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Intraocular Pressure Fluctuations during Scleral Buckling Surgery
Intraocular Pressure Fluctuations during Scleral Buckling Surgery Thomas W. Gardner, MD, 1 David A Quillen, MD, 1 George W. Blankenship, MD, 1 Wayne K. Marshall, MD2 Purpose: The purposes of this study are to measure real-time intraocular pressure (lOP) during scleral buckling and to determine the effects of elevated lOPs on ocular perfusion. Patients and Methods: A standard 4-mm, 20-gauge infusion cannula was inserted through the pars plana, connected to a standard hemodynamic monitoring unit with an electronic pressure transducer, and calibrated. The authors measured real-time lOP in 20 eyes undergoing scleral buckling surgery for primary rhegmatogenous retinal de tachments and determined the lOP required to close the central retinal artery. Pressure measurements were read from the monitor videoscreen intraoperatively and from a continuous paper tracing postoperatively. Results: The patients ranged in age from 24 to 88 years (mean, 59.7 years). The highest lOP elevations occurred during scleral depression and cryopexy, ranging up to 210 mmHg (mean, 116 mmHg). Pressures at which the central retinal artery closed ranged from 48 to 11 0 mmHg (mean, 79.2 mmHg). Manipulations of the globes caused lOPs greater than the central retinal artery perfusion pressures in 13 of the 20 patients. The duration of pressures in excess of the central retinal artery perfusion pressure ranged from 6 to 402 seconds (mean, 118.8 seconds). There were no intraoperative or postoperative complications from the infusion cannula. Conclusions: Conventional scleral buckling surgery causes wide fluctuations in lOP and may impair ocular perfusion. Additional studies are needed to determine the long-term consequences of these pressure elevations. Ophthalmology 1993; 100:1050-1054
Retinal reattachment may be accomplished in more than 90% of patients undergoing scleral buckling surgery. I-J However, visual results are generally less satisfactory than
Originally received: November 10, 1992. Revision accepted: February 5, 1993. 1 Department ofOphthalmology, Penn State University College of Med icine. Hershey, Pennsylvania. 2 Department of Anesthesia, Penn State University College of Medicine, Hershey, Pennsylvania. Presented as a poster at the American Academy of Ophthalmology An nual Meeting, Dallas, November 1992.
Supported by Research to Prevent Blindness, Inc, New York, New York. The authors have no proprietary interest in the products listed in this article. Reprint requests to Thomas W. Gardner, MD, Department of Oph thalmology, Penn State University College of Medicine, P.O. Box 850, Hershey, PA 17033.
1050
anatomic ,results, even in cases of retinal detachment without macular involvement.2 The reasons for decreased vision after apparently successful retinal reattachment are not completely understood. Elevated intraoperative in traocular pressure (lOP) with resultant optic nerve or ret inal vascular compromise may limit visual recovery, par ticularly in eyes with glaucoma or arterial insufficiency. Several experimental methods of monitoring intra operative lOP have been described, including anterior chamber cannulas, 4 •5 implantable sensors, 6 •7 and a variable resistance scleral buckle pressure gauge. 8 Although all of these methods allow for continuous monitoring of intra operative lOP, none is clinically applicable to scleral buckling surgery. We have previously described a method to monitor real-time lOP in human eye bank eyes using a pars plana infusion cannula connected to an electronic pressure transducer. 9 We now report the clinical application of this technique to characterize the lOP fluctuations that occur
Gardner et al · lOP and Scleral Buckling Surgery during scleral buckling surgery and the effects of these lOP variations on retinal vascular perfusion.
Patients and Methods Patients with primary rhegmatogenous detachments de termined to be repairable with scleral buckling were eli gible for the study. This study was approved by the Clinical Investigations Committee of the Penn State University College of Medicine; all patients received detailed infor mation before providing their consent. A standard 4-mm pars plana infusion cannula with 15-cm polyethylene tubing is connected to pressure-re sistant tubing and filled with balanced salt solution. The tubing system connects to an electronic pressure trans ducer (Spectromed DTX/Plus, Oxnard, CA) and recorder (Spacelabs 511 Patient Monitor, Hillsboro, OR). The cannula is placed at the patient's eye level and zeroed. The cannula is inserted through the pars plana (3.5 mm posterior to the corneal limbus) and secured with a 5-0 nylon suture (Fig 1). The position of the cannula within the eye is verified by direct observation. The baseline lOP is then determined by pneumotonometry, and the re corder is calibrated. Retinal reattachment is then performed with standard cryopexy, circumferential or radial silicone exoplants, subretinal fluid drainage, and intravitreal air injection as clinically indicated. The pressure at which the central ret inal artery closes, as observed by indirect ophthalmoscopy with a 20-diopter lens, is called the "central retinal artery closing pressure," and assumed to equal the retinal arterial systolic pressure. The amplitude and duration of pressure fluctuations that occur during scleral buckling surgery are monitored intraoperatively and quantified postoperatively during review of the hard copy data (Fig 2).
