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Postoperative visual loss following laparotomy
- Srikanth Chukkambotla, Sharon Smith, Consultant Anaesthetist.Whythenshawe Hospital, Manchester (25 October 2005)
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Postoperative visual loss: consider possible effects of anaesthetic agents on retrobulbar circulatio
- Thomas Geeraerts, Jean-Michel Devys (22 June 2005)
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Srikanth Chukkambotla, Specialist Registrar, Anaesthetics Whythenshawe Hospital, Manchester, Sharon Smith, Consultant Anaesthetist.Whythenshawe Hospital, Manchester
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We read with interest the case report ‘Postoperative visual loss following prone spinal surgery’ by D.Kamming and S Clarke [1] and would like to report another case of postoperative visual loss but with a probable different aetiology. A 62-year-old man with a history of diverticulitis presented with colonic obstruction and underwent an urgent laparotomy, right hemicolectomy and sigmoid colectomy. He had no significant past medical history, took Omeprazole for heartburn, smoked 15-20 cigarettes per day along with occasional intake of alcohol. Previous general anaesthetic about 25 years ago was uneventful. He was anaesthetised using total intravenous anaesthesia with propofol and remifentanil, and rocuronium . A thoracic epidural was inserted (awake) and perioperative analgesia provided with an infusion of 0.125% bupivacaine with fetanyl 2mcg/ml. An arterial line, central venous catheter and oesophageal doppler were used for cardiovascular monitoring. He was in the Lloyd-Davis position for the procedure which lasted 4 hours, with head down tilt (15-20 degrees) for some time. He received 5 litres of crystalloid and a litre of colloid. No blood products were required. There were no episodes of hypotension or arrhythmias. He had DVT prophylaxis with subcutaneous clexane and compression stockings. At the end of the operation his arterial blood gases were OK. He was nursed in HDU postoperatively for one night and made a good recovery over the next week. The patient noted reduced vision in the recovery period but didn’t complain during his hospital stay. However, he increasingly became aware of impaired vision to the left side of his visual field about a week after his discharge from hospital. He also complained of difficulties in reading and driving. He was referred to both a neurologist and an ophthalmologist. He was found to have a left homonymous upper quadrantonopia, otherwise ocular examination was unremarkable. No other neurological abnormalities were detected clinically. An MRI scan showed an infarction in the right occipital lobe and extensive white matter and vascular changes indicative of cerebrovascular disease. The ophthalmologist gave a poor prognosis for recovery and stated that in only 10-20% of cases was there likely to be any improvement in vision over a 12 -18 month period. No treatment was recommended. He underwent a second stage Hartman’s procedure 3 months later with no further deterioration in his vision. Though ischaemic optic neuropathy is the most frequently cited cause of postoperative visual loss (PVL) following general anaesthesia [2], in this particular case thromboembolism appears the most likely cause of PVL.There was no major blood loss, hypotension or anaemia and nothing obvious to explain PVL in this patient. Smoking, malignancy, major surgery and possibly patient position during surgery are the identified risk factors in this case which may have contributed to thromboembolism. The factors intrinsic to the patient (i.e. changes indicative of cerebrovascular disease which were subsequently shown on the MRI scan), combined with these other risk factors may have contributed to thromboembolism and resulted in PVL. Despite increased awareness of PVL, physicians remain helpless in preventing its occurrence because most of the cases have no proven etiology. The American Society of Anesthesiologists (ASA) Closed Claims Project established a Post-Operative Visual Loss Registry, to which 113 cases have been submitted since 1998 [3]. Although the preliminary data suggest unique etiologies for different types of ophthalmologic lesions causing postoperative visual loss, larger numbers of cases will be required before a meaningful statistical analysis can be performed [4]. It is important to highlight the need for reporting such rare but devastating complication. Such data collection and analysis would help to understand the etiology and mechanisms of PVL, so that perioperative strategies can be developed to prevent its occurrence. References: 1. D. Kamming and S. Clarke Postoperative visual loss following prone spinal surgery Br. J. Anaesth. 2005 95: 257-260; 2. Roth S, Thisted RA, Erickson JP, Balck S, Schreider BD: Eye injuries after nonocular surgery: A study of 60,965 anesthetics from 1988 to 1992. Anesthesiology 1996; 85: 1020-7 3. www.asaclosedclaims.org. Post-Operative Visual Loss Registry 4. Lee LA. ASA Postoperative Visual Loss Registry: Preliminary Analysis of Factors Associated with Spine Operations. ASA Newsletter 2003; 67(6): 7-8. Corresponding author e - mail: srikanth73@rediffmail.com Conflict of Interest:None declared |
