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[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Principios básicos  de la neuroanestesia
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Anesthesiology Clin N Am 20 (2002) 347– 359
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],EVALUACIÓN PREOPERATORIA Anesthesiology Clin N Am 20 (2002) 347– 359
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],PREMEDICACIÓN Anesthesiology Clin N Am 20 (2002) 347– 359
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Curr Opin Anaesthesiol 2005; 18:437–441.
[object Object],[object Object],[object Object],[object Object],[object Object],Neurosurgery 59:S3-66-S3-76, 2006
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Rev. Col. Anest. 31: 125, 2003
Neurosurgery 59:S3-66-S3-76, 2006 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],Neurosurgery 59:S3-66-S3-76, 2006
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Curr Opin Anaesthesiol 2005; 18:437–441.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Curr Opin Anaesthesiol 2005; 18:437–441.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Curr Opin Anaesthesiol 2005; 18:437–441.
[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Etomidato 0.2–0.6 mg/kg  o  Propofol 2 - 2.5 mg/kg  +  Midazolam 150–350 mcg/kg. Esmolol 0.5 - 1 mg/kg o lidocaína 1 mg/kg,  previa intubación.  Mantenimiento: Infusión propofol + inhalados. Máscara laríngea. ANESTESIA GENERAL Neurosurgery 59:S3-66-S3-76, 2006
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],Neurosurgery 59:S3-66-S3-76, 2006
[object Object],[object Object],[object Object],[object Object],[object Object],Neurosurgery 59:S3-66-S3-76, 2006
[object Object],[object Object],[object Object],SEDACIÓN CONSCIENTE:  INDICACIONES RELATIVAS Neurosurgery 59:S3-66-S3-76, 2006
[object Object],[object Object],[object Object],[object Object],[object Object],SEDACIÓN CONSCIENTE
[object Object],[object Object],[object Object],[object Object],DEXMEDETOMIDINA
 
Materiales empleados Br J Anaesth 2007; 99: 75–85 Agentes sólidos embólicos Agentes líquidos embólicos Trombolíticos/ antiplaquetarios Vasodilatadores Quimioterapia Coils PVA balloons gelfoam Etilen Vinil OH (OnyxTM)  NBCA Activador tisular plasminógeno streptokinasa Urokinasa abciximab ASA nimodipina nicardipina verapamilo papaverina nitratos
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Preferida anestesia general Inducción de hipotensión (contraste) y  luego inyección del material embólico. ,[object Object],[object Object],[object Object],MALFORMACIÓN ARTERIOVENOSA
[object Object],[object Object],[object Object]
 
[object Object],[object Object],[object Object],[object Object],[object Object],Sundeep Undeep Mangla. ASA 2006. Chapter 9. V olume 34. Curr Opin Anaesthesiol 2005; 18:437–441.
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],Angioplastia + stent
[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object]
TUMORES
TUMORES Neurosurgery 59:S3-251-S3-260, 2006
 
Br J Anaesth 2007; 99: 75–85 ,[object Object],[object Object],[object Object],[object Object],[object Object],Lenta, diluída Vía periférica Monitoría Protamina 5000 U / 5 ml / 50 mg  1 mg = 100 U ó 1 mg H Heparina 5000 U / ml / 50 mg
Br J Anaesth 2007; 99: 75–85 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
Br J Anaesth 2007; 99: 75–85 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object]
[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],NEFROPATÍA INDUCIDA POR MEDIO DE CONTRASTE Normovolemia
Br J Anaesth 2007; 99: 75–85 ,[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object],[object Object]

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neurointervencionismo

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  • 17. Etomidato 0.2–0.6 mg/kg o Propofol 2 - 2.5 mg/kg + Midazolam 150–350 mcg/kg. Esmolol 0.5 - 1 mg/kg o lidocaína 1 mg/kg, previa intubación. Mantenimiento: Infusión propofol + inhalados. Máscara laríngea. ANESTESIA GENERAL Neurosurgery 59:S3-66-S3-76, 2006
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  • 26. Materiales empleados Br J Anaesth 2007; 99: 75–85 Agentes sólidos embólicos Agentes líquidos embólicos Trombolíticos/ antiplaquetarios Vasodilatadores Quimioterapia Coils PVA balloons gelfoam Etilen Vinil OH (OnyxTM) NBCA Activador tisular plasminógeno streptokinasa Urokinasa abciximab ASA nimodipina nicardipina verapamilo papaverina nitratos
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Notas del editor

  1. Tratamiento de estados patológicos del SNC por medio de acceso vascular, con el propósito de administrar agentes terapéuticos, ya sean medicamentos o dispositivos Bases de tratamientos endovasculares. Oclusión selectiva vasos sanguíneos anormales Restablecimiento flujo sanguíneo Trombolisis, angioplastia, stents Administración arterial de qtx Localización centro lenguaje y memoria Embolización de fístulas y aneurismas
  2. Anesthetic considerations The anesthetic objectives in interventional neuroendovascular procedures are the same as those in traditional neurosurgery. However, because the cranium is not open, the management of intracranial pressure dynamics, blood pressure and intravascular volume, administration of proper pharmacologic agents, and PaCO2 control, become even more preeminent. The interventions of the anesthesiologist are critical, especially during microcatheter advancement, embolization, and in emergency treatment of complications. The patient’s neurological status during or immediately after the procedure needs to be evaluated. Of prime importance for this, is a rapid and smooth emergence from anesthesia, without hemodynamic stress, cough, or strain to prevent increases in intracranial pressure .These procedures are associated with significant potential complications, which frequently require postoperative intensive care support, such as vascular rupture, thrombosis, cerebral infarction, or anaphylactic reactions to contrast agents. 30 31 At TMH, patients are routinely admitted to the neurosurgical intensive care unit after undergoing most INR procedures. The goals of anesthetic management for INR procedures are: To safely render a patient immobile, painless and comfortable. To provide the neuroradiologist with optimum hemodynamic and intracerebral conditions for successful performance of the procedure. To allow for perioperative evaluation of neurologic function To assist in treating complications