Schreuder and Linssen 10 have demonstrated that ele vations in systemic blood pressure may result in concom itant elevations in lOP. For this reason, systemic blood pressure was carefully monitored during the scleral buck ling surgeries. All patients maintained stable intraoperative systemic blood pressures; therefore, we were able to elim inate this variable as a source of lOP fluctuation.
Results Twenty patients with primary rhegmatogenous retinal detachments were enrolled in the study. They ranged in age from 24 to 88 years (mean, 59.7 years). There were 14 right eyes and 6 left eyes; 10 eyes were phakic and 10 were pseudophakic. Thirteen of the 20 patients had a medical history of diabetes mellitus, hypertension, and/or atherosclerosis. The lOP fluctuations for the 20 eyes are shown in Table 1 and are represented graphically in Figure 3. The central retinal artery closing pressure ranged from 48 to 110 mmHg (mean, 79.2 mmHg). The highest lOPs occurred during scleral depression and cryopexy, ranging up to 210 mmHg (mean peak, 116 mmHg). Substantial elevations in lOP also occurred during placement of intrascleral su tures and the buckle elements. The peak intraoperative lOP exceeded the central retinal artery closing pressure in 13 of the 20 patients. The duration ofiOP in excess of the central retinal artery closing pressure ranged from 6 to 402 seconds (mean, 118.8 seconds). These times reflect the cumulative duration for which the central retinal ar tery closing pressure was exceeded during the entire scleral buckling procedure. The average age of the 13 patients who experienced lOP elevations in excess of the central retinal artery closing pressure was 67.2 years, compared with 50.1 years in those patients who did not have such elevations (P = 0.0 16; unpaired Student's t test). In ad-
Figure 1. Pars plana intraocu lar pressure monitoring sys tem. Intraocular pressure is monitored continuously via a pars plana infusion cannula connected to an electronic pressure transducer and re corder.
1051
Volume 100, Number 7, July 1993
Ophthalmology
180
Central Retilal Artery Ck>Wig Pr8SSU'e
0
r
180-
6 Sec.
t-----i
Muscle Slinging --~---
o180
Figure 2. Representative recording strip from the pars plana intraocular pressure monitoring system. The x axis is time plotted in seconds (6 seconds per mark) and the y-axis reflects the intraocular pressure in mmHg (0-180 mmHg).
o 180
f
6 Sec.
Suture Placement
!---------<
0
180 Cl
:r
Buckle Placement
6 Sec.
o---------i
~
dition, 69% ofthe patients who experienced lOP elevations in excess of their central retinal artery closing pressure had a medical history of diabetes mellitus, hypertension, and/or atherosclerosis. Individual lOP elevations in excess ofthe central retinal artery closing pressures were typically transient, lasting less than 45 seconds. However, patient l 0 had continuous central retinal artery closure for 4 minutes; and patients 6 and 18 each had continuous lOP elevations greater than the central retinal artery closing pressures for l minute. All of these lOP elevations occurred during cryopexy. There were no intraoperative or postoperative com plications from the infusion cannula. In particular, there were no new retinal tears or infections. However, in one eye with an inferior retinal detachment in which the in fusion cannula was placed in the inferotemporal quadrant, the retina initially did not settle onto the pigment epithe lium after subretinal fluid drainage. Intravitreal air injec tion facilitated retinal reattachment. The surgeon believed that vitreous traction to the infusion cannula may have impaired retinal reattachment.
