INTRAOCULAR gas may enter an eye in a variety of ways: penetrating injury, infection, rapid decompression, gas bubble disease, or from therapeutic interventions by ophthalmologists. 1Therapeutic use of intraocular gas provides internal retinal tamponade for retinal breaks or detachment, macular hole repair, and complicated diabetic vitrectomy. Unfortunately, gases used in intraocular surgery introduce a variety of potential problems. One problem is posed for patients requiring subsequent surgery (not necessarily ophthalmic) in the postoperative period while intraocular gas may still be present in the eye. We report three cases from three different centers where adverse events occurred after nitrous oxide (N2O)-induced general anesthesia in patients following recent vitrectomy with use of intraocular gas. A summary of principles of intraocular gases is provided, including recommendations for prevention and management of N2O-induced anesthesia-related intraocular gas complications.

Case 1

A 73-yr-old man underwent vitrectomy and internal drainage of a large subretinal hemorrhage at the right macula (table 1for summary of patient data). After fluid-air exchange, the eye (vitreous cavity) was filled with 14% perfluoropropane (C3F8) gas. Twenty-two days postoperatively, the patient underwent elective total hip replacement surgery during general anesthesia, which included N2O. The patient awoke from surgery with no perception of light (NPL) vision in the eye with intraocular gas. No visual recovery occurred and optic atrophy developed in the right eye.

Table 1. Pertinent Preoperative, Operative, and Postoperative Data from Each Case

Preoperative, intraoperative, and postoperative data relate to the second operation, not the initial vitrectomy.CF = counting fingers; HM = hand movements; NPL = no perception of light; PL = perception of light; IOP = intraocular pressure; CRAO = central retinal artery occlusion.

Table 1. Pertinent Preoperative, Operative, and Postoperative Data from Each Case
Table 1. Pertinent Preoperative, Operative, and Postoperative Data from Each Case

Case 2

An 80-yr-old man underwent vitrectomy for retinal detachment during general anesthesia. The eye was filled with 20% C3F8gas at the end of the procedure. The following day, examination showed a flat retina, normal intraocular pressure (IOP), and 70% gas fill (percentage vitreous cavity volume). Unfortunately urinary retention developed in the patient following the operation, requiring catheterization. Nine days postoperatively, the patient was progressing well, with hand movement visual acuity, 60% gas fill, and a flat inferior retina. He remained catheterized and transurethral prostate resection was performed during general anesthesia. N2O was used for the complete procedure. Overnight, the patient experienced ocular pain, but no emergent ophthalmic review was sought. When the ophthalmologist asked to see the patient the next day, the patient's IOP was slightly increased at 23 mmHg, and clinical features of total central retinal artery occlusion were present (marked relative afferent pupil defect, cherry red spot). Despite systemic and topical IOP-lowering agents, the patient's vision had deteriorated to NPL, which never recovered. Subsequent review confirmed development of optic atrophy.

Case 3

A 75-yr-old man underwent vitrectomy for macula hole and the eye filled with 20% C3F8gas. He then underwent emergency orthopedic surgery for a fractured neck of femur repair, with N2O use in general anesthesia 1 month later. Immediately after the orthopedic procedure, he reported loss of vision in his left eye to the staff in the recovery room. Examination 90 min after surgery revealed light perception visual acuity, a relative afferent pupil defect, and 50–60% gas bubble in the vitreous cavity. Fortunately visual acuity recovered to 6/24, though optic nerve pallor developed.

