POST OPERATIVE VISUAL LOSS Medical Presentation

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Published on : Jul 26, 2019 | Views : 2030 | Downloads : 14

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POST OPERATIVE VISUAL LOSS R. Aishwarya Durga
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Definition “perioperative visual loss” refers to permanent impairment or total loss of sight associated with a spine procedure during which general anesthesia is administered. The perioperative period includes the time from the immediate preoperative assessment through discharge from the acute healthcare facility. Conditions include posterior ischemic optic neuropathy, anterior ischemic optic neuropathy, central and branch retinal artery occlusion, cerebral visual loss, and posterior reversible encephalopathy syndrome.
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INCIDENCE ∼1/60 000–1/125 000 The highest frequencies were: Spine (3.09 per 10 000, 0.03%) and Cardiac surgery (8.64 per 10 000, 0.086%).
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Primary causes of POVL Retinal vascular occlusion (RVO) and Ischemic optic neuropathy (ION) Other sources are: Glycine toxicity during transurethral resection of the prostate, Acute angle closure glaucoma, Cortical blindness, and Expansion of an intraocular sulphur hexafluoride(perfluorocarbon gas tamponade) vitrectomy bubble by administration of nitrous oxide.
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Retinal ischemia: branch and central retinal artery occlusion Central retinal artery occlusion (CRAO) decreases blood supply to the entire retina, whereas branch retinal arterial occlusion (BRAO) affects a portion. These most commonly result in the perioperative period from improper patient positioning and external compression of the eye. Pressure within the orbit can also be increased internally after retrobulbar hemorrhage, associated with vascular injuries during sinus or nasal surgery. Retinal micro emboli, common during open-heart surgery, constitute another potential cause. Impaired venous drainage Arterial thrombosis due to a coagulation disorder Hypotension seems to be a rare cause
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Risk factors Facial structure –Asians with low nasal bridge Masks/ head rests- horse shoe Osteogenesis imperfecta Improper positioning
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Signs and symptoms Unilateral vision loss; No light perception; Afferent pupil defect; Periorbital, eyelid edema, or both; chemosis; Proptosis; ptosis; paresthesia of the supraorbital region; Hazy/cloudy cornea; and corneal abrasion. Loss of eye movements, ecchymosis, or other trauma near the eye was also reported FUNDUS :Macular/retinal edema, cherry red spot, or attenuated retinal vessels were typical.
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Mechanism Increased glutamate leading to increased cytosolic Ca2+ - activation of destruction pathways. External compression leading to retinal ischemia is worse due to simultaneous reduction in choroidal blood flow and retinal blood flow.
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NORMAL FUNDUS The macula lutea lies about 3-4mm temporal to and slightly below the optic disk. The fundus receives its uniform bright red coloration from the vessels of the choroid. Venous diameter is normally 1.5 times greater than arterial diameter.
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CRAO
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Branch Retinal Artery Occlusion BRAO is mainly due to emboli or vasospasm Retinal fluorescein angiography reveals microemboli during cardiopulmonary bypass. In animal studies, mechanisms include non-perfusion, vascular leakage and spasm, red blood cell sludging, and haemorrhage, blocked by perfluorocarbon priming. BRAO usually leads to permanent partial visual field loss.
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TREATMENT Ocular massage can lower IOP and possibly dislodge an embolus, if present, to more peripheral arterial branches, and can be instituted by the anaesthesiologist. I.V. acetazolamide can be administered to increase retinal blood flow, and 5% CO2 in oxygen inhaled to enhance dilation and increase O2delivery. A preliminary study showed that fibrinolysis via the ophthalmic artery within 6–8 h after spontaneous CRAO was associated with improved visual outcome. An ongoing multicentre study is testing efficacy. Localized application of hypothermia to the affected eye is a simple technique that decreased injury in animal studies after ischaemia,
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Prevention Because its most often caused by unintended pressure on the eye- Avoid pressure from anesthetic face masks Surgeons arm – not to rest on patients face Foam headrest for prone position with eyes properly placed In the space advisable to check every 20 minutes
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Prone view headrest
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Ischemic Optic neuropathy
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Pathogenic factors Hypotension Blood loss Hemodilution Altered venous hemodynamics Flow of CSF in the optic nerve Abnormal autoregulation Use of vasopressors
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Risk factors Male gender, small cup to disc ratio, abnormal anatomy -blood supply Vascular risk factors: 1) Hyertension, DM, Hyperlipidemia, atherosclerosis, 2) Obesity, Smoking History 3) Prone position, External pressure on the eye, lengthy surgery, Fluid resuscitation during surgery 4) OSA, Hypercoagulabilty 5) Para Nasal Sinus surgery
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ION Pathophysiology
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Presentation POVL within 24 to 48hrs after surgery. Frequently noted on awakening Painless visual loss, RAPD, complete visual loss, or visual field defects FUNDUS- In AION- Disc edema, hemorrhages, In PION- Normal fundus Over months Optic atrophy develops Mostly bilateral after spine surgery
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Treatment No proven treatment Acetazolamide, mannitol. Acute phase corticosteroids- careful Head up position if Raised IOP is suspected to be because of in adequate venous drainage. Urgent Lateral canthotomy to release pressure if its due to ocular compartment syndrome
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Cortical blindness Bilateral complete cortical blindness is rare. Cause- occipital lobe infarction Most commonly its localized and causes homonymous hemianopia. 80% of these are following cardiothoracic surgery Usually pupillary reflexes are preserved and vision improves over time. Treatment targeted towards reducing progression of stroke. Removal of air and particulate matter during valvular heart surgeries decreases the risk of embolism.