  3. Examen neurológico preoperatorio Orientación Glasgow, hunt y hess Patrón respiratorio Pupilas Movimientos anormales Déficit pares craneales Déficit motor ni sensitivo
  4. Sufficient space must be provided for an anesthesia machine, ventilator, supply cart, infusion pumps, and monitors. Anesthesia supplies such as extra gas cylinders, fluids, circuits, a difficult airway cart, and emergency medications must also be readily available. The anesthesia machine is best located on the opposite side of the radiologist, caudally to the patient’s head. In this location, the anesthesiologist and his equipment are not an obstacle, and imaging devices can rotate freely around the head. All anesthesia circuits, as well as I.V. tubing, monitoring cables, and lines must be long enough to reach the patient in all positions of the procedure table. Pressure transducers, IV poles, and infusion pumps can be mounted on the radiology table to move as the patient moves. The radiology table should turn so that the anesthesia equipment does not have to be moved when inducing general anesthesia. The supply hoses for oxygen, nitrous oxide, air, suction, and gas evacuation should preferably come from behind the anesthesia machine to avoid entanglements. There must be enough space behind the anesthesia machine to allow for cylinder changes, machine check-out, and monitor adjustments.
  5. Tendencia del ST The monitoring standards of the American Society of Anesthesiologists apply to all locations where anesthetics are administered. 8 9 These are considered a national standard of practice and should be followed, or medical-legal risk becomes paramount. 10 11 The only acceptable exceptions include nuclear magnetic resonance imaging (MRI), and external beam radiotherapy. 12 13 The quality of monitoring devices must be equal to that found in any major neurosurgical operating room. 14 Invasive blood pressure monitoring An arterial line is frequently indicated in these procedures and can be placed preoperatively, using local anesthesia, with minimum discomfort. 15 In our institution, we usually insert a radial artery catheter, preferably in the side closest to the anesthetist. In other centers, 16 the side port of the radiologist’s femoral artery sheath introducer is used to monitor arterial pressure. Pressures in the carotid or vertebral arteries as well as more distal pressures can be measured by transducing other ports of the radiologist’s coaxial catheter system. 17 This method accurately measures mean pressure, but tends to overestimate the diastolic pressure and underestimate the systolic. 18 In cases where thrombolytic therapy is used, hematoma formation at the site of arterial puncture can occur. In these cases, arterial pressure may be monitored from the femoral sheath introducer, instead of inserting a radial line, to avoid another arterial puncture and the possibility of hematoma formation.Indications for direct arterial line monitoring in interventional neuroradiology:Systemic heparinization with frequent monitoring of ACT Controlled hypotension Induced hypertension Hemodynamic instability Intracranial or spinal cord procedures Medically unstable patients Neuroradiologic technical considerations Neuroradiologists use the Seldinger wire technique to insert a 7.5 French gauge introducer sheath into the femoral artery, although the femoral vein and/or other vessels are also occasionally used. This catheter introducer has a side port that is used for irrigation with heparinized saline, but can also be used for arterial pressure monitoring. A coaxial catheter (also with a side port) is then advanced, under fluoroscopic guidance, through the introducer sheath into the carotid or vertebral arteries and cerebral angiography is performed.A superselective microcatheter is then inserted through the coaxial catheter and advanced with fluoroscopic guidance into the lesion. This catheter is used to deliver drugs or embolic materials into the lesion. Pulse oximetry In interventional radiology, the pulse oximeter is also used to detect arterial occlusion distal to the femoral arterial catheterization site by placing a probe on the ipsilateral toe. Since the oximeter amplifies the pulse signal, it will pick up a complete loss of a pulse, but not significant decreases. Therefore, a pulse oximeter will not detect decreasing perfusion, but will alarm only after the pulse is totally lost. 19 Temperature In the sedated patient, shivering can interfere with image quality. With severe hypothermia, neurologic signs may appear such as delirium, coma, or delayed awakening from anesthesia. 20 In our institution, perioperative hypothermia is unusual in adults since the neuroradiology suite is generally not as cold as an operating room, the patient is covered with warm blankets, and body cavities are not exposed. In small children however, significant heat loss can occur 21 while the patient is uncovered during induction of anesthesia, insertion of lines or while irrigating the angiography catheter with cold solutions. In children, we use a heat lamp while the patient is uncovered, and also warm irrigation fluids to prevent the development of hypothermia.Mild hypothermia has been reported to offer protection against ischemic injury to the brain and spinal cord. 22 23 Therefore, when due to the nature or location of the neuropathology, the neuroradiologist feels that the patient is at high risk for development of stroke, we do not warm the patient, but rather allow the temperature to drift down passively to 34 or 35 degrees centigrade.However, after successful completion of the procedure, these patients should be actively rewarmed before leaving the neuroradiology suite to avoid the risks of hypothermia in the postoperative period.
