Article Access Statistics | | Viewed | 3617 | | Printed | 101 | | Emailed | 0 | | PDF Downloaded | 144 | | Comments | [Add] | |
|

 Click on image for details.
|
|
|
Year : 2017
| Volume
: 10 | Issue : 3 | Page
: 234-239 |
|
Intraocular pressure in children after congenital heart surgery: A single-center study |
|
Sunali Goyal1, Paul H Phillips1, Lamonda A Corder2, Michael J Robertson3, Xiomara Garcia3, Michael L Schmitz4, Punkaj Gupta3
1 Department of Ophthalmology, Jones Eye Institute, University of Arkansas for Medical Sciences; Department of Pediatric Ophthalmology, Arkansas Children's Hospital, Little Rock, Arkansas, USA 2 Department of Pediatric Ophthalmology, Arkansas Children's Hospital, Little Rock, Arkansas, USA 3 Department of Pediatrics, Division of Pediatric Cardiology, Arkansas Children's Hospital, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA 4 Department of Anesthesia, Division of Pediatric Anesthesia, Arkansas Children's Hospital, University of Arkansas for Medical Sciences, Little Rock, Arkansas, USA
Click here for correspondence address and
email
Date of Web Publication | 21-Aug-2017 |
|
|
 |
|
Abstract | | |
Background: The impact of varied cardiac physiologies on intraocular pressure (IOP) among children undergoing heart operations is unknown. Aim: The aim of this study was to determine the IOP among children with varying cardiovascular physiologies and varying hemodynamics after their heart operation. Setting and Design: This was a prospective, observational study. Materials and Methods: Patients ≤18 years undergoing congenital heart surgery were included in this study. IOP measurement was performed by Icare® tonometer between 3 and 14 days after heart operation. Statistical Analysis: Summary statistics were estimated for all demographic, anthropometric, and clinical data. Results: A total of 116 eyes from 58 children were included. The mean and standard deviation age was 28.4 (45.8) months. Single-ventricle anatomy was present in 26 patients (45%). Despite similar heart rate and blood pressure, the mean IOP among the patients with single-ventricle anatomy was significantly elevated as compared to patients with two-ventricle anatomy (18 mm Hg vs. 12 mm Hg, P < 0.001). There was no difference in IOP measurements based on the complexity of operation performed. We noted that patients undergoing surgical palliation with central shunt (21 mm Hg), Fontan operation (19 mm Hg), bidirectional Glenn operation (19 mm Hg), Norwood operation (19 mm Hg), or definitive repairs such as tetralogy of Fallot repair (17 mm Hg), and atrioventricular canal repair (19 mm Hg) were associated with the highest IOPs in the study cohort. Conclusions: This study demonstrates that IOPs vary with varying cardiovascular physiology after pediatric cardiac surgery.
Keywords: Congenital heart surgery, heart defects, intraocular pressure, single ventricle anatomy
How to cite this article: Goyal S, Phillips PH, Corder LA, Robertson MJ, Garcia X, Schmitz ML, Gupta P. Intraocular pressure in children after congenital heart surgery: A single-center study. Ann Pediatr Card 2017;10:234-9 |
How to cite this URL: Goyal S, Phillips PH, Corder LA, Robertson MJ, Garcia X, Schmitz ML, Gupta P. Intraocular pressure in children after congenital heart surgery: A single-center study. Ann Pediatr Card [serial online] 2017 [cited 2022 May 16];10:234-9. Available from: https://www.annalspc.com/text.asp?2017/10/3/234/213367 |
Introduction | |  |
Children undergoing surgery for congenital heart disease often require cardiorespiratory support in the form of mechanical ventilation, inotropes, and extracorporeal membrane oxygenation (ECMO) after their heart operation. These patients are exposed to cardiopulmonary bypass (CPB), hypothermia, and general anesthetics in the operating room. In addition, these patients can experience hypoxia, hypercarbia, excessive ventilator pressures, and hypothermia after heart operation in the Intensive Care Unit (ICU). Many of these factors taken together or in isolation have the potential to alter intraocular pressure (IOP).[1],[2],[3],[4],[5],[6]
Patients undergoing cardiac surgery are associated with varying cardiovascular physiologies, such as functionally single-ventricle physiology, right ventricle dysfunction, low cardiac output, or pulmonary hypertension that can potentially include elevated central venous pressures (CVPs). The increase in CVP inhibits blood efflux from the intraocular vessels leading to increase in IOP.[6] A marked increase in IOP can result in reduced optic nerve perfusion, potentially causing disc ischemia and irreversible optic nerve atrophy.[7],[8] Although there is adult literature on the link between cardiac surgery and ischemic optic neuropathy, the impact of varied cardiac physiologies on IOP among children undergoing cardiac surgery is yet to be evaluated.[9] We thus sought to determine the IOP among children with varying cardiovascular physiologies and hemodynamics after heart surgery.