Intraocular Gas-Intraocular Pressure Relation

Whenever intraocular gas is used, the surgeon risks producing increased IOP from excessive volume and/or expansion of the intraocular gas. Gas expansion may cause ocular hypertension (increased IOP) in four circumstances: decreasing barometric pressure (altitude), influx of N2O, excessive concentration of an expanding gas, decreased facility of outflow (aqueous drainage) through the trabecular meshwork. 1 

As the eye is somewhat elastic and contains fluid and solids, the relation between ocular volume and gas pressure is more complex than is predicted by ideal gas laws (Boyle's, Charles’, Avagadro's and Dalton's laws). Nonetheless these laws allow an understanding of the behavior of intraocular gases in the clinical setting. Of perhaps greater relevance, Fick's law determines growth or shrinkage of gas bubbles in the eye. 1Essentially, behavior of an intraocular gas bubble after introduction into the globe depends on its solubility compared with atmospheric gases (room air). Thus, three types of gases may be introduced: room air; a gas that is less soluble or less diffusible than room air (e.g. , sulfurhexaflouride [SF6] and C3F8), which thus persists longer than air; a gas that is more soluble or diffusible than room air (e.g. , carbon dioxide and N2O) and thus disappears more quickly than air. 1 

Specific Gases Pertinent to the Ophthalmic- Anesthetic Situation

A variety of gases can be used in an ophthalmic setting. Filtered room air, SF6, and C3F8are those most commonly used. The duration of intraocular gas varies with the volume, concentration, and type of gas used. Larger more concentrated volumes of gases less soluble than air last longer. 2Air typically resorbs within a few days. SF6lasts 7–10 days; C3F8, 4–6 weeks; though C3F8durations of more than 70 days have been reported. 3C3F8, with its longer duration in the eye, has been shown to be superior to SF6in the management of complicated retinal detachments in which longer tamponade periods are required. 4Silicone oil is an alternate intraocular tamponade agent that avoids intraocular gas-related problems, while providing long-term tamponade protection. However, it introduces its own complications, requires an additional removal procedure, and does not provide tamponade protection sufficiently for its use in conditions such as macular hole. 4,5 

Unlike air, SF6and C3F8are expansile gases. During the expansion phase, nitrogen and other blood gases enter the bubble more rapidly than SF6or C3F8disappears, which leads to exponential expansion of the bubble. SF6and C3F8gases can be mixed with air and used in a nonexpansile (isovolumetric) concentrations or used in an expansile fashion depending on surgical factors and desired effects. One hundred percent SF6expands to twice the injected volume over 24 h, while 100% C3F8expands to four times the injected volume over 3–7 days. The expansion phase of SF6and C3F8gases is such that IOP is able to normalize faster than the rate of expansion of the gas and, by allowing smaller injection volumes, avoids potential problems of injecting larger volumes of nonexpansile gas (e.g. , air) into a closed eye. 1 

Effect of Intraocular Gas Injection on Intraocular Pressure

Injection of 0.3 ml gas (∼5% vitreal volume) is enough to increase the IOP to greater than 70 mmHg and close the central retinal artery; though usually IOP decreases to normal pressures within 15 min. 6Injection of larger volumes or expansile mixes can reach a much higher IOP and take longer before normalization of IOP. 16There is no precise duration of increased IOP greater than central retinal artery perfusion pressure that will lead to permanent visual loss; however, primate models suggest irreversible damage occurs if retinal artery obstruction is present for approximately 90 min. 7Clinically, increased IOP is known to close the central retinal artery and this can be visualized during the period of increased IOP. On resolution to normal IOP, however, fundal appearance can vary from normal reperfused vessels to the classic cherry red spot, which may take some hours to develop. 8,9Ultimately, however, an eye damaged by central retinal artery occlusion (CRAO) will typically show evidence of optic disc pallor, attenuated vessels, and nerve fiber layer loss in the months that follow. 8 

Influence of Nitrous Oxide on Intraocular Gas Behavior

Nitrous oxide is much more soluble than other gases and therefore exerts a potent effect on all intraocular gases. If N2O is used when gas is present in a closed eye (e.g. , after injection or in the postoperative period), then the volume of intraocular gas increases while N2O is being used and only stops expanding once N2O is discontinued. A more than threefold volume increase may be seen over 1 h of N2O use, 10which is easily sufficient to close the central retinal artery.

