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Print version ISSN 0034-7094
On-line version ISSN 1806-907X
Rev. Bras. Anestesiol. vol.56 no.3 Campinas May/June 2006
Optic nerve ischemia after spine surgery. Case report*
Isquemia del nervio óptico después de la intervención quirúrgica en la columna vertebral. Relato de caso
Clóvis Marcelo CorsoI; Pedro Paulo Tanaka, TSAII; Karina KhonIII
do Hospital Vita
IIProfessor Adjunto da Disciplina de Anestesiologia da UFPR. Responsável pelo CET/SBA do HC-UFPR, Anestesiologista do Hospital Vita
IIIME2 do HC-UFPR
OBJECTIVES: Visual loss is an uncommon complication in the postoperative
period of non-ocular procedures and its incidence may be confirmed by the increasing
number of studies in the international literature. This report aimed at describing
a case of anopsia after prone spinal procedure.
CASE REPORT: Male patient, 58 years old, body mass index of 37.6 scheduled for spinal cord decompression associated to lumbar spine arthrodesis. Clinical history of smoking and untreated hypertension. Normal physical, lab and cardiologic exams. Patient was anesthetized with general anesthesia associated to epidural catheter. There were no intraoperative complications. The day after, patient presented with ocular proptosis, conjunctival edema and left visual loss.
CONCLUSIONS: This case evidences the possibility of visual loss after prone spine surgery. Ischemic optic neuropathy results from the unbalance between optic nerve oxygen supply and demand as a consequence of increased intraocular pressure (IOP) as compared to systemic blood pressure, determining poor nervous tissue perfusion. Although the cause of this complication is still not explained, risk factors may be advanced age, atherosclerosis, diabetes mellitus, hypertension, smoking, changes in vascular supply and procedure duration.
Key Words: COMPLICATIONS: amauroses, ischemic optic neuropathy; DISEASES: arterial hypertension, obesidity; POSITION: ventral decubito; SURGERY, Neurosurgery: lumbar vertebral cord.
Y OBJETIVOS: La pérdida de la visión es una de las complicaciones
poco comunes que pueden ocurrir en el posoperatorio de operaciones no oftalmológicas,
y su incidencia puede ser constatada por el creciente número de estudios
disponibles en la literatura internacional. El objetivo de este relato fue el
de mostrar un caso de anopsia después de cirugía de columna vertebral
en posición prona.
RELATO DEL CASO: Paciente del sexo masculino, 58 años, índice de masa corporal de 37,6, con operación propuesta de descompresión medular asociada a la artrodesis de columna lumbar. Historial de tabaquismo e hipertensión arterial sin tratamiento. Exámenes físicos, de laboratorio y cardiológicos normales. La técnica anestésica utilizada fue la asociación de anestesia general con catéter peridural. No hubo ninguna complicación en el intraoperatorio. Al día siguiente, presentó proptosis ocular, edema conjuntival y pérdida visual en el ojo izquierdo.
CONCLUSIONES: El caso evidencia la posibilidad de la pérdida visual después de la intervención quirúrgica de columna con el paciente en posición prona. La neuropatía óptica isquémica es el resultado del desequilibrio entre la oferta y la demanda de oxígeno en el nervio óptico a causa del aumento de la presión intra ocular (PIO) con relación a la presión arterial sistémica, determinando la mala perfusión del tejido nervioso. Aunque todavía no esté clara la causa de esa complicación, pueden tenerse en cuenta como factores de riesgo, la avanzada edad, arteriosclerosis, diabetes melito, hipertensión arterial, tabaquismo, alteraciones en el suministro vascular y la duración del procedimiento.
Visual loss after non-ocular procedure, although uncommon, is one of the most devastating postoperative complications. Its incidence in general population is 1:125,000 1 being 75 times more frequent in patients submitted to cardiac procedures 2. Several reports were published in the last decade relating visual loss to prone spine surgery 3-5. This report aimed at describing a case of anopsia after prone spine surgery.
Male patient, physician, 58 years old, 114 kg, 1.74 m, scheduled for spinal cord decompression associated to arthrodesis (L2-L3-L4). Co-morbidities were smoking (15 cigarettes a day for 40 years) and untreated hypertension. Physical evaluation was normal with pressure levels of 120 x 80 mmHg. Lab tests with hemoglobin: 15 g/dL; hematocrit: 43%, platelets: 182,000/mm3; creatinine: 0.9 mg/dL; INR: 1.02 and normal ECG. Patient was anesthetized with general anesthesia associated to epidural catheter for postoperative analgesia.
