Acta Anaesthesiol Scand 2008; 52: 307309 Printed in Singapore.

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r 2007 The Authors Journal compilation r 2007 The Acta Anaesthesiologica Scandinavica Foundation ACTA ANAESTHESIOLOGICA SCANDINAVICA

doi: 10.1111/j.1399-6576.2007.01505.x

Case Report

Intraoperative anisocoria in a child during renal transplantation

1 Department of Anaesthesiology, Intensive Care Medicine and Pain Therapy, Knappschaftskrankenhaus Bochum Langendreer, University hospital, Bochum, Germany, 2Department of Anaesthesiology and 3Department of Paediatric Radiology, University Medical Center HamburgEppendorf, Hamburg, Germany

C. REMPF1,2, K. HELMKE3, A. GOTTSCHALK1, F. FAROKHZAD2 and M. A. BURMEISTER2

Anisocoria during anaesthesia may indicate a serious neurological condition. Assessment by physical examination and diagnostic imaging is limited during surgery and anaesthesia. We report a case of a boy undergoing renal transplantation, who suffered from anisocoria during general anaesthesia. A transcranial sonography was performed, showing no intracranial pathology. However, retinal hypoperfusion detected with orbital doppler sonography was a plausible explanation for anisocoria.

Accepted for publication 28 August 2007

Key words: Anisocoria; transcranial sonography; central artery blood ow.

r 2007 The Authors Journal compilation r 2007 The Acta Anaesthesiologica Scandinavica Foundation

EVELOPMENT of anisocoria during anaesthesia may indicate a cerebrovascular event, a mass lesion, cerebral trauma or oedema. Diagnosis of intracranial pathology may require a cranial computed tomography scan, which is costly, time consuming and requires the transfer of the patient to radiology. Interruption of surgery is sometimes not possible. Anisocoria may be caused by impaired ocular blood ow, which can result in blindness from ischaemic retinal cell damage. Evidence of elevated intracranial pressure and impaired ocular blood ow can be obtained by cranial ultrasound in the operating room. We report a case of anisocoria in a child during renal transplantation.

Case report
A 7-year-old boy was scheduled for a second renal transplantation caused by renal failure due to severe perinatal asphyxia. He further suffered from convulsions as well as growth and mental retardation. Renal support was initially performed by peritoneal dialysis complicated by peritonitis
This case occurred at the University hospital Hamburg Eppendorf, Germany.

and intermittent haemodialysis was necessary. A primary renal transplantation was performed 1 year ago. The transplanted kidney was rejected and explanted 6 weeks after the transplantation. Nine months later, the boy (ASA III; weight 17 kg, height 100 cm) was admitted for a second transplantation. His medication consisted of nifedipine 20 mg/day, prazosin 2 mg/day, ferric-II-ion 30 mg/ day, rifampicin 50 mg/day and dimeticone 80 mg/ day. The boy was normotensive pre-operatively (100/65 mmHg). The boy was orally pre-medicated with midazolam (6.8 mg). An intravenous access (18 G) had already been established on the right-mid-forearm at the ward. After IV atropine (0.25 mg), general anaesthesia was induced with IV etomidate (7 mg), sufentanil (7.5 mg) and cis-atracurium (2 mg). Following intubation with a 5.0 mm tracheal tube, anaesthesia was maintained with 40% oxygen in air and end-tidal sevourane concentration at 2.2 3.5. Additional sufentanil and cis-atracurium were administered as needed. A central venous catheter (CVC) was inserted in the right jugular vein using the anterior approach. The pupil size and reaction before and after induction of anaesthesia and insertion of the CVC were normal. The head of the supine-positioned patient was placed in a

