, and accountable for all aspects of the work.

Sashwanthi Mohan and Elham Sadeghi contributed equally to this work.