Despite numerous studies of the effect of N2O on bubble volume, secondary glaucoma is not commonly reported, though most anesthesiologists recognize that N2O is contraindicated if intraocular gas is present or planned to be used in a closed eye. 10–15Although IOP problems and CRAO are well-recognized complications of intraocular gas use, 6 16–19our case series represents the first reported cases of permanent visual loss through the postoperative use of N2O-induced general anesthesia in eyes with intraocular gas. Although not excluded in these cases, embolic phenomena (e.g. , fat emboli) typically occur as a shower and would likely have additional embolic findings, both in the affected eye and elsewhere. 8Similarly, other anesthetic factors have been implicated in visual loss, especially hemodynamic, such as hypotension, patient posturing, medications, and blood loss. 20–22These diseases typically would cause anterior or posterior ischemic optic neuropathy rather than CRAO. 21Aside from patient 2, who had intraoperative hypotension, no other factors implicated in visual loss were evident in these cases. Case 2 clearly showed CRAO as the mechanism of visual loss, making the hypotension, though possibly contributory, perhaps less significant than the gas-related mechanism. Although only case 2 showed clear evidence of CRAO, increased IOP in itself is not known to cause anterior or posterior ischemic optic neuropathy. However, anterior or posterior ischemic optic neuropathy can ultimately lead to disc pallor, and thus could not be excluded as causes in cases 1 and 3. 23 

It is important for anesthesiologists to be aware that an intraocular gas bubble can persist in the eye for up to 10 weeks after ocular surgery. Use of highly soluble gases, such as N2O, in the presence of intraocular gas can lead to significant visual complications. In the current patients, complications developed associated with N2O use 22, 9, and 30 days after eye surgery. This is because N2O rapidly enters the gas bubble, inducing an increase in gas volume inside the essentially rigid, closed eye. The rapid and extreme increase in pressure closes the central retinal artery, leading to the observed visual loss. Because the patient is anesthetized at the time this damage is presumably occurring, they do not report pain (as might normally be expected in an awake patient with extreme elevation of IOP). Presumably, IOP rapidly returns to asymptomatic values soon after anesthetic completion, as suggested experimentally. 11 

Methods to Reduce Risk of Nitrous Oxide Visual Loss


In the ophthalmic setting, communication between surgeon and anesthesiologist usually avoids gas-related complications, though, occasionally, inadvertent N2O problems have been detected intraoperatively. 1Clearly, surgeons have a responsibility to increase patient awareness regarding the risks of further surgery when intraocular gas has been used and to ensure adequate communication between surgeon and anesthesiologist preoperatively. In addition, we propose the use of a simple warning bracelet, for patients to wear in the postoperative period until the gas bubble has dissolved (fig. 1). The importance of such bracelets is even more relevant in the emergency situation when patients may be incapacitated and unable to relay intraocular gas history.

Fig. 1. Nitrous oxide warning bracelet placed at the time of intraocular gas injection and removed only after the gas has resorbed.

Fig. 1. Nitrous oxide warning bracelet placed at the time of intraocular gas injection and removed only after the gas has resorbed.

Close modal

Management of Acute Episode if Detected

If a problem is recognized intraoperatively, then immediate steps should be taken. N2O should be ceased immediately; ventilation, commenced with 100% oxygen. One hundred percent oxygen has been shown to lead to faster reversal of bubble expansion than room air alone. 24In addition, adequate systemic perfusion should be ensured. Urgent consultation with an ophthalmologist should be obtained, with ongoing emergency management guided by the ophthalmologist. If ophthalmology consultation is not available and if after 5 min the eye continues to feel hard during palpation (using other eye for comparison), then consideration of pars plana paracentesis should be given to vent excess gas from the eye. Using a short (1/2 in) needle (26–30 gauge), pierce the 1-mm thick sclera of the eye 3.5–4 mm from the limbus (junction between clear cornea and white sclera). The needle should be directed perpendicularly toward the center of the eye. A few seconds is typically enough to reduce IOP to safe pressures (removal of a precise amount is not essential).

The authors thank Jillian Blakley, R.N., Operating Theatre, Mercy Hospital, Auckland, New Zealand.

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