Patient was placed in the prone position with support over chest and hip, with lateral rotation of the head which was placed on a ring shape pad. Volume was replaced after procedure, which lasted 5 hours 30 minutes, with 3.5 liters of 0,9% saline solution. There was no hypotension or any other intraoperative complication and epidural 80 mg of 1% ropivacaine and 1 mg morphine were used in the intraoperative period. Back to the ward, patient referred left visual loss but attributed it to residual anesthesia. The day after, patient presented severe ocular proptosis, conjunctival edema and visual loss. Investigation consisted of eyegrounds, MRI, magnetic angioresonance and brain arteriography. Initial treatment consisted of manitol, acetazolamide and steroids.
A randomized study has shown that the incidence of visual deficit in spine surgery is 1:60,000 6. Blood supply to sensory parts of the eye comes from the central artery from retina, which is the first intracranial branch of the ophthalmic artery. Remaining irrigation comes from long and short posterior ciliary arteries irrigating the choroid with branches to the meninges involving the optic nerve 7.
Central artery of retina enters the optic nerve posteriorly bifurcating close to the optic disk. Central artery of retina is responsible for venous drainage and discharge at the cavernous sinus 7.
By definition, ischemic optic neuropathy results from the unbalance between optic nerve oxygen supply and demand, leading to nervous fibers injury. Visual deficit causes may be: a) anterior and posterior ischemic optic neuropathy, b) central artery or vein of retina occlusion, or c) cortical blindness of hypotensive or embolic cause 7.
Posterior optic nerve, located between the orbital foramen until central artery of retina bifurcation is the most susceptible region for ischemia because its blood supply comes solely from pia-mater vessels 7.
There are ischemic neuropathy-related etiologic factors and much of what is known comes from patients not submitted to surgical procedures. Among predisposing factors 7, one may stress advanced age, atherosclerosis, diabetes mellitus, hypertension, smoking and vascular supply changes. Our patient had history of untreated hypertension and smoking.
Others are considered triggering factors 7: a) venous obstruction by head positioning in rotation impairing venous return. In our case, rotation was minor and we checked to confirm the absence of external compression on the eye during surgery, since head was placed on a ring shape pad; b) intraoperative hypotension. There have been no significant blood pressure changes in our case, so that there was no need for vasopressors.
Decreased hematocrit and increased blood viscosity are also part of this list. In our case, immediate postoperative hematocrit was 29%. Major CSF loss was speculated as one possible explanation. Without CSF circulation in posterior optic nerve, there could be arterial flow impairment and consequent venous block 8.
The American Society of Anesthesiologists has normalized since 1999 the Record of visual loss during surgical procedures and 67% of reports were related to prone spine surgery 9.
In a study 10 comparing positioning effects on intraocular pressure (IOP) involving 20 patients submitted to prone spine surgery wit head fixation with pins and the head in the straight position, there has been significant IOP increase when patients' position was changed from supine to prone, suggesting that other factors, in addition to intraocular pressure, would be responsible for this increase.
In general, patients remain with the head slightly lower than body and this could lead to increased IOP. This pressure increase mechanism was proven by the evaluation of patients in the head-down position 10. The mechanism of this increase could be related to higher episcleral vessels pressure. It should always be reminded that ocular perfusion pressure is the result of the difference between mean blood pressure and IOP. So, a neutral head position with regard to body could decrease such effects.
Mechanically ventilated patients often present decreased expired CO2 with increased gradient 11. Hypocapnia could then be a hypothesis for ischemic neuropathy. However, Lee et al. 12 have shown that, paradoxically, decreased circulating CO2 leads to increased ophthalmic artery flow, evaluated by intracranial Doppler. However, an editorial related to the study states that normocapnia is a safe state 13.
High fluid volumes infusion may be related to increased eye venous pressure, which would reflect in increased intraocular pressure 14. This hypothesis would be one more factor commonly found in this type of procedure where crystalloid infusion has varied in the literature from 4 to 14 liters 15. Our patient received a total of 3.5 liters of 0.9% saline solution throughout the procedure.
Prolonged procedures, with mean duration of more than seven hours in reviewed studies 15, may also be considered a risk factor for the development of optic nerve ischemia. However, there is a report of a patient submitted to a 2-hour laminectomy procedure, without hypotension or excessive blood loss 9.
Early diagnosis of this complication is critical since adequate therapy may improve results, although not in all cases. Posterior ischemia is present in approximately 60% of cases in the first 24 postoperative hours 15, calling the attention for the need for immediate ophthalmologic evaluation if this complication is suspected. Maybe for being a health professional, our patient has only reported the fact the next day.
