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Table of Contents
LETTER TO EDITOR  
Year : 2012  |  Volume : 15  |  Issue : 1  |  Page : 88-90
Irreversible loss of vision in a paediatric patient due to occipital infarction after cardiopulmonary bypass


Department of Anaesthesiology and Intensive Care and Cardiothoracic and Vascular Surgery. G. B. Pant Hospital, New Delh, India

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Date of Web Publication5-Jan-2012
 

How to cite this article:
Datt V, Virmani S, Malik I, Agarwal S, Joshi CS, Dhingra A, Dutta R, Tomar AS. Irreversible loss of vision in a paediatric patient due to occipital infarction after cardiopulmonary bypass. Ann Card Anaesth 2012;15:88-90

How to cite this URL:
Datt V, Virmani S, Malik I, Agarwal S, Joshi CS, Dhingra A, Dutta R, Tomar AS. Irreversible loss of vision in a paediatric patient due to occipital infarction after cardiopulmonary bypass. Ann Card Anaesth [serial online] 2012 [cited 2019 Nov 17];15:88-90. Available from: http://www.annals.in/text.asp?2012/15/1/88/91474


The Editor,

Visual loss due to occipital infarction, following cardiac surgery under cardiopulmonary bypass (CPB) may be due to microembolism from the extracorporeal circulation. It may be associated with low hematocrit levels, hypoxia and perioperative use of epinephrine and amrinone besides prolonged duration of bypass which is responsible for not only increased inflammatory response, higher levels of endogenous catecholamines but also causes greater microembolic load to the brain. [1] We report a case of postoperative blindness in a three-year-old male child who presented with double outlet right ventricle (DORV), restrictive ventricular septal defect (VSD), sub-aortic membrane and severe right ventricular infundibular stenosis. The child was premedicated with morphine (2 mg) and promethazine (5 mg) intramuscularly 1 h prior to the operation. In the operating room, electrocardiogram electrodes and pulse oximetry probe were applied. Anesthesia was induced with sevoflurane (5-7%) in 100% oxygen using bag-mask ventilation, and intravenous access established. This was followed by administration of fentanyl (70 mg) and thiopentone sodium (15 mg). Muscle relaxation was achieved with pancuronium bromide (2 mg) and the trachea was intubated with 4.5 mm internal diameter cuffed endotracheal tube. A 20-G cannula in the left femoral artery and 5 F triple lumen central venous catheter (Arrow, USA) via the right internal jugular vein were inserted for hemodynamic monitoring. Anesthesia was maintained with intermittent fentanyl, midazolam and pancuronium bromide. The CPB machine with a roller pump and membrane oxygenator was primed with whole blood (400 ml), ringer's solution (300 ml), mannitol (65 ml) and methylprednisolone (300 mg). The patient underwent an uneventful intracardiac repair (during surgery, the VSD was enlarged and the left ventricle was routed to the aorta using a large intracardiac baffle. The aorta was opened to excise the sub-aortic membrane. Infundibular resection was performed via the right atrium) under hypothermic CPB wherein the pump flow was kept between 2.4-1.8 liters/m 2 at 25°C and mean arterial pressure was maintained between 40-60 mm Hg. Hematocrit, arterial blood gases, electrolytes, base excess and blood glucose values were maintained within normal limits throughout the procedure. The total CPB time was 188 min and ischemia time was 157 min. Patient was weaned off CPB uneventfully with inotropic support of dobutamine (5 mg/kg/min), nitroglycerine (1 mg/kg/min) and adrenaline (0.05 mg/kg/min). The patient received one unit of fresh blood and one unit plasma per operatively. The patient was transferred to the intensive care unit (ICU) and extubated 24 h after surgery. On the second postoperative day it was noticed that the child was not focusing with his eyes when called. A neurological and ophthalmological examination revealed bilateral normal pupils reacting to light, normal motor functions and a normal fundus. However, brain magnetic resonance imaging (MRI) revealed infarcts in the posterior cerebral artery and left middle cerebral artery regions bilaterally [Figure 1] and [Figure 2]. The inotropic support was gradually tapered and discontinued by the fourth postoperative day. The rest of the postoperative course was uneventful. He was discharged from the hospital on the 11 th postoperative day with no improvement in his visual acuity. In the last follow-up four months after the surgery patient had perception of light only (avoidance response to light).
Figure 1: MRI brain showing T2 flair hyperintensities noted involving cortical and sub-cortical white matter in bilateral cerebral hemispheres (left>right) showing restriction on diffusion-weighted images involving bilateral posterior cerebral-middle cerebral and anterior cerebral-middle cerebral arteries' watershed territories

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Figure 2: Evidence of restriction noted in diffusion-weighted images involving bilateral occipital and parietal regions