  6. Catéter femoral: subestima la presión sistólica y sobreestima la presión diastólica. Catéter coaxial: facilita el diagnostico de vasoespasmo o trombos intra arteriales. Indicaciones: Todos los casos de procedimientos intracraneales o de medula espinal (no compartida por todos los autores) Cuando se requiere hacer manipulación hemodinámica Uso de vasoactivos Procedimientos en fosa posterior o medula cervical Condiciones médicas asociadas que hagan necesario la medición exacta de la presión arterial.
  7. Central venous and pulmonary artery pressure measurement Although there are no procedure-specific indications, central venous lines are frequently inserted in patients undergoing high risk neurovascular invasive procedures. These patients often have serious coexisting medical problems and need vasoactive drug infusions or central access for forthcoming surgery.Invasive Neuroradiology; Principal Indications for CVP line insertion: Monitoring of cardiac filling pressures History of CHF History of renal insufficiency Strong possibility of surgery with CVP indication Use of vasoactive drugs Poor peripheral intravenous access At The Methodist Hospital of Houston ( TMH ), we prefer double lumen central venous catheters. One lumen can be a dedicated drug infusion line while the other can be used to monitor the central venous pressure. We usually insert these lines after induction of general anesthesia and the radiologist confirms the location with fluoroscopy. We prefer to use the subclavian approach in interventional neuroradiology because a carotid artery injury occurring during attempted internal jugular cannulation (1.9 to 3.6 percent incidence), 24 25 could jeopardize the procedure and imperil the patient. Some feel that central lines placed into the jugular veins can cause cerebral venous obstruction and should not be used in neurosurgery. 26 27 Although jugular vein catheterization is not our first choice, we use it, in the absence of increased intracranial pressure, when the subclavian route is difficult or contraindicated. Pulmonary artery catheterization Pulmonary artery flow- guided catheters (Swan-Ganz) are used in those cases where evaluation of left ventricular function is paramount. 28 29 At TMH, the two main indications are in: Patients who develop cerebral vasospasm and will be treated with intravascular volume expansion therapy and controlled hypertension. Patients in congestive heart failure, or with severe systemic disease, who have a neurovascular problem requiring immediate intervention . Care must be taken to insert these catheters only after the patients coagulation status is checked, and to confirm their position with fluoroscopy.
  8. Su indicación aún no está clara. TCA: activated clotting time activated partial thromboplastin time may be inaccurate, especially when high doses of heparin are used. United States Food and Drug Administration has recently approved the use of argatroban, a direct thrombin inhibitor, as an anticoagulant in patients with or at risk of heparin induced thrombocytopenia undergoing percutaneous coronary interventions. patients. The potential advantages of argatroban over heparin include a more predictable anticoagulant response and a minimal effect on platelets. Its use may expand into the neuroradiology suite in the future. Because of the inherently thrombogenic nature of the embolic materials and catheters, the neuroradiologist often requests systemic heparinization in high risk INR procedures to prevent the formation and propagation of intravascular thrombi. Often, heparinization is continued into the postoperative period, leaving the femoral arterial introducer sheath in place until the heparin is reversed. The specific indications and duration of heparinization are still controversial, although most centers heparinize when performing temporary balloon occlusion, or superselective catheterization.(88) Heparin can be administered either by intermittent IV boluses or by a bolus followed by a continuous infusion. In addition, heparin is used by the radiologist in the flush solution for the coaxial femoral arterial catheter system. The insertion of all invasive monitoring should be carried out before heparinization, and a control activated clotting time ( ACT ) obtained. Care should be taken that no residual heparin from the flush solution of the arterial line contaminates the ACT sample. Heparin can be given on a fixed dose, or titrated using a heparin dose-response curve as described by Bull et al.(89) Since there is individual variation in pharmacokinetics and patient sensitivity to heparin, individual titration and a low initial dose are clearly of value.