Materials and Methods | |  |
Study patients
We performed a single-center, prospective, observational study in a 15-bed pediatric cardiovascular ICU at the Arkansas Children's Hospital during February 2013 to March 2014. The study population included children ≤18 years undergoing heart surgery for congenital heart disease. The following patients were excluded from the study: identifiable underlying genetic disorders, intracranial bleeds and/or with increased intracranial pressure (ICP), seizure disorders, gestational ages ≤34 weeks, retinopathy of prematurity, high frequency oscillatory ventilation, positive end-expiratory pressure (PEEP) ≥10, ECMO or ventricular assist devices at the time of IOP measurement, orthotopic heart transplantation, glaucoma, and under sedation or anesthesia with ketamine.
We collected demographic and anthropometric data as well as data related to the heart operation, risk adjustment for congenital heart surgery (RACHS),[10] CPB time, and aortic cross-clamp time. We also collected data on the use of mechanical ventilation, presence of internal jugular central venous catheter, and hemodynamic data (such as heart rate, blood pressure, oxygen saturation, and respiratory rate) at the time of IOP measurement. The Institutional Review Board of the University of Arkansas for Medical Sciences approved the study. An informed consent and assent (if applicable) were obtained after cardiac surgery before measurement of IOP.
Methodology for intraocular pressure measurement
IOP measurement was performed by Icare ® tonometer (Icare, Inc., Helsinki, Finland) from 3 to 14 days after heart operation. No anesthetic drops were used for IOP measurement. The Icare ® tonometer is easily portable, well tolerated, and yields reproducible results.[11],[12] The Icare ® tonometer's disposable probe touches the cornea lightly for only a fraction of a second and the tonometer self-calibrates every time it is turned on.[11],[12] The IOP was attempted one time in both eyes to obtain measurements. However, the measurements were repeated if the health-care provider performing the IOP measurement questioned the reliability due to position variability and cooperation of the patient. To minimize the interrater variability, IOP was measured by the same provider in all our study patients.
Statistical analysis
Summary statistics (e.g., mean and standard deviation (SD) for continuous variables, frequency, and percentage for categorical variables) were estimated for all demographic, anthropometric, and clinical data. The frequency and incidence of patients who had elevated IOP after congenital heart surgery were calculated. The software packages used included R v. 2.15.0 (R Development Core Team, Vienna, Austria).
Results | |  |
A total of 116 eyes from 58 children were enrolled during the study. The mean and SD age of patients was 28.4 (45.8) months. Single-ventricle anatomy was present in 26 patients (45%). A majority of the study patients (85%) required CPB for their heart operation. The mean and SD CPB time for the study patients was 99.9 (53.4) min. Only 5 (9%) patients received mechanical ventilation at the time of IOP measurement. The internal jugular central venous line was present among 8 patients (14%) at IOP measurement. Based on the complexity of operations performed, the majority of the study patients (79%) underwent low complexity operations (RACHS-I Categories 1–3) [Table 1].