Management is optimized to reestablish optic nerve circulation. Manitol, acetazolamide and even timolol may be prescribed to decrease IOP and the two former drugs were used in our case. Due to the impossibility of performing eyeground tests, systemic steroid therapy was started, considering the differential diagnosis of arteritis 16. To rule out vascular diseases, both central artery and vein of retina occlusion, imaging tests were performed (magnetic angioresonance and brain arteriography) which have discarded the possibility. Some form of improvement is reported in 65% of patients 15. In our case, patient remained amaurotic. All approaches described were adopted because the possibility of complication by external compression was totally ruled out and confirmed by the evaluation by two well-known ophthalmologists.
Optic nerve ischemia seems to be a multifactorial problem without a well-established mechanism. The question is how to prevent a situation in which procedure duration, hypotension and volume loss are common conditions. Although there are still no confirming data, as it is the case with patients submitted to cardiac procedures, the suggestion is to prevent perioperative hypotension and anemia to decrease the possibility of ischemia. A protocol to handle blood pressure, bleeding and volume replacement is recommended in addition to a thorough evaluation when deliberate hypotension takes advantage of is worse than possible risks. Abdomen compression and head lower than body should be prevented and, in some cases, surgery should be performed in two stages 9,15. Immediate postoperative visual acuity should be evaluated in an attempt to obtain early diagnosis.
01. Warner ME, Warner MA, Garrity JA et al The frequency of perioperative loss. Anesth Analg, 2001;93:1417-1421. [ Links ]
02. Nuttall GA, Garrity JA, Dearani JA et al Risk factors for ischemic optic neuropathy after cardiopulmonary bypass: a matched case/control study. Anesth Analg, 2001;93:1410-1416. [ Links ]
03. Myers MA, Hamilton SR, Bogosian AJ et al Visual loss as a complication of spine surgery. A review of 37 cases. Spine, 1997;22:1325-1329. [ Links ]
04. Roth S, Nunez R, Schreider BD Unexplained visual loss after lumbar spinal fusion. J Neurosurg Anesthesiol, 1997;9:346-348. [ Links ]
05. Lee L, Lam A Unilateral blindness after prone lumbar spine surgery. Anesthesiology, 2001;95:793-795. [ Links ]
06. Roth S, Thisted RA, Erickson JP et al Eye injuries after nonocular surgery. A study of 60,965 anesthetics from 1988 to 1992. Anesthesiology, 1996;85:1020-1027. [ Links ]
07. Williams EL Postoperative blindness. Anesthesiol Clin North America, 2002;20:605-622. [ Links ]
08. Yi HJ, Kim DW Reversible unilateral blindness after lumbar spine surgery: a role for cerebrospinal fluid leakage? J Neurosurg Anesthesiol, 2004;16:322-323. [ Links ]
09. Warner MA - Perioperative neuropathies, blindness and positioning problems. ASA Annual Meeting Refresher Course Lectures, 2004;L117:1-7. [ Links ]
10. Cheng MA, Todorov A, Tempelhoff R et al The effect of prone positioning on intraocular pressure in anesthetized patients. Anesthesiology, 2001;95:1351-1355. [ Links ]
11. Wahba RW, Tessler MJ, Kardash KJ Carbon dioxide tensions during anesthesia in prone position. Anesth Analg, 1998;86: 668-669. [ Links ]
12. Lee LA, Vavilala MS, Lam AM et al Ophthalmic artery blood flow velocity increases during hypocapnia. Can J Anaesth, 2004; 51:388-392. [ Links ]
13. Tempelhoff R Ischemic optic neuropathy: "whodunit?". Can J Anaesth, 2004;51:286-289. [ Links ]
14. Lee LA, Lam AM, Roth S Causes of elevated introcular pressure during prone spine surgery. Anesthesiology, 2002;97:759-760. [ Links ]
15. Ho VT, Newman NJ, Song S et al Ischemic optic neuropathy following spine surgery. J Neurosurg Anesthesiol, 2005;17:38-44. [ Links ]
16. Hayreh SS Anterior ischemic optic neuropathy. Clin Neurosci, 1997;4:251-263. [ Links ]
Dr. Clóvis Marcelo Corso
Rua Machado de Assis, 290/403 - Juvevê
80030-370 Curitiba, PR
21 de setembro de 2006
Aceito para publicação 13 de fevereiro de 2006
* Received form do Serviço de Anestesiologia (CET/SBA) do Hospital de Clínicas da Universidade Federal do Paraná, Curitiba, PR.