Discussion We have developed a clinically applicable method to monitor real-time lOP using a standard pars plana infu
1052
sion cannula connected to an electronic pressure trans ducer. In a prior study on human eye bank eyes, we dem onstrated that the pars plana-lOP monitoring system re flects alterations in IOP. 9 In particular, the cannula does not alter scleral rigidity. The results of this current study confirm that the monitoring system provides accurate, sensitive measurements ofiOP in eyes undergoing scleral buckling surgery. The monitoring system is the same as that used to measure systemic arterial blood pressure and intracranial pressure and is readily available in most hos pitals. Similar to these methods, there is no net fluid flow through the tubing. Although the technique of pars plana infusion cannula insertion is generally safe and is per formed routinely during pars plana vitrectomy, it remains invasive with inherent risks (e.g., retinal or vitreous in carceration,
Gardner et al · lOP and Scleral Buckling Surgery Table 1. Intraocular Pressure Fluctuations during Scleral Buckling Surgery Patient
Age (yrs)
lOP (mmHg)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
78 70 62 41 75 57
22 6 20 12 8 24 10 25 6 12 9 12 9 18 9 12 18 15 18 12
No.
24
51 37 73 70 64 60 80 88 64 63 64
43
60
CRACP (mmHg)
Muscle (mmHg)
SD/CRYO (mmHg)
Suture (mmHg)
Buckle (mmHg)
Time lOP > CRACP (sees)
90
50 48 50 24 64
152 48 40 90 196 108 20 50
72 36 60 18 63 42 10 30 30 48 66 108 72 60 30 35 120 45 42 114
5 36 20 78 66 38 10 45 42 210 96 72 60 84
26
48 70 84
72 80 110 75 102 78 100 80 60 75 55 68 90
58 96 93
66
80 35 28 50 48 90 48 72 24 32 54 28 36 55
84
104 210 120 168 84 197 59 168 210 72 150
23
45 128 42 26 108
6 180 288
402 114 36 24 30 120 132 108 78
lOP = intraocular pressure (baseline); CRACP = central retinal artery closing pressure; Muscle =rectus muscle slinging; SD/CRYO =scleral depression/cryopexy; Suture = suture placement; Buckle =buckle element placement; Time lOP > CRACP = time in excess of the CRACP.
sclerosis had the lower central retinal artery closing pres sures. Likewise, older patients with concomitant vascular disease were significantly more Likely to have lOP eleva tions in excess of the central retinal artery perfusion pres sures. We could detect lOP fluctuations as low as I mmHg within I to 2 seconds in most patients. In two eyes, the tracing became dampened by the end of the procedure. Potential reasons for the decreased sensitivity include plugging of the infusion cannula by formed vitreous gel, leakage around the cannula site, or kinking of the poly ethylene tubing. In addition, eyes usually have a nearly normal lOP, ranging from I2 to 20 mmHg, in the early stages of the retinal reattachment procedure. However, scleral depression and cryopexy eventually soften the globe and increase the ocular capacitance (i.e., greater external force is required to cause a given increase in lOP than when the eye is firm). For this reason, fluctuations in lOP tended to diminish late in the operation. We continued our standard operative technique throughout this study. However, the surgeons were able to see the real-time lOP measurements intraoperatively. We cannot exClude the possibility that the surgeon or as sistant consciously or subconsciously altered their han dling of the eyes, particularly ifthe lOP was elevated. This may explain, in part, why the lOP elevations were typically transient. The surgeons did, in fact, use the lOP data dur ing surgery; for example, to avoid high lOP before sub-
retinal fluid drainage. Therefore, it is possible that the peak recorded lOPs underestimate the lOP elevations that would develop in the absence of the study. Fraunfelder and co-workers5 have previously described elevations ofiOP during scleral depression. They used an anterior chamber cannula and found peak lOPs ranging from I60 to 350 mmHg. These lOPs are generally higher than those found in this study. Potential sources of dif ferences include the method of measurement and the technique ofthe operating surgeons. Raizman and Beck 14 found lOPs ranging from 77 to 84 mmHg during extra ocular muscle manipulations for strabismus surgery using a pneumotonometer. Their data are consistent with the results of our study. The potential importance of lOP elevations during scleral buckling was initially addressed by Hilton. 15 In a 1986 survey of Retina Society members, he reported that 20 of 72 surgeons had never witnessed central retinal ar tery closure during scleral buckling without drainage. Forty-six surgeons had encountered approximately 775 cases in which the artery was closed for up to 5 minutes. None of the surgeons believed that intraoperative lOP elevations impaired postoperative visual recovery. Our data suggest that transient central artery occlusion is common during scleral buckling surgery. The consequences of increased lOPs on retinal vascular perfusion also have been studied in animals. In owl mon keys, lOPs greater than the ocular perfusion pressure de
1053
Ophthalmology
Volume 100, Number 7, July 1993
References
2so
0 200 +························+···························!···························+··········II···········+··························!···························+
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150
gj w
a: Q.