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Thomas Geeraerts, Anesthesiology and Intensive care Hopital de Bicętre and Fondation Rotschild, Paris, France, Jean-Michel Devys
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We read with interest the article by Kamming and Clarke on a case report of postoperative visual loss in a 60 yr-old man after prolonged decompressive laminectomy in the prone position.(1) We completely agree with the discussion about aetiology of postoperative visual loss, but we would like to add some commentaries on retrobulbar circulation physiology. The authors assumed that the vessels involved in vascular supply of the posterior portion of the optic nerve (branches of the ophthalmic artery) are “incapable of autoregulatory control”. As we discussed in a recent article published in the British Journal of Anaesthesia (2), although the ocular circulation does not have any autonomic nerve supply, the ophthalmic and central retinal arteries have an autoregulation of their own blood flow.(3,4) Central retinal artery is tightly autoregulated by retinal endothelium derived factors as prostaglandin or endothelin.(5) Ophthalmic artery may have a different autoregulatory mechanism and vasoreactivity seems to be lower but the autoregulation in this artery is also efficient.(6) Effects on anaesthetic agents (i.v. or inhalated) on retrobulbar circulation are not well known. We demonstrated in children that high alveolar concentrations of sevoflurane (2 MAC) may enhance alterations in ophthalmic artery blood flow.(2) At 2 MAC sevoflurane, end diastolic velocity in ophthalmic artery decreased to 70% from 1 MAC value, whereas mean arterial pressure decreases only to 4%. In the case reported by Kamming and Clarke (1), anaesthesia was induced with midazolam, propofol and remifentanil, and maintained with isoflurane (0.9-1.2%) and remifentanil for more than 6 h. In the presented case, considering the minor anaesthesia-related decrease in systolic blood pressure (to a worse of 90 mmHg), the oculo-vascular effect of inhalated anaesthetic like isoflurane may have contributed to alterations in ophthalmic artery blood flow, even if a major decrease in perfusion pressure to the eye did not occurred. In addition, isoflurane has a more important intrinsic cerebral vasodilatory effect compared to sevoflurane.(7) The specific oculo-vascular effect of isoflurane is unknown, but we can hypothesise a similar or greater effect than sevoflurane. The discussion of this case report should consider the possibility of important vasodilatory effect of isoflurane in ophthalmic artery. If perfusion pressure decreases in an artery vasodilated by isoflurane, the ocular blood flow will be compromised, and optic nerve ischemia may occur. In conclusion and addition to this carefully discussed case report of postoperative visual loss, we could suggest for a explanation of ischemic optic neuropathy, the possible isoflurane-induced alteration in ophthalmic artery autoregulation in combination with moderate hypotension, anaemia, and increased intraocular pressure. References 1. Kamming D, Clarke S: Postoperative visual loss following prone spinal surgery. Br J Anaesth 2005; doi: 10; 1093 2. Geeraerts T, Devys JM, Berges O, Dureau P, Plaud B: Sevoflurane effects on retrobulbar arteries blood flow in children. Br J Anaesth 2005; 94: 636-41 3. Best M, Gerstein D, Wlad N, Rabinovitz AZ, Hiller GH: Autoregulation of ocular blood flow. Arch Ophthalmol 1973; 89: 143-8 4. Tachibana H, Gotoh F, Ishikawa Y: Retinal vascular autoregulation in normal subjects. Stroke 1982; 13: 149-55 5. Delaey C, Van De Voorde J: Regulatory mechanisms in the retinal and choroidal circulation. Ophthalmic Res 2000; 32: 249-56 6. Bornstein NM, Gur AY, Geyer O, Almog Y: Vasomotor reactivity in the ophthalmic artery: different from or similar to intracerebral vessels? Eur J Ultrasound 2000; 11: 1-6 7. Matta BF, Heath KJ, Tipping K, Summors AC: Direct cerebral vasodilatory effects of sevoflurane and isoflurane. Anesthesiology 1999; 91: 677-80 Conflict of Interest:None declared |
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