  9. We know that many interdependent variables affect autoregulation of cerebral blood flow; yet, clinically, the lowest level of MAP that can be safely induced is not known. In our practice, we use a MAP of 50 mm Hg as the minimum allowable pressure for short periods of induced hypotension. For patients with a history of hypertension, we empirically use a MAP of 70 mmHg as a minimum. Many techniques are used to induce hypotension. The ideal agent would have a short onset and duration of action, be easily controlled and have no direct action on cerebral autoregulation. The principal agents used to induce hypotension are inhalation agents, b-blockers, vasodilators, ganglionic blocking agents, and calcium channel blocking agents. Inhalation anesthetic agents are effective and titratable, but increase cerebral blood flow unless hyperventilation is initiated prior to their use. However, when used in combination with other drugs, inhalation agents can be safely used to induce hypotension without increases in ICP.(77) Esmolol, a short acting b-blocker, does not increase CBF(78) and is effective in bolus doses of 0.5 to 1 mg/kg IV followed by an infusion. It is our agent of choice for induced hypotension, and is very effective and easily controllable, especially when used in combination with inhalation agents. Labetalol, a b-blocker with some -adrenergic antagonism is indicated at the end of the procedure in boluses of 10 - 20 mg IV to prevent postoperative hypertension.(79) . All vasodilators can potentially increase ICP by increasing cerebral blood volume. The magnitude of ICP increase with vasodilators is related to the speed of onset of their effect.(80) Thus, they must be titrated slowly to minimize their effect on ICP. When vasodilators are used in combination with other classes of hypotensive agents, their total dose can be reduced and so can their effect on ICP.(81) Sodium nitroprusside, nitroglycerin, and hydralazine are commonly used. Sodium nitroprusside is a very potent, rapid-onset arterial vasodilator, administered by intravenous infusion, which controls the blood pressure rapidly and effectively. The main drawbacks of sodium nitroprusside are rebound hypertension and tachycardia, which occur unless b-blockers are given concurrently; and cyanide toxicity, which can appear with prolonged therapy. Nitroglycerin, a vasodilator acting principally on capacitance and coronary vessels, is not associated with tachycardia, rebound hypertension, or cyanide toxicity, but is not as effective as sodium nitroprusside. Like sodium nitroprusside, it must be given via a constant infusion, and requires close titration. Hydralazine, an arterial vasodilator, has an onset of 20-30 minutes and, unlike nitroglycerin or sodium nitroprusside, cannot be given by infusion. We do not use it as a single agent for controlled hypotension, but find it useful in the postoperative period, or as an intraoperative adjuvant drug in combination with b-blockers. In our practice, we use vasodilators only when b-blockers are contraindicated or ineffective , usually in combination with inhalation agents. Trimetaphan, a ganglionic blocking agent, does not cause an increase in CBV, but has been largely abandoned because it causes mydriasis, which can confuse the neurologic exam; and is associated with a high incidence of tachyphylaxis. Nicardipine is a calcium channel blocker for intravenous administration by infusion. It has theoretical advantages when used as a hypotensive agent for INR. Although it can increase ICP,(82) it may provide cerebral protection in the event of cerebral ischemia,(83) produces significant decreases in systemic and cerebral vascular resistance with only mild tachycardia, increases coronary blood flow, and causes no myocardial depression.(84) It is administered by intravenous infusion at a rate of 5mg/hr - 50mg/hr. In INR, we have empirically used this drug in several patients, as the sole agent, and in combination with inhalation anesthetics, for induced hypotension and found it to be effective and easy to titrate. Technique of induced hypotension for INR Prior to inducing hypotension in the intubated patient, we decrease the level of ventilation to reach a PetCO2 of 30 - 35 mmHg, since cerebral ischemia can result when hypotension is combined with hyperventilation. Once the PaCO2 level is stable, we begin by increasing the inspired concentration of inhaled anesthetic agent.. In most patients, inhalation agents alone, or in combination with b-blocke If the end-tidal concentration reaches a level higher than 1 MAC (minimum alveolar concentration) for isoflurane or desflurane, we give a 0.5 - 1 mg/kg bolus of esmolol and start an infusion at 0.5 mg/kg/min while maintaining the inspired concentration of isoflurane or desflurane at 1 MAC or below. The esmolol infusion is then titrated to the desired pressure rs, are all that is needed, but calcium channel blocking agents can be added or used alone if necessary. Patients under MAC will require significantly higher doses of b-blockers, vasodilators, or calcium channel blockers, to reach the same level of hypotension when compared to patients under general anesthesia. When the interventional procedure is completed, the pressure is allowed to drift up by decreasing the dose of the inhalation agent and/or b-blocker. Towards the end of the procedure we administer intermittent boluses of labetalol 5-10 mg IV, or enalaprilat (an injectable converting enzyme inhibitor) 1.25 - 2.5 mg IV, to maintain the blood pressure empirically 10- 20 percent lower than control during the postoperative period. If a vasodilator infusion is being used, it is continued into the postoperative period, titrating the dose down and substituting it as soon as possible with longer- acting antihypertensive drugs.
