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Retina & Vitreous

Suprachoroidal Hemorrhage

Suprachoroidal hemorrhage (SCH) is a condition in which the long and short posterior ciliary arteries rupture, causing blood to accumulate in the potential space between the choroid and sclera (the suprachoroidal space)1). The accumulated blood clot pushes the intraocular contents forward, leading to severe effects on intraocular structures.

The incidence during cataract surgery is reported to be approximately 0.03–0.1%3). It can occur more frequently during glaucoma surgery than during cataract surgery1). Delayed SCH after Xen45 microstent implantation has also been reported1), and attention is increasing with the spread of minimally invasive glaucoma surgery (MIGS).

Spontaneous cases also exist. Honzawa et al. (2024) reported a case of spontaneous expulsive SCH in a 50-year-old man with severe hypertension (blood pressure 228/124 mmHg) and intraocular pressure of 70 mmHg, in a cumulative report of 55 cases of spontaneous SCH2). Spontaneous cases occur without a history of ophthalmic surgery, so caution is needed in diagnosis.

Acute Expulsive

Timing of onset: During ophthalmic surgery (when the wound is open)

Mechanism: Sudden drop in intraocular pressure → vascular rupture

Features: Rapid progression of anterior chamber loss, loss of red reflex, and iris prolapse. Can lead to devastating visual impairment.

Delayed-onset

Timing: Days to weeks after surgery

Mechanism: Persistent low intraocular pressure → chronic stress on vessel walls

Features: More common after Xen45 implantation or trabeculectomy. Often noticed due to eye pain and elevated intraocular pressure1)

Spontaneous

Timing: No history of surgery

Mechanism: Severe hypertension, vascular fragility

Features: Rare. Occurs as part of hypertensive eye disease. A cumulative report of 55 cases exists2)

The incidence by main surgical procedure is shown below.

ProcedureIncidenceNotes
Cataract surgery0.03–0.1%Rare3)
TrabeculectomyHigher than cataractCases after Xen reported1)
Spontaneous onsetRareReported in severe hypertension cases2)
Q Does suprachoroidal hemorrhage only occur during surgery?
A

Suprachoroidal hemorrhage occurs not only during surgery (acute expulsive) but also as delayed onset days to weeks after surgery, and spontaneous cases without prior surgery have been reported1, 2). In particular, delayed SCH after trabeculectomy or Xen45 implantation is easy to overlook, so attention should be paid to postoperative eye pain and elevated intraocular pressure.

The subjective symptoms of SCH vary depending on the mode of onset.

  • Sudden eye pain: In acute expulsive cases, it appears suddenly during surgery. In spontaneous cases, severe eye pain can be the initial symptom2)
  • Rapid vision loss and visual field defects: Caused by compression of intraocular structures by the blood clot
  • Headache and nausea: Systemic symptoms associated with high intraocular pressure or vagal reflex
  • Shallow or flat anterior chamber: Forward displacement of intraocular contents due to blood clot
  • Loss of red reflex: Fundus reflex is no longer obtainable
  • Prolapse of iris and intraocular contents: Extrusion through the open wound; immediate cessation of surgery is required
  • Sudden rise in intraocular pressure: Elevated intraocular pressure due to hemorrhage
  • Elevated intraocular pressure: Reported to reach 70 mmHg in spontaneous cases2)
  • Hard eye: Firm consistency even on palpation
  • Shallow or flat anterior chamber: Due to compression by blood clot
  • Kissing choroidal detachment: Apposition of contralateral choroidal elevations in the center4)
Q If the eye suddenly becomes painful after surgery, should suprachoroidal hemorrhage be suspected?
A

Acute ocular pain and elevated intraocular pressure after trabeculectomy or Xen45 implantation may indicate delayed SCH1). Perform B-mode ultrasonography to confirm hemorrhagic choroidal elevation. For details, see the Diagnosis and Examination Methods section.

The risk of SCH increases when multiple risk factors are present.