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Acute glaucoma Women and elderly patients No correlation between anesthetic drug or technique and acute glaucoma Painful red eye, blurred vision. Pupil mid dilated.
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TURP Excessive fluid absorption- hyponatremia, cerebral edema, seizures, coma, cardiac failure. Glycine- the smallest amino acid- easily crosses the BBB and depresses the spontaneous activity of the retinal neurons and hyperpolarizes cells through the blockade of chloride channels Threshold for visual symptoms with glycine- plasma conc. of 4000micromol/L
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Advisory Recommendations for Preoperative Patient Evaluation and Preparation Review a patient’s preoperative history and perform an appropriate examination to identify patients with conditions such as preoperative anemia, vascular risk factors (e.g., hypertension, diabetes, peripheral vascular disease, coronary artery disease, previous stroke, carotid artery stenosis, tobacco use), and obesity. Inform patients that certain preoperative conditions may increase their risk of perioperative visual loss in spine surgery. These include, but are not limited to, those who are male, obese, or have vascular disease risk factors such as hypertension and peripheral vascular disease. Inform patients in whom prolonged procedures, substantial blood loss, or both are anticipated that there may be an increased risk of perioperative visual loss. Determine on a case-by-case basis whether or not to inform patients who are not anticipated to be “high-risk” for visual loss.
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Intraoperative Management Intraoperative management topics consist of (1) blood pressure management, (2) management of blood loss and administration of fluids, (3) use of vasopressors, (4) patient and head positioning, and (5) staging of surgical procedures.
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Advisory Recommendations for Intraoperative Management: Blood Pressure Management Assess the patient’s baseline blood pressure. Continually monitor systemic blood pressure in high-risk patients. Determine on a case-by case basis whether deliberate hypotension should be used in high-risk patients. Check for the presence of preoperative hypertension, its degree of control, the preoperative use of antihypertensive drugs, and the patient’s risk of end-organ damage before using deliberate hypotension in a high-risk patient. Discuss with the surgeon whether deliberate hypotension is necessary. Maintain arterial pressure at higher levels in hypertensive patients to prevent risks to end organs. Use deliberate hypotension in high-risk patients only when the anesthesiologist and surgeon agree that its use is essential. Treat prolonged significant decreases in blood pressure.
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Management of Blood Loss and Administration of Fluids Periodically monitor hemoglobin or hematocrit values during surgery in high-risk patients who experience substantial blood loss. Use transfusions of blood as deemed appropriate. Crystalloids or colloids alone or in combination may be used to maintain adequate replacement of intravascular volume.
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Vasopressors Use of Vasopressors Adrenergic agonists may be used on a case-by-case basis when it is necessary to correct for hypotension.
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Patient and Head Positioning Devices Position the high-risk patient so that the head is level with or higher than the rest of the body when possible. Maintain the high-risk patient’s head in a neutral forward position (e.g., without significant neck flexion, extension, lateral flexion, or rotation) when possible. Avoid direct pressure on the eye to prevent retinal artery occlusion. A head holder may be applied by the spine surgeon in patients in whom head positioning is challenging. Check the position of the eyes periodically during surgery to ensure the head has not moved and there is no eye compression.
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Post operative management Advisory Recommendations for Postoperative Management Assess the vision of a high-risk patient when the patient becomes alert (e.g., in the recovery room, intensive care unit, or nursing floor). If there is concern regarding potential visual loss, obtain an urgent ophthalmologic consultation to determine its cause. Computerized tomography or magnetic resonance imaging may be used on a case-by-case basis to rule out intracranial causes of visual loss as well as to visualize an abnormal optic nerve. Additional management may include optimizing hemoglobin or hematocrit values, hemodynamic status, and arterial oxygenation.
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