Pretutorial
    Assessment

Tutorial
Introduction
Incidence
Causes
Pathogenesis
Clinical Manifestations
Differential Diagnosis
Management
References

Slides

Suprachoroidal Hemorrhage and Effusion

Luis W. Lu, MD, FACS

Introduction

Intraoperative suprachoroidal hemorrhage and the consequential expulsive hemorrhage that can occur constitute the most serious complication in ocular surgery. The conversion to phacoemulsification has decreased the occurrence of this condition. Predisposing risk factors for a suprachoroidal hemorrhage and effusion include:

• Advanced age
• Arterial hypertension
• Arteriosclerosis
• Polycytemia
• Diabetes
• Glaucoma
• Increased intraocular pressure (IOP)
• High myopia
• Intraoperative vitreous loss
• Sudden ocular decompression
• Elevated intraoperative pulse rate
• Vascular fragility
• Choroidal congestion
• Necrosis of intraocular arterioles
• Vascular sclerosis
• Previous suprachoroidal hemorrhage
• Prolonged intraocular hypotony
• Scleral manipulation in eyes that have undergone a second surgery
• Extensive use of cryotherapy and photocoagulation with the trans scleral mode

Incidence

Fortunately, the incidence of this severe complication, which in many cases causes total loss of visual function in the affected eye, is relatively low and varies between 0.05% and 0.4% according to statistics from different authors.¹ It has been said that every ocular surgeon will face this serious complication at least once in his or her career.

The incidence of limited acute intraoperative suprachoroidal hemorrhage (AISH) has been reported to be 1.2% in planned extracapsular cataract extraction (ECCE) by nucleus expression and 0.81% in phacoemulsification procedures using an iris plane superior nuclear pole prolapse technique.²

Massive suprachoroidal hemorrhage (MSH), cases in which more than 50% of the vitreous cavity is occupied by the bleeding, occurs in 1.9% of intraocular surgeries.³

Causes

Expulsive hemorrhage is due to two principal causes, the choroidal hemorrhage and the massive choroidal effusion. In both cases, there is a rapid collection of blood and/or fluid in the suprachoroidal space, which consequently increases the IOP. If the problem cannot be controlled in a timely manner, it can lead to the total expulsion of the intraocular contents through the operative wound, unless the incision is promptly closed.

With improvements in wound architecture, most small incisions are now self-sealing. This improved wound design and newer phacoemulsification techniques have contributed to the decreased incidence of suprachoroidal hemorrhage. Total expulsion of the intraocular contents has not been reported in the presence of a well-constructed, small, self-sealing incision.

Ocular trauma is the most frequent cause (35%) of massive suprachoroidal hemorrhage, followed by cataract surgery (30%), glaucoma surgery (17%), penetrating keratoplasty (6%), pars plana vitrectomy (3%), secondary IOL surgery (3%) and other etiologies (4%).⁴

Some factors increase the risk of suprachoroidal hemorrhage, the most important of which is high myopia with axial length greater than 25 mm. In those eyes, scleral rigidity is decreased, and choroidal vascular fragility is increased. Of all patients with massive suprachoroidal hemorrhage, 52% are myopes.⁵

Pathogenesis

A choroidal hemorrhage generally begins from the short posterior ciliary arteries at the point at which they penetrate the globe through the sclera surrounding the optic nerve. Histopathologic studies reveal that in many cases, the cause of the hemorrhage is the rupture of necrotic areas in the wall of the vessels.⁶ With regard to this, it is useful to remember some physiopathologic details related to choroidal vessels. First, these arteries and arterioles share characteristics with those of the spleen, with the frequent showing of hyaline enlargement and sclerosis of the middle layer in the absence of general vascular illness. Unlike other blood vessels that support a low external pressure, the intraocular vessels (both choroidal and retinal) are subjected to IOP, which can be approximately 20 mm Hg, or even higher in cases of glaucoma. These conditions can even cause vascular collapse, especially at the level of the arterioles where the intravascular pressure drops considerably.

The direct result of this phenomenon is a sluggish circulation at this vascular level, reducing the blood supply to the vascular walls. In addition, the choroidal arterioles do not have vasa vasorum and rely exclusively on diffusion for their nutrition.⁷

If we accept the mechanism of alteration of the wall of the choroidal vessels as a predisposing factor in choroidal hemorrhage, any patient with circulatory impairment could be prediposed to this complication. Risk factors include arterial hypertension, glaucoma, general arteriolosclerosis, high myopia, vascular fragility, and diabetes. The risk factors identified and reported in a 1986 study of ECCE cases included advanced age, the presence of glaucoma with an axial length greater than 25 mm, and manual, large incision ECCE. One case-control study of risk factors for intraoperative suprachoroidal expulsive hemorrhage identified age, glaucoma, increased IOP, increased axial length, and elevated intraoperative pulse as risk factors.³ If a patient developed a choroidal hemorrhage in the first operated eye, the second eye is at higher risk for developing this same complication.