The mean IOP for all patients was 12 (4) mm Hg in the right eye and 11 (4) mm Hg in the left eye [Table 2]. Despite similar heart rate and blood pressure, the mean IOP for patients with single-ventricle anatomy was significantly elevated as compared to patients with two-ventricle anatomy (single ventricle vs. two ventricle, 18 (6) mm Hg vs. 12 (3) mm Hg, P < 0.001). The mean CVPs in patients with single-ventricle anatomy were higher than patients with two-ventricle anatomy (single ventricle vs. two ventricle, 17 (4) mm Hg vs. 8 (3) mm Hg, P < 0.001). Oxygen saturations were significantly lower for patients with single-ventricle anatomy, as compared to those with two-ventricle anatomy (P < 0.001). The mean IOP for patients with right ventricle dysfunction, such as those after tetralogy of Fallot repair, was 16 (5) mm Hg. There was no difference in the IOP measurements based on the complexity of operation performed. The mean IOP for patients undergoing low complexity operations (RACHS-I Categories 1–3) was 14 (4) mm Hg, compared to mean IOP of 15 (4) for high complexity operations (RACHS-I Categories 4–6). | Table 2: Intraocular pressure measurements and hemodynamic parameters among the study patients
Click here to view |
[Table 3] depicts the patients with maximum IOPs in our study population. We noted that patients undergoing surgical palliation with central shunt, Fontan operation, bidirectional Glenn operation, Norwood operation, or definitive repairs such as for tetralogy of Fallot and AVC, were associated with highest IOPs in the study cohort. To note, none of these patients was receiving mechanical ventilation or inotropes at the time of IOP measurement. One patient after atrioventricular canal repair had an internal jugular central venous catheter in place at the time of IOP measurement. The patients with elevated IOPs had stable hemodynamics at the time of IOP measurement. [Figure 1] depicts schematic representation of pathophysiological mechanism of elevated IOP after the bidirectional Glenn operation. | Figure 1: Schematic representation of pathophysiological mechanism of elevated intraocular pressure after bidirectional Glenn operation
Click here to view |
Discussion | |  |
This single-center study demonstrates that IOPs may vary with cardiovascular physiology after pediatric cardiac surgery. Our study demonstrates that certain cardiovascular physiologies, such as occur with single-ventricle anatomy and right ventricle dysfunction are prone to elevated IOPs after heart surgery. We also demonstrate that variation in IOP after heart operation is not dependent on the complexity of the heart operation performed.
The IOP of the eye is determined by the balance between the production of aqueous humor by the eye and the ease with which it exits the eye. The relationship between IOP, aqueous humor formation, and venous pressure is described by the formula IOP = F/C + EVP, where F is the aqueous humor formation rate, C is the outflow rate, and EVP is the episcleral venous pressure.[13] EVP is an important factor that regulates IOP. Normal EVP is 8–10 mm Hg, but it can be raised by clinical entities that obstruct venous outflow such as obstruction of superior vena cava or superior vena cava syndrome, thyroid ophthalmopathy, retro-orbital tumors, cavernous sinus thrombosis, or orbital vein thrombosis.[13],[14],[15],[16] Theoretically, factors such as tension pneumothorax, pleural effusion, cardiac tamponade, mechanical ventilation and PEEP, pulmonary hypertension, and pulmonary embolism are associated with elevated CVPs, thereby leading to elevated IOP.[17] In addition, other conditions such as low cardiac output (e.g., in ventricular failure) results in elevated preload in the central venous circulation and elevated CVPs.[17] In our study, only one patient with elevated IOP was mechanically ventilated at the time of IOP measurement. To the best of our knowledge, none of our study patients with elevated IOP had medical conditions such as pneumothorax, pleural effusion, or pulmonary embolus at the time of IOP measurement. However, it is possible that some of our patients with elevated IOPs had cardiac dysfunction after heart operation leading to elevated IOP.
In patients with single-ventricle anatomy, one adequately-sized functional ventricle (right or left) is available to pump blood into both systemic and pulmonary circulations. The blood flow in patients with single-ventricle anatomy depends on various factors such as flow across the atrial septum, myocardial contractility, systemic vascular resistance, pulmonary vascular resistance, atrioventricular valve regugitation, cardiac output, end-diastolic volume, rate of venous return, and/or obstruction to venous return.[18],[19] Derangement of any of these factors in patients with single-ventricle anatomy can potentially lead to compromised venous return leading to elevated IOP. In certain single-ventricle physiologies, such as bidirectional Glenn circulation or Fontan circulation, pulmonary blood flow is passive and is dependent on rate of venous return. In these patients, compromised pulmonary circulation, hypervolemia, or ventricular dysfunction can lead to elevated CVP, that in turn, can lead to elevated IOP.[20] In our study, patients with elevated IOPs were also associated with higher CVPs.