~
::;)
100
~ ~
50
lOP
CRACP
MUSClE
SD/CRYO
SUTURE
BUCKLE
Figure 3. Intraocular pressure fluctuations during scleral buckling surgery. The baseline intraocular pressure (lOP), central retinal artery closing pressure (CRACP), and the lOP fluctuations during scleral buckling surgery (Muscle= muscle slinging; SD/Cryo =scleral depression/cryo therapy; Suture = suture placement; Buckle = buckle element placement) are summerized for all20 patients. The bars represent the range of lOPs, the boxes contain 50% of the lOP values, and the horizontal line in each box is the mean lOP for each maneuver.
pressed the electroretinogram, but there was complete electroretinogram recovery when the duration ofiOP ele vation was less than 60 minutes. 16 Ernest and Potts 17 studied optic disc perfusion in rhesus monkeys with flu orescein angiography at baseline lOP and when the lOP was maintained at 80 mmHg. Comparison of arterial phase angiograms showed that the majority of small disc vessels were nonperfused in the eyes subjected to increased lOP, but not in the normotensive eyes. Two clinical conditions provide additional evidence for deleterious effects oftransient lOP elevations on optic disc function. First, anterior ischemic optic neuropathy after cataract extraction is thought to result from lOP spikes in eyes with vulnerable optic nerve head circula tion. 18 Second, a high lOP after argon laser trabeculoplasty can lead to central visual loss in eyes with glaucomatous optic nerve damage. 19 The relationship ofiOP elevations to retinal and optic nerve function, and to ultimate visual recovery after scleral buckling in humans, remains un known. Studies to determine the visual consequences of these lOP fluctuations are in progress.
1054
I. Burton TC, Lambert RW Jr. A predictive model for visual recovery following retinal detachment surgery. Ophthal mology 1978;85:619-25. 2. Tani P, Robertson DM, Langworthy A. Rhegmatogenous retinal detachment without macular involvement treated with scleral buckling. Am J Ophthalmol 1980;90:503-8. 3. Tani P, Robertson DM, Langworthy A. Prognosis for central vision and anatomic reattachment in rhegmatogenous ret inal detachment with macula detached. Am J Ophtha1mol 1981 ;92:611-20. 4. Blumenthal M, Cahane M, Ashkenazi I. Direct intraoper ative continuous monitoring of intraocular pressure. Ophthalmic Surg 1992;23: 132-4. 5. Fraunfelder FT, Boozman FW III, Wilson RS, Thomas AH. No-touch technique for intraocular malignant melanomas. Arch Ophthalmol 1977;95:1616-20. 6. Honda Y, Kawano S, Negi A, Koizumi K. Pressure profile of ophthalmic surgical procedures: an experimental study on the rabbit eye. Ophthalmic Surg 1982;13:387-91. 7. Moorhead LC, Armeniades CD. Variations in intraocular pressure during closed-system surgical procedures. Arch Ophthalmol 1986; 104:269-72. 8. Wolbarsht ML, Wortman J, Schwartz B, Cook D. A scleral buckle pressure gauge for continuous monitoring of intra ocular pressure. Int Ophthalmol 1980;3: 11-17. 9. Quillen DA, Gardner TW, Blankenship GW, Marshall WK. A method for real-time intraocular pressure measurement during scleral buckling. Graefe's Arch Clin Exp Ophthalmol (in press). I0. Schreuder M, Linssen GH. Intra-ocular pressure and an aesthesia. Direct measurements by needling the anterior chamber in the monkey. Anaesthesia 1972;27:165-70. II. Oyakawa RT, Schachat AP, Michels RG, Rice TA. Com plications of vitreous surgery for diabetic retinopathy. I. In traoperative complications. Ophthalmology 1983;90:517 21. 12. Faulborn J, Conway BP, Machemer R. Surgical complica tions ofpars plana vitreous surgery. Ophthalmology 1978;85: 116-25. 13. Blankenship GW. Endophthalmitis following pars plana vi trectomy. Am J Ophthalmoll977;84:815-17. 14. Raizman MB, Beck RW. Sustained increases in intraocular pressure during strabismus surgery. Am J Ophthalmol 1986;101:308-9. 15. Hilton GF. Planned elevation of intraocular pressure with temporary occlusion of the central retinal artery during ret inal surgery [letter]. Arch Ophthalmol 1986;104:975. 16. Gerstle CL, Anderson DR, Hamasaki DI. Pressure effect on ERG and optic nerve conduction ofvisual impulse: short term effects in owl monkeys. Arch Ophthalmol 1973;90: 121-4. 17. Ernest JT, Potts AM. Pathophysiology of the distal portion ofthe optic nerve. II. Vascular relationships. Am J Ophthal mol 1968;66:380-7. 18. Hayreh SS. Anterior ischemic optic neuropathy. IV. Oc currence after cataract extraction. Arch Ophthalmol 1980;98: 1410-16. 19. Thomas JV, Simmons RJ, Belcher CD III. Argon laser tra beculoplasty in the presurgical glaucoma patient. Ophthal mology 1982;89: 187-97.