  10. In invasive neuroradiology, controlled hypertension is used in cases of iatrogenic vascular occlusion and in cases of acute thromboembolic stroke. The goal is to increase cerebral perfusion pressure to ischemic areas via collateral circulation through the circle of Willis and external carotid to internal carotid communicators. If a cerebrovascular occlusion occurs during an INR procedure, induced hypertension may reverse or prevent a neurologic deficit . Several drugs can be used to elevate the blood pressure. Young et al (85) suggest a phenylephrine drip as a first line agent. It is titrated to empirically increase the pressure 30-40 percent above the baseline,(86) until the neurologic deficit is reversed. Phenylephrine is a pure a-1 agonist vasoconstrictor and causes no direct cardiac stimulation, but can cause coronary artery vasoconstriction and reflex bradycardia. Norepinephrine, a potent inotrope and vasoconstrictor, also causes reflex bradycardia, but is more potent and has a shorter duration of action than neosynephrine, and for this reason is our drug of choice in this situation. If the patient already has bradycardia, dopamine can added to phenylephrine or çorepinephrine. If dopamine is used alone, tachycardia often becomes a difficult clinical problem. Some patients with acute thromboembolic stroke are candidates for intracerebral arterial thrombolysis.(87) They are usually hypertensive, and often have coronary artery disease. An increase in afterload or tachycardia during induced hypertension, places those patients with coronary artery disease at risk for developing coronary ischemia or pulmonary edema and may limit the level of hypertension that is safely tolerated. Monitoring of the ECG for ischemia with ST segment trending, if available, is particularly important in these cases . A pulmonary artery catheter needs to be considered, especially in those with a history of poor myocardial performance.
  11. Intraoperative management of ventilation By changing the PaCO2, cerebral blood flow (CBF), cerebral blood volume (CBV), and intracranial pressure can be modified. A high PaCO2 causes cerebral vasodilation, increasing CBF and to a lesser extent CBV. Between a PaCO2 of 18 mmHG and a PaCO2 of 80 mm Hg, CBF varies directly with the PaCO2. The lowest CBF that can be obtained by hyperventilation occurs at a PaCO2 of 18 - 20 mmHg. In INR procedures, PaCO2 control has two objectives: (1) to modify cerebral blood flow: A decrease in cerebral blood flow is useful for imaging since contrast transit time is decreased, and better contrast visualization will result. In embolization of intracerebral AVM’s, lowering of the CBF can decrease shunt flow and allow the embolic liquid adhesive more time to polymerize inside the AVM, decreasing the possibility of distal embolization . If the neuroradiologist requests it, ventilation can be increased, preferably by increasing respiratory rate, until he or she is satisfied with the velocity of contrast flow, or until the PaCO2 is 20 to 25 mmHg. When controlled hypotension and hyperventilation are used concurrently, cerebral ischemia will occur at a higher level of blood pressure than it would if the PaCO2 was normal. Hyperventilation also augments the CBV- lowering effects of hypotension induced by b-blockers. Accordingly, we avoid using hyperventilation simultaneously with controlled hypotension, and maintain either normocapnia, or mild hyperventilation (PaCO2 30 to 35 mmHg) during controlled hypotension. (2) to control intracranial pressure In cases of cerebral edema or in the presence of mass lesions, hyperventilation is used to decrease the ICP. The PaCO2 should be maintained close to 20 mmHG to effect the maximum decrease in CBV. Hyperventilation, however, will not reduce the ICP if there is cerebral venous outflow obstruction. Thus, all constrictions around the neck, such as crossing EKG cables, or gowns, must be loosened. If possible, the head of the bed should be raised in cases of elevated ICP to facilitate venous outflow. All inhalation anesthesia agents, to different degrees, cause a dose-dependent increase in CBF; however, when hyperventilation is begun prior to the introduction of the inhaled anesthetic, and the end -tidal anesthetic concentration is kept close to 1 MAC, the ICP is not increased. To manage ventilation, the PaCO2 can be obtained from a blood gas, or deduced from the PetCO2. Ventilatory adjustments should be made by changing respiratory rate, keeping tidal volume constant , because changes in tidal volume can alter physiologic dead space and change the PetCO2 - PaCO2 relationship. Increasing the ventilation by using large tidal volumes can also elevate intracerebral venous pressure. Most patients for INR are ventilated to a PaCO2 of around 35 mmHg. However, we change the level of ventilation in conjunction with blood pressure control to fit the clinical situation. Deliberate hypercapnia According to Young et al,(75) hypercapnia, to a PaCO2 of 50 to 60 mmHg has been used in cases of facial AVM’s or dural fistulas to decrease the possibility of inadvertent intracerebral embolization when embolic agents are injected from the venous side into the malformation. The elevated PaCO2 increases CBF and cerebral venous outflow to a greater degree than extracranial venous outflow. Presumably, pressure gradients, clinically demonstrable but not measured, are created that impede extracranial to intracerebral flow