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The overall incidence of perioperative vision loss (POVL) after all types of surgeries varies from 0.1 to 1%, while the frequency of POVL is 8.64/10,000 after cardiac procedures and approximately 0.024% is due to ischemic optic neuropathy (ION). The incidence estimate for POVL due to cortical blindness is about 81% in patients undergoing cardiac surgery involving CPB. [2],[3] There are various proposed etiological theories for ION. It may develop secondary to an interruption of oxygen supply to the optic nerve head anterior to the lamina cribrosa due to critically reduced blood supply or oxygen-carrying capacity. Several surgical and patient factors have been implicated in the reduction of blood flow in the posterior ciliary arteries and so inducing ischemia in the watershed zones. Embolism in the form of gaseous micro-bubbles, particulate micro-emboli and platelet-fibrin micro-aggregates is another etiological possibility. Cerebral embolism may be of pump origin or induced by the anesthetist. One of the main causes of cortical blindness is the use of extracorporeal circulation during cardiac surgery. Although heparin prevents thrombus formation, it does not prevent coagulum formation. Coagulum is heat-denatured fibrinogen which results from overheating at the cautery electrode tip and may embolise or form a nidus for thrombus formation. [4] In addition, a severe decrease in blood pressure, low hematocrit (<8.5 g/dl), emboli and thrombus mid or post surgery and vascular spasm in the presence of high catecholamine levels during hypothermic cardiopulmonary bypass can cause an infarction in the occipital cortex, which can lead to cortical blindness. [5],[6] In the present case, the development of bilateral visual loss is most likely due to the synergistic effect of a combination of factors like prolonged duration of CPB (188 min), complex cardiac procedure, perioperative use of epinephrine, and hypothermic (25°C) bypass. In addition microembolisation from the extracorporeal circulation or particulate matter from the roughened VSD edge or excised sub-aortic membrane or the large baffle used to route the VSD could have contributed to infarction of the occipital lobe.

In order to reduce the chances of neural sequelae after paediatric cardiac surgery, it is important to choose the CPB machine's circuit very carefully to minimize microembolisation. Acid base balance must be maintained preferably by the pH-stat method and whole blood or packed cells should be used for pump priming. Diagnosis of vision loss in a paediatric patient may be delayed or difficult as the patient may not communicate appropriately. Therefore, postoperative eye examination i.e. visual acuity, pupillary reaction, external ocular examination and tonometry should be performed to confirm loss of vision in both eyes. Evaluation by electroencephalogram, flash visual evoked potential, angiography and fundoscopy can assist in confirming the diagnosis. Transcranial Doppler has been reported to detect microembolic signals in the right middle cerebral artery in the patients with neural sequelae than without. [7] Recovery has been reported to begin after 28 days, [8] but in the present case even four months postoperatively, restoration of vision was only up to the perception of light.

In conclusion, visual loss due to occipital infarction should be kept in mind during complex cardiac surgery involving CPB. We also suggest an early ophthalmic evaluation in the paediatric age group. In addition, active efforts should be made to reduce embolic load, prolonged bypass time, low hematocrit, hypoxia and use of high-dose epinephrine.

 
   References Top

1.Blauth CI, Arnold JV, Schulenberg WE, McCartney AC, Taylor KM. Cerebral microembolism during cardiopulmonary bypass: Retinal microvascular studies in vivo with fluorescein angiography. J Thorac Cardiovasc Surg 1988;5:668-76.  Back to cited text no. 1
    
2.Williams EL, Hart WM Jr, Tempelhoff R. Postoperative ischemic optic neuropathy. Anesth Analg 1995;80:1018-29  Back to cited text no. 2
    
3.Berg KT, Harrison AR, Lee MS. Perioperative visual loss in ocular and nonocular surgery. Clin Ophthalmol 2010; 4:531-46.  Back to cited text no. 3
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4.Asirvatham SJ. Ablation for atrial fibrillation: Can we decrease thromboembolism without increasing the risk for bleeding. Circulation 2007;116:2517-9.  Back to cited text no. 4
[PUBMED]  [FULLTEXT]  
5.Bagheri J, Mandegar MH, Sarzaeem MR, Chitsaz S. Transient bilateral cortical visual loss after coronary artery bypass grafting in a normotensive risk-free patient. Heart Surg Forum 2008;11:E248-51.  Back to cited text no. 5
[PUBMED]  [FULLTEXT]  
6.Trittenwein G, Nardi A, Pansi H, Golj J, Burda G, Hermon M, et al. Early postoperative prediction of cerebral damage after cardiac surgery. Ann ThoracSurg 2003;76:576-80.  Back to cited text no. 6
    
7.Braekken SK, Russel D, Brucher R, Abdelnoor M, Svennevig JL. Cerebral microembolic signals during cardiopulmonary bypass surgery. Frequency, time of occurrence and association with patient and surgical characteristics. Stroke 1997;28:1988-92.  Back to cited text no. 7
    
8.Shin YD, Lim SW, Bae JH, Lee DH, Baek DH, Hoong JS. Transient cortical blindness after heart surgery in a child patient-A case report. Korean J Anesthesiol 2010;59:61-4.  Back to cited text no. 8
    

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Correspondence Address:
Vishnu Datt
Department of Anaesthesiolgy and Intensive Care, Academic Block, Room No. 619, G. B. Pant Hospital, New Delhi 110 002
India
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Source of Support: None, Conflict of Interest: None


DOI: 10.4103/0971-9784.91474

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