  • Advanced age: Weakening of blood vessel walls and progression of arteriosclerosis2, 3)
  • Hypertension: Chronic stress on blood vessel walls. In spontaneous cases, blood pressure of 228/124 mmHg has been reported2)
  • Diabetes mellitus (DM): Increased fragility due to vascular lesions3)
  • Anticoagulants and antiplatelet drugs: Increase the risk of intraoperative bleeding
  • Glaucoma: Exposure to low intraocular pressure and vulnerability of choroidal blood flow3)
  • Long axial length (axial myopia): Stretching of the choroid makes blood vessels fragile3)
  • Aphakia or history of vitrectomy: Loss of intraocular structural support
  • Preoperative high intraocular pressure: Greater intraocular pressure drop during surgery
  • Rapid decrease in intraocular pressure: A sudden drop in intraocular pressure at the open wound is the greatest trigger
  • Prolonged surgery time: Long-term stress on blood vessels
  • Intraoperative hypotension: Local ischemia due to systemic circulatory failure

The classification of risk factors is shown below.

CategoryMain risk factorsEvidence
SystemicHypertension, diabetes mellitus, advanced ageReports 2)3)
Ocular localGlaucoma, long axial lengthReport 3)
IntraoperativeRapid intraocular pressure dropCommon knowledge

This is the central examination method for diagnosing SCH.

  • Acute phase findings: High-intensity, homogeneous suprachoroidal elevation. Blood is liquid and shows uniform brightness.
  • Subacute phase (7–14 days): Formation of a blood clot results in a heterogeneous hyperechoic image. This phase is the appropriate timing for drainage 3, 4)
  • Confirmation of contact: It is important to confirm the “kissing” type, where the contralateral choroidal elevations touch in the center 4)
  • Follow-up: Useful for evaluating liquefaction and absorption of the blood clot. Essential for determining the timing of drainage

It is necessary to differentiate SCH from diseases that may be confused with it.

DiseaseUltrasound FindingsKey Differentiating Points
Choroidal effusionHypoechoic, homogeneousNo hemorrhage, mobile
Rhegmatogenous retinal detachmentThin membrane-like elevationConfirmation of retinal break
Choroidal tumorHeterogeneous, solidEnlarging tendency, blood flow present
  • Fundus examination: Evaluates the extent of bleeding and impact on the retina. However, in severe cases, visualization may be difficult.
  • Intraocular pressure measurement: Important for follow-up monitoring.
  • Anterior chamber depth assessment: Confirmation of shallow anterior chamber using slit-lamp microscopy.

Intraoperative Management (Acute Expulsive SCH)

Section titled “Intraoperative Management (Acute Expulsive SCH)”

If SCH is suspected during surgery, the following steps should be taken.

  • Immediate wound closure: Quickly close the open wound to restore intraocular pressure.
  • Posterior sclerotomy: Consider performing to decompress intraocular pressure depending on the situation.
  • Surgery interruption: Stabilize intraocular structures before deciding on further management.

For mild to moderate SCH, conservative management is performed.

  • Systemic steroids: Suppress inflammation and reduce exudation1, 2)
  • Mydriatics (cycloplegics): Relieve ciliary spasm and manage inflammation1, 2)
  • Intraocular pressure management: Use eye drops or oral medications for high intraocular pressure.
  • Rest and observation: Wait for the blood clot to liquefy (usually 7–14 days)

If conservative treatment does not improve, or in cases of kissing SCH, surgical drainage is performed.

Drainage via posterior sclerotomy. Blood is drained through the incision, but the procedure is complex and carries a risk of secondary complications.

A minimally invasive drainage method using a trocar reported by Pericak et al. (2022)4).

A method was reported in which a 23G trocar is inserted into the suprachoroidal space via an inferotemporal approach, and blood is drained while maintaining an intraocular perfusion pressure of 60 mmHg4). The inferotemporal region is anatomically favorable for avoiding large vessels and is considered a safe access site.

  • Approach site: Inferotemporal is optimal4)
  • Intraocular pressure management: Maintaining a perfusion pressure of 60 mmHg is recommended4)
  • Advantages: Simple procedure and easy control of bleeding

Injection of tPA has been reported to be effective in dissolving clotted blood3).

A systematic review by Ribeiro et al. (2024) organized multiple treatment methods for perioperative SCH, including conservative management, sclerotomy drainage, and vitrectomy3). The timing of intervention is determined based on the coagulation state of the hemorrhage and the presence of retinal contact.

Conventional drainage

Method: Drain blood through posterior sclerotomy

Indication: After clot liquefaction (7–14 days later)

Challenges: Complexity of procedure and risk of secondary complications

Trocar Method (23G)

Method: Minimally invasive access with a 23G trocar

Site: Inferotemporal quadrant is optimal4)

Perfusion pressure: Safe drainage maintained at 60 mmHg4)

tPA-Assisted Drainage

Method: Liquefy the clot with tPA before drainage

Advantage: Can handle even hard clots

Evidence: Reported in cases of SCH after cataract surgery3)

When performing tamponade in cases requiring vitrectomy, air tamponade has been reported to carry a risk of postoperative rebleeding, so materials with long-term tamponade effect such as silicone oil may be considered4).