Retinal reattachment may be accomplished in more than 90% of patients undergoing scleral buckling surgery. I-J However, visual results are generally less satisfactory than
Originally received: November 10, 1992. Revision accepted: February 5, 1993. 1 Department ofOphthalmology, Penn State University College of Med icine. Hershey, Pennsylvania. 2 Department of Anesthesia, Penn State University College of Medicine, Hershey, Pennsylvania. Presented as a poster at the American Academy of Ophthalmology An nual Meeting, Dallas, November 1992.
Supported by Research to Prevent Blindness, Inc, New York, New York. The authors have no proprietary interest in the products listed in this article. Reprint requests to Thomas W. Gardner, MD, Department of Oph thalmology, Penn State University College of Medicine, P.O. Box 850, Hershey, PA 17033.
1050
anatomic ,results, even in cases of retinal detachment without macular involvement.2 The reasons for decreased vision after apparently successful retinal reattachment are not completely understood. Elevated intraoperative in traocular pressure (lOP) with resultant optic nerve or ret inal vascular compromise may limit visual recovery, par ticularly in eyes with glaucoma or arterial insufficiency. Several experimental methods of monitoring intra operative lOP have been described, including anterior chamber cannulas, 4 •5 implantable sensors, 6 •7 and a variable resistance scleral buckle pressure gauge. 8 Although all of these methods allow for continuous monitoring of intra operative lOP, none is clinically applicable to scleral buckling surgery. We have previously described a method to monitor real-time lOP in human eye bank eyes using a pars plana infusion cannula connected to an electronic pressure transducer. 9 We now report the clinical application of this technique to characterize the lOP fluctuations that occur
Gardner et al · lOP and Scleral Buckling Surgery during scleral buckling surgery and the effects of these lOP variations on retinal vascular perfusion.
Patients and Methods Patients with primary rhegmatogenous detachments de termined to be repairable with scleral buckling were eli gible for the study. This study was approved by the Clinical Investigations Committee of the Penn State University College of Medicine; all patients received detailed infor mation before providing their consent. A standard 4-mm pars plana infusion cannula with 15-cm polyethylene tubing is connected to pressure-re sistant tubing and filled with balanced salt solution. The tubing system connects to an electronic pressure trans ducer (Spectromed DTX/Plus, Oxnard, CA) and recorder (Spacelabs 511 Patient Monitor, Hillsboro, OR). The cannula is placed at the patient's eye level and zeroed. The cannula is inserted through the pars plana (3.5 mm posterior to the corneal limbus) and secured with a 5-0 nylon suture (Fig 1). The position of the cannula within the eye is verified by direct observation. The baseline lOP is then determined by pneumotonometry, and the re corder is calibrated. Retinal reattachment is then performed with standard cryopexy, circumferential or radial silicone exoplants, subretinal fluid drainage, and intravitreal air injection as clinically indicated. The pressure at which the central ret inal artery closes, as observed by indirect ophthalmoscopy with a 20-diopter lens, is called the "central retinal artery closing pressure," and assumed to equal the retinal arterial systolic pressure. The amplitude and duration of pressure fluctuations that occur during scleral buckling surgery are monitored intraoperatively and quantified postoperatively during review of the hard copy data (Fig 2).
Schreuder and Linssen 10 have demonstrated that ele vations in systemic blood pressure may result in concom itant elevations in lOP. For this reason, systemic blood pressure was carefully monitored during the scleral buck ling surgeries. All patients maintained stable intraoperative systemic blood pressures; therefore, we were able to elim inate this variable as a source of lOP fluctuation.