Another cause of an expulsive event is a massive choroidal effusion, as first described by Girard.⁸ This idiopathic entity is characterized by a rapid collection of clear liquid in the suprachoroidal space, which can cause the same serious expulsive consequences as a choroidal hemorrhage.

In the presence of predisposing risk factors, certain circumstances can provoke the occurrence of an expulsive hemorrhage. Such factors include inadequate local or general anesthesia and a sudden ocular decompression during cataract surgery.

Clinical Manifestations

A suprachoroidal hemorrhage usually occurs during the actual surgical procedure, while the operative wound is open. However, this complication has also been reported hours to days after a cataract extraction. In its intraoperative presentation, the eye becomes firm and the patient usually complains of severe pain. The sudden onset of pain has been called the hallmark of suprachoroidal hemorrhage. If the wound opens, the iris prolapses and if the lens will extrude spontaneously. This may be followed by vitreous, blood, and the remainder of the ocular contents. Sometimes, the onset is more gradual; beginning with a decrease of the red reflex and followed by the appearance of an opaque mass in the vitreous space. As the mass expands in size, it is accompanied by obvious signs of increased IOP (Slides 1 through 6).

SLIDE 1	SLIDE 2	SLIDE 3
SLIDE 4	SLIDE 5	SLIDE 6

Davison defined intraoperative suprachoroidal hemorrhage during extracapsular cataract surgery using the following intraoperative criteria: a progressive shallowing of the anterior segment; a globe that becomes firm to tactile pressure; and confirmation of a dark, bulging suprachoroidal by indirect ophthalmoscopy.²

It should be emphasized that the clinical picture, the behavior of the eye, and the outcome of this complication can differ dramatically, depending upon whether surgery is performed through a large or small incision. With phacomemulsification, maintenance of a closed chamber is primarily responsible for the decreased incidence of suprachoroidal hemorrhage. In contrast, a larger ECCE incision permits the intraocular contents to be expulsed with relative ease as a result of posterior volumes. When an expulsive hemorrhage appears during a planned ECCE, there may be insufficient time to close the wound. In contrast, if a posterior mass effect occurs during phaco, the internal lip of the self-sealing incision will close, causing the IOP to rise. Increased IOP in the presence of a small incision can tamponade the intraocular bleeding and prevent escape of intraocular contents.

Differential Diagnosis

The differential diagnosis of sudden intraoperative anterior chamber shallowing with elevated IOP is difficult, and often confronted under duress. Potential causes depend on the type of surgery and the patient’s predisposing factors.

Intraoperative aqueous misdirection syndrome or posterior misdirection of irrigating fluid is usually associated with short eyes.⁹ The tendency for eyes with short axial lengths to develop uveal effusion syndrome is also well known and thought to be the result of an abnormally thick sclera. A sudden decrease in IOP or the development of intraocular inflammation may predispose such an eye to a relative or absolute vortex vein obstruction. Another possible cause of increased intraoperative IOP is a retrobulbar hemorrhage following a retrobulbar or peribulbar anesthetic injection.

Management

Unfortunately, it is difficult to predict when this severe surgical complication will occur. Therefore, it is important for surgeons to be aware of the predisposing factors.

Patients with arterial hypertension, generalized arteriolosclerosis, glaucoma, high myopia, vascular fragility, coagulation problems, or diabetes must be considered at high risk for a suprachoroidal hemorrhage. If necessary, these patients can be referred to a general practitioner to stabilize their condition prior to the elective surgical procedure.

Such risk factors would indicate surgery through a small, self-sealing incision. However, suprachoroidal hemorrhage has even been reported in children and young adults in the absence of risk factors. Obviously, there are some other unknown causative factors.¹⁰ 

If a shadow appears during surgery, raising the suspicion of a choroidal effusion or hemorrhage, immediate closure of the eye is critical. Closure of the surgical wound stops the bleeding. It is not advisable to perform an emergency drainage sclerotomy as this procedure induces transit ocular hypotony, increasing the risk of rebleeding. The choroidal manipulation necessary to perform a sclerotomy may result in the rupture of other choroidal vessels and the sudden egress of choroidal blood in presence of high IOP may produce retinal incarceration at the sclerotomy site. Also, the clotted blood cannot exit through the sclerostomy. If the pressure is severely elevated, intravenous (IV) acetazolamide 500 mg is given. Parenteral acetazolamide starts working within 5 to 10 minutes with duration of action of 2 hours. Mannitol 20% (0.5 to 2 g/kg) can also be administered intravenously for severe cases but the onset of action takes 30 to 60 minutes and lasts approximately 6 hours.