  12. Puede ser necesaria la apnea en Roadmapping en procedimientos en columna (ajuste de ventilador). There are many advantages to this technique. With newer induction and inhalation agents, general anesthesia can be rapidly induced with minimum hemodynamic changes, the depth readily controlled , and a smooth and rapid emergence obtained.(66) (67) Under general anesthesia, PaCO2 can be regulated, and management of induced hypotension is facilitated. Respiratory immobility is essential with certain imaging techniques; when apnea is requested by the neuroradiologist it can be induced at will with general anesthesia. When a neurologic emergency such as thrombosis or hemorrhage occurs, no time is lost in securing the airway and the anesthesiologist can immediately begin to control hemodynamics . The main disadvantage of general anesthesia is that awake neurologic assessments cannot be readily performed, but as discussed above, we feel this is only of prime importance in selected cases. Other disadvantages are that endotracheal intubation can cause hypertension, while extubation can lead to straining, airway obstruction, and coughing. However, with careful anesthetic management, these disadvantages can be minimized. We do not give sedatives or narcotics if intraoperative neurophysiologic assessment with somatosensory- evoked potentials (SSEP), or electroencephalography (EEG) is contemplated until baseline studies are obtained and the anesthetic plan has been discussed with the neurophysiologist. We obtain peripheral intravenous access with a single 16 or 18 gauge IV catheter and a multiple port extension, preferably on the arm nearest to the anesthetist. This is usually adequate, unless the neuroradiologist feels that there is a high probability of serious complications. In such a case, two peripheral IV’s or a central line and a peripheral IV are inserted. Particular attention must be given to fluid balance since large amounts of irrigating solutions and contrast media are often used by the neuroradiologist. A urinary catheter is always inserted, either after induction of anesthesia or under sedation. Glucose- containing solutions are avoided because of their deleterious effect on brain ischemia. (68) In diabetics, we strictly control blood sugar levels perioperatively, with intravenous insulin, to maintain blood sugar levels between 150 and 200 mg percent.
  13. Ninguna evidencia sugiere que deba ser diferente en NRI. Etomidate, although effective, may also increase the incidence of postoperative nausea and vomiting In general, we recommend the induction of mild hypothermia at the time of treatment of the aneurysm (coil or clip), and the duration should not exceed the timeframe associated with the occurrence of secondary neurological deficits (delayed ischemic neurological deficit secondary to vasospasm). Propofol infusion: Propofol should be combined with fentanyl and/or midazolam for adequate amnesia. If used by itself, propofol can cause patients to wake up and move unexpectedly as the infusion is titrated down. Patients can also develop sudden airway obstruction, ( usually at a critical point in the procedure ! ) and one may need to insert an airway, which will usually cause the patient to move or cough. For airway management, we prefer a low profile RAE endotracheal tube, or a regular endotracheal tube with the extraoral end cut short. Cutting the tube short keeps the extraoral end from being pushed in or kinked by the image intensifier, which moves close to the patient’s face. We have recently used a laryngeal mask airway (LMA) for airway management. This device allows for control of the airway with minimal stimulation, hypertension, or cough, and a smooth emergence under light general anesthesia.(69) (70) In our experience, however, the head movement that sometimes occurs when using an LMA with spontaneous ventilation has impaired radiographic imaging; and the PaC02 levels have been higher than ideal. Muscle relaxants and controlled ventilation can be used with an LMA, and thus avoid these problems, but only as long as airway pressures are not greater than 20 cm H20.(71) More experience is needed in order to recommend routine use of LMA’s in this setting. For maintenance of anesthesia we use a continuous infusion of propofol plus low inspired concentrations of isoflurane or desflurane. Inhalation anesthetics allow rapid changes of anesthetic depth and blood pressure, but increase ICP with concentrations higher than 1 MAC and normocapnia.(72) We do not advocate the routine use of nitrous oxide for these cases since nitrous oxide increases cerebral blood flow from 60 to 100 percent; and can increase ICP to a variable degree.(73) Nitrous oxide could also theoretically enlarge air bubbles that may be accidentally introduced into the arterial circulation by the radiologist.(74) Minimal amounts of intravenous narcotics should be used because these procedures are not painful, and excessive doses of narcotics will only delay emergence . The blood pressure should be controlled during emergence and after the procedure. we extubate the patient while still under deep anesthesia, reverse the muscle relaxants, and wake the patient breathing oxygen via face mask If an LMA was used, the patient is allowed to wake up with the device in place, to be removed once the patient responds to commands. This awake extubation with an LMA is remarkably well tolerated, with little cough, straining, or hypertension.