Results Twenty patients with primary rhegmatogenous retinal detachments were enrolled in the study. They ranged in age from 24 to 88 years (mean, 59.7 years). There were 14 right eyes and 6 left eyes; 10 eyes were phakic and 10 were pseudophakic. Thirteen of the 20 patients had a medical history of diabetes mellitus, hypertension, and/or atherosclerosis. The lOP fluctuations for the 20 eyes are shown in Table 1 and are represented graphically in Figure 3. The central retinal artery closing pressure ranged from 48 to 110 mmHg (mean, 79.2 mmHg). The highest lOPs occurred during scleral depression and cryopexy, ranging up to 210 mmHg (mean peak, 116 mmHg). Substantial elevations in lOP also occurred during placement of intrascleral su tures and the buckle elements. The peak intraoperative lOP exceeded the central retinal artery closing pressure in 13 of the 20 patients. The duration ofiOP in excess of the central retinal artery closing pressure ranged from 6 to 402 seconds (mean, 118.8 seconds). These times reflect the cumulative duration for which the central retinal ar tery closing pressure was exceeded during the entire scleral buckling procedure. The average age of the 13 patients who experienced lOP elevations in excess of the central retinal artery closing pressure was 67.2 years, compared with 50.1 years in those patients who did not have such elevations (P = 0.0 16; unpaired Student's t test). In ad-
Figure 1. Pars plana intraocu lar pressure monitoring sys tem. Intraocular pressure is monitored continuously via a pars plana infusion cannula connected to an electronic pressure transducer and re corder.
1051
Volume 100, Number 7, July 1993
Ophthalmology
180
Central Retilal Artery Ck>Wig Pr8SSU'e
0
r
180-
6 Sec.
t-----i
Muscle Slinging --~---
o180
Figure 2. Representative recording strip from the pars plana intraocular pressure monitoring system. The x axis is time plotted in seconds (6 seconds per mark) and the y-axis reflects the intraocular pressure in mmHg (0-180 mmHg).
o 180
f
6 Sec.
Suture Placement
!---------<
0
180 Cl
:r
Buckle Placement
6 Sec.
o---------i
~
dition, 69% ofthe patients who experienced lOP elevations in excess of their central retinal artery closing pressure had a medical history of diabetes mellitus, hypertension, and/or atherosclerosis. Individual lOP elevations in excess ofthe central retinal artery closing pressures were typically transient, lasting less than 45 seconds. However, patient l 0 had continuous central retinal artery closure for 4 minutes; and patients 6 and 18 each had continuous lOP elevations greater than the central retinal artery closing pressures for l minute. All of these lOP elevations occurred during cryopexy. There were no intraoperative or postoperative com plications from the infusion cannula. In particular, there were no new retinal tears or infections. However, in one eye with an inferior retinal detachment in which the in fusion cannula was placed in the inferotemporal quadrant, the retina initially did not settle onto the pigment epithe lium after subretinal fluid drainage. Intravitreal air injec tion facilitated retinal reattachment. The surgeon believed that vitreous traction to the infusion cannula may have impaired retinal reattachment.
Discussion We have developed a clinically applicable method to monitor real-time lOP using a standard pars plana infu
1052
sion cannula connected to an electronic pressure trans ducer. In a prior study on human eye bank eyes, we dem onstrated that the pars plana-lOP monitoring system re flects alterations in IOP. 9 In particular, the cannula does not alter scleral rigidity. The results of this current study confirm that the monitoring system provides accurate, sensitive measurements ofiOP in eyes undergoing scleral buckling surgery. The monitoring system is the same as that used to measure systemic arterial blood pressure and intracranial pressure and is readily available in most hos pitals. Similar to these methods, there is no net fluid flow through the tubing. Although the technique of pars plana infusion cannula insertion is generally safe and is per formed routinely during pars plana vitrectomy, it remains invasive with inherent risks (e.g., retinal or vitreous in carceration,
Gardner et al · lOP and Scleral Buckling Surgery Table 1. Intraocular Pressure Fluctuations during Scleral Buckling Surgery Patient
Age (yrs)
lOP (mmHg)
1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20
78 70 62 41 75 57
22 6 20 12 8 24 10 25 6 12 9 12 9 18 9 12 18 15 18 12
No.