The following management is suggested:

1. If a sudden intraoperative increase of IOP occurs, the surgeon should examine the fundus with an ophthalmoscope. If no choroidal effusion or hemorrhage is found, a diagnosis of infusion misdirection syndrome is more likely. Conservative treatment with IV acetazolamide, IV mannitol, and cycloplegic drops usually alleviates the situation within 30 minutes. Phacoemulsification can then be completed following this precautionary delay.¹¹
2. 
   
   SLIDE 7
   If a diagnosis of choroidal effusion and hemorrhage is considered, closing the incision and assessing the clinical situation are mandatory. Use of IV acetazolamide and topical steroids is indicated postoperatively. A B scan ultrasound should be performed. If a suprachoroidal hemorrhage is present on B scan, it is advisable to wait 11 to 14 days or the necessary time to allow the hemorrhage to be reabsorbed. The cataract extraction and IOL insertion can be completed after complete resorption of the clot. Simultaneous drainage of the hemorrhage may be required due to persistent anterior chamber shallowing or the belief that the macula is involved. Some delay in performing secondary surgery may be recommended to decrease the risk of recurrent bleeding (Slide 7).
3. The surgical management will differ when the choroidal hemorrhage is considered to be sectorial or massive. In presence of a sectorial hemorrhage, medical control of the IOP and inflammation are indicated until the choroidal detachment is resolved, except in cases when there is vitreous incarceration in the wound, retained lens fragments, vitreous hemorrhage or a retinal detachment.
4. In the interim, oral steroids (1 mg/kg per day) are continued until the surgeon tries to complete the previous surgical procedure under general anesthesia (some prefer local anesthesia), consider simultaneous drainage of the suprachoroidal hemorrhage if a shallow anterior chamber persists, or drain the hemorrhage first, and later perform a pars plana vitrectomy and lensectomy under general anesthesia with a posterior chamber intraocular lens placed in the sulcus.

If infusion misdirection syndrome (negative ultrasound) is the cause, it usually resolves spontaneously and the phacoemulsification procedure can be completed by the following day.

Most patients have poor outcomes if a massive suprachoroidal hemorrhage is left untreated, as they may develop retinal detachment, proliferative vitreoretinopathy, neovascular glaucoma, and phthisis bulbi. ^12-15

References

1. Jaffe NS. Expulsive hemorrhage. In: Welsh RC, Welsh J, eds. The Second Report in Cataract Surgery. Miami, Fla: Educational Press; 1971:119-121.
2. Davison JA. Acute intraoperative suprachoroidal hemorrhage in capsular bag phacoemulsification. J Cataract Refract Surg. 1993;19:534-537.
3. Speaker MG, Guerriero PN, Met JA, et al. A case-control study of risks factors for intraoperative suprachoroidal expulsive hemorrhage. Ophthalmology. 1991;98:202-210.
4. Reynolds MG, Haimovici R, Flynn HW Jr, et al. Suprachoroidal hemorrhage: Clinical features and results of secondary surgical management. Ophthalmology. 1993;100:460-465.
5. Srinivasan M. Expulsive choroidal haemorrhage. Indian J Ophthalmol. 1992;40:100-102.
6. Manschot WA. The pathology of expulsive hemorrhage. Am J Ophthalmol. 1955;40:15-24.
7. Muller H. Expulsive hemorrhage. Trans Ophthalmol Soc UK. 1959;79:621-634.
8. Girard LJ. Expulsive hemorrhage during cataract surgery. Emergency treatment in five cases. In: Paton D, ed. Current Concepts in Cataract Surgery. Proceedings of the Third Biennial Cataract Congress. St. Louis, Mo: Mosby; 1974:612.
9. Mackool R. Infusion misdirection syndrome. J Cataract Refract Surg. 1994;20:9.
10. Pereira G, Lu LW. Phacoemulsification in patients with high risk of choroidal hemorrhage. In: Lu LW, Fine IH, eds. Phacoemulsification In Difficult and Challenging Cases. New York, NY: Thieme; 1999:173-176.
11. Rhee DJ, Pyfer MF. Malignant glaucoma. In: Rhee DJ, Pyfer MF, eds. The Wills Eye Manual, 3rd ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 1999:266-268.
12. Welch JC, Spaeth GL, Benson WE. Massive suprachoroidal hemorrhage: Follow up and outcome of 30 cases. Ophthalmology. 1988;95:1202-1206.
13. Lakhanpal V, Schoket SS, Elman MJ, Nirankari VS. A new modified vitreoretinal surgical approach in the management of massive suprachoroidal hemorrhage. Ophthalmology. 1989;96:793-800.
14. Gressel MG, Parrish RK II, Heuer DK. Delayed nonexpulsive suprachoroidal hemorrhage. Arch Ophthalmol. 1984;102:1757-1760.
15. Spaeth G, Baez K. Long term prognosis of eyes having had operative suprachoroidal expulsive hemorrhage. Ger J Ophthalmol. 1994;3:159-163.

Acknowledgment
Special thanks to Luis Izquierdo Jr., MD, for providing a case for the tutorial.