It has been suggested that IOP may be a surrogate measure of ICP.[21],[22] Increased IOPs may cause engorgement of the orbital compartments through pressure-induced dilation of the episcleral veins, manifesting as increased IOP.[21],[22] In a recent study, 76 concurrent ICP and IOP measurements in 27 patients in emergency medicine settings were correlated.[21] All patients with an abnormal ICP had an abnormal IOP; similarly, all patients with a normal ICP had a normal IOP. The authors' concluded that an abnormal IOP, as measured with the handheld tonometer, is an excellent indicator of abnormal ICP.[21] It is possible that patients with elevated IOPs in our study also had elevated ICP. However, this is just a speculation, as we do not have any definitive data on ICP in our study patients.
The results from this study are subject to the limitations of all observational analyses, including selection bias, residual confounding, and measurement by error. The small sample size and single-center study may limit the generalizability of our results. Another limitation is related to the heterogeneity of patient populations undergoing heart operation and differences in diagnoses that may affect the IOP measurements. Our study patients did not have objective measurements for cardiac output that could have provided a better insight into the pathophysiology of the increased IOP. Our study also lacked data on ICPs that precluded us from making any meaningful association between ICP and IOP after pediatric cardiac surgery. Our study also lacked follow-up among patients with elevated IOP. Our study lacked IOP measurements before cardiac surgery. It is possible that certain patient populations (such with single-ventricle anatomy, right ventricle dysfunction) had elevated IOP even before the cardiac surgery. Given the small number of patients with elevated IOP in our study, we could not perform multivariable models to study risk factors associated with elevated IOP in children undergoing heart operations.
The purpose of this study was to compare IOPs among varied cardiovascular physiologies after pediatric cardiac surgery with an attempt to tease out associations between varied cardiovascular physiologies and IOP measurement. Even though the IOPs for majority of the study patients fell within normal limits, the IOPs in certain cardiovascular physiologies were higher, as compared to patients with other physiologies. Given the limitations of our study, this study should be considered as hypothesis generating. Based on these results, we recommend obtaining a complete ophthalmologic examination (including posterior chamber, optic nerve, optic disc) among patients with potential for elevated IOPs, both before and after their heart operation. As there can be multiple factors associated with elevated IOP during acute illness, we recommend that care providers managing these patients provide timely evaluation and intervention (if needed). As increased IOP can result in optic nerve damage, close ophthalmology follow-up is needed among certain patient populations (such as patients with single-ventricle anatomy and patients with right ventricle dysfunction) even after hospital discharge until the IOP is normalized. In case of persistent elevation of IOP, a glaucoma specialist should evaluate these children.
Conclusions | |  |
This study demonstrates that IOPs may be altered by varying cardiovascular physiology after congenital heart surgery. Certain cardiovascular physiologies, such as single-ventricle anatomy and right ventricle dysfunction are prone for higher IOP after heart operation, as compared to other physiologies, such as two-ventricle physiology. We recommend future studies with invasive hemodynamic monitoring to understand the pathophysiological mechanisms of elevated IOP after congenital heart surgery. We also recommend a future study with a larger number of patients in individual surgical categories to substantiate the results and determine the pathophysiological mechanisms responsible for altering the IOP in patients that undergo cardiac surgery.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Runciman JC, Bowen-Wright RM, Welsh NH, Downing JW. Intra-ocular pressure changes during halothane and enflurance anaesthesia. Br J Anaesth 1978;50:371-4.  [ PUBMED] |
