Open-Eye Injury

Theresa T. Kudlak

A. Medical Disease and Differential Diagnosis

Why is this patient a particular challenge to the anesthesiologist?
What are the determinants of intraocular pressure (IOP) under normal circumstances? What is the normal range? What was the expected IOP in this patient’s injured eye?
How is aqueous humor formed and eliminated?
How is IOP affected by arterial PCO₂, systemic blood pressure, coughing and vomiting, deep inspiration, and hypoxemia?
What is the role of the central nervous system (CNS) on IOP?
What is glaucoma?
Is atropine contraindicated in patients with glaucoma?
How do carbonic anhydrase inhibitors work to decrease IOP? By what mechanism may osmotic agents decrease IOP?
Are carbonic anhydrase inhibitors or osmotic diuretics indicated in open-globe injuries?
Are topically applied ophthalmic medications absorbed systemically? How can this absorption be reduced? Which eyedrops may have effects that are of concern to the anesthesiologist?

B. Preoperative Evaluation and Preparation

Is an open-globe injury always a surgical emergency?
What preoperative evaluation would you require?
The patient ate shortly before the accident. Would you attempt to pass a nasogastric tube or to administer emetics to empty the stomach?
Could this case be done with topical anesthesia or a retrobulbar block?
How would you premedicate this patient?

C. Intraoperative Management

What are some factors that may increase the risk of vitreous herniation during induction and maintenance of anesthesia?
Will you intubate this patient? Would you consider a laryngeal mask airway? How does intubation affect IOP? How can this effect be minimized?
Would you consider an awake intubation?
Is succinylcholine contraindicated in open-globe injuries? How does succinylcholine affect IOP?
Does pretreatment with nondepolarizing muscle relaxants prevent the succinylcholine-induced elevation in IOP?
How do nondepolarizing muscle relaxants affect IOP?
How will you perform a rapid sequence induction and intubation without using succinylcholine?
What are the effects of ketamine on the eye?
Would you consider the use of etomidate as an induction agent? What about propofol?
How do inhalation agents affect IOP and by what mechanism?
During the procedure, the patient’s pulse suddenly dropped to 40 beats per minute. What do you think was happening? What is the oculocardiac reflex (OCR)?
What are the afferent and efferent pathways of the OCR?
What factors contribute to the incidence of the OCR?
How do you diagnose and treat the OCR?
Is atropine useful for the OCR?
Can a retrobulbar block prevent the OCR? Is it appropriate in this patient?

D. Postoperative Management

Would you reverse the neuromuscular blockade in this patient?
Do reversal doses of atropine affect IOP?
What would you do before extubating this patient?
When would you extubate this patient?
The patient awakened in the recovery room and complained of pain and tearing in the opposite eye. The conjunctiva was inflamed. What was the likely cause?
Will taping the eyes shut or applying ointment prevent corneal abrasions? Are there any contributing factors?
What should you do when you suspect your patient might have a corneal abrasion?
A month after the surgical repair, the patient complained of impaired vision in the operative eye. He was examined and found to have a detached retina. As part of the surgical treatment, the ophthalmologist injected a gas bubble into the patient’s posterior chamber. Why is this important to an anesthesiologist?

A. Medical Disease and Differential Diagnosis

A.1. Why is this patient a particular challenge to the anesthesiologist?

The combination of a full stomach and an open-globe injury presents a unique challenge to the anesthesiologist. In addition to the increased risk of aspiration of gastric contents, any drug or maneuver that raises IOP in the injured, open eye may cause extrusion of the vitreous humor and loss of vision when the globe is opened.

Cunningham AJ, Barry P. Intraocular pressure—physiology and implications for anaesthetic management. Can Anaesth Soc J. 1986;33:195-208.

Holloway KB. Control of the eye during general anaesthesia for intraocular surgery. Br J Anaesth. 1980;52:671-679.

Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2521.

A.2. What are the determinants of intraocular pressure (IOP) under normal circumstances? What is the normal range? What was the expected IOP in this patient’s injured eye?

IOP is determined by the balance between production and drainage of aqueous humor, by changes in choroidal blood volume, and by vitreous volume and extraocular muscle tone. Resistance to outflow of aqueous humor in the trabecular tissue is probably the factor that maintains IOP within physiologic range, but the mechanism of homeostasis is unknown.

Normal IOP is 12 to 16 torr in the upright posture and increases by 2 to 4 torr in the supine position. IOP has been observed to nearly double in steep head-down position in the operating room.

When the globe is open, the IOP is lowered and may be as low as ambient pressure. The concern in this case is for the relative volume of choroid and vitreous humor within the eye. If this volume increases while the eye is open, the vitreous humor may be lost. Any deformation of the eye by external pressure in the globe may cause an increase in IOP.