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neutral forward position. His eyes were treated with an ophthalmic ointment (dexpanthenol eye salve) and taped. Direct pressure on the eyes was avoided during the whole procedure. Immune suppression was started with prednisolone 175 mg IV. According to institutional preference, uid therapy was started with 0.9% saline in a continuous-rate infusion of 99 ml/h to elevate the central venous and aterial pressures. Adhesions led to prolonged surgery and uid boli became necessery to keep haemodynamic variables within 20% of values recorded before anaesthesia. A total of 1500 ml NaCl 0.9% and 50 ml human albumin 5% were infused over a period of 7 h. Central venous pressure (CVP) varied between 4 and 11 mmHg. Systolic blood pressure remained between 110 and 80 mmHg during surgery and the heart rate varied between 80 and 110 beats per minute. The lowest mean blood pressure was 50 mmHg. High potassium levels (6.3 mmol/l) were treated with glucose (20 ml G5% and 20 ml G20%) and insulin (10 IE). Additionally, calcium chloride (10%, 12 ml) and sodium bicarbonate (8.4%, 58 ml) were administered. Four hours after induction of anaesthesia the left pupil was found to be larger than the right. However, mydriasis slowly developed on both sides, but was more pronounced for the left pupil. Both pupils reacted poorly to direct light stimulus. The patient showed a bilateral conjunctival chemosis. Additional dosages of sufentanil (a total of 45 mg IV in 30 min) were administered and the exspiratory concentration of sevourane was increased from 2.2 up to 3.0 vol%. The surgeons were informed and it was decided that the transplantation could not be interrupted for a computed tomographic head scan. A transcranial ultrasound was performed intraoperatively (Philips ATL-HDI 5000, 12 MHz linear array probe; Phillips Medizin Systeme, Hamburg, Germany) by a paediatric radiologist. Intracranial ventricular dimensions and parenchyma were normal without any midline shift. Cerebral blood ow velocity by transcranial doppler mode in the major arteries of the circle of Willisi was not impaired. Orbital ultrasound showed no papilloedema and a normal diameter of the optic nerve sheath. Blood ow in both central retinal arteries was severely impaired with no holodiastolic and a reduced systolic ow velocity (Fig. 1). The arterial pressure was increased with administration of norepinephrine (0.030.06 mg/Kg min) and the pupil size and reaction returned to normal within a few minutes.

Fig. 1. Orbital spectral waveforms obtained from the right artery centralis retinae of the patient during surgery. The circulation of the right as well as the left eye (data not shown) was characterized by reduced blood ow velocity. During the diastolic phase, the blood ow velocity decreases continuously reaching zero value, and straight away there is a reversion of ow direction.

Sonography after surgery conrmed a normal cerebral and retinal perfusion without any intracranial pathology. On awaking, the boy did not require norepinephrine. After extubation, his alertness did not differ from the status documented before induction of anaesthesia and vision was not impaired.

Discussion
During renal re-transplantation we observed an impairment of retinal blood ow, indicated by a missing holodiastolic and reduced systolic ow velocity that probably resulted in alteration of the afferent limb of the pupillary reex leading to initial anisocoria. There are two sources of blood supply to the retina (1). The central retinal artery supplies blood to the inner layers and the choriocappillaris to the outer layers. Hence, the sphincter pupillae muscle is not innervated by parasympathic bres arising in the EdingerWestphal nucleus and the sympathetic nerve supply to the dilator pupillae muscle received intact nerve activity via the superior cervical ganglion. The patients retinal vascular occlusive disease could be associated with the use of large volumes of crystalloids increasing intraoperative ocular pressure (2) and decreased retinal perfusion. Moreover, decreased perfusion pressure in the retina may be inuenced by increased central venous pressure. In addition, a minimum mean systolic

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blood pressure of 50 mmHg may not be sufcient for retinal perfusion in a patient with arterial hypertension and potentially abnormal autoregulation. However, because the posterior ciliary arteries were not identied using colour Doppler sonography and an opthalmological examination was not performed, we cannot distinguish between ischaemic optic neuropathy and ischemia by impairment of retinal blood ow, even if a papilloedema was not detectable by sonography. Cranial and orbital ultrasound should be considered during surgery to screen for elevated intracranial pressure (3) when wake-up test or emergency computerized tomography of the brain are not possible.

References
1. Bill A. Blood circulation and uid dynamics in the eye. Physiol Rev 1975; 55: 383417. 2. Abbott MA, McLaren AD, Algie T. Intra-ocular pressure during cardiopulmonary bypass a comparison of crystalloid and colloid priming solutions. Anaesthesia 1994; 49: 3436. 3. Helmke K, Burdelski M, Hansen HC. Detection and monitoring of intracranial pressure dysregulation in liver failure by ultrasound. Transplantation 2000; 70: 3925. Address: Dr Christian Rempf Department of Anaesthesiology Intensive Care Medicine and Pain Therapy Knappschaftskrankenhaus Bochum Langendreer University hospital In der Schornau 23-25 44892 Bochum Germany e-mail: rempf@anaesthesia.de

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