  14. Definición: estado que permite a un paciente tolerar un procedimiento no placentero, manteniendo su función cardiorrespiratoria y con capacidad de responder a comandos verbales o al estímulo táctil. The demands placed on the anesthesiologist by an interventional neuroradiology (INR) procedure are much greater than those of simple diagnostic angiography.(57) The anesthesiologist must keep the patient immobile and calm, sometimes for many hours, and manage hemodynamics, cerebral perfusion, and coagulation; yet, on demand, the patient may need to be responsive enough for a neurologic examination. In selected procedures with cooperative patients, managed anesthesia care with intravenous sedation (MAC) can provide excellent conditions for performance of endovascular interventional procedures. Its main advantage is the ease with which an awake neurologic examination can be carried out during the procedure. There are also significant disadvantages associated with this approach: Advantages of Intravenous sedation: Easier to perform neurologic testing repeatedly No hemodynamic changes associated with intubation or emergence Potential disadvantages: 1. Poor control of the airway, with potential for: Hypoxemia Hypercapnia Stertorous breathing and movement 2. Side effects of IV sedatives Dysphoria Prolonged somnolence Extrapyramidal symptoms 3. Poor tolerance of induced hypotension in awake patient. 4. Nausea and vomiting 5. Vagal reactions 6. Delays and complications if neurologic emergency occurs Need to intubate acutely Hemodynamic changes at wrong time 7. No protection from aspiration 8. May need to interrupt the procedure and induce general anesthesia if the patient is unable to tolerate sedation.
  15. Sonda vesical
  16. Procedimientos no dolorosos (escleroterapia y quimioterapia). Es estresante (riesgo de muerte o evento agudo). El movimiento del paciente daña la sustracción, o puede provocar una complicación (ruptura).
  17. INDICATIONS FOR MAC There are specific procedures during which the patient must be fully awake, with minimal or no sedation: 1.- Test occlusions of major cerebral vessels:(58) When a major vascular supply to the brain must be permanently or temporarily interrupted, a test occlusion of the vessel is performed to asses the adequacy of collateral flow and the consequences of occlusion. The patient must be awake because an ongoing neurologic evaluation is of primary importance to asses neurologic integrity during the period of occlusion. 2.- Performance of the Wada-Rasmussen test:(59) Amobarbital, a short acting barbiturate, is directly injected into the carotid circulation while the patient undergoes electrophysiologic and neurobehavioral exams in this test used to determine cerebral dominance, cognitive, and language function, and to locate seizure foci prior to surgical ablation . Usually, no premedication or sedation is given during this procedure because it interferes with interpretation of the test.
  18. RELATIVE INDICATIONS FOR MAC These procedures are usually performed under MAC in our institution: 1.- Simple procedures: When they are of short duration, the patient is amenable and absolute immobility is not crucial (e.i., diagnostic angiography) 2.- Intra-arterial chemotherapy of brain tumors with cis-platinum: This procedure is essentially the same as a diagnostic angiogram, except that a catheter is placed in a branch of the carotid or vertebral system to infuse chemotherapy in direct proximity to an intracranial tumor. The procedure typically lasts two to three hours, but absolute immobility is not crucial. 3.- Preoperative embolization of intracranial and extracranial tumors or, arterio-venous malformations which are perfused by the external carotid circulation. These procedures are usually of short duration, do not often require hemodynamic management, and although sometimes painful, are usually well tolerated with MAC. However, in patients with large extracerebral to intracerebral vascular anastomosis, embolic material can pass into the brain from the extracerebral circulation. In these cases, as discussed before,Young et al advocate increasing cerebral blood flow, by increasing the PaCO2, to establish a pressure gradient that opposes intracerebral embolization. Hypercapnia is produced by adding CO2 to the circuit, or by decreasing the minute ventilation. Control of ventilation for production of hypercapnia is accomplished best with general anesthesia 4.- Embolization of intracranial arterio-venous malformations (AVM’s):
  19. Propofol Tiempo medio sensible al contexto muy corto Posee un estrecho rango entre sedación y anestesia Dosis recomendadas para sedación 25 – 200  gr/kg/min Propofol bolo 40 - 60 mg IV previo a punción femoral. Goteo Propofol: iniciar 20 ųg /Kg/min, y ajustar según sedación. Sistemas de TCI REMI Seguro en pacientes con enfermedad hepática y renal Su metabolito no se altera en pacientes con deficiencia de pseudocolinesterasa Ketamina : Sistemas de infusión controlada Concentración plasmática 100 - 200 ng/ml asociado a opiode produce rápido inicio – Excelente sedación Recomendada en niños. Fentanil 2 - 3 ųg /Kg IV + midazolam 2 - 3 mg IV
  20. Aprobada desde 1980’s para sedación en ICU (24 h).
  21. This is a challenging procedure for both neuroradiologist and anesthesiologist. It had previously been performed under MAC to evaluate the patient’s neurologic status during the procedure. However, in our institution, general anesthesia has superseded MAC for these cases because our team feels that the advantages of general anesthesia outweigh those of MAC. Superselective flow-guided catheterization of the feeding vessels of the AVM, can place the tip of the embolizing catheter in the nidus of the AVM. Using liquid adhesive with the catheter in this position, the deposition of embolic material can be precisely controlled, such that the possibility of compromising normal neural tissue is decreased. Placement of the catheter in this position requires a motionless patient, and hemodynamic management by the anesthesiologist.