Cunningham AJ, Barry P. Intraocular pressure—physiology and implications for anaesthetic management. Can Anaesth Soc J. 1986;33:195-208.

Jay JL. Functional organization of the human eye. Br J Anaesth. 1980;52:649-654.

Kohli R, Ramsingh H, Makkad B. The anesthetic management of ocular trauma. Int Anesthesiol Clin. 2007;45:83-98.

Kumar C, Dodds C, Fanning G, eds. Ophthalmic Anaesthesia. Lisse, The Netherlands: Swets & Zeitlinger BV; 2002:23-25.

LeMay M. Aspects of measurement in ophthalmology. Br J Anaesth. 1980;52:655-662.

Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2513-2514.

A.3. How is aqueous humor formed and eliminated?

Aqueous humor is a clear fluid that occupies the anterior and posterior chambers of the eye. Its total volume is 0.3 mL. Aqueous humor is produced primarily by an active secretory process from the ciliary body in the posterior chambers at an equilibrium rate of 2 µL per minute. The aqueous humor then circulates through the pupil to the anterior chamber, passes through the trabeculated Fontana spaces, and enters Schlemm canal. From here, the fluid drains into the episcleral veins and finally into the cavernous sinus or jugular venous systems (Fig. 34.1).

Cunningham AJ, Barry P. Intraocular pressure—physiology and implications for anaesthetic management. Can Anaesth Soc J. 1986;33:195-208.

Jay JL. Functional organization of the human eye. Br J Anaesth. 1980;52:649-654.

LeMay M. Aspects of measurement in ophthalmology. Br J Anaesth. 1980;52:655-662.

McGoldrick K, ed. Anesthesia for Ophthalmic and Otolaryngologic Surgery. Philadelphia, PA: WB Saunders; 1992:180-182.

Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2513-2514.

A.4. How is IOP affected by arterial PCO₂, systemic blood pressure, coughing and vomiting, deep inspiration, and hypoxemia?

The choroidal arterioles vasodilate in response to hypercapnia and constrict during hypocapnia, thereby changing intraocular volume and pressure. However, the effect is minimal within the normal physiologic range of PCO₂.

Minor fluctuations in arterial blood pressure also have minimal effects on IOP, although IOP may be seen to increase when hypertension is sustained and can fall significantly with induced hypotension. Changes in venous pressure, on the other hand, have a major impact on IOP. Vomiting, coughing, and bucking on the endotracheal tube cause a dramatic increase in IOP by 30 to 40 torr. These actions, and also Valsalva maneuver, cause congestion in the venous system, which impedes the outflow of aqueous humor and increases the volume of choroidal blood. A deep inspiration may reduce IOP by 5 torr. Hypoxemia may increase IOP through choroidal vasodilatation.

Beulen P, Rotteveel J, de Haan A, et al. Ultrasonographic assessment of congestion of the choroid plexus in relation to the carbon dioxide pressure. Eur J Ultrasound. 2000;11:25-29.

Calobrisi BL, Lebowitz P. Muscle relaxants and the open globe. Int Anesthesiol Clin. 1990;28(2):83-88.

Cunningham AJ, Barry P. Intraocular pressure—physiology and implications for anaesthetic management. Can Anaesth Soc J. 1986;33:195-208.

Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2513-2514.

Murphy DF. Anesthesia and intraocular pressure. Anesth Analg. 1985;64:520-530.

FIGURE 34.1 Sites of formation, circulation, and drainage of aqueous humor. (Modified from Cunningham AJ, Barry P. Intraocular pressure—physiology and implications for anaesthetic management. Can Anaesth Soc J. 1986;33:197, with permission.)

A.5. What is the role of the central nervous system (CNS) on IOP?

The CNS influences IOP through alterations in extraocular muscle tone or, indirectly, by hormonal or hemodynamic changes.

Cunningham AJ, Barry P. Intraocular pressure—physiology and implications for anaesthetic management. Can Anaesth Soc J. 1986;33:195-208.

Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2513-2514.

A.6. What is glaucoma?

Glaucoma is a pathologic elevation of IOP caused by increased resistance to outflow of aqueous humor from the anterior chamber of the eye. It is classified as either open- or closed-angle glaucoma, depending on the anatomy and pathophysiology. Chronic elevation of IOP interferes with the intraocular blood supply and normal metabolism of the cornea. It can result in corneal opacities or decreased retinal blood flow.