24
51 37 73 70 64 60 80 88 64 63 64
43
60
CRACP (mmHg)
Muscle (mmHg)
SD/CRYO (mmHg)
Suture (mmHg)
Buckle (mmHg)
Time lOP > CRACP (sees)
90
50 48 50 24 64
152 48 40 90 196 108 20 50
72 36 60 18 63 42 10 30 30 48 66 108 72 60 30 35 120 45 42 114
5 36 20 78 66 38 10 45 42 210 96 72 60 84
26
48 70 84
72 80 110 75 102 78 100 80 60 75 55 68 90
58 96 93
66
80 35 28 50 48 90 48 72 24 32 54 28 36 55
84
104 210 120 168 84 197 59 168 210 72 150
23
45 128 42 26 108
6 180 288
402 114 36 24 30 120 132 108 78
lOP = intraocular pressure (baseline); CRACP = central retinal artery closing pressure; Muscle =rectus muscle slinging; SD/CRYO =scleral depression/cryopexy; Suture = suture placement; Buckle =buckle element placement; Time lOP > CRACP = time in excess of the CRACP.
sclerosis had the lower central retinal artery closing pres sures. Likewise, older patients with concomitant vascular disease were significantly more Likely to have lOP eleva tions in excess of the central retinal artery perfusion pres sures. We could detect lOP fluctuations as low as I mmHg within I to 2 seconds in most patients. In two eyes, the tracing became dampened by the end of the procedure. Potential reasons for the decreased sensitivity include plugging of the infusion cannula by formed vitreous gel, leakage around the cannula site, or kinking of the poly ethylene tubing. In addition, eyes usually have a nearly normal lOP, ranging from I2 to 20 mmHg, in the early stages of the retinal reattachment procedure. However, scleral depression and cryopexy eventually soften the globe and increase the ocular capacitance (i.e., greater external force is required to cause a given increase in lOP than when the eye is firm). For this reason, fluctuations in lOP tended to diminish late in the operation. We continued our standard operative technique throughout this study. However, the surgeons were able to see the real-time lOP measurements intraoperatively. We cannot exClude the possibility that the surgeon or as sistant consciously or subconsciously altered their han dling of the eyes, particularly ifthe lOP was elevated. This may explain, in part, why the lOP elevations were typically transient. The surgeons did, in fact, use the lOP data dur ing surgery; for example, to avoid high lOP before sub-
retinal fluid drainage. Therefore, it is possible that the peak recorded lOPs underestimate the lOP elevations that would develop in the absence of the study. Fraunfelder and co-workers5 have previously described elevations ofiOP during scleral depression. They used an anterior chamber cannula and found peak lOPs ranging from I60 to 350 mmHg. These lOPs are generally higher than those found in this study. Potential sources of dif ferences include the method of measurement and the technique ofthe operating surgeons. Raizman and Beck 14 found lOPs ranging from 77 to 84 mmHg during extra ocular muscle manipulations for strabismus surgery using a pneumotonometer. Their data are consistent with the results of our study. The potential importance of lOP elevations during scleral buckling was initially addressed by Hilton. 15 In a 1986 survey of Retina Society members, he reported that 20 of 72 surgeons had never witnessed central retinal ar tery closure during scleral buckling without drainage. Forty-six surgeons had encountered approximately 775 cases in which the artery was closed for up to 5 minutes. None of the surgeons believed that intraoperative lOP elevations impaired postoperative visual recovery. Our data suggest that transient central artery occlusion is common during scleral buckling surgery. The consequences of increased lOPs on retinal vascular perfusion also have been studied in animals. In owl mon keys, lOPs greater than the ocular perfusion pressure de
1053
Ophthalmology
Volume 100, Number 7, July 1993
References
2so
0 200 +························+···························!···························+··········II···········+··························!···························+
¥ E
§. w a: ::;)
150
gj w
a: Q.
~
::;)
100
~ ~
50
lOP
CRACP
MUSClE
SD/CRYO
SUTURE
BUCKLE
Figure 3. Intraocular pressure fluctuations during scleral buckling surgery. The baseline intraocular pressure (lOP), central retinal artery closing pressure (CRACP), and the lOP fluctuations during scleral buckling surgery (Muscle= muscle slinging; SD/Cryo =scleral depression/cryo therapy; Suture = suture placement; Buckle = buckle element placement) are summerized for all20 patients. The bars represent the range of lOPs, the boxes contain 50% of the lOP values, and the horizontal line in each box is the mean lOP for each maneuver.