2. | Dear GD, Hammerton M, Hatch DJ, Taylor D. Anaesthesia and intra-ocular pressure in young children. A study of three different techniques of anaesthesia. Anaesthesia 1987;42:259-65.  [ PUBMED] |
3. | Potter DE, Rowland JM. Adrenergic drugs and intraocular pressure: Effects of selective beta-adrenergic agonists. Exp Eye Res 1978;27:615-25.  [ PUBMED] |
4. | Buehner E, Pietsch UC, Bringmann A, Foja C, Wiedemann P, Uhlmann S. Effects of propofol and isoflurane anesthesia on the intraocular pressure and hemodynamics of pigs. Ophthalmic Res 2011;45:42-6.  [ PUBMED] |
5. | Samuel JR, Beaugié A. Effect of carbon dioxide on the intraocular pressure in man during general anaesthesia. Br J Ophthalmol 1974;58:62-7. |
6. | Teba L, Viti A, Banks DE, Fons A, Barbera M, Hshieh PB. Intraocular pressure during mechanical ventilation with different levels of positive end-expiratory pressure. Crit Care Med 1993;21:867-70.  [ PUBMED] |
7. | Chauhan BC, Pan J, Archibald ML, LeVatte TL, Kelly ME, Tremblay F. Effect of intraocular pressure on optic disc topography, electroretinography, and axonal loss in a chronic pressure-induced rat model of optic nerve damage. Invest Ophthalmol Vis Sci 2002;43:2969-76.  [ PUBMED] |
8. | Grozdanic SD, Betts DM, Sakaguchi DS, Kwon YH, Kardon RH, Sonea IM. Temporary elevation of the intraocular pressure by cauterization of vortex and episcleral veins in rats causes functional deficits in the retina and optic nerve. Exp Eye Res 2003;77:27-33.  [ PUBMED] |
9. | Tice DA. Ischemic optic neuropathy and cardiac surgery. Ann Thorac Surg 1987;44:677.  [ PUBMED] |
10. | Jenkins KJ, Gauvreau K, Newburger JW, Spray TL, Moller JH, Iezzoni LI. Consensus-based method for risk adjustment for surgery for congenital heart disease. J Thorac Cardiovasc Surg 2002;123:110-8.  [ PUBMED] |
11. | Flemmons MS, Hsiao YC, Dzau J, Asrani S, Jones S, Freedman SF. Icare rebound tonometry in children with known and suspected glaucoma. J AAPOS 2011;15:153-7.  [ PUBMED] |
12. | Flemmons MS, Hsiao YC, Dzau J, Asrani S, Jones S, Freedman SF. Home tonometry for management of pediatric glaucoma. Am J Ophthalmol 2011;152:470-8.e2. |
13. | Rhee DJ, Gupta M, Moncavage MB, Moster ML, Moster MR. Idiopathic elevated episcleral venous pressure and open-angle glaucoma. Br J Ophthalmol 2009;93:231-4.  [ PUBMED] |
14. | Greenfield DS. Glaucoma associated with elevated episcleral venous pressure. J Glaucoma 2000;9:190-4.  [ PUBMED] |
15. | Weinreb RN, Karwatowski WS. Glaucoma associated with elevated episcleral venous pressure. The Glaucomas. St. Louis: Mosby; 1996. p. 1143-55. |
16. | Ho YJ, Yeh CH, Lai CC, Huang JC, Chuang LH. ExPRESS miniature glaucoma shunt for intractable secondary glaucoma in superior vena cava syndrome - A case report. BMC Ophthalmol 2016;16:125. |
17. | Luecke T, Pelosi P. Clinical review: Positive end-expiratory pressure and cardiac output. Crit Care 2005;9:607-21.  [ PUBMED] |
18. | Ohye RG, Sleeper LA, Mahony L, Newburger JW, Pearson GD, Lu M, et al. Comparison of shunt types in the Norwood procedure for single-ventricle lesions. N Engl J Med 2010;362:1980-92.  [ PUBMED] |
19. | Lee TM, Aiyagari R, Hirsch JC, Ohye RG, Bove EL, Devaney EJ. Risk factor analysis for second-stage palliation of single ventricle anatomy. Ann Thorac Surg 2012;93:614-8.  [ PUBMED] |
20. | Schwartz SM, Lu M, Ohye RG, Hill KD, Atz AM, Naim MY, et al. Risk factors for prolonged length of stay after the stage 2 procedure in the single-ventricle reconstruction trial. J Thorac Cardiovasc Surg 2014;147:1791-8, 1798.e1-4. |
21. | Lashutka MK, Chandra A, Murray HN, Phillips GS, Hiestand BC. The relationship of intraocular pressure to intracranial pressure. Ann Emerg Med 2004;43:585-91.  [ PUBMED] |
22. | Spentzas T, Henricksen J, Patters AB, Chaum E. Correlation of intraocular pressure with intracranial pressure in children with severe head injuries. Pediatr Crit Care Med 2010;11:593-8.  [ PUBMED] |

Correspondence Address: Punkaj Gupta Department of Pediatrics, Arkansas Children's Hospital, University of Arkansas for Medical Sciences, One Children's Way, Slot 512-3, Little Rock, Arkansas USA
 Source of Support: None, Conflict of Interest: None  | Check |
DOI: 10.4103/apc.APC_41_17

[Figure 1]
[Table 1], [Table 2], [Table 3] |
|
|
|
 |
 |
|
|
|