The pathophysiology in open-angle glaucoma involves increased resistance to the flow of aqueous humor through Fontana spaces as a result of scarring of the trabecular network or thickening of the endothelial covering of these channels. In closed-angle glaucoma, the iris bulges forward blocking the access of aqueous humor to the trabecular network. This may occur with pupillary dilation or an acutely swollen lens.

Johnson DH, Brubaker RF. Glaucoma: an overview. Mayo Clin Proc. 1986;61:59-67.

LeMay M. Aspects of measurement in ophthalmology. Br J Anaesth. 1980;52:655-662.

A.7. Is atropine contraindicated in patients with glaucoma?

Topical atropine in the eye is generally contraindicated in patients with glaucoma, especially in those with closed-angle glaucoma. Atropine, studied in a single dose of 0.01 mg per kg, administered intramuscularly (IM), or given orally as 0.6 mg in two doses 4 hours apart,
caused no increase in IOP in either open- or closed-angle glaucoma because by calculation, only approximately 0.0001 mg reaches the eye, which is far less than topical dose. Intravenous atropine is associated with mydriasis and might be contraindicated in patients with glaucoma; however, preemptive topical use of pupillary constrictors such as pilocarpine and timolol avoid this problem.

Adams AK, Jones RM. Anaesthesia for eye surgery: general considerations. Br J Anaesth. 1980;52:663-669.

Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013:1376-1377.

Greenstein SH, Abramson DH, Pitts WR III. Systemic atropine and glaucoma. Bull N Y Acad Med. 1984;60:961-968.

Miller RD, Cohen NH, Eriksson LI, et al, eds. Miller’s Anesthesia. 8th ed. Philadelphia, PA: Elsevier Saunders; 2015:2513-2514.

Schwartz B. Current concepts in ophthalmology: the glaucomas. N Engl J Med. 1978;299:182-184.

A.8. How do carbonic anhydrase inhibitors work to decrease IOP? By what mechanism may osmotic agents decrease IOP?

Carbonic anhydrase inhibitors, such as acetazolamide, interfere with the sodium-pump mechanism necessary for secretion of aqueous humor. An intravenous dose acts in 5 minutes, with maximal effect in 20 to 30 minutes. Chronic acetazolamide therapy may result in potassium depletion.

Osmotic agents, such as mannitol, increase plasma oncotic pressure relative to that of aqueous humor and produce an acute, transient drop in IOP. The maximum reduction in IOP occurs after 30 to 45 minutes and the effect lasts 5 to 6 hours.

Barash PG, Cullen BF, Stoelting RK, et al, eds. Clinical Anesthesia. 7th ed. Philadelphia, PA: Lippincott Williams & Wilkins; 2013:1376.

McGoldrick KE. Ocular drugs and anesthesia. Int Anesthesiol Clin. 1990;28(2):72-77.

A.9. Are carbonic anhydrase inhibitors or osmotic diuretics indicated in open-globe injuries?

No. If the globe is open, the IOP is low and these agents are not useful. In addition, they may cause transient choroidal congestion, which could lead to loss of ocular contents.

Smith GB. Ophthalmic Anaesthesia. Baltimore: University Park Press; 1983.

A.10. Are topically applied ophthalmic medications absorbed systemically? How can this absorption be reduced? Which eyedrops may have effects that are of concern to the anesthesiologist?

Topical ophthalmic drugs may be absorbed through the conjunctiva or may drain through the nasolacrimal duct and be absorbed through the nasal mucosa. Absorption is increased when the eye is instrumented, diseased, or traumatized. Finger pressure on the inner canthus for a few minutes after instillation of eyedrops will impede absorption by occluding the nasolacrimal duct.

Usage of the following topical medications may have implications for the anesthesiologist:

Atropine

Atropine is used to produce mydriasis and cycloplegia. The 1% solution contains 0.2 to 0.5 mg of atropine per drop. Systemic reactions, seen primarily in children and older adults, include tachycardia, flushing, thirst, dry skin, and agitation. Atropine is contraindicated in closed-angle glaucoma.

Scopolamine

One drop of the 0.5% solution has 0.2 mg of scopolamine. CNS excitement can be treated with physostigmine, 0.015 mg per kg intravenously (IV), repeated one or two times in a 15-minute period. Scopolamine is contraindicated in closed-angle glaucoma.

Cyclopentolate (Cyclogyl)

Cyclopentolate, a short-acting mydriatic and cycloplegic, may cause transient neurotoxic effects such as incoherence, visual hallucinations, slurred speech, ataxia, and seizures. It is contraindicated in closed-angle glaucoma.

Tropicamide (Mydriacyl)

Tropicamide is used to produce mydriasis for refraction or funduscopic examination. It may have CNS effects and can elevate IOP in closed-angle glaucoma.

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