  22. The hemodynamic and respiratory management is designed to help the radiologist “float” the superselective catheter into position and to decrease the possibility of neurologic damage. We feel that controlled hypotension or induced hypertension with PaCO2-related adjustments of cerebral blood flow and cerebral vascular tone are best managed with the patient under general anesthesia. The complications associated with MAC, such as nausea and vomiting during the critical part of the procedure, are thus avoided. Our colleagues in neuroradiology also feel that awake neurologic assessment is no longer of prime importance because they are able to control the deposition of embolic material more exactly with the conditions provided by general anesthesia.(60) However, if the lesion cannot be reached with a superselective catheter, or embolization with particulate material must be carried out from a more distal location, the procedure is more safely carried out with MAC.This allows for performance of a superselective anesthesia functional examination (SAFE),(61) (62) which helps to decide whether the catheter is positioned in a hazardous position, proximal to a vessel irrigating expressive regions of the brain, or if the area can be embolized without neurologic sequelae. At TMH, SAFE is performed with minimal or no sedation. A neurophysiologic exam with EEG is performed as a baseline, followed by sodium amytal injection via the superselective catheter into the vessel. After injection the neurophysiologic exam is repeated to evaluate the area of irrigation. Thus, the choice of anesthesia, general or MAC, depends not only on the procedure and the patient, but also on the vascular anatomy, the type of embolization material and catheter system used by the neuroradiologist
  23. El catéter se puede adherir al vaso (es el momento crítico de la qx).
  24. The concept of endovascular embolization of an aneurysm is relatively straight- straightforward and elegant in its simplicity. The generally believed pathophysiology of an forward intracranial aneurysm is as follows: An inherent possibly genetic genetic or environmentally induced weakness (associations with smoking and hypertension suggested) 10,11 in the wall of the artery produces a defect most commonly at a vascular branching point or bifurcation. Over some period of time, this wall defect slowly expands and a thin- thin walled (thinned or absent smooth muscle media layer) outpouching develops. At some walled future point, an incident event may occur that results in perforation of the aneurysmal outpouching resulting in life-threatening SAH. The goal of microsurgical clipping is to exclude this thin-walled aneurysm from the native normal circulation by externally clamping the neck of the aneurysm . Embolization also excludes the aneurysm from the native circulation, but achieves this goal by an endovascular placement of mechan- mechanical blocking/filling materials within the aneurysm sac to achieve complete oblitera- ical obliteration of the aneurysm. In addition, physiologically active materials are being placed on tion the newer coils (2000–2005) in an effort to promote endoluminal healing and scarring at the aneurysm neck. The early results suggest that the endovascular technique may result in greater vascular durability and prolonged protective effect. 12
  25. The neurologic complications of INR are an anesthetic emergency. The management of these is similar to that of intraoperative complications in open neurosurgical procedures. There are two main types of immediate vascular complications. One is a vascular occlusion, due to emboli, thrombosis, arterial dissection, or vasospasm, that can lead to brain ischemia or infarction. The second is a vascular perforation leading to cerebral or subarachnoid hemorrhage. Primary management in either case consists of obtaining control of the airway with endotracheal intubation. Etomidate is our induction agent of choice for intubation since it does not cause cardiovascular depression and may protect the brain .(91) Thiopental is used if the patient is hypertensive and cerebral hemorrhage is suspected. Initially, the most important decision is to differentiate between an occlusive and a hemorrhagic event since the specific treatment for each is different. When a complication occurs, the radiologist should immediately report to the anesthesiologist which one is suspected so that the appropriate treatment can be started immediately.
  26. Contrast-medium–induced nephropathy is usually transient, with serum creatinine levels peaking at 3 days after administration of the medium and returning to baseline within 10 days after administration.8,10 Appreciable nephropathy is unlikely to develop if the serum creatinine level does not increase by more than 0.5 mg per deciliter within 24 hours However, the association between these outcomes and the decline in function may be explained at least in part by coexisting conditions, acuteness of illness, or other causes of acute kidney failure, such as atheroembolism.
  27. Patients with normal kidney function and no recognized risk factors for contrast-medium–induced nephropathy do not require routine testing or prophylactic intervention before angiography. For patients likely to have reduced kidney function, such as the man described in the vignette, we recommend measurement of the serum creatinine level and estimation of the glomerular filtration rate. If the glomerular filtration rate is less than 50 ml per minute per 1.73 m2, particularly in combination with other risk factors, consideration should be given to alternative imaging approaches. If infusing contrast medium is thought to be warranted, a low-osmolar agent should be used at the minimal dose necessary. and measurement of the serum creatinine level should be repeated 24 to 48 hours after the administration of the contrast medium. Nonsteroidal antiinflammatory drugs and diuretics should be withheld for at least 24 hours before and after exposure to contrast medium, if possible. Metformin should be withheld for 48 hours before the administration of contrast medium and until it is certain that contrast-medium–induced nephropathy has not occurred. Additional fluids should be given; although the optimal regimen is uncertain, available data support a regimen of 0.9 percent saline at 1 ml per kilogram per hour intravenously from up to 12 hours before administration of contrast medium and for up to 12 hours after, with careful observation of fluid balance. The use of N -acetylcysteine is not recommended routinely, given the inconsistent results of clinical trials.