pressed the electroretinogram, but there was complete electroretinogram recovery when the duration ofiOP ele vation was less than 60 minutes. 16 Ernest and Potts 17 studied optic disc perfusion in rhesus monkeys with flu orescein angiography at baseline lOP and when the lOP was maintained at 80 mmHg. Comparison of arterial phase angiograms showed that the majority of small disc vessels were nonperfused in the eyes subjected to increased lOP, but not in the normotensive eyes. Two clinical conditions provide additional evidence for deleterious effects oftransient lOP elevations on optic disc function. First, anterior ischemic optic neuropathy after cataract extraction is thought to result from lOP spikes in eyes with vulnerable optic nerve head circula tion. 18 Second, a high lOP after argon laser trabeculoplasty can lead to central visual loss in eyes with glaucomatous optic nerve damage. 19 The relationship ofiOP elevations to retinal and optic nerve function, and to ultimate visual recovery after scleral buckling in humans, remains un known. Studies to determine the visual consequences of these lOP fluctuations are in progress.
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I. Burton TC, Lambert RW Jr. A predictive model for visual recovery following retinal detachment surgery. Ophthal mology 1978;85:619-25. 2. Tani P, Robertson DM, Langworthy A. Rhegmatogenous retinal detachment without macular involvement treated with scleral buckling. Am J Ophthalmol 1980;90:503-8. 3. Tani P, Robertson DM, Langworthy A. Prognosis for central vision and anatomic reattachment in rhegmatogenous ret inal detachment with macula detached. Am J Ophtha1mol 1981 ;92:611-20. 4. Blumenthal M, Cahane M, Ashkenazi I. Direct intraoper ative continuous monitoring of intraocular pressure. Ophthalmic Surg 1992;23: 132-4. 5. Fraunfelder FT, Boozman FW III, Wilson RS, Thomas AH. No-touch technique for intraocular malignant melanomas. Arch Ophthalmol 1977;95:1616-20. 6. Honda Y, Kawano S, Negi A, Koizumi K. Pressure profile of ophthalmic surgical procedures: an experimental study on the rabbit eye. Ophthalmic Surg 1982;13:387-91. 7. Moorhead LC, Armeniades CD. Variations in intraocular pressure during closed-system surgical procedures. Arch Ophthalmol 1986; 104:269-72. 8. Wolbarsht ML, Wortman J, Schwartz B, Cook D. A scleral buckle pressure gauge for continuous monitoring of intra ocular pressure. Int Ophthalmol 1980;3: 11-17. 9. Quillen DA, Gardner TW, Blankenship GW, Marshall WK. A method for real-time intraocular pressure measurement during scleral buckling. Graefe's Arch Clin Exp Ophthalmol (in press). I0. Schreuder M, Linssen GH. Intra-ocular pressure and an aesthesia. Direct measurements by needling the anterior chamber in the monkey. Anaesthesia 1972;27:165-70. II. Oyakawa RT, Schachat AP, Michels RG, Rice TA. Com plications of vitreous surgery for diabetic retinopathy. I. In traoperative complications. Ophthalmology 1983;90:517 21. 12. Faulborn J, Conway BP, Machemer R. Surgical complica tions ofpars plana vitreous surgery. Ophthalmology 1978;85: 116-25. 13. Blankenship GW. Endophthalmitis following pars plana vi trectomy. Am J Ophthalmoll977;84:815-17. 14. Raizman MB, Beck RW. Sustained increases in intraocular pressure during strabismus surgery. Am J Ophthalmol 1986;101:308-9. 15. Hilton GF. Planned elevation of intraocular pressure with temporary occlusion of the central retinal artery during ret inal surgery [letter]. Arch Ophthalmol 1986;104:975. 16. Gerstle CL, Anderson DR, Hamasaki DI. Pressure effect on ERG and optic nerve conduction ofvisual impulse: short term effects in owl monkeys. Arch Ophthalmol 1973;90: 121-4. 17. Ernest JT, Potts AM. Pathophysiology of the distal portion ofthe optic nerve. II. Vascular relationships. Am J Ophthal mol 1968;66:380-7. 18. Hayreh SS. Anterior ischemic optic neuropathy. IV. Oc currence after cataract extraction. Arch Ophthalmol 1980;98: 1410-16. 19. Thomas JV, Simmons RJ, Belcher CD III. Argon laser tra beculoplasty in the presurgical glaucoma patient. Ophthal mology 1982;89: 187-97.