Q When is it appropriate to perform drainage of suprachoroidal hemorrhage?
A

In principle, drainage is performed after confirming liquefaction of the clot by B-mode ultrasound, usually around 7–14 days after onset 3, 4). If performed too early, the clot is difficult to expel and the risk of rebleeding is high. In cases of kissing choroidals or persistent high intraocular pressure, earlier intervention may be necessary.

6. Pathophysiology and Detailed Mechanism of Onset

Section titled “6. Pathophysiology and Detailed Mechanism of Onset”

The central mechanism of SCH is a combination of intraocular pressure reduction and vascular wall fragility.

When intraocular pressure drops rapidly, the transmural pressure on choroidal vessels increases. In normal eyes, the lumen of the ciliary arteries is moderately compressed by intraocular pressure, but when intraocular pressure falls sharply, the outward pressure on the vessel wall increases, causing fragile posterior ciliary arteries to rupture 1).

In some cases, choroidal effusion precedes hemorrhage 2). It is thought that the effusion expands the suprachoroidal space, increasing traction on blood vessels and leading to hemorrhage. Pathophysiological analysis of spontaneous cases suggests the importance of this mechanism.

A report by Pham et al. (2023) showed that some cases of SCH after Xen45 implantation do not have clear hypotony immediately after surgery 1). In this type, vascular wall fragility and local inflammatory reaction are considered the main causes, suggesting that hypotony alone may not explain all cases of SCH.

The suprachoroidal space is normally a closed potential space, extending from the ciliary body to the vortex veins. When hemorrhage occurs here, the clot expands rapidly, compressing the retina, vitreous, and lens system anteriorly. In eyes with long axial length, the suprachoroidal space is wide, and blood tends to accumulate extensively.


SCH after MIGS and Minimally Invasive Management

Section titled “SCH after MIGS and Minimally Invasive Management”

With the spread of MIGS, reports of SCH after minimally invasive glaucoma surgery such as the Xen45 microstent have been accumulating.

Pham et al. (2023) reported delayed-onset SCH after Xen45 implantation 1). Even with MIGS, severe hemorrhagic complications can rarely occur, so careful observation for postoperative hypotony and eye pain is necessary.

The minimally invasive drainage method using a 23G trocar has been reported as a promising approach, but the number of cases is still limited.

Pericak et al. (2022) achieved safe drainage using a 23G trocar via an inferotemporal approach while maintaining a perfusion pressure of 60 mmHg 4). If standardized, it may become widely adopted as a minimally invasive alternative to conventional posterior sclerotomy.

Ribeiro et al. (2024) summarized the need to select a surgical technique based on a comprehensive assessment of clot status, retinal contact, and presence of vitreous hemorrhage in the surgical management of SCH 3). Establishing treatment selection criteria according to clot characteristics is a future challenge.

Q How will the treatment of suprachoroidal hemorrhage change in the future?
A

The combination of minimally invasive drainage using the trocar method (23G) and tPA clot lysis is attracting attention 3, 4). Additionally, developing management guidelines for delayed-onset SCH associated with the spread of MIGS is also a challenge 1). These are still in the research stage, and further accumulation of evidence is needed for establishment as standard treatment.


  1. Pham AH, Junk AK. Delayed suprachoroidal hemorrhage after Xen45 gel stent. J Glaucoma. 2023;32(4):e33-e35. doi:10.1097/IJG.0000000000002181. PMID: 36795516.
  2. Honzawa Y, Inoue T, Ikeda Y, et al. Spontaneous expulsive suprachoroidal hemorrhage in a hypertensive patient. Am J Ophthalmol Case Rep. 2024;34:102059.
  3. Ribeiro M, Monteiro DM, Moleiro AF, et al. Perioperative suprachoroidal hemorrhage and its surgical management: a systematic review. Int J Retina Vitreous. 2024;10:55. doi:10.1186/s40942-024-00577-x. PMID: 39169423.
  4. Pericak O, Chin EK, Almeida DRP. Trocar-based surgical approach to suprachoroidal hemorrhage drainage. J Vitreoretin Dis. 2022;6(6):501-503. doi:10.1177/24741264211057674. PMID: 37009544.

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